Preface - SIZ-Nursing

Resuscitation (2005) 67S1, S1—S2PrefaceThis supplement of Resuscitation contains the EuropeanResuscitation Council (ERC) Guidelines forResuscitation 2005. It is derived from the 2005International Consensus Conference on CardiopulmonaryResuscitation and Emergency CardiovascularCare Science with Treatment Recommendationsproduced by the International Liaison Committeeon Resuscitation (ILCOR) published simultaneouslyin an issue of Resuscitation.The European representatives at that Conference,held in Dallas in January 2005, more thanpulled their weight in the process of producing theConsensus on Science conclusions arising as a resultof presentations and debate. Their names are listedat the end of this Foreword, and the resuscitationcommunity in Europe and beyond is most gratefulto them for their talent, dedication and selflesshard work. In addition, they, and many others fromEurope, also produced worksheets addressing theevidence for and against every conceivable detailof resuscitation theory and practice.The ERC Guidelines contain recommendationsthat, by consensus of the European representatives,are suitable for European practice in the light oftoday’s conclusions agreed in the Consensus on Science.As with the Consensus on Science document,they represent an enormous amount of work bymany people who have worked against the clockto produce the Guidelines for Europe. Each sectionof the Guidelines has been masterminded and coordinatedby the leaders of the ERC working groupsand areas of special interest.Such ventures do not happen without leadership,and we are grateful to Vinay Nadkarni, BillMontgomery, Peter Morley, Mary Fran Hazinski, ArnoZaritsky, and Jerry Nolan for guiding the Consensuson Science process through to completion. It wouldnot be invidious to single out Jerry Nolan, the ILCORco-chairman, for thanks and praise. He is universallyrespected and popular, and has proved to bea wonderful ambassador for Europe. His scientificcredibility and understanding are beyond doubt andhis integrity, dedication, sheer hard work, patienceand meticulous attention to detail and sensitivitieshave won the admiration of all. He has led the Consensuson Science process on our behalf, and hasbeen the lead co-ordinator in producing the EuropeanGuidelines.Finally we thank our publishers, Elsevier, throughthe Publishing Editor for Resuscitation, Anne Lloydand her colleagues, for their professionalism, toleranceand patience in these endeavours.Representatives from Europe at theInternational Consensus Conferenceheld in Dallas, USA, in January 2005Hans-Richard Arntz (Germany), Dennis Azzopardi(UK), Jan Bahr (Germany), Gad Bar-Joseph (Israel),Peter Baskett (UK), Michael Baubin (Austria),Dominique Biarent (Belgium), Bob Bingham (UK),Bernd Böttiger (Germany), Leo Bossaert (Belgium),Steven Byrne (UK), Pierre Carli (France), PascalCassan (France), Sian Davies (UK), Charles Deakin(UK), Burkhard Dirks (Germany), Volker Doerges(Germany), Hans Domanovits (Austria), ChristophEich (Germany), Lars Ekstrom (Sweden), PeterFenici (Italy), F. Javier Garcia-Vega (Spain), HenrikGervais (Germany) Anthony Handley (UK), JohanHerlitz (Sweden), Fulvio Kette (Italy), RudolphKoster (Netherlands), Kristian Lexow (Norway),Perttu Lindsberg (Finland), Freddy Lippert (Denmark),Vit Marecek (Czech Republic), KoenraadMonsieurs (Belgium), Jerry Nolan (UK), Narcisco0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.doi:10.1016/j.resuscitation.2005.10.001

S2PrefacePerales (Spain), Gavin Perkins (UK), Sam Richmond(UK), Antonio Rodriquez Nunez (Spain), StenRubertsson (Sweden), Sebastian Russo (Germany),Jas Soar (UK), Eldar Soreide (Norway), Petter Steen(Norway), Benjamin Stenson (UK), Kjetil Sunde(Norway), Caroline Telion (France), Andreas Thierbach(Germany), Christian Torp Pederson (Denmark),Volker Wenzel (Austria), Lars Wik (Norway),Benno Wolke (Germany), Jonathan Wyllie (UK),David Zideman (UK).Peter BaskettDavid Zideman

Resuscitation (2005) 67S1, S3—S6European Resuscitation Council Guidelines forResuscitation 2005Section 1. IntroductionJerry NolanIt is five years since publication of the Guidelines2000 for Cardiopulmonary Resuscitation (CPR)and Emergency Cardiovascular Care (ECC). 1 TheEuropean Resuscitation Council (ERC) based itsown resuscitation guidelines on this document,and these were published as a series of papersin 2001. 2—7 Resuscitation science continues toadvance, and clinical guidelines must be updatedregularly to reflect these developments and advisehealthcare providers on best practice. In betweenmajor guideline updates (about every five years),interim advisory statements can inform the healthcareprovider about new therapies that might influenceoutcome significantly; 8 we anticipate thatfurther advisory statements will be published inresponse to important research findings.The guidelines that follow do not define theonly way that resuscitation should be achieved;they merely represent a widely accepted view ofhow resuscitation can be undertaken both safelyand effectively. The publication of new and revisedtreatment recommendations does not imply thatcurrent clinical care is either unsafe or ineffective.Consensus on scienceThe International Liaison Committee on Resuscitation(ILCOR) was formed in 1993. 9 Its mission isto identify and review international science andknowledge relevant to CPR, and to offer consensuson treatment recommendations. The processfor the latest resuscitation guideline update beganin 2003, when ILCOR representatives establishedsix task forces: basic life support; advanced cardiaclife support; acute coronary syndromes; paediatriclife support; neonatal life support; and aninterdisciplinary task force to address overlappingtopics, such as educational issues. Each task forceidentified topics requiring evidence evaluation, andappointed international experts to review them.To ensure a consistent and thorough approach, aworksheet template was created containing stepby-stepdirections to help the experts documenttheir literature review, evaluate studies, determinelevels of evidence and develop recommendations. 10A total of 281 experts completed 403 worksheets on276 topics; 380 people from 18 countries attendedthe 2005 International Consensus Conference onECC and CPR Science with Treatment Recommendations(C2005), which took place in Dallas inJanuary 2005. 11 Worksheet authors presented theresults of their evidence evaluations and proposedsummary scientific statements. After discussionamong all participants, these statements wererefined and, whenever possible, supported by treatmentrecommendations. These summary sciencestatements and treatment recommendations havebeen published in the 2005 International Consensuson Cardiopulmonary Resuscitation and EmergencyCardiovascular Care Science with Treatment Recommendations(CoSTR). 120300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.doi:10.1016/j.resuscitation.2005.10.002

S4From science to guidelinesThe resuscitation organisations forming ILCOR willpublish individual resuscitation guidelines that areconsistent with the science in the consensus document,but will also consider geographic, economicand system differences in practice, and the availabilityof medical devices and drugs. These 2005ERC Resuscitation Guidelines are derived from theCoSTR document but represent consensus amongmembers of the ERC Executive Committee. TheERC Executive Committee considers these new recommendationsto be the most effective and easilylearned interventions that can be supportedby current knowledge, research and experience.Inevitably, even within Europe, differences in theavailability of drugs, equipment, and personnel willnecessitate local, regional and national adaptationof these guidelines.DemographicsIschaemic heart disease is the leading cause ofdeath in the world. 13—17 Sudden cardiac arrest isresponsible for more than 60% of adult deathsfrom coronary heart disease. 18 Based on data fromScotland and from five cities in other parts ofEurope, the annual incidence of resuscitation forout-of-hospital cardiopulmonary arrest of cardiacaetiology is 49.5—66 per 100,000 population. 19,20The Scottish study includes data on 21,175 outof-hospitalcardiac arrests, and provides valuableinformation on aetiology (Table 1.1). The incidenceof in-hospital cardiac arrest is difficult to assessbecause it is influenced heavily by factors such asthe criteria for hospital admission and implementationof a do-not-attempt-resuscitation (DNAR) policy.In a general hospital in the UK, the incidenceof primary cardiac arrest (excluding those withDNAR and those arresting in the emergency department)was 3.3/1000 admissions; 21 using the sameexclusion criteria, the incidence of cardiac arrestin a Norwegian University hospital was 1.5/1000admissions. 22The Chain of SurvivalThe actions linking the victim of sudden cardiacarrest with survival are called the Chain of Survival.They include early recognition of the emergencyand activation of the emergency services,early CPR, early defibrillation and early advancedlife support. The infant-and-child Chain of SurvivalJerry NolanTable 1.1 Out-of-hospital cardiopulmonary arrests(21,175) by aetiology. 19Aetiology Number (%)Presumed cardiac disease 17451 (82.4)Non-cardiac internal aetiologies 1814 (8.6)Lung disease 901 (4.3)Cerebrovascular disease 457 (2.2)Cancer 190 (0.9)Gastrointestinal haemorrhage 71 (0.3)Obstetric/paediatric 50 (0.2)Pulmonary embolism 38 (0.2)Epilepsy 36 (0.2)Diabetes mellitus 30 (0.1)Renal disease 23 (0.1)Non-cardiac external aetiologies 1910 (9.0)Trauma 657 (3.1)Asphyxia 465 (2.2)Drug overdose 411 (1.9)Drowning 105 (0.5)Other suicide 194 (0.9)Other external 50 (0.2)Electric shock/lightning 28 (0.1)includes prevention of conditions leading to thecardiopulmonary arrest, early CPR, early activationof the emergency services and early advancedlife support. In hospital, the importance of earlyrecognition of the critically ill patient and activationof a medical emergency team (MET) is now wellaccepted. 23 Previous resuscitation guidelines haveprovided relatively little information on treatmentof the patient during the post-resuscitation carephase. There is substantial variability in the waycomatose survivors of cardiac arrest are treatedin the initial hours and first few days after returnof spontaneous circulation (ROSC). Differences intreatment at this stage may account for some ofthe interhospital variability in outcome after cardiacarrest. 24 The importance of recognising criticalillness and/or angina and preventing cardiacarrest (in- or out-of-hospital), and post resuscitationcare has been highlighted by the inclusion ofthese elements in a new four-ring Chain of Survival.The first link indicates the importance ofrecognising those at risk of cardiac arrest and callingfor help in the hope that early treatment canprevent arrest. The central links in this new chaindepict the integration of CPR and defibrillation asthe fundamental components of early resuscitationin an attempt to restore life. The final link, effectivepost resuscitation care, is targeted at preservingfunction, particularly of the brain and heart(Figure 1.1). 25,26

European Resuscitation Council Guidelines for Resuscitation 2005S5Figure 1.1ERC Chain of Survival.The universal algorithmThe adult basic, adult advanced and paediatricresuscitation algorithms have been updated toreflect changes in the ERC Guidelines. Every efforthas been made to keep these algorithms simpleyet applicable to cardiac arrest victims in mostcircumstances. Rescuers begin CPR if the victimis unconscious or unresponsive, and not breathingnormally (ignoring occasional gasps). A singlecompression—ventilation (CV) ratio of 30:2 is usedfor the single rescuer of an adult or child (excludingneonates) out of hospital, and for all adult CPR.This single ratio is designed to simplify teaching,promote skill retention, increase the number ofcompressions given and decrease interruption tocompressions. Once a defibrillator is attached, ifa shockable rhythm is confirmed, a single shockis delivered. Irrespective of the resultant rhythm,chest compressions and ventilations (2 min with aCV ratio of 30:2) are resumed immediately after theshock to minimise the ‘no-flow’ time. Advanced lifesupport interventions are outlined in a box at thecentre of the ALS algorithm (see Section 4). Oncethe airway is secured with a tracheal tube, laryngealmask airway (LMA) or Combitube, the lungsare ventilated at a rate of 10 min −1 without pausingduring chest compressions.Quality of CPRInterruptions to chest compressions must be minimised.On stopping chest compressions, the coronaryflow decreases substantially; on resumingchest compressions, several compressions are necessarybefore the coronary flow recovers to itsprevious level. 27 Recent evidence indicates thatunnecessary interruptions to chest compressionsoccur frequently both in and out of hospital. 28—31Resuscitation instructors must emphasise theimportance of minimising interruptions to chestcompressions.SummaryIt is intended that these new guidelines willimprove the practice of resuscitation and, ultimately,the outcome from cardiac arrest. Theuniversal ratio of 30 compressions to two ventilationsshould decrease the number of interruptionsin compression, reduce the likelihood of hyperventilation,simplify instruction for teaching andimprove skill retention. The single-shock strategyshould minimise ‘no-flow’ time. Resuscitationcourse materials are being updated to reflect thesenew guidelines.References1. American Heart Association, In collaboration with InternationalLiaison Committee on Resuscitation. Guidelines forcardiopulmonary resuscitation and emergency cardiovascularcare—–an international consensus on science. Resuscitation2000;46:3—430.2. Handley AJ, Monsieurs KG, Bossaert LL, European ResuscitationCouncil Guidelines 2000 for Adult Basic Life Support.A statement from the Basic Life Support and AutomatedExternal Defibrillation Working Group. Resuscitation2001;48:199—205.3. Monsieurs KG, Handley AJ, Bossaert LL, European ResuscitationCouncil Guidelines 2000 for Automated External Defibrillation.A statement from the Basic Life Support and AutomatedExternal Defibrillation Working Group. Resuscitation2001;48:207—9.4. de Latorre F, Nolan J, Robertson C, Chamberlain D, BaskettP, European Resuscitation Council Guidelines 2000 for AdultAdvanced Life Support. A statement from the Advanced LifeSupport Working Group. Resuscitation 2001;48:211—21.

S65. Phillips B, Zideman D, Garcia-Castrillo L, Felix M, Shwarz-Schwierin U, European Resuscitation Council Guidelines2000 for Basic Paediatric Life Support. A statement fromthe Paediatric Life Support Working Group. Resuscitation2001;48:223—9.6. Phillips B, Zideman D, Garcia-Castrillo L, Felix M, Shwarz-Schwierin V, European Resuscitation Council Guidelines2000 for Advanced Paediatric Life Support. A statementfrom Paediatric Life Support Working Group. Resuscitation2001;48:231—4.7. Phillips B, Zideman D, Wyllie J, Richmond S, van ReemptsP, European Resuscitation Council Guidelines 2000 for NewlyBorn Life Support. A statement from the Paediatric Life SupportWorking Group. Resuscitation 2001;48:235—9.8. Nolan JP, Morley PT, Vanden Hoek TL, Hickey RW. Therapeutichypothermia after cardiac arrest. An advisory statementby the Advancement Life support Task Force of the InternationalLiaison committee on Resuscitation. Resuscitation2003;57:231—5.9. The Founding Members of the International Liaison Committeeon Resuscitation. The International Liaison Committeeon Resuscitation (ILCOR)—–past, present and future. Resuscitation2005;67:157—61.10. Morley P, Zaritsky A. The evidence evaluation process for the2005 International Consensus on Cardiopulmonary Resuscitationand Emergency Cardiovascular Care Science With TreatmentRecommendations. Resuscitation 2005;67:167—70.11. Nolan JP, Hazinski MF, Steen PA, Becker LB. Controversialtopics from the 2005 International Consensus Conference onCardiopulmonary Resuscitation and Emergency CardiovascularCare Science with treatment recommendations. Resuscitation2005;67:175—9.12. International Liaison Committee on Resuscitation. 2005International Consensus on Cardiopulmonary Resuscitationand Emergency Cardiovascular Care Science with TreatmentRecommendations. Resuscitation 2005;67:157—341.13. Murray CJ, Lopez AD. Mortality by cause for eight regionsof the world: global burden of disease study. Lancet1997;349:1269—76.14. Sans S, Kesteloot H, Kromhout D. The burden of cardiovasculardiseases mortality in Europe. Task Force of the EuropeanSociety of Cardiology on Cardiovascular Mortality andMorbidity Statistics in Europe. Eur Heart J 1997;18:1231—48.15. Kesteloot H, Sans S, Kromhout D. Evolution of all-causesand cardiovascular mortality in the age-group 75—84 yearsin Europe during the period 1970—1996; a comparison withworldwide changes. Eur Heart J 2002;23:384—98.16. Fox R. Trends in cardiovascular mortality in Europe. Circulation1997;96:3817.Jerry Nolan17. Levi F, Lucchini F, Negri E, La Vecchia C. Trends in mortalityfrom cardiovascular and cerebrovascular diseases inEurope and other areas of the world. Heart 2002;88:119—24.18. Zheng ZJ, Croft JB, Giles WH, Mensah GA. Sudden cardiacdeath in the United States, 1989 to 1998. Circulation2001;104:2158—63.19. Pell JP, Sirel JM, Marsden AK, Ford I, Walker NL, Cobbe SM.Presentation, management, and outcome of out of hospitalcardiopulmonary arrest: comparison by underlying aetiology.Heart 2003;89:839—42.20. Herlitz J, Bahr J, Fischer M, Kuisma M, Lexow K, ThorgeirssonG. Resuscitation in Europe: a tale of five European regions.Resuscitation 1999;41:121—31.21. Hodgetts TJ, Kenward G, Vlackonikolis I, et al. Incidence,location and reasons for avoidable in-hospital cardiac arrestin a district general hospital. Resuscitation 2002;54:115—23.22. Skogvoll E, Isern E, Sangolt GK, Gisvold SE. In-hospital cardiopulmonaryresuscitation. 5 years’ incidence and survivalaccording to the Utstein template. Acta Anaesthesiol Scand1999;43:177—84.23. The MERIT study investigators. Introduction of the medicalemergency team (MET) system: a cluster-randomised controlledtrial. Lancet 2005;365:2091—7.24. Langhelle A, Tyvold SS, Lexow K, Hapnes SA, Sunde K, SteenPA. In-hospital factors associated with improved outcomeafter out-of-hospital cardiac arrest. A comparison betweenfour regions in Norway. Resuscitation 2003;56:247—63.25. Langhelle A, Nolan J, Herlitz J, et al. Recommended guidelinesfor reviewing, reporting, and conducting research onpost-resuscitation care: The Utstein style. Resuscitation2005;66:271—83.26. Perkins GD, Soar J. In hospital cardiac arrest: missing linksin the chain of survival. Resuscitation 2005;66:253—5.27. Kern KB, Hilwig RW, Berg RA, Ewy GA. Efficacy of chestcompression-only BLS CPR in the presence of an occludedairway. Resuscitation 1998;39:179—88.28. Wik L, Kramer-Johansen J, Myklebust H, et al. Quality ofcardiopulmonary resuscitation during out-of-hospital cardiacarrest. JAMA 2005;293:299—304.29. Abella BS, Alvarado JP, Myklebust H, et al. Quality of cardiopulmonaryresuscitation during in-hospital cardiac arrest.JAMA 2005;293:305—10.30. Abella BS, Sandbo N, Vassilatos P, et al. Chest compressionrates during cardiopulmonary resuscitation are suboptimal:a prospective study during in-hospital cardiac arrest. Circulation2005;111:428—34.31. Valenzuela TD, Kern KB, Clark LL, et al. Interruptions of chestcompressions during emergency medical systems resuscitation.Circulation 2005;112:1259—65.

Resuscitation (2005) 67S1, S7—S23European Resuscitation Council Guidelines forResuscitation 2005Section 2. Adult basic life support and use ofautomated external defibrillatorsAnthony J. Handley, Rudolph Koster, Koen Monsieurs, Gavin D. Perkins,Sian Davies, Leo BossaertBasic life support (BLS) refers to maintaining airwaypatency and supporting breathing and the circulation,without the use of equipment other than aprotective device. 1 This section contains the guidelinesfor adult BLS by lay rescuers and for the useof an automated external defibrillator (AED). Italso includes recognition of sudden cardiac arrest,the recovery position and management of choking(foreign-body airway obstruction). Guidelines forin-hospital BLS and the use of manual defibrillatorsmay be found in Sections 3 and 4b.IntroductionSudden cardiac arrest (SCA) is a leading cause ofdeath in Europe, affecting about 700,000 individualsa year. 2 At the time of the first heart rhythmanalysis, about 40% of SCA victims have ventricularfibrillation (VF). 3—6 It is likely that many more victimshave VF or rapid ventricular tachycardia (VT)at the time of collapse but, by the time the firstECG is recorded, their rhythm has deteriorated toasystole. 7,8 VF is characterized by chaotic, rapiddepolarisation and repolarisation. The heart losesits coordinated function and stops pumping bloodeffectively. 9 Many victims of SCA can survive ifbystanders act immediately while VF is still present,but successful resuscitation is unlikely once therhythm has deteriorated to asystole. 10 The optimumtreatment for VF cardiac arrest is immediatebystander CPR (combined chest compression andrescue breathing) plus electrical defibrillation. Thepredominant mechanism of cardiac arrest in victimsof trauma, drug overdose, drowning, and in manychildren is asphyxia; rescue breaths are critical forresuscitation of these victims.The following concept of the Chain of Survivalsummarises the vital steps needed for successfulresuscitation (Figure 1.1). Most of these linksare relevant for victims of both VF and asphyxialarrest. 111. Early recognition of the emergency and callingfor help: activate the emergency medicalservices (EMS) or local emergency response system,e.g. ‘‘phone 112’’. 12,13 An early, effectiveresponse may prevent cardiac arrest.2. Early bystander CPR: immediate CPR can doubleor triple survival from VF SCA. 10,14—173. Early defibrillation: CPR plus defibrillationwithin 3—5 min of collapse can produce survivalrates as high as 49—75%. 18—25 Each minute of0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.doi:10.1016/j.resuscitation.2005.10.007

S8A.J. Handley et al.delay in defibrillation reduces the probability ofsurvival to discharge by 10—15%. 14,174. Early advanced life support and postresuscitationcare: the quality of treatmentduring the post-resuscitation phase affectsoutcome. 26In most communities, the time from EMS call toEMS arrival (response interval) is 8 min or longer. 27During this time the victim’s survival is dependenton early initiation by bystanders of the first threeof the links of the Chain of Survival.Victims of cardiac arrest need immediate CPR.This provides a small but critical blood flow to theheart and brain. It also increases the likelihoodthat a defibrillatory shock will terminate VF andenable the heart to resume an effective rhythm andeffective systemic perfusion. Chest compression isespecially important if a shock cannot be deliveredsooner than 4 or 5 min after collapse. 28,29 Defibrillationinterrupts the uncoordinated depolarisationrepolarisationprocess that occurs during VF. Ifthe heart is still viable, its normal pacemakersthen resume their function and produce an effectiverhythm and resumption of circulation. In thefirst few minutes after successful defibrillation, therhythm may be slow and ineffective; chest compressionsmay be needed until adequate cardiacfunction returns. 30Lay rescuers can be trained to use an automatedexternal defibrillator (AED) to analyse the victim’scardiac rhythm and deliver a shock if VF is present.An AED uses voice prompts to guide the rescuer. Itanalyses the ECG rhythm and informs the rescuerif a shock is needed. AEDs are extremely accurateand will deliver a shock only when VF (or its precursor,rapid ventricular tachycardia) is present. 31 AEDfunction and operation are discussed in Section 3.Several studies have shown the benefit on survivalof immediate CPR, and the detrimental effectof delay before defibrillation. For every minutewithout CPR, survival from witnessed VF decreasesby 7—10%. 10 When bystander CPR is provided, thedecline in survival is more gradual and averages3—4% min −1 . 10,14,17 Overall, bystander CPR doublesor triples survival from witnessed cardiacarrest. 10,14,32Figure 2.1Adult basic life support algorithm.• gently shake his shoulders and ask loudly:‘‘Are you all right?’’3a If he responds• leave him in the position in which you find himprovided there is no further danger• try to find out what is wrong with him and gethelp if needed• reassess him regularlyAdult BLS sequenceBLS consists of the following sequence of actions(Figure 2.1).1 Make sure you, the victim and any bystandersare safe.2 Check the victim for a response (Figure 2.2).Figure 2.2 Check the victim for a response. © 2005European Resuscitation Council.

European Resuscitation Council Guidelines for Resuscitation 2005S9Figure 2.3 Shout for help. © 2005 European ResuscitationCouncil.3b If he does not respond• shout for help (Figure 2.3)• turn the victim onto his back and thenopen the airway using head tilt and chin lift(Figure 2.4)◦ place your hand on his forehead and gentlytilt his head back keeping your thumb andFigure 2.5 Head tilt and chin lift in detail. © 2005 EuropeanResuscitation Council.index finger free to close his nose if rescuebreathing is required (Figure 2.5)◦ with your fingertips under the point of thevictim’s chin, lift the chin to open the airway4 Keeping the airway open, look, listen and feelfor normal breathing (Figure 2.6).• Look for chest movement.• Listen at the victim’s mouth for breathsounds.• Feel for air on your cheek.In the first few minutes after cardiac arrest, avictim may be barely breathing, or taking infrequent,noisy gasps. Do not confuse this withnormal breathing. Look, listen, and feel for noFigure 2.4 Head tilt and chin lift. © 2005 EuropeanResuscitation Council.Figure 2.6 Look listen and feel for normal breathing.© 2005 European Resuscitation Council.

S10A.J. Handley et al.Figure 2.7The recovery position. © 2005 European Resuscitation Council.more than 10 s to determine whether the victimis breathing normally. If you have any doubtwhether breathing is normal, act as if it is notnormal.5a If he is breathing normally• turn him into the recovery position (seebelow) (Figure 2.7)• send or go for help/call for an ambulance• check for continued breathing5b If he is not breathing normally• send someone for help or, if you are on yourown, leave the victim and alert the ambulanceservice; return and start chest compressionas follows:◦ kneel by the side of the victim◦ place the heel of one hand in the centre ofthe victim’s chest (Figure 2.8)◦ place the heel of your other hand on top ofthe first hand (Figure 2.9)◦ interlock the fingers of your hands andensure that pressure is not applied over thevictim’s ribs (Figure 2.10). Do not apply anypressure over the upper abdomen or thebottom end of the bony sternum (breastbone)◦ position yourself vertically above the victim’schest and, with your arms straight,press down on the sternum 4—5 cm(Figure 2.11)◦ after each compression, release all thepressure on the chest without losing contactbetween your hands and the sternum;repeat at a rate of about 100 min −1 (a littleless than 2 compressions s −1 )◦ compression and release should take equalamounts of time6a Combine chest compression with rescuebreaths.• After 30 compressions open the airway againusing head tilt and chin lift (Figure 2.12).• Pinch the soft part of the nose closed, usingthe index finger and thumb of your hand onthe forehead.• Allow the mouth to open, but maintain chinlift.• Take a normal breath and place your lipsaround his the mouth, making sure that youhave a good seal.• Blow steadily into the mouth while watchingfor the chest to rise (Figure 2.13), takingabout 1 s as in normal breathing; this is aneffective rescue breath.• Maintaining head tilt and chin lift, take yourmouth away from the victim and watch for thechest to fall as air passes out (Figure 2.14).Figure 2.8 Place the heel of one hand in the centre ofthe victim’s chest. © 2005 European Resuscitation Council.Figure 2.9 Place the heel of your other hand on top ofthe first hand. © 2005 European Resuscitation Council.

European Resuscitation Council Guidelines for Resuscitation 2005S11Figure 2.10 Interlock the fingers of your hands. © 2005European Resuscitation Council.Figure 2.11 Press down on the sternum 4—5 cm. © 2005European Resuscitation Council.• Take another normal breath and blow into thevictim’s mouth once more, to achieve a totalof two effective rescue breaths. Then returnyour hands without delay to the correct positionon the sternum and give a further 30chest compressions.• Continue with chest compressions and rescuebreaths in a ratio of 30:2.• Stop to recheck the victim only if he startsbreathing normally; otherwise do not interruptresuscitation.If your initial rescue breath does not make thechest rise as in normal breathing, then beforeyour next attempt:• check the victim’s mouth and remove anyobstruction• recheck that there is adequate head tilt andchin lift• do not attempt more than two breaths eachtime before returning to chest compressionsIf there is more than one rescuer present,another should take over CPR every 1—2 min toprevent fatigue. Ensure the minimum of delayduring the changeover of rescuers.Figure 2.12 After 30 compressions open the airwayagain using head tilt and chin lift. © 2005 European ResuscitationCouncil.6b Chest-compression-only CPR may be used as follows.• If you are not able or are unwilling to giverescue breaths, give chest compressions only.

S12Figure 2.13 Blow steadily into his mouth whilst watchingfor his chest to rise. © 2005 European ResuscitationCouncil.• If chest compressions only are given, theseshould be continuous, at a rate of 100 min −1 .• Stop to recheck the victim only if he startsbreathing normally; otherwise do not interruptresuscitation.7 Continue resuscitation until• qualified help arrives and takes over• the victim starts breathing normally• you become exhaustedRisk to the rescuerThe safety of both rescuer and victim areparamount during a resuscitation attempt. Therehave been few incidents of rescuers sufferingFigure 2.14 Take your mouth away from the victim andwatch for his chest to fall as air comes out. © 2005 EuropeanResuscitation Council.A.J. Handley et al.adverse effects from undertaking CPR, with onlyisolated reports of infections such as tuberculosis(TB) 33 and severe acute respiratory distress syndrome(SARS). 34 Transmission of HIV during CPRhas never been reported. There have been nohuman studies to address the effectiveness of barrierdevices during CPR; however, laboratory studieshave shown that certain filters, or barrierdevices with one-way valves, prevent oral bacterialtransmission from the victim to the rescuer duringmouth-to-mouth ventilation. 35,36 Rescuers shouldtake appropriate safety precautions where feasible,especially if the victim is known to have aserious infection, such as TB or SARS. During anoutbreak of a highly infectious condition such asSARS, full protective precautions for the rescuer areessential.Opening the airwayThe jaw thrust is not recommended for lay rescuersbecause it is difficult to learn and performand may itself cause spinal movement. 37 Therefore,the lay rescuer should open the airway using a headtilt-chin lift manoeuvre for both injured and noninjuredvictims.Recognition of cardiorespiratory arrestChecking the carotid pulse is an inaccuratemethod of confirming the presence or absenceof circulation. 38 However, there is no evidencethat checking for movement, breathing or coughing(‘signs of a circulation’) is diagnostically superior.Healthcare professionals as well as lay rescuershave difficulty determining the presence or absenceof adequate or normal breathing in unresponsivevictims. 39,40 This may be because the airway isnot open 41 or because the victim is making occasional(agonal) gasps. When bystanders are askedby ambulance dispatchers over the telephone ifbreathing is present, they often misinterpret agonalgasps as normal breathing. This erroneous informationcan result in the bystander withholding CPRfrom a cardiac arrest victim. 42 Agonal gasps arepresent in up to 40% of cardiac arrest victims.Bystanders describe agonal gasps as barely breathing,heavy or laboured breathing, or noisy or gaspingbreathing. 43Laypeople should, therefore, be taught to beginCPR if the victim is unconscious (unresponsive) andnot breathing normally. It should be emphasisedduring training that agonal gasps occur commonlyin the first few minutes after SCA. They are an indicationfor starting CPR immediately and should notbe confused with normal breathing.

European Resuscitation Council Guidelines for Resuscitation 2005S13Initial rescue breathsDuring the first few min after non-asphyxial cardiacarrest the blood oxygen content remains high, andmyocardial and cerebral oxygen delivery is limitedmore by the diminished cardiac output than a lackof oxygen in the lungs. Ventilation is, therefore,initially less important than chest compression. 44It is well recognised that skill acquisition andretention is aided by simplification of the BLSsequence of actions. 45 It is also recognized thatrescuers are frequently unwilling to carry outmouth-to-mouth ventilation for a variety of reasons,including fear of infection and distaste for theprocedure. 46—48 For these reasons, and to emphasisethe priority of chest compressions, it is recommendedthat in adults CPR should start with chestcompression rather than initial ventilation.VentilationDuring CPR the purpose of ventilation is to maintainadequate oxygenation. The optimal tidal volume,respiratory rate and inspired oxygen concentrationto achieve this, however, are not fully known. Thecurrent recommendations are based on the followingevidence:1. During CPR, blood flow to the lungs is substantiallyreduced, so an adequate ventilationperfusionratio can be maintained with lowertidal volumes and respiratory rates thannormal. 492. Not only is hyperventilation (too many breathsor too large a volume) unnecessary, but it isharmful because it increases intrathoracic pressure,thus decreasing venous return to the heartand diminishing cardiac output. Survival is consequentlyreduced. 503. When the airway is unprotected, a tidal volumeof 1 l produces significantly more gastric distentionthan a tidal volume of 500 ml. 514. Low minute-ventilation (lower than normal tidalvolume and respiratory rate) can maintaineffective oxygenation and ventilation duringCPR. 52—55 During adult CPR, tidal volumes ofapproximately 500—600 ml (6—7 ml kg −1 ) shouldbe adequate.5. Interruptions in chest compression (for exampleto give rescue breaths) have a detrimentaleffect on survival. 56 Giving rescue breaths overa shorter time will help to reduce the durationof essential interruptions.The current recommendation is, therefore, forrescuers to give each rescue breath over about 1 s,with enough volume to make the victim’s chestrise, but to avoid rapid or forceful breaths Thisrecommendation applies to all forms of ventilationduring CPR, including mouth-to-mouth and bagvalve-mask(BVM) with and without supplementaryoxygen.Mouth-to-nose ventilation is an effective alternativeto mouth-to-mouth ventilation. 57 It may beconsidered if the victim’s mouth is seriously injuredor cannot be opened, the rescuer is assisting a victimin the water, or a mouth-to-mouth seal is difficultto achieve.There is no published evidence on thesafety, effectiveness or feasibility of mouthto-tracheostomyventilation, but it may be usedfor a victim with a tracheostomy tube or trachealstoma who requires rescue breathing.To use bag-mask ventilation requires considerablepractice and skill. 58,59 The lone rescuer hasto be able to open the airway with a jaw thrustwhile simultaneously holding the mask to the victim’sface. It is a technique that is appropriateonly for lay rescuers who work in highly specialisedareas, such as where there is a risk of cyanide poisoningor exposure to other toxic agents. Thereare other specific circumstances in which nonhealthcareproviders receive extended training infirst aid which could include training, and retraining,in the use of bag-mask ventilation. The samestrict training that applies to healthcare professionalsshould be followed.Chest compressionChest compressions produce blood flow by increasingthe intrathoracic pressure and by directly compressingthe heart. Although chest compressionsperformed properly can produce systolic arterialpressure peaks of 60—80 mmHg, diastolic pressureremains low and mean arterial pressure in thecarotid artery seldom exceeds 40 mmHg. 60 Chestcompressions generate a small but critical amountof blood flow to the brain and myocardium andincrease the likelihood that defibrillation will besuccessful. They are especially important if the firstshock is delivered more than 5 min after collapse. 61Much of the information about the physiology ofchest compression and the effects of varying thecompression rate, compression-to-ventilation ratioand duty cycle (ratio of time chest is compressedto total time from one compression to the next) isderived from animal models. However, the conclusionsof the 2005 Consensus Conference 62 includedthe following:(1) Each time compressions are resumed, the rescuershould place his hands without delay ‘‘inthe centre of the chest’’. 63

S14(2) Compress the chest at a rate of about100 min −1 . 64—66(3) Pay attention to achieving the full compressiondepth of 4—5 cm (for an adult). 67,68(4) Allow the chest to recoil completely after eachcompression. 69,70(5) Take approximately the same amount of timefor compression and relaxation.(6) Minimise interruptions in chest compression.(7) Do not rely on a palpable carotid or femoralpulse as a gauge of effective arterial flow. 38,71There is insufficient evidence to support a specifichand position for chest compression during CPRin adults. Previous guidelines have recommended amethod of finding the middle of the lower half ofthe sternum by placing one finger on the lower endof the sternum and sliding the other hand down toit. 72 It has been shown that for healthcare professionalsthe same hand position can be found morequickly if rescuers are taught to ‘‘place the heelof your hand in the centre of the chest with theother hand on top’’, provided the teaching includesa demonstration of placing the hands in the middleof the lower half of the sternum. 63 It is reasonableto extend this to laypeople.Compression rate refers to the speed at whichcompressions are given, not the total number deliveredin each minute. The number delivered isdetermined by the rate, but also by the numberof interruptions to open the airway, deliver rescuebreaths and allow AED analysis. In one outof-hospitalstudy rescuers recorded compressionrates of 100—120 min −1 but, the mean number ofcompressions was reduced to 64 min −1 by frequentinterruptions. 68Compression—ventilation ratioInsufficient evidence from human outcome studiesexists to support any given compression:ventilationratio. Animal data support an increase in the ratioabove 15:2. 73—75 A mathematical model suggeststhat a ratio of 30:2 would provide the best compromisebetween blood flow and oxygen delivery. 76,77A ratio of 30 compressions to two ventilations isrecommended for the single rescuer attemptingresuscitation on an adult or child out of hospital.This should decrease the number of interruptionsin compression, reduce the likelihoodof hyperventilation, 50,78 simplify instruction forteaching and improve skill retention.Compression-only CPRA.J. Handley et al.Healthcare professionals as well as lay rescuersadmit to being reluctant to perform mouth-tomouthventilation in unknown victims of cardiacarrest. 46,48 Animal studies have shown that chestcompression-only CPR may be as effective as combinedventilation and compression in the first fewminutes after non-asphyxial arrest. 44,79 In adults,the outcome of chest compression without ventilationis significantly better than the outcome ofgiving no CPR. 80 If the airway is open, occasionalgasps and passive chest recoil may provide some airexchange. 81,82 A low minute-ventilation may be allthat is necessary to maintain a normal ventilationperfusionratio during CPR.Laypeople should, therefore, be encouraged toperform compression-only CPR if they are unableor unwilling to provide rescue breaths, althoughcombined chest compression and ventilation is thebetter method of CPR.CPR in confined spacesOver-the-head CPR for single rescuers and straddleCPR for two rescuers may be considered for resuscitationin confined spaces. 83,84Recovery positionThere are several variations of the recovery position,each with its own advantages. No single positionis perfect for all victims. 85,86 The positionshould be stable, near a true lateral position withthe head dependent, and with no pressure on thechest to impair breathing. 87The ERC recommends the following sequenceof actions to place a victim in the recoveryposition:• Remove the victim’s spectacles.• Kneel beside the victim and make sure that bothlegs are straight.• Place the arm nearest to you out at right angles tothe body, elbow bent with the hand palm uppermost(Figure 2.15).• Bring the far arm across the chest, and hold theback of the hand against the victim’s cheek nearestto you (Figure 2.16).• With your other hand, grasp the far leg just abovethe knee and pull it up, keeping the foot on theground (Figure 2.17).• Keeping his hand pressed against his cheek, pullon the far leg to roll the victim towards you ontohis side.• Adjust the upper leg so that both hip and kneeare bent at right angles.• Tilt the head back to make sure the airwayremains open.

European Resuscitation Council Guidelines for Resuscitation 2005S15Figure 2.15 Place the arm nearest to you out at rightangles to his body, elbow bent with the hand palm uppermost.© 2005 European Resuscitation Council.Figure 2.18 The recovery position. © 2005 EuropeanResuscitation Council.• Adjust the hand under the cheek, if necessary, tokeep the head tilted (Figure 2.18).• Check breathing regularly.Figure 2.16 Bring the far arm across the chest, and holdthe back of the hand against the victim’s cheek nearestto you. © 2005 European Resuscitation Council.If the victim has to be kept in the recovery positionfor more than 30 min turn him to the oppositeside to relieve the pressure on the lower arm.Foreign-body airway obstruction (choking)Figure 2.17 With your other hand, grasp the far leg justabove the knee and pull it up, keeping the foot on theground. © 2005 European Resuscitation Council.Foreign-body airway obstruction (FBAO) is anuncommon but potentially treatable cause of accidentaldeath. 88 Each year approximately 16,000adults and children in the UK receive treatment inan emergency department for FBAO. Fortunately,less than 1% of these incidents are fatal. 89 Thecommonest cause of choking in adults is airwayobstruction caused by food such as fish, meat orpoultry. 89 In infants and children, half the reportedepisodes of choking occur while eating (mostly confectionery),and the remaining choking episodesoccur with non-food items such as coins or toys. 90Deaths from choking are rare in infants and children;24 deaths a year on average were reportedin the UK between 1986 and 1995, and over half ofthese children were under 1 year. 90

S16A.J. Handley et al.Table 2.1Differentiation between mild and severe foreign body airway obstruction (FBAO) aSign Mild obstruction Severe obstruction‘‘Are you choking?’’ ‘‘Yes’’ Unable to speak, may nodOther signs Can speak, cough, breathe Cannot breathe/wheezy breathing/silentattempts to cough/unconsciousnessa General signs of FBAO: attack occurs while eating; victim may clutch at neck.As most choking events are associated with eating,they are commonly witnessed. Thus, there isoften the opportunity for early intervention whilethe victim is still responsive.RecognitionBecause recognition of airway obstruction is the keyto successful outcome, it is important not to confusethis emergency with fainting, heart attack,seizure or other conditions that may cause suddenrespiratory distress, cyanosis or loss of consciousness.Foreign bodies may cause either mild orsevere airway obstruction. The signs and symptomsenabling differentiation between mild and severeairway obstruction are summarised in Table 2.1. Itis important to ask the conscious victim ‘Are youchoking?’Adult FBAO (choking) sequence(This sequence is also suitable for use in childrenover the age of 1 year) (Figure 2.19).1 If the victim shows signs of mild airway obstruction• Encourage him to continue coughing but donothing else2 If the victim shows signs of severe airway obstructionand is conscious• Apply up to five back blows as follows.◦ Stand to the side and slightly behind the victim.◦ Support the chest with one hand and leanthe victim well forwards so that when theobstructing object is dislodged it comes outof the mouth rather than goes further downthe airway.◦ Give up to five sharp blows between theshoulder blades with the heel of your otherhand• Check to see if each back blow has relieved theairway obstruction. The aim is to relieve theobstruction with each slap rather than necessarilyto give all five.• If five back blows fail to relieve the airwayobstruction, give up to five abdominal thrustsas follows:◦ Stand behind the victim and put both armsround the upper part of his abdomen.◦ Lean the victim forwards.◦ Clench your fist and place it between theumbilicus and xiphisternum.◦ Grasp this hand with your other hand andpull sharply inwards and upwards.◦ Repeat up to five times.• If the obstruction is still not relieved, continuealternating five back blows with five abdominalthrusts.3 If the victim at any time becomes unconscious.Figure 2.19Adult foreign body airway obstruction treatment algorithm.

European Resuscitation Council Guidelines for Resuscitation 2005S17• Support the victim carefully to the ground.• Immediately activate EMS.• Begin CPR (from 5b of the adult BLS sequence).Healthcare providers, trained and experiencedin feeling for a carotid pulse, should initiatechest compressions, even if a pulse is presentin the unconscious choking victim.FBAO causing mild airway obstructionCoughing generates high and sustained airway pressuresand may expel the foreign body. Aggressivetreatment, with back blows, abdominal thrusts andchest compression, may cause potentially seriouscomplications and could worsen the airway obstruction.It should be reserved for victims who havesigns of severe airway obstruction. Victims withmild airway obstruction should remain under continuousobservation until they improve, as severeairway obstruction may develop.FBAO with severe airway obstructionThe clinical data on choking are largely retrospectiveand anecdotal. For conscious adults and childrenover 1 year with a complete FBAO, case reportsdemonstrate the effectiveness of back blows or‘slaps’, abdominal thrusts and chest thrusts. 91Approximately 50% of episodes of airway obstructionare not relieved by a single technique. 92 Thelikelihood of success is increased when combinationsof back blows or slaps, and abdominal andchest thrusts are used. 91A randomised trial in cadavers 93 and twoprospective studies in anaesthetised volunteers 94,95showed that higher airway pressures can be generatedusing chest thrusts compared with abdominalthrusts. Since chest thrusts are virtually identicalto chest compressions, rescuers should be taughtto start CPR if a victim of known or suspectedFBAO becomes unconscious. During CPR, each timethe airway is opened the victim’s mouth should bequickly checked for any foreign body that has beenpartly expelled. The incidence of unsuspectedchoking as a cause of unconsciousness or cardiacarrest is low; therefore, during CPR routinelychecking the mouth for foreign bodies is notnecessary.The finger sweepNo studies have evaluated the routine use of a fingersweep to clear the airway in the absence of visibleairway obstruction, 96—98 and four case reports havedocumented harm to the victim 96,99 or rescuer. 91Therefore, avoid use of a blind finger sweep andmanually remove solid material in the airway onlyif it can be seen.Aftercare and referral for medical reviewFollowing successful treatment for FBAO, foreignmaterial may nevertheless remain in the upper orlower respiratory tract and cause complicationslater. Victims with a persistent cough, difficultyswallowing or the sensation of an object being stillstuck in the throat, should therefore be referred fora medical opinion.Abdominal thrusts can cause serious internalinjuries, and all victims treated with abdominalthrusts should be examined for injury by adoctor. 91Resuscitation of children (see alsoSection 6) and victims of drowning (seealso Section 7c)Both ventilation and compression are importantfor victims of cardiac arrest when the oxygenstores become depleted—–about 4—6 min after collapsefrom VF and immediately after collapsefrom asphyxial arrest. Previous guidelines tried totake into account the difference in pathophysiology,and recommended that victims of identifiableasphyxia (drowning; trauma; intoxication) and childrenshould receive 1 min of CPR before the lonerescuer left the victim to get help. The majorityof cases of SCA out of hospital, however, occur inadults, and are of cardiac origin due to VF. Theseadditional recommendations, therefore, added tothe complexity of the guidelines while affectingonly a minority of victims.It is important to be aware that many childrendo not receive resuscitation because potential rescuersfear causing harm. This fear is unfounded;it is far better to use the adult BLS sequence forresuscitation of a child than to do nothing. Forease of teaching and retention, therefore, laypeopleshould be taught that the adult sequence mayalso be used for children who are not responsiveand not breathing.The following minor modifications to the adultsequence will, however, make it even more suitablefor use in children.• Give five initial rescue breaths before startingchest compressions (adult sequence of actions,5b).

S18• A lone rescuer should perform CPR for approximately1 min before going for help.• Compress the chest by approximately one thirdof its depth; use two fingers for an infant under1 year; use one or two hands for a child over 1year as needed to achieve an adequate depth ofcompression.The same modifications of five initial breaths, and1 min of CPR by the lone rescuer before gettinghelp, may improve outcome for victims of drowning.This modification should be taught only tothose who have a specific duty of care to potentialdrowning victims (e.g. lifeguards). Drowning iseasily identified. It can be difficult, on the otherhand, for a layperson to determine whether cardiorespiratoryarrest is a direct result of traumaor intoxication. These victims should, therefore, bemanaged according to the standard protocol.Use of an automated externaldefibrillatorSection 3 discusses the guidelines for defibrillationusing both automated external defibrillators (AEDs)and manual defibrillators. However, there are somespecial considerations when an AED is to be used bylay or non-healthcare rescuers.Standard AEDs are suitable for use in childrenolder than 8 years. For children between 1 and 8years use paediatric pads or a paediatric mode ifavailable; if these are not available, use the AED asit is. Use of AEDs is not recommended for childrenless than 1 year.Sequence for use of an AEDSee Figure 2.20.(1) Make sure you, the victim, and any bystandersare safe.(2) If the victim is unresponsive and not breathingnormally, send someone for the AED and to callfor an ambulance.(3) Start CPR according to the guidelines for BLS.(4) As soon as the defibrillator arrives• switch on the defibrillator and attach theelectrode pads. If more than one rescuer ispresent, CPR should be continued while thisis carried out• follow the spoken/visual directions• ensure that nobody touches the victim whilethe AED is analysing the rhythm5a If a shock is indicated• ensure that nobody touches the victimA.J. Handley et al.• push shock button as directed (fully automaticAEDs will deliver the shock automatically)• continue as directed by the voice/visualprompts5b If no shock indicated• immediately resume CPR, using a ratio of 30compressions to 2 rescue breaths• continue as directed by the voice/visualprompts6 Continue to follow the AED prompts until• qualified help arrives and takes over• the victim starts to breathe normally• you become exhaustedCPR before defibrillationImmediate defibrillation, as soon as an AEDbecomes available, has always been a key elementin guidelines and teaching, and considered ofparamount importance for survival from ventricularfibrillation. This concept has been challengedbecause evidence suggests that a period of chestcompression before defibrillation may improve survivalwhen the time between calling for the ambulanceand its arrival exceeds 5 min. 28,61,100 Onestudy 101 did not confirm this benefit, but the weightof evidence supports a period of CPR for victims ofprolonged cardiac arrest before defibrillation.In all of these studies CPR was performed byparamedics, who protected the airway by intubationand delivered 100% oxygen. Such high-qualityventilation cannot be expected from lay rescuersgiving mouth-to-mouth ventilation. Secondly, thebenefit from CPR occurred only when the delay fromcall to the availability of a defibrillator was greaterthan 5 min; the delay from collapse to arrival of therescuer with an AED will rarely be known with certainty.Thirdly, if good bystander CPR is already inprogress when the AED arrives, it does not seemlogical to continue it any further. For these reasonsthese guidelines recommend an immediate shock,as soon as the AED is available. The importance ofearly uninterrupted external chest compression isemphasised.Voice promptsIn several places, the sequence of actions states‘follow the voice/visual prompts’. The prompts areusually programmable, and it is recommended thatthey be set in accordance with the sequence ofshocks and timings for CPR given in Section 2. Theseshould include at least:

European Resuscitation Council Guidelines for Resuscitation 2005S19Figure 2.20Algorithm for use of an automated external defibrillator.(1) a single shock only, when a shockable rhythm isdetected(2) no rhythm check, or check for breathing or apulse, after the shock(3) a voice prompt for immediate resumption ofCPR after the shock (giving chest compressionsin the presence of a spontaneous circulation isnot harmful)(4) two minutes for CPR before a prompt to assessthe rhythm, breathing or a pulse is givenThe shock sequence and energy levels are discussedin Section 3.Fully-automatic AEDsHaving detected a shockable rhythm, a fullyautomaticAED will deliver a shock without furtherinput from the rescuer. One manikin study showedthat untrained nursing students committed fewersafety errors using a fully-automatic AED ratherthan a semi-automatic AED. 102 There are no humandata to determine whether these findings can beapplied to clinical use.Public access defibrillation programmesPublic access defibrillation (PAD) and first responderAED programmes may increase the number of victimswho receive bystander CPR and early defibrillation,thus improving survival from out-of-hospitalSCA. 103 These programmes require an organisedand practised response with rescuers trained andequipped to recognise emergencies, activate theEMS system, provide CPR and use the AED. 104,105 Layrescuer AED programmes with very rapid response

S20times in airports, 22 on aircraft 23 or in casinos, 25 anduncontrolled studies using police officers as firstresponders, 106,107 have achieved reported survivalrates as high as 49—74%.The logistic problem for first responder programmesis that the rescuer needs to arrive notjust earlier than the traditional EMS, but within5—6 min of the initial call, to enable attempteddefibrillation in the electrical or circulatory phaseof cardiac arrest. 108 With longer delays, the survivalcurve flattens; 10,17 a few minutes’ gain in time willhave little impact when the first responder arrivesmore than 10 min after the call 27,109 or when a firstresponder does not improve on an already shortEMS response time. 110 However, small reductionsin response intervals achieved by first-responderprogrammes that have an impact on many residentialvictims may be more cost effective than thelarger reductions in response interval achieved byPAD programmes that have an impact on fewer cardiacarrest victims. 111,112Recommended elements for PAD programmesinclude:• a planned and practised response• training of anticipated rescuers in CPR and use ofthe AED• link with the local EMS system• programme of continuous audit (quality improvement)Public access defibrillation programmes are mostlikely to improve survival from cardiac arrestif they are established in locations where witnessedcardiac arrest is likely to occur. 113 Suitablesites might include those where the probabilityof cardiac arrest occurring is at least oncein every 2 years (e.g., airports, casinos, sportsfacilities). 103 Approximately 80% of out-of-hospitalcardiac arrests occur in private or residentialsettings; 114 this fact inevitably limits the overallimpact that PAD programmes can have on survivalrates. There are no studies documenting effectivenessof home AED deployment.ReferencesA.J. Handley et al.1. Recommended guidelines for uniform reporting of datafrom out-of-hospital cardiac arrest: the ‘Utstein style’.Prepared by a Task Force of Representatives from theEuropean Resuscitation Council, American Heart Association.Heart and Stroke Foundation of Canada, AustralianResuscitation Council. Resuscitation 1991;22:1—26.2. Sans S, Kesteloot H, Kromhout D. The burden of cardiovasculardiseases mortality in Europe. Task Force of theEuropean Society of Cardiology on Cardiovascular Mortalityand Morbidity Statistics in Europe. Eur Heart J1997;18:1231—48.3. Cobb LA, Fahrenbruch CE, Olsufka M, Copass MK. Changingincidence of out-of-hospital ventricular fibrillation,1980—2000. JAMA 2002;288:3008—13.4. Rea TD, Eisenberg MS, Sinibaldi G, White RD. Incidence ofEMS-treated out-of-hospital cardiac arrest in the UnitedStates. Resuscitation 2004;63:17—24.5. Vaillancourt C, Stiell IG. Cardiac arrest care andemergency medical services in Canada. Can J Cardiol2004;20:1081—90.6. Waalewijn RA, de Vos R, Koster RW. Out-of-hospital cardiacarrests in Amsterdam and its surrounding areas:results from the Amsterdam resuscitation study (ARREST)in ‘Utstein’ style. Resuscitation 1998;38:157—67.7. Cummins R, Thies W. Automated external defibrillators andthe Advanced Cardiac Life Support Program: a new initiativefrom the American Heart Association. Am J Emerg Med1991;9:91—3.8. Waalewijn RA, Nijpels MA, Tijssen JG, Koster RW. Preventionof deterioration of ventricular fibrillation by basic lifesupport during out-of-hospital cardiac arrest. Resuscitation2002;54:31—6.9. Page S, Meerabeau L. Achieving change through reflectivepractice: closing the loop. Nurs Educ Today2000;20:365—72.10. Larsen MP, Eisenberg MS, Cummins RO, Hallstrom AP.Predicting survival from out-of-hospital cardiac arrest: agraphic model. Ann Emerg Med 1993;22:1652—8.11. Cummins RO, Ornato JP, Thies WH, Pepe PE. Improvingsurvival from sudden cardiac arrest: the ‘‘chain of survival’’concept. A statement for health professionals fromthe Advanced Cardiac Life Support Subcommittee and theEmergency Cardiac Care Committee, American Heart Association.Circulation 1991;83:1832—47.12. Calle PA, Lagaert L, Vanhaute O, Buylaert WA. Do victimsof an out-of-hospital cardiac arrest benefit from a trainingprogram for emergency medical dispatchers? Resuscitation1997;35:213—8.13. Curka PA, Pepe PE, Ginger VF, Sherrard RC, Ivy MV,Zachariah BS. Emergency medical services priority dispatch.Ann Emerg Med 1993;22:1688—95.14. Valenzuela TD, Roe DJ, Cretin S, Spaite DW, LarsenMP. Estimating effectiveness of cardiac arrest interventions:a logistic regression survival model. Circulation1997;96:3308—13.15. Holmberg M, Holmberg S, Herlitz J. Factors modifying theeffect of bystander cardiopulmonary resuscitation on survivalin out-of-hospital cardiac arrest patients in Sweden.Eur Heart J 2001;22:511—9.16. Holmberg M, Holmberg S, Herlitz J, Gardelov B. Survivalafter cardiac arrest outside hospital in Sweden. SwedishCardiac Arrest Registry. Resuscitation 1998;36:29—36.17. Waalewijn RA, De Vos R, Tijssen JGP, Koster RW. Survivalmodels for out-of-hospital cardiopulmonary resuscitationfrom the perspectives of the bystander, the first responder,and the paramedic. Resuscitation 2001;51:113—22.18. Weaver WD, Hill D, Fahrenbruch CE, et al. Use of the automaticexternal defibrillator in the management of out-ofhospitalcardiac arrest. N Engl J Med 1988;319:661—6.19. Auble TE, Menegazzi JJ, Paris PM. Effect of out-ofhospitaldefibrillation by basic life support providers oncardiac arrest mortality: a metaanalysis. Ann Emerg Med1995;25:642—58.20. Stiell IG, Wells GA, DeMaio VJ, et al. Modifiable factorsassociated with improved cardiac arrest survival in a multicenterbasic life support/defibrillation system: OPALS

European Resuscitation Council Guidelines for Resuscitation 2005S21Study Phase I results. Ontario Prehospital Advanced LifeSupport. Ann Emerg Med 1999;33:44—50.21. Stiell IG, Wells GA, Field BJ, et al. Improved out-of-hospitalcardiac arrest survival through the inexpensive optimizationof an existing defibrillation program: OPALS studyphase II. Ontario Prehospital Advanced Life Support. JAMA1999;281:1175—81.22. Caffrey S. Feasibility of public access to defibrillation. CurrOpin Crit Care 2002;8:195—8.23. O’Rourke MF, Donaldson E, Geddes JS. An airline cardiacarrest program. Circulation 1997;96:2849—53.24. Page RL, Hamdan MH, McKenas DK. Defibrillation aboarda commercial aircraft. Circulation 1998;97:1429—30.25. Valenzuela TD, Roe DJ, Nichol G, Clark LL, Spaite DW,Hardman RG. Outcomes of rapid defibrillation by securityofficers after cardiac arrest in casinos. N Engl J Med2000;343:1206—9.26. Langhelle A, Nolan JP, Herlitz J, et al. Recommended guidelinesfor reviewing, reporting, and conducting researchon post-resuscitation care: the Utstein style. Resuscitation2005;66:271—83.27. van Alem AP, Vrenken RH, de Vos R, Tijssen JG, Koster RW.Use of automated external defibrillator by first respondersin out of hospital cardiac arrest: prospective controlledtrial. BMJ 2003;327:1312—7.28. Cobb LA, Fahrenbruch CE, Walsh TR, et al. Influenceof cardiopulmonary resuscitation prior to defibrillation inpatients with out-of-hospital ventricular fibrillation. JAMA1999;281:1182—8.29. Wik L, Myklebust H, Auestad BH, Steen PA. Retention ofbasic life support skills 6 months after training with anautomated voice advisory manikin system without instructorinvolvement. Resuscitation 2002;52:273—9.30. White RD, Russell JK. Refibrillation, resuscitation andsurvival in out-of-hospital sudden cardiac arrest victimstreated with biphasic automated external defibrillators.Resuscitation 2002;55:17—23.31. Kerber RE, Becker LB, Bourland JD, et al. Automatic externaldefibrillators for public access defibrillation: recommendationsfor specifying and reporting arrhythmia analysisalgorithm performance, incorporating new waveforms,and enhancing safety. A statement for health professionalsfrom the American Heart Association Task Force on AutomaticExternal Defibrillation, Subcommittee on AED Safetyand Efficacy. Circulation 1997;95:1677—82.32. Holmberg M, Holmberg S, Herlitz J. Effect of bystandercardiopulmonary resuscitation in out-of-hospital cardiacarrest patients in Sweden. Resuscitation 2000;47:59—70.33. Heilman KM, Muschenheim C. Primary cutaneous tuberculosisresulting from mouth-to-mouth respiration. N Engl JMed 1965;273:1035—6.34. Christian MD, Loutfy M, McDonald LC, et al. Possible SARScoronavirus transmission during cardiopulmonary resuscitation.Emerg Infect Dis 2004;10:287—93.35. Cydulka RK, Connor PJ, Myers TF, Pavza G, Parker M.Prevention of oral bacterial flora transmission by usingmouth-to-mask ventilation during CPR. J Emerg Med1991;9:317—21.36. Blenkharn JI, Buckingham SE, Zideman DA. Prevention oftransmission of infection during mouth-to-mouth resuscitation.Resuscitation 1990;19:151—7.37. Aprahamian C, Thompson BM, Finger WA, Darin JC. Experimentalcervical spine injury model: evaluation of airwaymanagement and splinting techniques. Ann Emerg Med1984;13:584—7.38. Bahr J, Klingler H, Panzer W, Rode H, Kettler D. Skillsof lay people in checking the carotid pulse. Resuscitation1997;35:23—6.39. Ruppert M, Reith MW, Widmann JH, et al. Checkingfor breathing: evaluation of the diagnostic capability ofemergency medical services personnel, physicians, medicalstudents, and medical laypersons. Ann Emerg Med1999;34:720—9.40. Perkins GD, Stephenson B, Hulme J, Monsieurs KG. Birminghamassessment of breathing study (BABS). Resuscitation2005;64:109—13.41. Domeier RM, Evans RW, Swor RA, Rivera-Rivera EJ, FrederiksenSM. Prospective validation of out-of-hospital spinalclearance criteria: a preliminary report. Acad Emerg Med1997;4:643—6.42. Hauff SR, Rea TD, Culley LL, Kerry F, Becker L,Eisenberg MS. Factors impeding dispatcher-assisted telephonecardiopulmonary resuscitation. Ann Emerg Med2003;42:731—7.43. Clark JJ, Larsen MP, Culley LL, Graves JR, Eisenberg MS.Incidence of agonal respirations in sudden cardiac arrest.Ann Emerg Med 1992;21:1464—7.44. Kern KB, Hilwig RW, Berg RA, Sanders AB, Ewy GA.Importance of continuous chest compressions duringcardiopulmonary resuscitation: improved outcome duringa simulated single lay-rescuer scenario. Circulation2002;105:645—9.45. Handley JA, Handley AJ. Four-step CPR—–improving skillretention. Resuscitation 1998;36:3—8.46. Ornato JP, Hallagan LF, McMahan SB, Peeples EH, RostafinskiAG. Attitudes of BCLS instructors about mouth-to-mouthresuscitation during the AIDS epidemic. Ann Emerg Med1990;19:151—6.47. Brenner BE, Van DC, Cheng D, Lazar EJ. Determinants ofreluctance to perform CPR among residents and applicants:the impact of experience on helping behavior. Resuscitation1997;35:203—11.48. Hew P, Brenner B, Kaufman J. Reluctance of paramedicsand emergency medical technicians to perform mouth-tomouthresuscitation. J Emerg Med 1997;15:279—84.49. Baskett P, Nolan J, Parr M. Tidal volumes which are perceivedto be adequate for resuscitation. Resuscitation1996;31:231—4.50. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al.Hyperventilation-induced hypotension during cardiopulmonaryresuscitation. Circulation 2004;109:1960—5.51. Wenzel V, Idris AH, Banner MJ, Kubilis PS, Williams JLJ.Influence of tidal volume on the distribution of gasbetween the lungs and stomach in the nonintubatedpatient receiving positive-pressure ventilation. Crit CareMed 1998;26:364—8.52. Idris A, Gabrielli A, Caruso L. Smaller tidal volume is safeand effective for bag-valve-ventilation, but not for mouthto-mouthventilation: an animal model for basic life support.Circulation 1999;100(Suppl. I):I-644.53. Idris A, Wenzel V, Banner MJ, Melker RJ. Smaller tidal volumesminimize gastric inflation during CPR with an unprotectedairway. Circulation 1995;92(Suppl.):I-759.54. Dorph E, Wik L, Steen PA. Arterial blood gases with 700ml tidal volumes during out-of-hospital CPR. Resuscitation2004;61:23—7.55. Winkler M, Mauritz W, Hackl W, et al. Effects of half thetidal volume during cardiopulmonary resuscitation on acidbasebalance and haemodynamics in pigs. Eur J Emerg Med1998;5:201—6.56. Eftestol T, Sunde K, Steen PA. Effects of interruptingprecordial compressions on the calculated probability of

S22defibrillation success during out-of-hospital cardiac arrest.Circulation 2002;105:2270—3.57. Ruben H. The immediate treatment of respiratory failure.Br J Anaesth 1964;36:542—9.58. Elam JO. Bag-valve-mask O 2 ventilation. In: Safar P, ElamJO, editors. Advances in cardiopulmonary resuscitation:the Wolf Creek Conference on Cardiopulmonary Resuscitation.New York, NY: Springer-Verlag, Inc.; 1977. p. 73—9.59. Dailey RH. The airway: emergency management. St. Louis,MO: Mosby Year Book; 1992.60. Paradis NA, Martin GB, Goetting MG, et al. Simultaneousaortic, jugular bulb, and right atrial pressures during cardiopulmonaryresuscitation in humans. Insights into mechanisms.Circulation 1989;80:361—8.61. Wik L, Hansen TB, Fylling F, et al. Delaying defibrillation togive basic cardiopulmonary resuscitation to patients without-of-hospital ventricular fibrillation: a randomized trial.JAMA 2003;289:1389—95.62. International Liaison Committee on Resuscitation. Internationalconsensus on cardiopulmonary resuscitation andemergency cardiovascular care science with treatment recommendations.Resuscitation 2005:67.63. Handley AJ. Teaching hand placement for chestcompression—–a simpler technique. Resuscitation2002;53:29—36.64. Yu T, Weil MH, Tang W, et al. Adverse outcomes of interruptedprecordial compression during automated defibrillation.Circulation 2002;106:368—72.65. Swenson RD, Weaver WD, Niskanen RA, Martin J, DahlbergS. Hemodynamics in humans during conventional andexperimental methods of cardiopulmonary resuscitation.Circulation 1988;78:630—9.66. Kern KB, Sanders AB, Raife J, Milander MM, Otto CW,Ewy GA. A study of chest compression rates during cardiopulmonaryresuscitation in humans: the importanceof rate-directed chest compressions. Arch Intern Med1992;152:145—9.67. Abella BS, Alvarado JP, Myklebust H, et al. Quality ofcardiopulmonary resuscitation during in-hospital cardiacarrest. JAMA 2005;293:305—10.68. Wik L, Kramer-Johansen J, Myklebust H, et al. Quality ofcardiopulmonary resuscitation during out-of-hospital cardiacarrest. JAMA 2005;293:299—304.69. Aufderheide TP, Pirrallo RG, Yannopoulos D, et al. Incompletechest wall decompression: a clinical evaluationof CPR performance by EMS personnel and assessmentof alternative manual chest compression—decompressiontechniques. Resuscitation 2005;64:353—62.70. Yannopoulos D, McKnite S, Aufderheide TP, et al. Effectsof incomplete chest wall decompression during cardiopulmonaryresuscitation on coronary and cerebral perfusionpressures in a porcine model of cardiac arrest. Resuscitation2005;64:363—72.71. Ochoa FJ, Ramalle-Gomara E, Carpintero JM, Garcia A, SaraleguiI. Competence of health professionals to check thecarotid pulse. Resuscitation 1998;37:173—5.72. Handley AJ, Monsieurs KG, Bossaert LL. European ResuscitationCouncil Guidelines 2000 for Adult Basic Life Support.A statement from the Basic Life Support and AutomatedExternal Defibrillation Working Group(1) and approved bythe Executive Committee of the European ResuscitationCouncil. Resuscitation 2001;48:199—205.73. Sanders AB, Kern KB, Berg RA, Hilwig RW, HeidenrichJ, Ewy GA. Survival and neurologic outcomeafter cardiopulmonary resuscitation with four differentchest compression-ventilation ratios. Ann Emerg Med2002;40:553—62.A.J. Handley et al.74. Dorph E, Wik L, Stromme TA, Eriksen M, Steen PA. Qualityof CPR with three different ventilation:compression ratios.Resuscitation 2003;58:193—201.75. Dorph E, Wik L, Stromme TA, Eriksen M, Steen PA. Oxygendelivery and return of spontaneous circulation with ventilation:compressionratio 2:30 versus chest compressionsonly CPR in pigs. Resuscitation 2004;60:309—18.76. Babbs CF, Kern KB. Optimum compression to ventilationratios in CPR under realistic, practical conditions:a physiological and mathematical analysis. Resuscitation2002;54:147—57.77. Fenici P, Idris AH, Lurie KG, Ursella S, Gabrielli A. What isthe optimal chest compression—ventilation ratio? Curr OpinCrit Care 2005;11:204—11.78. Aufderheide TP, Lurie KG. Death by hyperventilation: acommon and life-threatening problem during cardiopulmonaryresuscitation. Crit Care Med 2004;32:S345—51.79. Chandra NC, Gruben KG, Tsitlik JE, et al. Observations ofventilation during resuscitation in a canine model. Circulation1994;90:3070—5.80. Becker LB, Berg RA, Pepe PE, et al. A reappraisal of mouthto-mouthventilation during bystander-initiated cardiopulmonaryresuscitation. A statement for healthcare professionalsfrom the Ventilation Working Group of the Basic LifeSupport and Pediatric Life Support Subcommittees, AmericanHeart Association. Resuscitation 1997;35:189—201.81. Berg RA, Kern KB, Hilwig RW, et al. Assisted ventilationdoes not improve outcome in a porcine model of singlerescuerbystander cardiopulmonary resuscitation. Circulation1997;95:1635—41.82. Berg RA, Kern KB, Hilwig RW, Ewy GA. Assisted ventilationduring ‘bystander’ CPR in a swine acute myocardialinfarction model does not improve outcome. Circulation1997;96:4364—71.83. Handley AJ, Handley JA. Performing chest compressions ina confined space. Resuscitation 2004;61:55—61.84. Perkins GD, Stephenson BT, Smith CM, Gao F. A comparisonbetween over-the-head and standard cardiopulmonaryresuscitation. Resuscitation 2004;61:155—61.85. Turner S, Turner I, Chapman D, et al. A comparative studyof the 1992 and 1997 recovery positions for use in the UK.Resuscitation 1998;39:153—60.86. Handley AJ. Recovery position. Resuscitation1993;26:93—5.87. Anonymous. Guidelines 2000 for cardiopulmonary resuscitationand emergency cardiovascular care—–an internationalconsensus on science. Resuscitation 2000;46:1—447.88. Fingerhut LA, Cox CS, Warner M. International comparativeanalysis of injury mortality. Findings from the ICE oninjury statistics. International collaborative effort on injurystatistics. Adv Data 1998;12:1—20.89. Industry DoTa. Choking. In: Home and leisure accidentreport. London: Department of Trade and Industry; 1998,p. 13—4.90. Industry DoTa. Choking risks to children. London: Departmentof Trade and Industry; 1999.91. International Liaison Committee on Resuscitation. Part2. Adult basic life support. 2005 international consensuson cardiopulmonary resuscitation and emergency cardiovascularcare science with treatment recommendations.Resuscitation 2005;67:187—200.92. Redding JS. The choking controversy: critique of evidenceon the Heimlich maneuver. Crit Care Med 1979;7:475—9.93. Langhelle A, Sunde K, Wik L, Steen PA. Airway pressure withchest compressions versus Heimlich manoeuvre in recentlydead adults with complete airway obstruction. Resuscitation2000;44:105—8.

European Resuscitation Council Guidelines for Resuscitation 2005S2394. Guildner CW, Williams D, Subitch T. Airway obstructedby foreign material: the Heimlich maneuver. JACEP1976;5:675—7.95. Ruben H, Macnaughton FI. The treatment of food-choking.Practitioner 1978;221:725—9.96. Hartrey R, Bingham RM. Pharyngeal trauma as a result ofblind finger sweeps in the choking child. J Accid Emerg Med1995;12:52—4.97. Elam JO, Ruben AM, Greene DG. Resuscitation of drowningvictims. JAMA 1960;174:13—6.98. Ruben HM, Elam JO, Ruben AM, Greene DG. Investigation ofupper airway problems in resuscitation. 1. Studies of pharyngealX-rays and performance by laymen. Anesthesiology1961;22:271—9.99. Kabbani M, Goodwin SR. Traumatic epiglottis followingblind finger sweep to remove a pharyngeal foreign body.Clin Pediatr (Phila) 1995;34:495—7.100. Eftestol T, Wik L, Sunde K, Steen PA. Effects of cardiopulmonaryresuscitation on predictors of ventricular fibrillationdefibrillation success during out-of-hospital cardiacarrest. Circulation 2004;110:10—5.101. Jacobs IG, Finn JC, Oxer HF, Jelinek GA. CPR before defibrillationin out-of-hospital cardiac arrest: a randomized trial.Emerg Med Australas 2005;17:39—45.102. Monsieurs KG, Vogels C, Bossaert LL, Meert P, Calle PA.A study comparing the usability of fully automatic versussemi-automatic defibrillation by untrained nursing students.Resuscitation 2005;64:41—7.103. The Public Access Defibrillation Trial Investigators.Public-access defibrillation and survival after out-ofhospitalcardiac arrest. N Engl J Med 2004;351:637—46.104. Priori SBL, Chamberlain D, Napolitano C, Arntz HR, KosterR, Monsieurs K, Capucci A, Wellens H. Policy Statement:ESC-ERC recommendations for the use of AEDs in Europe.Eur Heart J 2004;25:437—45.105. Priori SG, Bossaert LL, Chamberlain DA, et al. Policy statement:ESC-ERC recommendations for the use of automatedexternal defibrillators (AEDs) in Europe. Resuscitation2004;60:245—52.106. White RD, Bunch TJ, Hankins DG. Evolution of a communitywideearly defibrillation programme experience over 13years using police/fire personnel and paramedics as responders.Resuscitation 2005;65:279—83.107. Mosesso Jr VN, Davis EA, Auble TE, Paris PM, Yealy DM. Useof automated external defibrillators by police officers fortreatment of out-of-hospital cardiac arrest. Ann Emerg Med1998;32:200—7.108. Weisfeldt M, Becker L. Resuscitation after cardiac arrest.A 3-phase time-sensitive model. JAMA 2002;288:3035—8.109. Groh WJ, Newman MM, Beal PE, Fineberg NS, Zipes DP. Limitedresponse to cardiac arrest by police equipped withautomated external defibrillators: lack of survival benefitin suburban and rural Indiana—–the police as responderautomated defibrillation evaluation (PARADE). Acad EmergMed 2001;8:324—30.110. Sayre M, Evans J, White L, Brennan T. Providing automatedexternal defibrillators to urban police officers in additionto fire department rapid defibrillation program is not effective.Resuscitation 2005;66:189—96.111. Nichol G, Hallstrom AP, Ornato JP, et al. Potential costeffectivenessof public access defibrillation in the UnitedStates. Circulation 1998;97:1315—20.112. Nichol G, Valenzuela T, Roe D, Clark L, Huszti E, Wells GA.Cost effectiveness of defibrillation by targeted respondersin public settings. Circulation 2003;108:697—703.113. Becker L, Eisenberg M, Fahrenbruch C, Cobb L. Public locationsof cardiac arrest: implications for public access defibrillation.Circulation 1998;97:2106—9.114. Becker DE. Assessment and management of cardiovascularurgencies and emergencies: cognitive and technical considerations.Anesth Progress 1988;35:212—7.

Resuscitation (2005) 67S1, S25—S37European Resuscitation Council Guidelines forResuscitation 2005Section 3. Electrical therapies: Automatedexternal defibrillators, defibrillation,cardioversion and pacingCharles D. Deakin, Jerry P. NolanIntroductionThis section presents guidelines for defibrillationusing both automated external defibrillators (AEDs)and manual defibrillators. All healthcare providersand lay responders can use AEDs as an integral componentof basic life support. Manual defibrillation isused as part of advanced life support (ALS) therapy.In addition, synchronised cardioversion and pacingare ALS functions of many defibrillators and are alsodiscussed in this section.Defibrillation is the passage across the myocardiumof an electrical current of sufficient magnitudeto depolarise a critical mass of myocardium andenable restoration of coordinated electrical activity.Defibrillation is defined as the termination offibrillation or, more precisely, the absence of ventricularfibrillation/ventricular tachycardia (VF/VT)at 5 s after shock delivery; however, the goal ofattempted defibrillation is to restore spontaneouscirculation.Defibrillator technology is advancing rapidly. AEDinteraction with the rescuer through voice promptsis now established, and future technology mayenable more specific instructions to be given byvoice prompt. The ability of defibrillators to assessthe rhythm while CPR is in progress is required toprevent unnecessary delays in CPR. Waveform analysismay also enable the defibrillator to calculatethe optimal time at which to give a shock.A vital link in the chain of survivalDefibrillation is a key link in the Chain of Survivaland is one of the few interventions that have beenshown to improve outcome from VF/VT cardiacarrest. The previous guidelines, published in 2000,rightly emphasised the importance of early defibrillationwith minimum delay. 1The probability of successful defibrillation andsubsequent survival to hospital discharge declinesrapidly with time 2,3 and the ability to deliverearly defibrillation is one of the most importantfactors in determining survival from cardiacarrest. For every minute that passes followingcollapse and defibrillation, mortality increases7%—10% in the absence of bystander CPR. 2—4 EMSsystems do not generally have the capability todeliver defibrillation through traditional paramedicresponders within the first few minutes of a call,and the alternative use of trained lay responders0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.doi:10.1016/j.resuscitation.2005.10.008

S26to deliver prompt defibrillation using AEDs is nowwidespread. EMS systems that have reduced time todefibrillation following cardiac arrest using trainedlay responders have reported greatly improvedsurvival-to-discharge rates, 5—7 some as high as75% if defibrillation is performed within 3 min ofcollapse. 8 This concept has also been extended toin-hospital cardiac arrests where staff, other thandoctors, are also being trained to defibrillate usingan AED before arrival of the cardiac arrest team.When bystander CPR is provided, the reduction insurvival rate is more gradual and averages 3%—4%per minute from collapse to defibrillation; 2—4bystander CPR can double 2,3,9 or treble 10 survivalfrom witnessed out-of-hospital cardiacarrest.All healthcare providers with a duty to performCPR should be trained, equipped, and encouragedto perform defibrillation and CPR. Early defibrillationshould be available throughout all hospitals,outpatient medical facilities and public areas ofmass gathering (see Section 2). Those trained inAED use should also be trained to deliver at leastexternal chest compressions before the arrival ofALS providers, to optimise the effectiveness of earlydefibrillation.Automated external defibrillatorsAutomated external defibrillators are sophisticated,reliable computerised devices that use voiceand visual prompts to guide lay rescuers and healthcareprofessionals to safely attempt defibrillationin cardiac arrest victims. Automated defibrillatorshave been described as ‘‘... the single greatestadvance in the treatment of VF cardiac arrest sincethe development of CPR.’’ 11 Advances in technology,particularly with respect to battery capacity,and software arrhythmia analysis have enabled themass production of relatively cheap, reliable andeasily operated portable defibrillators. 12—15 Use ofAEDs by lay or non-healthcare rescuers is coveredin Section 2.Automated rhythm analysisAutomated external defibrillators have microprocessorsthat analyse several features of the ECG,including frequency and amplitude. Some AEDs areprogrammed to detect spontaneous movement bythe patient or others. Developing technology shouldsoon enable AEDs to provide information aboutfrequency and depth of chest compressions duringCPR that may improve BLS performance by allrescuers. 16,17C.D. Deakin, J.P. NolanAutomated external defibrillators have beentested extensively against libraries of recordedcardiac rhythms and in many trials in adults 18,19and children. 20,21 They are extremely accurate inrhythm analysis. Although AEDs are not designed todeliver synchronised shocks, all AEDs will recommendshocks for VT if the rate and R-wave morphologyexceed preset values.In-hospital use of AEDsAt the time of the 2005 Consensus Conference,there were no published randomised trialscomparing in-hospital use of AEDs with manualdefibrillators. Two lower level studies of adultswith in-hospital cardiac arrest from shockablerhythms showed higher survival-to-hospital dischargerates when defibrillation was providedthrough an AED programme than with manual defibrillationalone. 22,23 A manikin study showed thatuse of an AED significantly increased the likelihoodof delivering three shocks, but increased the timeto deliver the shocks when compared with manualdefibrillators. 24 In contrast, a study of mock arrestsin simulated patients showed that use of monitoringleads and fully automated defibrillators reducedtime to defibrillation when compared with manualdefibrillators. 25Delayed defibrillation may occur when patientssustain cardiac arrest in unmonitored hospital bedsand in outpatient departments. In these areas severalminutes may elapse before resuscitation teamsarrive with a defibrillator and deliver shocks. 26Despite limited evidence, AEDs should be consideredfor the hospital setting as a way to facilitateearly defibrillation (a goal of

European Resuscitation Council Guidelines for Resuscitation 2005S27significant burns to the patient. The risk of fire duringattempted defibrillation can be minimised bytaking the following precautions.• Take off any oxygen mask or nasal cannulae andplace them at least 1 m away from the patient’schest.• Leave the ventilation bag connected to the trachealtube or other airway adjunct. Alternatively,disconnect any bag-valve device from thetracheal tube (or other airway adjunct such asthe laryngeal mask airway, combitube or laryngealtube), and remove it at least 1 m from thepatient’s chest during defibrillation.• If the patient is connected to a ventilator, forexample in the operating room or critical careunit, leave the ventilator tubing (breathing circuit)connected to the tracheal tube unless chestcompressions prevent the ventilator from deliveringadequate tidal volumes. In this case, theventilator is usually substituted for a ventilationbag, which can itself be left connected ordetached and removed to a distance of at least1 m. If the ventilator tubing is disconnected,ensure it is kept at least 1 m from the patientor, better still, switch the ventilator off; modernventilators generate massive oxygen flowswhen disconnected. During normal use, whenconnected to a tracheal tube, oxygen from a ventilatorin the critical care unit will be vented fromthe main ventilator housing well away from thedefibrillation zone. Patients in the critical careunit may be dependent on positive end expiratorypressure (PEEP) to maintain adequate oxygenation;during cardioversion, when the spontaneouscirculation potentially enables blood to remainwell oxygenated, it is particularly appropriate toleave the critically ill patient connected to theventilator during shock delivery.• Minimise the risk of sparks during defibrillation.Theoretically, self-adhesive defibrillation padsare less likely to cause sparks than manual paddles.The technique for electrode contact withthe chestOptimal defibrillation technique aims to delivercurrent across the fibrillating myocardium in thepresence of minimal transthoracic impedance.Transthoracic impedance varies considerably withbody mass, but is approximately 70—80 inadults. 33,34 The techniques described below aim toplace external electrodes (paddles or self-adhesivepads) in an optimal position using techniques thatminimise transthoracic impedance.Shaving the chestPatients with a hairy chest have air trappingbeneath the electrode and poor electrode-to-skinelectrical contact. This causes high impedance,reduced defibrillation efficacy, risk of arcing(sparks) from electrode to skin and electrodeto electrode and is more likely to cause burnsto the patient’s chest. Rapid shaving of thearea of intended electrode placement may benecessary, but do not delay defibrillation if ashaver is not immediately available. Shaving thechest per se may reduce transthoracic impedanceslightly and has been recommended for elective DCcardioversion. 35Paddle forceIf using paddles, apply them firmly to the chestwall. This reduces transthoracic impedance byimproving electrical contact at the electrode—skininterface and reducing thoracic volume. 36 Thedefibrillator operator should always press firmlyon handheld electrode paddles, the optimal forcebeing 8 kg in adults 37 and 5 kg in children aged1—8 years when using adult paddles 38 ; 8-kg forcemay be attainable only by the strongest membersof the cardiac arrest team, and therefore itis recommended that these individuals apply thepaddles during defibrillation. Unlike self-adhesivepads, manual paddles have a bare metal plate thatrequires a conductive material placed between themetal and patient’s skin to improve electrical contact.Use of bare metal paddles alone creates hightransthoracic impedance and is likely to increasethe risk of arcing and to worsen cutaneous burnsfrom defibrillation.Electrode positionNo human studies have evaluated the electrodeposition as a determinant of return of spontaneouscirculation (ROSC) or survival from VF/VT cardiacarrest. Transmyocardial current during defibrillationis likely to be maximal when the electrodesare placed so that the area of the heart that is fibrillatinglies directly between them, i.e., ventriclesin VF/VT, atria in atrial fibrillation (AF). Therefore,the optimal electrode position may not be the samefor ventricular and atrial arrhythmias.More patients are presenting with implantablemedical devices (e.g., permanent pacemaker,automatic implantable cardioverter defibrillator(AICD)). MedicAlert bracelets are recommended forsuch patients. These devices may be damaged duringdefibrillation if current is discharged through

S28electrodes placed directly over the device. Placethe electrode away from the device or use an alternativeelectrode position as described below. Ondetecting VF/VT, AICD devices will discharge nomore than six times. Further discharges will occuronly if a new episode of VF/VT is detected. Rarely,a faulty device or broken lead may cause repeatedfiring; in these circumstances, the patient is likelyto be conscious, with the ECG showing a relativelynormal rate. A magnet placed over the AICD willdisable the defibrillation function in these circumstances.AICD discharge may cause pectoral musclecontraction, but an attendant touching the patientwill not receive an electric shock. AICD and pacingfunction should always be re-evaluated followingexternal defibrillation, both to check the deviceitself and to check pacing/defibrillation thresholdsof the device leads.Transdermal drug patches may prevent goodelectrode contact, causing arcing and burns if theelectrode is placed directly over the patch duringdefibrillation. 39,40 Remove medication patches andwipe the area before applying the electrode.For ventricular arrhythmias, place electrodes(either pads or paddles) in the conventionalsternal—apical position. The right (sternal) electrodeis placed to the right of the sternum, belowthe clavicle. The apical paddle is placed in the midaxillaryline, approximately level with the V6 ECGelectrode or female breast. This position shouldbe clear of any breast tissue. It is important thatthis electrode is placed sufficiently laterally. Otheracceptable pad positions include:• each electrode on the lateral chest wall, oneon the right and the other on the left side (biaxillary);• one electrode in the standard apical position andthe other on the right or left upper back;• one electrode anteriorly, over the left precordium,and the other electrode posterior to theheart just inferior to the left scapula.It does not matter which electrode (apex/sternum) is placed in either position.Transthoracic impedance has been shown to beminimised when the apical electrode is not placedover the female breast. 41 Asymmetrically shapedapical electrodes have a lower impedance whenplaced longitudinally rather than transversely. 42The long axis of the apical paddle should thereforebe orientated in a craniocaudal direction.Atrial fibrillation is maintained by functionalre-entry circuits anchored in the left atrium. Asthe left atrium is located posteriorly in the thorax,an anteroposterior electrode position may bemore efficient for external cardioversion of atrialC.D. Deakin, J.P. Nolanfibrillation. 43 Most, 44,45 but not all, 46,47 studieshave shown that anteroposterior electrode placementis more effective than the traditional anteroapicalposition in elective cardioversion of atrialfibrillation. Efficacy of cardioversion may be lessdependent on electrode position when using biphasicimpedance-compensated waveforms. 48 Eitherposition is safe and effective for cardioversion ofatrial arrhythmias.Respiratory phaseTransthoracic impedance varies during respiration,being minimal at end expiration. If possible, defibrillationshould be attempted at this phase ofthe respiratory cycle. Positive end-expiratory pressure(PEEP) increases transthoracic impedance andshould be minimised during defibrillation. Auto-PEEP (gas trapping) may be particularly high inasthmatics and may necessitate higher than usualenergy levels for defibrillation. 49Electrode sizeThe Association for the Advancement of MedicalInstrumentation recommends a minimum electrodesize of for individual electrodes and thesum of the electrode areas should be a minimumof 150 cm 2 . 50 Larger electrodes have lowerimpedance, but excessively large electrodes mayresult in less transmyocardial current flow. 51 Foradult defibrillation, both handheld paddle electrodesand self-adhesive pad electrodes 8—12 cmin diameter are used and function well. Defibrillationsuccess may be higher with electrodesof 12-cm diameter compared with those of 8-cmdiameter. 34,52Standard AEDs are suitable for use in childrenover the age of 8 years. In children between 1 and8 years, use paediatric pads with an attenuatorto reduce delivered energy, or a paediatric mode,if they are available; if not, use the unmodifiedmachine, taking care to ensure that the adult padsdo not overlap. Use of AEDs is not recommended inchildren less than 1 year.Coupling agentsIf using manual paddles, gel pads are preferableto electrode pastes and gels because the lattercan spread between the two paddles, creating thepotential for a spark. Do not use bare electrodeswithout a coupling material, because this causeshigh transthoracic impedance and may increase theseverity of any cutaneous burns. Do not use medicalgels or pastes of poor electrical conductivity

European Resuscitation Council Guidelines for Resuscitation 2005S29(e.g., ultrasound gel). Electrode pads are preferredto electrode gel because they avoid the risk ofsmearing gel between the two paddles and the subsequentrisk of arcing and ineffective defibrillation.Pads versus paddlesSelf-adhesive defibrillation pads are safe and effectiveand are preferable to standard defibrillationpaddles. 52 Consideration should be given to useof self-adhesive pads in peri-arrest situations andin clinical situations where patient access is difficult.They have a similar transthoracic impedance 51(and therefore efficacy) 53,54 to manual paddles,and enable the operator to defibrillate the patientfrom a safe distance rather than leaning over thepatient (as occurs with paddles). When used for initialmonitoring of a rhythm, both pads and paddlesenable quicker delivery of the first shock comparedwith standard ECG electrodes, but pads are quickerthan paddles. 55When gel pads are used with paddles, the electrolytegel becomes polarised and thus is a poorconductor after defibrillation. This can cause spuriousasystole that may persist for 3—4 min whenused to monitor the rhythm; a phenomenon notreported with self-adhesive pads. 56,57 When usinga gel pad/paddle combination, confirm a diagnosisof asystole with independent ECG electrodes ratherthan the paddles.Fibrillation waveform analysisIt is possible to predict, with varying reliability,the success of defibrillation from the fibrillationwaveform. 58—77 If optimal defibrillation waveformsand the optimal timing of shock delivery can bedetermined in prospective studies, it should be possibleto prevent the delivery of unsuccessful highenergyshocks and minimise myocardial injury. Thistechnology is under active development and investigation.CPR versus defibrillation as the initialtreatmentAlthough the previous guidelines have recommendedimmediate defibrillation for all shockablerhythms, recent evidence has suggested that aperiod of CPR before defibrillation may be beneficialafter prolonged collapse. In clinical studieswhere response times exceeded 4—5 min, a periodof 1.5—3 min of CPR by paramedics or EMS physiciansbefore shock delivery improved ROSC, survivalto hospital discharge 78,79 and 1-year survival 79for adults with out-of-hospital VF or VT, comparedwith immediate defibrillation. In contrast, a singlerandomised study in adults with out-of-hospitalVF or VT failed to show improvements in ROSC orsurvival following 1.5 min of paramedic CPR. 80 Inanimal studies of VF lasting at least 5 min, CPRbefore defibrillation improved haemodynamics andsurvival. 81—83 It may not be possible to extrapolatethe outcomes achieved by paramedic-providedCPR, which includes intubation and delivery of 100%oxygen, 79 to those that may be achieved by laypeopleproviding relative poor-quality CPR with mouthto-mouthventilation.It is reasonable for EMS personnel to give a periodof about 2 min of CPR (i.e., about five cycles at30:2) before defibrillation in patients with prolongedcollapse (>5 min). The duration of collapseis frequently difficult to estimate accurately, and itmay be simplest if EMS personnel are instructed toprovide this period of CPR before attempted defibrillationin any cardiac arrest they have not witnessed.Given the relatively weak evidence available,individual EMS directors should determinewhether to implement a CPR-before-defibrillationstrategy; inevitably, protocols will vary dependingon the local circumstances.Laypeople and first responders using AEDS shoulddeliver the shock as soon as possible.There is no evidence to support or refute CPRbefore defibrillation for in-hospital cardiac arrest.We recommend shock delivery as soon as possiblefollowing in-hospital cardiac arrest (see Section 4band c).The importance of early uninterrupted externalchest compression is emphasised throughout theseguidelines. In practice, it is often difficult to ascertainthe exact time of collapse and, in any case,CPR should be started as soon as possible. The rescuerproviding chest compressions should interruptchest compressions only for rhythm analysis andshock delivery, and should be prepared to resumechest compressions as soon as a shock is delivered.When two rescuers are present, the rescuer operatingthe AED should apply the electrodes while CPRis in progress. Interrupt CPR only when it is necessaryto assess the rhythm and deliver a shock.The AED operator should be prepared to deliver ashock as soon as analysis is complete and the shockis advised, ensuring all rescuers are not in contactwith the victim. The single rescuer should practicecoordination of CPR with efficient AED operation.One-shock versus three-shock sequenceThere are no published human or animal studiescomparing a single-shock protocol with a three-

S30stacked-shock protocol for treatment of VF cardiacarrest. Animal studies show that relativelyshort interruptions in external chest compressionto deliver rescue breaths 84,85 or perform rhythmanalysis 86 are associated with post-resuscitationmyocardial dysfunction and reduced survival.Interruptions in external chest compression alsoreduce the chances of converting VF to anotherrhythm. 87 Analysis of CPR performance during outof-hospital16,88 and in-hospital 17 cardiac arrest hasshown that significant interruptions are common,with external chest compressions comprising nomore than 51% 16 to 76% 17 of total CPR time.In the context of a three-shock protocol beingrecommended in the 2000 guidelines, interruptionsin CPR to enable rhythm analysis by AEDs weresignificant. Delays of up to 37 s between deliveryof shocks and recommencing chest compressionshave been reported. 89 With first shock efficacy ofbiphasic waveforms exceeding 90%, 90—93 failure tocardiovert VF successfully is more likely to suggestthe need for a period of CPR rather than a furthershock. Thus, immediately after giving a singleshock, and without reassessing the rhythm or feelingfor a pulse, resume CPR (30 compressions:2 ventilations)for 2 min before delivering another shock(if indicated) (see Section 4c). Even if the defibrillationattempt is successful in restoring a perfusingrhythm, it is very rare for a pulse to be palpableimmediately after defibrillation, and the delay intrying to palpate a pulse will further compromisethe myocardium if a perfusing rhythm has not beenrestored. 89 In one study of AEDs in out-of-hospitalVF cardiac arrest, a pulse was detected in only 2.5%(12/481) of patients with the initial post shock pulsecheck, though a pulse was detected sometime afterthe initial shock sequence (and before a secondshock sequence) in 24.5% (118/481) of patients. 93 Ifa perfusing rhythm has been restored, giving chestcompressions does not increase the chance of VFrecurring. 94 In the presence of post-shock asystolechest compressions may induce VF. 94This single shock strategy is applicable to bothmonophasic and biphasic defibrillators.Figure 3.1(MDS).C.D. Deakin, J.P. NolanMonophasic damped sinusoidal waveformof repetitive shocks, which in turn limits myocardialdamage. 95After a cautious introduction a decade ago,defibrillators delivering a shock with a biphasicwaveform are now preferred. Monophasic defibrillatorsare no longer manufactured, although manyremain in use. Monophasic defibrillators deliver currentthat is unipolar (i.e., one direction of currentflow). There are two main types of monophasicwaveform. The commonest waveform is themonophasic damped sinusoidal (MDS) waveform(Figure 3.1) which gradually returns to zero currentflow. The monophasic truncated exponential (MTE)waveform is electronically terminated before currentflow reaches zero (Figure 3.2). Biphasic defibrillators,in contrast, deliver current that flows ina positive direction for a specified duration beforereversing and flowing in a negative direction for theremaining milliseconds of the electrical discharge.There are two main types of biphasic waveform: thebiphasic truncated exponential (BTE) (Figure 3.3)and rectilinear biphasic (RLB) (Figure 3.4). Biphasicdefibrillators compensate for the wide variationsin transthoracic impedance by electronicallyWaveforms and energy levelsDefibrillation requires the delivery of sufficientelectrical energy to defibrillate a critical mass ofmyocardium, abolish the wavefronts of VF andenable restoration of spontaneous synchronisedelectrical activity in the form of an organisedrhythm. The optimal energy for defibrillation isthat which achieves defibrillation while causing theminimum of myocardial damage. 33 Selection of anappropriate energy level also reduces the numberFigure 3.2 Monophasic truncated exponential waveform(MTE).

European Resuscitation Council Guidelines for Resuscitation 2005S31Figure 3.3(BTE).Biphasic truncated exponential waveformadjusting the waveform magnitude and duration.The optimal ratio of first-phase to second-phaseduration and leading-edge amplitude has not beenestablished. Whether different waveforms have differingefficacy for VF of differing durations is alsounknown.All manual defibrillators and AEDs that allowmanual override of energy levels should be labelledto indicate their waveform (monophasic or biphasic)and recommended energy levels for attempteddefibrillation of VF/VT. First-shock efficacy forlong-duration VF/VT is greater with biphasic thanmonophasic waveforms, 96—98 and therefore use ofthe former is recommended whenever possible.Optimal energy levels for both monophasic andbiphasic waveforms are unknown. The recommendationsfor energy levels are based on a consensusfollowing careful review of the current literature.Although energy levels are selected for defibrillation,it is the transmyocardial current flow thatachieves defibrillation. Current correlates well withthe successful defibrillation and cardioversion. 99Figure 3.4Rectilinear biphasic waveform (RLB).The optimal current for defibrillation using amonophasic waveform is in the range of 30—40 A.Indirect evidence from measurements during cardioversionfor atrial fibrillation suggest that the currentduring defibrillation using biphasic waveformsis in the range of 15—20 A. 100 Future technologymay enable defibrillators to discharge according totransthoracic current: a strategy that may lead togreater consistency in shock success. Peak currentamplitude, average current and phase duration allneed to be studied to determine optimal values,and manufacturers are encouraged to explore furtherthis move from energy-based to current-baseddefibrillation.First shockFirst-shock efficacy for long-duration cardiac arrestusing monophasic defibrillation has been reportedas 54%—63% for a 200-J monophasic truncatedexponential (MTE) waveform 97,101 and 77%—91%using a 200-J monophasic damped sinusoidal (MDS)waveform. 96—98,101 Because of the lower efficacyof this waveform, the recommended initial energylevel for the first shock using a monophasic defibrillatoris 360 J. Although higher energy levels riska greater degree of myocardial injury, the benefitsof earlier conversion to a perfusing rhythm areparamount. Atrioventricular block is more commonwith higher monophasic energy levels, but is generallytransient and has been shown not to affectsurvival to hospital discharge. 102 Only 1 of 27 animalstudies demonstrated harm caused by attempteddefibrillation using high-energy shocks. 103There is no evidence that one biphasic waveformor device is more effective than another. Firstshockefficacy of the BTE waveform using 150—200 Jhas been reported as 86%—98%. 96,97,101,104,105 Firstshockefficacy of the RLB waveform using 120 J is upto 85% (data not published in the paper but suppliedby personnel communication). 98 The initialbiphasic shock should be no lower than 120 J forRLB waveforms and 150 J for BTE waveforms. Ideally,the initial biphasic shock energy should be atleast 150 J for all waveforms.Manufacturers should display the effective waveformdose range on the face of the biphasic device.If the provider is unaware of the effective doserange of the device, use a dose of 200 J for thefirst shock. This 200 J default energy has been chosenbecause it falls within the reported range ofselected doses that are effective for first and subsequentbiphasic shocks and can be provided by everybiphasic manual defibrillator available today. It isa consensus default dose and not a recommendedideal dose. If biphasic devices are clearly labelled

S32and providers are familiar with the devices they usein clinical care, there will be no need for the default200 J dose. Ongoing research is necessary to firmlyestablish the most appropriate initial settings forboth monophasic and biphasic defibrillators.Second and subsequent shocksWith monophasic defibrillators, if the initial shockhas been unsuccessful at 360 J, second and subsequentshocks should all be delivered at 360 J.With biphasic defibrillators there is no evidence tosupport either a fixed or escalating energy protocol.Both strategies are acceptable; however, if thefirst shock is not successful and the defibrillator iscapable of delivering shocks of higher energy, itis rational to increase the energy for subsequentshocks. If the provider is unaware of the effectivedose range of the biphasic device and has used thedefault 200 J dose for the first shock, use eitheran equal or higher dose for second or subsequentshocks, depending on the capabilities of the device.If a shockable rhythm (recurrent ventricular fibrillation)recurs after successful defibrillation (withor without ROSC), give the next shock with theenergy level that had previously been successful.Other related defibrillation topicsDefibrillation of childrenCardiac arrest is less common in children. Aetiologyis generally related to hypoxia and trauma. 106—108VF is relatively rare compared with adult cardiacarrest, occurring in 7%—15% of paediatric and adolescentarrests. 108—112 Common causes of VF inchildren include trauma, congenital heart disease,long QT interval, drug overdose and hypothermia.Rapid defibrillation of these patients may improveoutcome. 112,113The optimal energy level, waveform and shocksequence are unknown but, as with adults, biphasicshocks appear to be at least as effective as,and less harmful than, monophasic shocks. 114—116The upper limit for safe defibrillation is unknown,but doses in excess of the previously recommendedmaximum of 4 J kg −1 (as high as 9 J kg −1 ) havedefibrillated children effectively without significantadverse effects. 20,117,118 The recommendedenergy level for manual monophasic defibrillationis 4Jkg −1 for the initial shock and for subsequentshocks. The same energy level is recommended formanual biphasic defibrillation. 119 As with adults, ifa shockable rhythm recurs, use the energy level fordefibrillation that had previously been successful.Blind defibrillationC.D. Deakin, J.P. NolanDelivery of shocks without a monitor or an ECGrhythm diagnosis is referred to as ‘‘blind’’ defibrillation.Blind defibrillation is unnecessary. Handheldpaddles with ‘‘quick-look’’ monitoring capabilitieson modern manually operated defibrillators arewidely available. AEDs use reliable and proven decisionalgorithms to identify VF.Spurious asystole and occult ventricularfibrillationRarely, coarse VF can be present in some leads, withvery small undulations seen in the orthogonal leads,which is called occult VF. A flat line that may resembleasystole is displayed; examine the rhythm intwo leads to obtain the correct diagnosis. Of moreimportance, one study noted that spurious asystole,a flat line produced by technical errors (e.g., nopower, leads unconnected, gain set to low, incorrectlead selection, or polarisation of electrolytegel (see above)), was far more frequent than occultVF. 120There is no evidence that attempting to defibrillatetrue asystole is beneficial. Studies inchildren 121 and adults 122 have failed to show benefitfrom defibrillation of asystole. On the contrary,repeated shocks will cause myocardial injury.Precordial thumpThere are no prospective studies that evaluateuse of precordial (chest) thump. The rationale forgiving a thump is that the mechanical energy ofthe thump is converted to electrical energy, whichmay be sufficient to achieve cardioversion. 123The electrical threshold of successful defibrillationincreases rapidly after the onset of the arrhythmia,and the amount of electrical energy generated fallsbelow this threshold within seconds. A precordialthump is most likely to be successful in convertingVT to sinus rhythm. Successful treatment ofVF by precordial thump is much less likely: in allthe reported successful cases, the precordial thumpwas given within the first 10 s of VF. 123 Althoughthree case series 124—126 reported that VF or pulselessVT was converted to a perfusing rhythm bya precordial thump, there are occasional reportsof thump causing deterioration in cardiac rhythm,such as rate acceleration of VT, conversion of VTinto VF, complete heart block or asystole. 125,127—132Consider giving a single precordial thump whencardiac arrest is confirmed rapidly after a witnessed,sudden collapse and a defibrillator is notimmediately to hand. These circumstances are

European Resuscitation Council Guidelines for Resuscitation 2005S33most likely to occur when the patient is monitored.Precordial thump should be undertaken immediatelyafter confirmation of cardiac arrest and onlyby healthcare professionals trained in the technique.Using the ulnar edge of a tightly clenchedfist, a sharp impact is delivered to the lower half ofthe sternum from a height of about 20 cm, followedby immediate retraction of the fist, which createsan impulse-like stimulus.CardioversionIf electrical cardioversion is used to convert atrialor ventricular tachyarrhythmias, the shock must besynchronised to occur with the R wave of the electrocardiogramrather than with the T wave: VF canbe induced if a shock is delivered during the relativerefractory portion of the cardiac cycle. 133Synchronisation can be difficult in VT because ofthe wide-complex and variable forms of ventriculararrhythmia. If synchronisation fails, give unsynchronisedshocks to the unstable patient in VT to avoidprolonged delay in restoring sinus rhythm. Ventricularfibrillation or pulseless VT requires unsynchronisedshocks. Conscious patients must be anaesthetisedor sedated before attempting synchronisedcardioversion.Atrial fibrillationBiphasic waveforms are more effective thanmonophasic waveforms for cardioversion ofAF 100,134,135 ; when available, use a biphasic defibrillatorin preference to a monophasic defibrillator.Monophasic waveformsA study of electrical cardioversion for atrial fibrillationindicated that 360-J MDS shocks weremore effective than 100-J or 200-J MDS shocks. 136Although a first shock of 360-J reduces overallenergy requirements for cardioversion, 360 J maycause greater myocardial damage than occurs withlower monophasic energy levels, and this must betaken into consideration. Commence cardioversionof atrial fibrillation using an initial energy level of200 J, increasing in a stepwise manner as necessary.Biphasic waveformsMore data are needed before specific recommendationscan be made for optimal biphasic energylevels. First-shock efficacy of a 70-J biphasic waveformhas been shown to be significantly greater thanthat with a 100-monophasic waveform. 100,134,135 Arandomised study comparing escalating monophasicenergy levels to 360 J and biphasic energy levels to200 J found no difference in efficacy between thetwo waveforms. 137 An initial shock of 120—150 J,escalating if necessary, is a reasonable strategybased on current data.Atrial flutter and paroxysmalsupraventricular tachycardiaAtrial flutter and paroxysmal SVT generallyrequire less energy than atrial fibrillation forcardioversion. 138 Give an initial shock of 100-Jmonophasic or 70—120 J biphasic waveform. Givesubsequent shocks using stepwise increases inenergy. 99Ventricular tachycardiaThe energy required for cardioversion of VTdepends on the morphological characteristics andrate of the arrhythmia. 139 Ventricular tachycardiawith a pulse responds well to cardioversion usinginitial monophasic energies of 200 J. Use biphasicenergy levels of 120—150 J for the initial shock.Give stepwise increases if the first shock fails toachieve sinus rhythm. 139PacingConsider pacing in patients with symptomaticbradycardia refractory to anticholinergic drugs orother second-line therapy (see Section 4f). Immediatepacing is indicated, especially when the block isat or below the His—Purkinje level. If transthoracicpacing is ineffective, consider transvenous pacing.Whenever a diagnosis of asystole is made, check theECG carefully for the presence of P waves, becausethis may respond to cardiac pacing. Do not attemptpacing for asystole; it does not increase short-termor long-term survival in or out of hospital. 140—148References1. American Heart Association in collaboration with InternationalLiaison Committee on Resuscitation. Guidelines2000 for Cardiopulmonary Resuscitation and EmergencyCardiovascular Care, Part 6: Advanced CardiovascularLife Support: Section 2: Defibrillation. Circulation2000;102(Suppl.):I90—4.2. Larsen MP, Eisenberg MS, Cummins RO, Hallstrom AP.Predicting survival from out-of-hospital cardiac arrest: agraphic model. Ann Emerg Med 1993;22:1652—8.3. Valenzuela TD, Roe DJ, Cretin S, Spaite DW, LarsenMP. Estimating effectiveness of cardiac arrest interventions:a logistic regression survival model. Circulation1997;96:3308—13.

S34C.D. Deakin, J.P. Nolan4. Waalewijn RA, de Vos R, Tijssen JGP, Koster RW. Survivalmodels for out-of-hospital cardiopulmonary resuscitationfrom the perspectives of the bystander, the first responder,and the paramedic. Resuscitation 2001;51:113—22.5. Myerburg RJ, Fenster J, Velez M, et al. Impact ofcommunity-wide police car deployment of automatedexternal defibrillators on survival from out-of-hospital cardiacarrest. Circulation 2002;106:1058—64.6. Capucci A, Aschieri D, Piepoli MF, Bardy GH, IconomuE, Arvedi M. Tripling survival from sudden cardiacarrest via early defibrillation without traditional educationin cardiopulmonary resuscitation. Circulation2002;106:1065—70.7. van Alem AP, Vrenken RH, de Vos R, Tijssen JG, Koster RW.Use of automated external defibrillator by first respondersin out of hospital cardiac arrest: prospective controlledtrial. BMJ 2003;327:1312.8. Valenzuela TD, Bjerke HS, Clark LL, et al. Rapid defibrillationby nontraditional responders: the Casino Project. AcadEmerg Med 1998;5:414—5.9. Swor RA, Jackson RE, Cynar M, et al. Bystander CPR,ventricular fibrillation, and survival in witnessed, unmonitoredout-of-hospital cardiac arrest. Ann Emerg Med1995;25:780—4.10. Holmberg M, Holmberg S, Herlitz J. Effect of bystandercardiopulmonary resuscitation in out-of-hospital cardiacarrest patients in Sweden. Resuscitation 2000;47:59—70.11. Monsieurs KG, Handley AJ, Bossaert LL. European ResuscitationCouncil Guidelines 2000 for Automated ExternalDefibrillation. A statement from the Basic Life Support andAutomated External Defibrillation Working Group (1) andapproved by the Executive Committee of the EuropeanResuscitation Council. Resuscitation 2001;48:207—9.12. Cummins RO, Eisenberg M, Bergner L, Murray JA. Sensitivityaccuracy, and safety of an automatic external defibrillator.Lancet 1984;2:318—20.13. Davis EA, Mosesso Jr VN. Performance of police firstresponders in utilizing automated external defibrillationon victims of sudden cardiac arrest. Prehosp Emerg Care1998;2:101—7.14. White RD, Vukov LF, Bugliosi TF. Early defibrillation bypolice: initial experience with measurement of criticaltime intervals and patient outcome. Ann Emerg Med1994;23:1009—13.15. White RD, Hankins DG, Bugliosi TF. Seven years’ experiencewith early defibrillation by police and paramedicsin an emergency medical services system. Resuscitation1998;39:145—51.16. Wik L, Kramer-Johansen J, Myklebust H, et al. Quality ofcardiopulmonary resuscitation during out-of-hospital cardiacarrest. JAMA 2005;293:299—304.17. Abella BS, Alvarado JP, Myklebust H, et al. Quality ofcardiopulmonary resuscitation during in-hospital cardiacarrest. JAMA 2005;293:305—10.18. Kerber RE, Becker LB, Bourland JD, et al. Automatic externaldefibrillators for public access defibrillation: recommendationsfor specifying and reporting arrhythmia analysisalgorithm performance, incorporating new waveforms,and enhancing safety. A statement for health professionalsfrom the American Heart Association Task Force on AutomaticExternal Defibrillation, Subcommittee on AED Safetyand Efficacy. Circulation 1997;95:1677—82.19. Dickey W, Dalzell GW, Anderson JM, Adgey AA. The accuracyof decision-making of a semi-automatic defibrillatorduring cardiac arrest. Eur Heart J 1992;13:608—15.20. Atkinson E, Mikysa B, Conway JA, et al. Specificity andsensitivity of automated external defibrillator rhythm analysisin infants and children. Ann Emerg Med 2003;42:185—96.21. Cecchin F, Jorgenson DB, Berul CI, et al. Is arrhythmiadetection by automatic external defibrillator accurate forchildren? Sensitivity and specificity of an automatic externaldefibrillator algorithm in 696 pediatric arrhythmias.Circulation 2001;103:2483—8.22. Zafari AM, Zarter SK, Heggen V, et al. A program encouragingearly defibrillation results in improved in-hospitalresuscitation efficacy. J Am Coll Cardiol 2004;44:846—52.23. Destro A, Marzaloni M, Sermasi S, Rossi F. Automatic externaldefibrillators in the hospital as well? Resuscitation1996;31:39—43.24. Domanovits H, Meron G, Sterz F, et al. Successful automaticexternal defibrillator operation by people trained only inbasic life support in a simulated cardiac arrest situation.Resuscitation 1998;39:47—50.25. Cusnir H, Tongia R, Sheka KP, et al. In hospital cardiacarrest: a role for automatic defibrillation. Resuscitation2004;63:183—8.26. Kaye W, Mancini ME, Richards N. Organizing and implementinga hospital-wide first-responder automated externaldefibrillation program: strengthening the in-hospitalchain of survival. Resuscitation 1995;30:151—6.27. Miller PH. Potential fire hazard in defibrillation. JAMA1972;221:192.28. Hummel IIIrd RS, Ornato JP, Weinberg SM, Clarke AM. Sparkgeneratingproperties of electrode gels used during defibrillation.A potential fire hazard. JAMA 1988;260:3021—4.29. Fires from defibrillation during oxygen administration.Health Devices 1994;23:307—9.30. Lefever J, Smith A. Risk of fire when using defibrillation inan oxygen enriched atmosphere. Medical Devices AgencySafety Notices 1995;3:1—3.31. Ward ME. Risk of fires when using defibrillators in an oxygenenriched atmosphere. Resuscitation 1996;31:173.32. Theodorou AA, Gutierrez JA, Berg RA. Fire attributableto a defibrillation attempt in a neonate. Pediatrics2003;112:677—9.33. Kerber RE, Kouba C, Martins J, et al. Advance prediction oftransthoracic impedance in human defibrillation and cardioversion:importance of impedance in determining thesuccess of low-energy shocks. Circulation 1984;70:303—8.34. Kerber RE, Grayzel J, Hoyt R, Marcus M, Kennedy J.Transthoracic resistance in human defibrillation. Influenceof body weight, chest size, serial shocks, paddle sizeand paddle contact pressure. Circulation 1981;63:676—82.35. Sado DM, Deakin CD, Petley GW, Clewlow F. Comparisonof the effects of removal of chest hair with not doing sobefore external defibrillation on transthoracic impedance.Am J Cardiol 2004;93:98—100.36. Deakin CD, Sado DM, Petley GW, Clewlow F. Differentialcontribution of skin impedance and thoracic volumeto transthoracic impedance during external defibrillation.Resuscitation 2004;60:171—4.37. Deakin C, Sado D, Petley G, Clewlow F. Determining theoptimal paddle force for external defibrillation. Am J Cardiol2002;90:812—3.38. Deakin C, Bennetts S, Petley G, Clewlow F. What is the optimalpaddle force for paediatric defibrillation? Resuscitation2002;55:59.39. Panacek EA, Munger MA, Rutherford WF, Gardner SF. Reportof nitropatch explosions complicating defibrillation. Am JEmerg Med 1992;10:128—9.40. Wrenn K. The hazards of defibrillation through nitroglycerinpatches. Ann Emerg Med 1990;19:1327—8.

European Resuscitation Council Guidelines for Resuscitation 2005S3541. Pagan-Carlo LA, Spencer KT, Robertson CE, Dengler A, BirkettC, Kerber RE. Transthoracic defibrillation: importanceof avoiding electrode placement directly on the femalebreast. J Am Coll Cardiol 1996;27:449—52.42. Deakin CD, Sado DM, Petley GW, Clewlow F. Is the orientationof the apical defibrillation paddle of importanceduring manual external defibrillation? Resuscitation2003;56:15—8.43. Kirchhof P, Borggrefe M, Breithardt G. Effect of electrodeposition on the outcome of cardioversion. Card ElectrophysiolRev 2003;7:292—6.44. Kirchhof P, Eckardt L, Loh P, et al. Anterior-posterior versusanterior-lateral electrode positions for external cardioversionof atrial fibrillation: a randomised trial. Lancet2002;360:1275—9.45. Botto GL, Politi A, Bonini W, Broffoni T, Bonatti R. Externalcardioversion of atrial fibrillation: role of paddle positionon technical efficacy and energy requirements. Heart1999;82:726—30.46. Alp NJ, Rahman S, Bell JA, Shahi M. Randomised comparisonof antero-lateral versus antero-posterior paddle positionsfor DC cardioversion of persistent atrial fibrillation. Int JCardiol 2000;75:211—6.47. Mathew TP, Moore A, McIntyre M, et al. Randomised comparisonof electrode positions for cardioversion of atrialfibrillation. Heart 1999;81:576—9.48. Walsh SJ, McCarty D, McClelland AJ, et al. Impedance compensatedbiphasic waveforms for transthoracic cardioversionof atrial fibrillation: a multi-centre comparison ofantero-apical and antero-posterior pad positions. Eur HeartJ 2005.49. Deakin CD, McLaren RM, Petley GW, Clewlow F, Dalrymple-Hay MJ. Effects of positive end-expiratory pressure ontransthoracic impedance—–implications for defibrillation.Resuscitation 1998;37:9—12.50. American National Standard: Automatic External Defibrillatorsand Remote Controlled Defibrillators (DF39). Arlington,Virgina: Association for the Advancement of MedicalInstrumentation; 1993.51. Deakin CD, McLaren RM, Petley GW, Clewlow F, Dalrymple-Hay MJ. A comparison of transthoracic impedance usingstandard defibrillation paddles and self-adhesive defibrillationpads. Resuscitation 1998;39:43—6.52. Stults KR, Brown DD, Cooley F, Kerber RE. Self-adhesivemonitor/defibrillation pads improve prehospital defibrillationsuccess. Ann Emerg Med 1987;16:872—7.53. Kerber RE, Martins JB, Kelly KJ, et al. Self-adhesive preappliedelectrode pads for defibrillation and cardioversion. JAm Coll Cardiol 1984;3:815—20.54. Kerber RE, Martins JB, Ferguson DW, et al. Experimentalevaluation and initial clinical application ofnew self-adhesive defibrillation electrodes. Int J Cardiol1985;8:57—66.55. Perkins GD, Roberts C, Gao F. Delays in defibrillation: influenceof different monitoring techniques. Br J Anaesth2002;89:405—8.56. Bradbury N, Hyde D, Nolan J. Reliability of ECG monitoringwith a gel pad/paddle combination after defibrillation.Resuscitation 2000;44:203—6.57. Chamberlain D. Gel pads should not be used for monitoringECG after defibrillation. Resuscitation 2000;43:159—60.58. Callaway CW, Sherman LD, Mosesso Jr VN, Dietrich TJ, HoltE, Clarkson MC. Scaling exponent predicts defibrillationsuccess for out-of-hospital ventricular fibrillation cardiacarrest. Circulation 2001;103:1656—61.59. Eftestol T, Sunde K, Aase SO, Husoy JH, Steen PA. Predictingoutcome of defibrillation by spectral characterizationand nonparametric classification of ventricular fibrillationin patients with out-of-hospital cardiac arrest. Circulation2000;102:1523—9.60. Eftestol T, Wik L, Sunde K, Steen PA. Effects of cardiopulmonaryresuscitation on predictors of ventricular fibrillationdefibrillation success during out-of-hospital cardiacarrest. Circulation 2004;110:10—5.61. Weaver WD, Cobb LA, Dennis D, Ray R, Hallstrom AP, CopassMK. Amplitude of ventricular fibrillation waveform and outcomeafter cardiac arrest. Ann Intern Med 1985;102:53—5.62. Brown CG, Dzwonczyk R. Signal analysis of the human electrocardiogramduring ventricular fibrillation: frequencyand amplitude parameters as predictors of successful countershock.Ann Emerg Med 1996;27:184—8.63. Callaham M, Braun O, Valentine W, Clark DM, Zegans C. Prehospitalcardiac arrest treated by urban first-responders:profile of patient response and prediction of outcomeby ventricular fibrillation waveform. Ann Emerg Med1993;22:1664—77.64. Strohmenger HU, Lindner KH, Brown CG. Analysis ofthe ventricular fibrillation ECG signal amplitude and frequencyparameters as predictors of countershock successin humans. Chest 1997;111:584—9.65. Strohmenger HU, Eftestol T, Sunde K, et al. The predictivevalue of ventricular fibrillation electrocardiogram signalfrequency and amplitude variables in patients with outof-hospitalcardiac arrest. Anesth Analg 2001;93:1428—33.66. Podbregar M, Kovacic M, Podbregar-Mars A, Brezocnik M.Predicting defibrillation success by ‘genetic’ programmingin patients with out-of-hospital cardiac arrest. Resuscitation2003;57:153—9.67. Menegazzi JJ, Callaway CW, Sherman LD, et al. Ventricularfibrillation scaling exponent can guide timing of defibrillationand other therapies. Circulation 2004;109:926—31.68. Povoas HP, Weil MH, Tang W, Bisera J, Klouche K, BarbatsisA. Predicting the success of defibrillation by electrocardiographicanalysis. Resuscitation 2002;53:77—82.69. Noc M, Weil MH, Tang W, Sun S, Pernat A, Bisera J. Electrocardiographicprediction of the success of cardiac resuscitation.Crit Care Med 1999;27:708—14.70. Strohmenger HU, Lindner KH, Keller A, Lindner IM, PfenningerEG. Spectral analysis of ventricular fibrillation andclosed-chest cardiopulmonary resuscitation. Resuscitation1996;33:155—61.71. Noc M, Weil MH, Gazmuri RJ, Sun S, Biscera J, Tang W.Ventricular fibrillation voltage as a monitor of the effectivenessof cardiopulmonary resuscitation. J Lab Clin Med1994;124:421—6.72. Lightfoot CB, Nremt P, Callaway CW, et al. Dynamic natureof electrocardiographic waveform predicts rescue shockoutcome in porcine ventricular fibrillation. Ann Emerg Med2003;42:230—41.73. Marn-Pernat A, Weil MH, Tang W, Pernat A, Bisera J. Optimizingtiming of ventricular defibrillation. Crit Care Med2001;29:2360—5.74. Hamprecht FA, Achleitner U, Krismer AC, et al. Fibrillationpower, an alternative method of ECG spectral analysisfor prediction of countershock success in a porcine modelof ventricular fibrillation. Resuscitation 2001;50:287—96.75. Amann A, Achleitner U, Antretter H, et al. Analysing ventricularfibrillation ECG-signals and predicting defibrillationsuccess during cardiopulmonary resuscitation employingN(alpha)-histograms. Resuscitation 2001;50:77—85.76. Brown CG, Griffith RF, Van Ligten P, et al. Medianfrequency—–a new parameter for predicting defibrillationsuccess rate. Ann Emerg Med 1991;20:787—9.

S3677. Amann A, Rheinberger K, Achleitner U, et al. The predictionof defibrillation outcome using a new combination ofmean frequency and amplitude in porcine models of cardiacarrest. Anesth Analg 2002;95:716—22.78. Cobb LA, Fahrenbruch CE, Walsh TR, et al. Influenceof cardiopulmonary resuscitation prior to defibrillation inpatients with out-of-hospital ventricular fibrillation. JAMA1999;281:1182—8.79. Wik L, Hansen TB, Fylling F, et al. Delaying defibrillation togive basic cardiopulmonary resuscitation to patients without-of-hospital ventricular fibrillation: a randomized trial.JAMA 2003;289:1389—95.80. Jacobs IG, Finn JC, Oxer HF, Jelinek GA. CPR before defibrillationin out-of-hospital cardiac arrest: a randomized trial.Emerg Med Australas 2005;17:39—45.81. Berg RA, Hilwig RW, Kern KB, Ewy GA. Precountershockcardiopulmonary resuscitation improves ventricular fibrillationmedian frequency and myocardial readiness for successfuldefibrillation from prolonged ventricular fibrillation:a randomized, controlled swine study. Ann Emerg Med2002;40:563—70.82. Berg RA, Hilwig RW, Ewy GA, Kern KB. Precountershockcardiopulmonary resuscitation improves initial responseto defibrillation from prolonged ventricular fibrillation:a randomized, controlled swine study. Crit Care Med2004;32:1352—7.83. Kolarova J, Ayoub IM, Yi Z, Gazmuri RJ. Optimal timing forelectrical defibrillation after prolonged untreated ventricularfibrillation. Crit Care Med 2003;31:2022—8.84. Berg RA, Sanders AB, Kern KB, et al. Adverse hemodynamiceffects of interrupting chest compressions forrescue breathing during cardiopulmonary resuscitationfor ventricular fibrillation cardiac arrest. Circulation2001;104:2465—70.85. Kern KB, Hilwig RW, Berg RA, Sanders AB, Ewy GA.Importance of continuous chest compressions duringcardiopulmonary resuscitation: improved outcome duringa simulated single lay-rescuer scenario. Circulation2002;105:645—9.86. Yu T, Weil MH, Tang W, et al. Adverse outcomes of interruptedprecordial compression during automated defibrillation.Circulation 2002;106:368—72.87. Eftestol T, Sunde K, Steen PA. Effects of interrupting precordialcompressions on the calculated probability of defibrillationsuccess during out-of-hospital cardiac arrest. Circulation2002;105:2270—3.88. Valenzuela TD, Kern KB, Clark LL, et al. Interruptionsof chest compressions during emergency medical systemsresuscitation. Circulation 2005;112:1259—65.89. van Alem AP, Sanou BT, Koster RW. Interruption of cardiopulmonaryresuscitation with the use of the automatedexternal defibrillator in out-of-hospital cardiac arrest. AnnEmerg Med 2003;42:449—57.90. Bain AC, Swerdlow CD, Love CJ, et al. Multicenter studyof principles-based waveforms for external defibrillation.Ann Emerg Med 2001;37:5—12.91. Poole JE, White RD, Kanz KG, et al. Low-energy impedancecompensatingbiphasic waveforms terminate ventricularfibrillation at high rates in victims of out-of-hospital cardiacarrest. LIFE Investigators. J Cardiovasc Electrophysiol1997;8:1373—85.92. Schneider T, Martens PR, Paschen H, et al. Multicenter,randomized, controlled trial of 150-J biphasic shocks comparedwith 200- to 360-J monophasic shocks in the resuscitationof out-of-hospital cardiac arrest victims. OptimizedResponse to Cardiac Arrest (ORCA) Investigators. Circulation2000;102:1780—7.C.D. Deakin, J.P. Nolan93. Rea TD, Shah S, Kudenchuk PJ, Copass MK, Cobb LA. Automatedexternal defibrillators: to what extent does the algorithmdelay CPR? Ann Emerg Med 2005;46:132—41.94. Hess EP, White RD. Ventricular fibrillation is not provokedby chest compression during post-shock organizedrhythms in out-of-hospital cardiac arrest. Resuscitation2005;66:7—11.95. Joglar JA, Kessler DJ, Welch PJ, et al. Effects of repeatedelectrical defibrillations on cardiac troponin I levels. Am JCardiol 1999;83:270—2. A6.96. van Alem AP, Chapman FW, Lank P, Hart AA, KosterRW. A prospective, randomised and blinded comparisonof first shock success of monophasic and biphasicwaveforms in out-of-hospital cardiac arrest. Resuscitation2003;58:17—24.97. Carpenter J, Rea TD, Murray JA, Kudenchuk PJ, EisenbergMS. Defibrillation waveform and post-shock rhythm in outof-hospitalventricular fibrillation cardiac arrest. Resuscitation2003;59:189—96.98. Morrison LJ, Dorian P, Long J, et al. Out-of-hospital cardiacarrest rectilinear biphasic to monophasic damped sinedefibrillation waveforms with advanced life support interventiontrial (ORBIT). Resuscitation 2005;66:149—57.99. Kerber RE, Martins JB, Kienzle MG, et al. Energy, current,and success in defibrillation and cardioversion: clinicalstudies using an automated impedance-based method ofenergy adjustment. Circulation 1988;77:1038—46.100. Koster RW, Dorian P, Chapman FW, Schmitt PW, O’GradySG, Walker RG. A randomized trial comparing monophasicand biphasic waveform shocks for external cardioversion ofatrial fibrillation. Am Heart J 2004;147:e20.101. Martens PR, Russell JK, Wolcke B, et al. Optimal Responseto Cardiac Arrest study: defibrillation waveform effects.Resuscitation 2001;49:233—43.102. Weaver WD, Cobb LA, Copass MK, Hallstrom AP. Ventriculardefibrillation: a comparative trial using 175-J and 320-Jshocks. N Engl J Med 1982;307:1101—6.103. Tang W, Weil MH, Sun S, et al. The effects ofbiphasic and conventional monophasic defibrillation onpostresuscitation myocardial function. J Am Coll Cardiol1999;34:815—22.104. Gliner BE, Jorgenson DB, Poole JE, et al. Treatment of outof-hospitalcardiac arrest with a low-energy impedancecompensatingbiphasic waveform automatic external defibrillator.The LIFE Investigators. Biomed Instrum Technol1998;32:631—44.105. White RD, Blackwell TH, Russell JK, Snyder DE, JorgensonDB. Transthoracic impedance does not affect defibrillation,resuscitation or survival in patients with out-of-hospitalcardiac arrest treated with a non-escalating biphasic waveformdefibrillator. Resuscitation 2005;64:63—9.106. Kuisma M, Suominen P, Korpela R. Paediatric out-of-hospitalcardiac arrests: epidemiology and outcome. Resuscitation1995;30:141—50.107. Sirbaugh PE, Pepe PE, Shook JE, et al. A prospective,population-based study of the demographics, epidemiology,management, and outcome of out-of-hospitalpediatric cardiopulmonary arrest. Ann Emerg Med1999;33:174—84.108. Hickey RW, Cohen DM, Strausbaugh S, Dietrich AM. Pediatricpatients requiring CPR in the prehospital setting. AnnEmerg Med 1995;25:495—501.109. Appleton GO, Cummins RO, Larson MP, Graves JR. CPR andthe single rescuer: at what age should you ‘‘call first’’rather than ‘‘call fast’’? Ann Emerg Med 1995;25:492—4.110. Ronco R, King W, Donley DK, Tilden SJ. Outcome and costat a children’s hospital following resuscitation for out-of-

European Resuscitation Council Guidelines for Resuscitation 2005S37hospital cardiopulmonary arrest. Arch Pediatr Adolesc Med1995;149:210—4.111. Losek JD, Hennes H, Glaeser P, Hendley G, Nelson DB.Prehospital care of the pulseless, nonbreathing pediatricpatient. Am J Emerg Med 1987;5:370—4.112. Mogayzel C, Quan L, Graves JR, Tiedeman D, FahrenbruchC, Herndon P. Out-of-hospital ventricular fibrillation in childrenand adolescents: causes and outcomes. Ann EmergMed 1995;25:484—91.113. Safranek DJ, Eisenberg MS, Larsen MP. The epidemiologyof cardiac arrest in young adults. Ann Emerg Med1992;21:1102—6.114. Berg RA, Chapman FW, Berg MD, et al. Attenuated adultbiphasic shocks compared with weight-based monophasicshocks in a swine model of prolonged pediatric ventricularfibrillation. Resuscitation 2004;61:189—97.115. Tang W, Weil MH, Jorgenson D, et al. Fixed-energy biphasicwaveform defibrillation in a pediatric model of cardiacarrest and resuscitation. Crit Care Med 2002;30:2736—41.116. Clark CB, Zhang Y, Davies LR, Karlsson G, Kerber RE. Pediatrictransthoracic defibrillation: biphasic versus monophasicwaveforms in an experimental model. Resuscitation2001;51:159—63.117. Gurnett CA, Atkins DL. Successful use of a biphasic waveformautomated external defibrillator in a high-risk child.Am J Cardiol 2000;86:1051—3.118. Atkins DL, Jorgenson DB. Attenuated pediatric electrodepads for automated external defibrillator use in children.Resuscitation 2005;66:31—7.119. Gutgesell HP, Tacker WA, Geddes LA, Davis S, Lie JT, McNamaraDG. Energy dose for ventricular defibrillation of children.Pediatrics 1976;58:898—901.120. Cummins RO, Austin Jr D. The frequency of ‘occult’ ventricularfibrillation masquerading as a flat line in prehospitalcardiac arrest. Ann Emerg Med 1988;17:813—7.121. Losek JD, Hennes H, Glaeser PW, Smith DS, Hendley G. Prehospitalcountershock treatment of pediatric asystole. AmJ Emerg Med 1989;7:571—5.122. Martin DR, Gavin T, Bianco J, et al. Initial countershock inthe treatment of asystole. Resuscitation 1993;26:63—8.123. Kohl P, King AM, Boulin C. Antiarrhythmic effects of acutemechanical stiumulation. In: Kohl P, Sachs F, Franz MR, editors.Cardiac mechano-electric feedback and arrhythmias:form pipette to patient. Philadelphia: Elsevier Saunders;2005. p. 304—14.124. Befeler B. Mechanical stimulation of the heart; its therapeuticvalue in tachyarrhythmias. Chest 1978;73:832—8.125. Volkmann HKA, Kühnert H, Paliege R, Dannberg G,Siegert K. Terminierung von Kammertachykardien durchmechanische Herzstimulation mit Präkordialschlägen.(‘‘Termination of Ventricular Tachycardias by MechanicalCardiac Pacing by Means of Precordial Thumps’’).Zeitschrift für Kardiologie 1990;79:717—24.126. Caldwell G, Millar G, Quinn E. Simple mechanical methodsfor cardioversion: Defence of the precordial thump andcough version. Br Med J 1985;291:627—30.127. Morgera T, Baldi N, Chersevani D, Medugno G, Camerini F.Chest thump and ventricular tachycardia. Pacing Clin Electrophysiol1979;2:69—75.128. Rahner E, Zeh E. Die Regularisierung von Kammertachykardiendurch präkordialen Faustschlag. (‘‘The Regularizationof Ventricular Tachycardias by Precordial Thumping’’).Medizinsche Welt 1978;29:1659—63.129. Gertsch M, Hottinger S, Hess T. Serial chest thumps for thetreatment of ventricular tachycardia in patients with coronaryartery disease. Clin Cardiol 1992;15:181—8.130. Krijne R. Rate acceleration of ventricular tachycardia aftera precordial chest thump. Am J Cardiol 1984;53:964—5.131. Sclarovsky S, Kracoff OH, Agmon J. Acceleration of ventriculartachycardia induced by a chest thump. Chest1981;80:596—9.132. Yakaitis RW, Redding JS. Precordial thumping during cardiacresuscitation. Crit Care Med 1973;1:22—6.133. Lown B. Electrical reversion of cardiac arrhythmias. BrHeart J 1967;29:469—89.134. Mittal S, Ayati S, Stein KM, et al. Transthoracic cardioversionof atrial fibrillation: comparison of rectilinear biphasicversus damped sine wave monophasic shocks. Circulation2000;101:1282—7.135. Page RL, Kerber RE, Russell JK, et al. Biphasic versusmonophasic shock waveform for conversion of atrial fibrillation:the results of an international randomized, doubleblindmulticenter trial. J Am Coll Cardiol 2002;39:1956—63.136. Joglar JA, Hamdan MH, Ramaswamy K, et al. Initial energyfor elective external cardioversion of persistent atrial fibrillation.Am J Cardiol 2000;86:348—50.137. Alatawi F, Gurevitz O, White R. Prospective, randomizedcomparison of two biphasic waveforms for the efficacy andsafety of transthoracic biphasic cardioversion of atrial fibrillation.Heart Rhythm 2005;2:382—7.138. Pinski SL, Sgarbossa EB, Ching E, Trohman RG. A comparisonof 50-J versus 100-J shocks for direct-current cardioversionof atrial flutter. Am Heart J 1999;137:439—42.139. Kerber RE, Kienzle MG, Olshansky B, et al. Ventriculartachycardia rate and morphology determine energy andcurrent requirements for transthoracic cardioversion. Circulation1992;85:158—63.140. Hedges JR, Syverud SA, Dalsey WC, Feero S, Easter R, ShultzB. Prehospital trial of emergency transcutaneous cardiacpacing. Circulation 1987;76:1337—43.141. Barthell E, Troiano P, Olson D, Stueven HA, Hendley G. Prehospitalexternal cardiac pacing: a prospective, controlledclinical trial. Ann Emerg Med 1988;17:1221—6.142. Cummins RO, Graves JR, Larsen MP, et al. Out-of-hospitaltranscutaneous pacing by emergency medical techniciansin patients with asystolic cardiac arrest. N Engl J Med1993;328:1377—82.143. Ornato JP, Peberdy MA. The mystery of bradyasystoleduring cardiac arrest. Ann Emerg Med 1996;27:576—87.144. Niemann JT, Adomian GE, Garner D, Rosborough JP. Endocardialand transcutaneous cardiac pacing, calcium chloride,and epinephrine in postcountershock asystole andbradycardias. Crit Care Med 1985;13:699—704.145. Quan L, Graves JR, Kinder DR, Horan S, Cummins RO.Transcutaneous cardiac pacing in the treatment of outof-hospitalpediatric cardiac arrests. Ann Emerg Med1992;21:905—9.146. Dalsey WC, Syverud SA, Hedges JR. Emergency departmentuse of transcutaneous pacing for cardiac arrests. Crit CareMed 1985;13:399—401.147. Knowlton AA, Falk RH. External cardiac pacing during inhospitalcardiac arrest. Am J Cardiol 1986;57:1295—8.148. Ornato JP, Carveth WL, Windle JR. Pacemaker insertion forprehospital bradyasystolic cardiac arrest. Ann Emerg Med1984;13:101—3.

Resuscitation (2005) 67S1, S39—S86European Resuscitation Council Guidelines forResuscitation 2005Section 4. Adult advanced life supportJerry P. Nolan, Charles D. Deakin, Jasmeet Soar,Bernd W. Böttiger, Gary Smith4a. Prevention of in-hospital cardiacarrestThe problemThis new section of the guidelines stresses theimportance of preventing in-hospital cardiac arrest.Fewer than 20% of patients suffering an in-hospitalcardiac arrest will survive to go home. 1,2 Most survivorshave a witnessed and monitored VF arrest,primary myocardial ischaemia as the cause, andreceive immediate defibrillation.Cardiac arrest in patients in unmonitored wardareas is not usually a sudden unpredictable event,nor is it usually caused by primary cardiac disease.These patients often have slow and progressivephysiological deterioration, involving hypoxia andhypotension, that is unnoticed by staff, or is recognisedbut poorly treated. 3,4 The underlying cardiacarrest rhythm in this group is usually non-shockableand survival to hospital discharge is very poor. 1,5The records of patients who have a cardiacarrest or unanticipated intensive care unit (ICU)admission often contain evidence of unrecognised,or untreated, breathing and circulationproblems. 3,4,6—8 The ACADEMIA study showedE-mail address: jerry.nolan@ukgateway.net (J.P. Nolan).antecedents in 79% of cardiac arrests, 55% of deathsand 54% of unanticipated ICU admissions. 4 Early andeffective treatment of seriously ill patients mightprevent some cardiac arrests, deaths and unanticipatedICU admissions. A third of patients who havea false cardiac arrest call die subsequently. 9Nature of the deficiencies in acute careThese often involve simple aspects of care including:the failure to treat abnormalities of thepatient’s airway, breathing and circulation, incorrectuse of oxygen therapy, failure to monitorpatients, failure to involve experienced seniorstaff, poor communication, lack of teamwork andinsufficient use of treatment limitation plans. 3,7Several studies show that medical and nursingstaff lack knowledge and skills in acute care.For example, trainee doctors may lack knowledgeabout oxygen therapy, 10 fluid and electrolytebalance, 11 analgesia, 12 issues of consent, 13 pulseoximetry 14 and drug doses. 15 Medical studentsmay be unable to recognise abnormal breathingpatterns. 16 Medical school training provides poorpreparation for doctors’ early careers, and fails toteach them the essential aspects of applied physiologyand acute care. 17 There is also little to suggestthat the acute care training and knowledge of0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.doi:10.1016/j.resuscitation.2005.10.009

S40senior medical staff is better. 18,19 Staff often lackconfidence when dealing with acute care problems,and rarely use a systematic approach to the assessmentof critically ill patients. 20Recognising the critically ill patientIn general, the clinical signs of acute illness aresimilar whatever the underlying process, as theyreflect failing respiratory, cardiovascular and neurologicalsystems. Abnormal physiology is commonon general wards, 21 yet the measurementand recording of important physiological observationsof sick patients occurs less frequently thanis desirable. 3,4,8 This is surprising, as respiratoryrate abnormalities may predict cardiorespiratoryarrest. 22 To assist in the early detection of criticalillness, many hospitals now use early warningscores (EWS) or calling criteria. 23—25 Early warningscoring systems allocate points to routine vital signsmeasurements on the basis of their derangementfrom an arbitrarily agreed ‘normal’ range. 23—25 Theweighted score of one or more vital sign observations,or the total EWS, may be used to suggestincreasing the frequency of vital signs monitoring tonurses, or to call ward doctors or critical care outreachteams to the patient. Alternatively, systemsincorporating ‘calling criteria’ are based on routineobservations, which activate a response whenone or more variables reach an extremely abnormalvalue. 23,26 There are no data to establish the superiorityof one system over another, but it may bepreferable to use an EWS system, which can trackchanges in physiology and warn of impending physiologicalcollapse, rather than the ‘‘calling criteria’’approach, which is triggered only when an extremevalue of physiology has been reached.There is a clinical rationale to the use of EWSor calling criteria systems to identify sick patientsearly. However, their sensitivity, specificity andaccuracy in predicting clinical outcomes has yet tobe validated convincingly. 27,28 Several studies haveidentified abnormalities of heart rate, blood pressure,respiratory rate and conscious level as markersof impending critical events. 22,23,29 The suggestionthat their incidence has predictive value mustbe questioned, as not all important vital signs are,or can be, recorded continuously in general wardareas. Several studies show that charting of vitalsigns is poor, with gaps in data recording. 3,4,8,30Although the use of physiological systems canincrease the frequency of vital signs monitoring, 31they will be useful for outcome prediction onlyif widespread monitoring of hospitalised patientsbecomes available. Even when medical staff areJ.P. Nolan et al.alerted to a patient’s abnormal physiology, thereis often delay in attending the patient or referringto higher levels of care. 3,4,7 Whereas the use of awarning score based on physiological abnormalitiesis attractive, it is possible that a more subjectiveapproach, based on staff experience and expertise,may also be effective. 32Response to critical illnessThe traditional response to cardiac arrest is areactive one in which hospital staff (‘the cardiacarrest team’) attend the patient after the cardiacarrest has occurred. Cardiac arrest teams appearto improve survival after cardiac arrest in circumstanceswhere no team has previously existed. 33However, the role of the cardiac arrest team hasbeen questioned. In one study, only patients whohad return of spontaneous circulation before thecardiac arrest team arrived were discharged fromhospital alive. 34 When combined with the poorsurvival rate after in-hospital cardiac arrest, thisemphasises the importance of early recognition andtreatment of critically ill patients to prevent cardiacarrest. The name ‘cardiac arrest team’ impliesthat the team will be called only after cardiacarrest has occurred.In some hospitals the cardiac arrest team hasbeen replaced by a medical emergency team (MET)that responds, not only to patients in cardiacarrest, but also to those with acute physiologicaldeterioration. 26 The MET usually comprises medicaland nursing staff from intensive care and generalmedicine. and responds to specific calling criteria.Any member of the healthcare team can initiatea MET call. Early involvement of the METmay reduce cardiac arrests, deaths and unanticipatedICU admissions. 35,36 The MET may also beuseful in detecting medical error, improving treatmentlimitation decisions and reducing postoperativeward deaths. 37,38 MET interventions ofteninvolve simple tasks such as starting oxygen therapyand intravenous fluids. 39 A circadian pattern ofMET activation has been reported, which may suggestthat systems for identifying and responding tomedical emergencies may not be uniform throughoutthe 24-h period. 40 Studying the effect of theMET on patient outcomes is difficult. Many of thestudy findings to date can be criticised becauseof poor study design. A recent, well-designed,cluster-randomised controlled trial of the MET systemdemonstrated that the introduction of a METincreased the calling incidence for the team. However,it failed to show a reduction in the incidenceof cardiac arrest, unexpected death or unplannedICU admission. 41

European Resuscitation Council Guidelines for Resuscitation 2005S41In the UK, a system of pre-emptive wardcare, based predominantly on individual or teamsof nurses known as critical care outreach, hasdeveloped. 42 Outreach services exist in manyforms, ranging from a single nurse to a 24-h, 7 daysper week multiprofessional team. An outreach teamor system may reduce ward deaths, postoperativeadverse events, ICU admissions and readmissions,and increase survival. 43—45Other attempts to improve the general wardcare of patients and prevent physiological deteriorationand cardiac arrest include new admissionprocesses, early physiological monitoring and clinicalintervention in the emergency department (ED),and the appointment of new grades of emergencyphysicians. Many of these models attempt to supportthe primary admitting team with the skillsof ‘resuscitation’ specialists. 46 Medical and surgicalassessment units act as a single location for allacute admissions until their required level of careis evaluated. Patients are monitored and observedfor periods of up to 72 h, and there is usuallyrapid access to senior medical staff, diagnostics andurgent treatment. 47 The single location provides acentral focus for on-call medical, nursing and physiotherapystaff, in contrast to the traditional systemin which staff and patients are dispersed throughoutthe hospital.Many acutely ill patients present to hospital viathe ED and are obviously in need of immediateICU-type interventions. Early goal-directed therapyin the ED reverses physiological derangement andappears to improve patient survival. 48Appropriate placement of patientsIdeally, the sickest patients should be admittedto an area that can provide the greatest supervisionand the highest level of organ support andnursing care. This often occurs, but some patientsare placed incorrectly. 49 International organisationshave offered definitions of levels of care andproduced admission and discharge criteria for highdependency units (HDUs) and ICUs. 50,51Staffing levelsHospital staffing tends to be at its lowest during thenight and at weekends. This may influence patientmonitoring, treatment and outcomes. Admission toa general medical ward after 17:00 h 52 or to hospitalat weekends 53 is associated with increasedmortality. Patients who are discharged from ICUsto general wards at night have an increased risk ofin-hospital death compared with those dischargedduring the day and those discharged to HDUs. 54 Onestudy shows that higher nurse staffing is associatedwith reduction in cardiac arrest rates, as well asrates of pneumonia, shock and death. 55Resuscitation decisionsConsider ‘do not attempt resuscitation’ (DNAR)when the patient:• does not wish to have CPR• will not survive cardiac arrest even if CPR isattemptedHospital staff often fail to consider whetherresuscitation attempts are appropriate and resuscitationattempts in futile cases are common. 37Even when there is clear evidence that cardiacarrest or death is likely, ward staff rarely makedecisions about the patient’s resuscitation status. 4Many European countries have no formal policy forrecording DNAR decisions and the practice of consultingpatients about the decision is variable. 56Improved knowledge, training and DNAR decisionmakingshould improve patient care and preventfutile CPR attempts (see Section 8).Guidelines for prevention of in-hospitalcardiac arrestThe following strategies may prevent avoidable inhospitalcardiac arrests.1. Provide care for patients who are critically illor at risk of clinical deterioration in appropriateareas, with the level of care provided matchedto the level of patient sickness.2. Critically ill patients need regular observations:match the frequency and type of observations tothe severity of illness or the likelihood of clinicaldeterioration and cardiopulmonary arrest. Oftenonly simple vital sign observations (pulse, bloodpressure, respiratory rate) are needed.3. Use an EWS system to identify patients who arecritically ill and or at risk of clinical deteriorationand cardiopulmonary arrest.4. Use a patient charting system that enables theregular measurement and recording of EWS.5. Have a clear and specific policy that requiresa clinical response to EWS systems. This shouldinclude advice on the further clinical managementof the patient and the specific responsibilitiesof medical and nursing staff.6. The hospital should have a clearly identifiedresponse to critical illness. This may includea designated outreach service or resuscitationteam (e.g. MET) capable of responding to acuteclinical crises identified by clinical triggers or

S42other indicators. This service must be available24 h per day.7. Train all clinical staff in the recognition, monitoringand management of the critically illpatient. Include advice on clinical managementwhile awaiting the arrival of more experiencedstaff.8. Identify patients for whom cardiopulmonaryarrest is an anticipated terminal event and inwhom CPR is inappropriate, and patients whodo not wish to be treated with CPR. Hospitalsshould have a DNAR policy, based on nationalguidance, which is understood by all clinicalstaff.9. Ensure accurate audit of cardiac arrest, ‘falsearrest’, unexpected deaths and unanticipatedICU admissions using common datasets. Auditalso the antecedents and clinical response tothese events.4b. In-hospital resuscitationAfter in-hospital cardiac arrest, the divisionbetween basic life support and advanced life supportis arbitrary; in practice, the resuscitation processis a continuum and is based on common sense.The public expect that clinical staff can undertakecardiopulmonary resuscitation (CPR). For allin-hospital cardiac arrests, ensure that:• cardiorespiratory arrest is recognised immediately• help is summoned using a standard telephonenumber• CPR is started immediately using airwayadjuncts, e.g. a pocket mask and, if indicated,defibrillation attempted within 3 minThe exact sequence of actions after in-hospitalcardiac arrest will depend on many factors, including:• location (clinical/non-clinical area; monitored/unmonitoredarea)• training of the first responders• number of responders• equipment available• hospital response system to cardiac arrest andmedical emergencies, (e.g. MET) cardiac arrestteamLocationPatients who have monitored arrests are usuallydiagnosed rapidly. Ward patients may havehad a period of deterioration and an unwitnessedarrest. 3,4,6—8 Ideally, all patients who are at highJ.P. Nolan et al.risk of cardiac arrest should be cared for in a monitoredarea where facilities for immediate resuscitationare available.Training of first respondersAll healthcare professionals should be able torecognise cardiac arrest, call for help and start CPR.Staff should do what they have been trained to do.For example, staff in critical care and emergencymedicine will have more advanced resuscitationskills than staff who are not involved regularly inresuscitation in their normal clinical role. Hospitalstaff who attend a cardiac arrest may have differentlevels of skill to manage the airway, breathingand circulation. Rescuers must undertake the skillsin which they are trained and competent.Number of respondersThe single responder must ensure that help is coming.If other staff are nearby, several actions can beundertaken simultaneously.Equipment availableAll clinical areas should have immediate accessto resuscitation equipment and drugs to facilitaterapid resuscitation of the patient in cardiopulmonaryarrest. Ideally, the equipment used for CPR(including defibrillators) and the layout of equipmentand drugs should be standardised throughoutthe hospital. 57Resuscitation teamThe resuscitation team may take the form of a traditionalcardiac arrest team, which is called onlywhen cardiac arrest is recognised. Alternatively,hospitals may have strategies to recognise patientsat risk of cardiac arrest and summon a team (e.g.,MET) before cardiac arrest occurs. 35,36,39,41,58 Theterm ‘resuscitation team’ reflects the range ofresponse teams. In hospital cardiac arrests arerarely sudden or unexpected. A strategy of recognisingpatients at risk of cardiac arrest may enablesome of these arrests to be prevented, or may preventfutile resuscitation attempts in those who areunlikely to benefit from CPR.Immediate actions for a collapsed patient ina hospitalAn algorithm for the initial management of inhospitalcardiac arrest is shown in Figure 4.1.

European Resuscitation Council Guidelines for Resuscitation 2005S43Figure 4.1Algorithm for the treatment of in-hospital cardiac arrest.• Ensure personal safety.• Check the victim for a response.• When healthcare professionals see a patient collapseor find a patient apparently unconscious ina clinical area, they should first shout for help,then assess if the patient is responsive. Gentlyshake the shoulders and ask loudly: ‘‘Are you allright?’’• If other members of staff are nearby, it will bepossible to undertake actions simultaneously.The responsive patientUrgent medical assessment is required. Dependingon the local protocols, this may take the form of aresuscitation team (e.g., MET). While awaiting thisteam, give the patient oxygen, attach monitoringand insert an intravenous cannula.The unresponsive patientThe exact sequence will depend on the trainingof staff and experience in assessment of breathingand circulation. Trained healthcare staff cannotassess the breathing and pulse sufficiently reliablyto confirm cardiac arrest. 16,59,60 Agonal breathing(occasional gasps, slow, laboured or noisy breathing)is common in the early stages of cardiac arrestand is a sign of cardiac arrest and should not beconfused as a sign of life/circulation.• Shout for help (if not already)Turn the victim on to his back and then open theairway:• Open Airway and check breathing:◦ Open the airway using a head tilt chin lift◦ Look in the mouth. If a foreign body or debrisis visible attempt to remove with forceps orsuction as appropriate◦ If you suspect that there may have been aninjury to the neck, try to open the airway usinga jaw thrust. Remember that maintaining anairway and adequate ventilation is the overridingpriority in managing a patient with a suspectedspinal injury. If this is unsuccessful, usejust enough head tilt to clear the airway. Usemanual in-line stabilisation to minimise headmovement if sufficient rescuers are available.Keeping the airway open, look, listen, and feelfor normal breathing (an occasional gasp, slow,laboured or noisy breathing is not normal):• Look for chest movement• Listen at the victim’s mouth for breath sounds• Feel for air on your cheekLook, listen, and feel for no more than 10 s todetermine if the victim is breathing normally• Check for signs of a circulation:◦ It may be difficult to be certain that there is nopulse. If the patient has no signs of life (lackof movement, normal breathing, or coughing),start CPR until more experience help arrives orthe patient shows signs of life.◦ Those experienced in clinical assessmentshould assess the carotid pulse whilst simultaneouslylooking for signs of life for not morethan 10 s.◦ If the patient appears to have no signs of life, orif there is doubt, start CPR immediately. Delays

S44in diagnosis of cardiac arrest and starting CPRwill adversely effect survival must be avoided.If there is a pulse or signs of life, urgent medicalassessment is required. Depending on the localprotocols, this may take the form of a resuscitationteam. While awaiting this team, give thepatient oxygen, attach monitoring, and insert anintravenous cannula.If there is no breathing, but there is a pulse (respiratoryarrest), ventilate the patient’s lungs andcheck for a circulation every 10 breaths.Starting in-hospital CPR• One person starts CPR as others call the resuscitationteam and collect the resuscitation equipmentand a defibrillator. If only one memberof staff is present, this will mean leaving thepatient.• Give 30 chest compressions followed by 2 ventilations.• Undertaking chest compressions properly is tiring;try to change the person doing chest compressionsevery 2 min.• Maintain the airway and ventilate the lungs withthe most appropriate equipment immediately tohand. A pocket mask, which may be supplementedwith an oral airway, is usually readilyavailable. Alternatively, use a laryngeal mask airway(LMA) and self-inflating bag, or bag-mask,according to local policy. Tracheal intubationshould be attempted only by those who aretrained, competent and experienced in this skill.• Use an inspiratory time of 1 s and give enoughvolume to produce a normal chest rise. Add supplementaloxygen as soon as possible.• Once the patient’s trachea has been intubated,continue chest compressions uninterrupted(except for defibrillation or pulse checks whenindicated), at a rate of 100 min −1 , and ventilatethe lungs at approximately 10 breaths min −1 .Avoid hyperventilation.• If there is no airway and ventilation equipmentavailable, give mouth-to-mouth ventilation. Ifthere are clinical reasons to avoid mouth-tomouthcontact, or you are unwilling or unableto do this, do chest compressions until help orairway equipment arrives.• When the defibrillator arrives, apply the paddlesto the patient and analyse the rhythm. Ifself-adhesive defibrillation pads are available,apply these without interrupting chest compressions.Pause briefly to assess the heart rhythm. Ifindicated, attempt either manual or automatedexternal defibrillation (AED).J.P. Nolan et al.• Recommence chest compressions immediatelyafter the defibrillation attempt. Minimise interruptionsto chest compressions.• Continue resuscitation until the resuscitationteam arrives or the patient shows signs of life.Follow the voice prompts if using an AED. If usinga manual defibrillator, follow the universal algorithmfor advanced life support (Section 4c).• Once resuscitation is underway, and if there aresufficient staff present, prepare intravenous cannulaeand drugs likely to be used by the resuscitationteam (e.g. adrenaline).• Identify one person to be responsible for handoverto the resuscitation team leader. Locatethe patient’s records.• The quality of chest compressions during inhospitalCPR is frequently sub-optimal. 61,62 Theteam leader should monitor the quality of CPRand change CPR providers if the quality of CPRis poor. The person providing chest compressionsshould be changed every 2 min.The monitored and witnessed cardiac arrestIf a patient has a monitored and witnessed cardiacarrest, act as follows.• Confirm cardiac arrest and shout for help.• Consider a precordial thump if the rhythm isVF/VT and a defibrillator is not immediatelyavailable.• If the initial rhythm is VF/VT and a defibrillatoris immediately available, give a shock first. Theuse of adhesive electrode pads or a ‘quick-look’paddles technique will enable rapid assessmentof heart rhythm compared with attaching ECGelectrodes. 63Training for healthcare professionalsThe Immediate Life Support course trains healthcareprofessionals in the skills required to startresuscitation, including defibrillation, and to bemembers of a cardiac arrest team (see Section 9). 64The Advanced Life Support (ALS) course teaches theskills required for leading a resuscitation team. 65,664c. ALS treatment algorithmIntroductionHeart rhythms associated with cardiac arrest aredivided into two groups: shockable rhythms (ventricularfibrillation/pulseless ventricular tachycardia(VF/VT)) and non-shockable rhythms (asystole

European Resuscitation Council Guidelines for Resuscitation 2005S45Figure 4.2Advanced life support cardiac arrest algorithm.and pulseless electrical activity (PEA)). The principaldifference in the management of these twogroups of arrhythmias is the need for attempteddefibrillation in those patients with VF/VT. Subsequentactions, including chest compressions, airwaymanagement and ventilation, venous access,administration of adrenaline and the identificationand correction of reversible factors, are common toboth groups.Although the ALS cardiac arrest algorithm(Figure 4.2) is applicable to all cardiac arrests,additional interventions may be indicated for cardiacarrest caused by special circumstances (Section7).The interventions that unquestionably contributeto improved survival after cardiac arrest areearly defibrillation for VF/VT and prompt and effectivebystander basic life support (BLS). Advancedairway intervention and the delivery of drugs havenot been shown to increase survival to hospitaldischarge after cardiac arrest, although they arestill included among ALS interventions. Thus, duringadvanced life support, attention must be focusedon early defibrillation and high-quality, uninterruptedBLS.Shockable rhythms (ventricularfibrillation/pulseless ventriculartachycardia)In adults, the commonest rhythm at the time ofcardiac arrest is VF, which may be preceded by aperiod of VT or even supraventricular tachycardia(SVT). 67 Having confirmed cardiac arrest, summonhelp (including the request for a defibrillator) andstart CPR, beginning with external chest compression,with a compression:ventilation (CV) ratio of30:2. As soon as the defibrillator arrives, diagnosethe rhythm by applying paddles or self-adhesivepads to the chest.

S46If VF/VT is confirmed, charge the defibrillatorand give one shock (150—200-J biphasic or 360-J monophasic). Without reassessing the rhythm orfeeling for a pulse, resume CPR (CV ratio 30:2)immediately after the shock, starting with chestcompressions. Even if the defibrillation attempt issuccessful in restoring a perfusing rhythm, it is veryrare for a pulse to be palpable immediately afterdefibrillation, 68 and the delay in trying to palpatea pulse will further compromise the myocardiumif a perfusing rhythm has not been restored. 69 Ifa perfusing rhythm has been restored, giving chestcompressions does not increase the chance of VFrecurring. 70 In the presence of post-shock asystole,chest compressions may usefully induce VF. 70 ContinueCPR for 2 min, then pause briefly to check themonitor: if there is still VF/VT, give a second shock(150—360-J biphasic or 360-J monophasic). ResumeCPR immediately after the second shock.Pause briefly after 2 min of CPR to check themonitor: if there is still VF/VT, give adrenalinefollowed immediately by a third shock (150—360-J biphasic or 360-J monophasic) and resumptionof CPR (drug-shock-CPR-rhythm check sequence).Minimise the delay between stopping chest compressionsand delivery of the shock. The adenalinethat is given immediately before the shock will becirculated by the CPR that immediately follows theshock. After drug delivery and 2 min of CPR, analysethe rhythm and be prepared to deliver anothershock immediately if indicated. If VF/VT persistsafter the third shock, give an intravenous bolus ofamiodarone 300 mg. Inject the amiodarone duringthe brief rhythm analysis before delivery of thefourth shock.When the rhythm is checked 2 min after givinga shock, if a nonshockable rhythm is present andthe rhythm is organised (complexes appear regularor narrow), try to palpate a pulse. Rhythm checksmust be brief, and pulse checks undertaken onlyif an organised rhythm is observed. If an organisedrhythm is seen during a 2 min period of CPR,do not interrupt chest compressions to palpate apulse unless the patient shows signs of life suggestingROSC. If there is any doubt about the presenceof a pulse in the presence of an organised rhythm,resume CPR. If the patient has ROSC, begin postresuscitationcare. If the patient’s rhythm changesto asystole or PEA, see non-shockable rhythmsbelow.During treatment of VF/VT, healthcare providersmust practice efficient coordination between CPRand shock delivery. When VF is present for morethan a few minutes, the myocardium is depletedof oxygen and metabolic substrates. A briefperiod of chest compressions will deliver oxygenJ.P. Nolan et al.and energy substrates and increase the probabilityof restoring a perfusing rhythm after shockdelivery. 71 Analyses of VF waveform characteristicspredictive of shock success indicate thatthe shorter the time between chest compressionand shock delivery, the more likely the shockwill be successful. 71,72 Reduction in the intervalfrom compression to shock delivery by even afew seconds can increase the probability of shocksuccess. 73Regardless of the arrest rhythm, give adrenaline1 mg every 3—5 min until ROSC is achieved; thiswill be once every two loops of the algorithm. Ifsigns of life return during CPR (movement, normalbreathing, or coughing), check the monitor: if anorganised rhythm is present, check for a pulse. If apulse is palpable, continue post-resuscitation careand/or treatment of peri-arrest arrhythmia. If nopulse is present, continue CPR. Providing CPR witha CV ratio of 30:2 is tiring; change the individualundertaking compressions every 2 min.Precordial thumpConsider giving a single precordial thump when cardiacarrest is confirmed rapidly after a witnessed,sudden collapse and a defibrillator is not immediatelyto hand (Section 3). 74 These circumstancesare most likely to occur when the patient is monitored.A precordial thump should be undertakenimmediately after confirmation of cardiac arrestand only by healthcare professionals trained inthe technique. Using the ulnar edge of a tightlyclenched fist, deliver a sharp impact to the lowerhalf of the sternum from a height of about 20 cm,then retract the fist immediately to create animpulse-like stimulus. A precordial thump is mostlikely to be successful in converting VT to sinusrhythm. Successful treatment of VF by precordialthump is much less likely: in all the reportedsuccessful cases, the precordial thump was givenwithin the first 10 s of VF. 75 There are very rarereports of a precordial thump converting a perfusingto a non-perfusing rhythm. 76Airway and ventilationDuring the treatment of persistent VF, ensure goodqualitychest compressions between defibrillationattempts. Consider reversible causes (4 H’s and 4T’s) and, if identified, correct them. Check theelectrode/defibrillating paddle positions and contacts,and the adequacy of the coupling medium,e.g. gel pads. Tracheal intubation provides themost reliable airway, but should be attemptedonly if the healthcare provider is properly trained

European Resuscitation Council Guidelines for Resuscitation 2005S47and has adequate ongoing experience with thetechnique. Personnel skilled in advanced airwaymanagement should attempt laryngoscopy withoutstopping chest compressions; a brief pause inchest compressions may be required as the tubeis passed through the vocal cords. Alternatively, toavoid any interruptions in chest compressions, theintubation attempt may be deferred until returnof spontaneous circulation. No intubation attemptshould take longer than 30 s: if intubation has notbeen achieved after this time, recommence bagmaskventilation. After intubation, confirm correcttube position and secure it adequately. Oncethe patient’s trachea has been intubated, continuechest compressions, at a rate of 100 min −1 ,without pausing during ventilation. Ventilate thelungs at 10 breaths min −1 ; do not hyperventilatethe patient. A pause in the chest compressionsallows the coronary perfusion pressure to fall substantially.On resuming compressions there is somedelay before the original coronary perfusion pressureis restored, thus chest compressions that arenot interrupted for ventilation result in a substantiallyhigher mean coronary perfusion pressure.In the absence of personnel skilled in trachealintubation, acceptable alternatives are the Combitube,laryngeal mask airway (LMA), ProSeal LMA,or Laryngeal Tube (Section 4d). Once one of theseairways has been inserted, attempt to deliver continuouschest compressions, uninterrupted duringventilation. If excessive gas leakage causes inadequateventilation of the patient’s lungs, chest compressionswill have to be interrupted to enable ventilation(using a CV ratio of 30:2).During continuous chest compressions, ventilatethe lungs at 10 breaths min −1 .Intravenous access and drugsPeripheral versus central venous drug delivery.Establish intravenous access if this has not alreadybeen achieved. Although peak drug concentrationsare higher and circulation times are shorter whendrugs are injected into a central venous cathetercompared with a peripheral cannula, 77 insertion ofa central venous catheter requires interruption ofCPR and is associated with several complications.Peripheral venous cannulation is quicker, easier toperform and safer. Drugs injected peripherally mustbe followed by a flush of at least 20 ml of fluid andelevation of the extremity for 10—20 s to facilitatedrug delivery to the central circulation.Intraosseous route. If intravenous access is difficultor impossible, consider the intraosseous route.Although normally considered as an alternativeroute for vascular access in children, it can also beeffective in adults. 78 Intraosseous injection of drugsachieves adequate plasma concentrations in a timecomparable with injection through a central venouscatheter. The intraosseous route also enables withdrawalof marrow for venous blood gas analysis andmeasurement of electrolytes and haemoglobin concentration.Tracheal route. If neither intravenous norintraosseous access can be established, somedrugs can be given by the tracheal route. However,unpredictable plasma concentrations areachieved when drugs are given via a tracheal tube,and the optimal tracheal dose of most drugs isunknown. During CPR, the equipotent dose ofadrenaline given via the trachea is three to tentimes higher than the intravenous dose. 79,80 Someanimal studies suggest that the lower adrenalineconcentrations achieved when the drug is given viathe trachea may produce transient beta-adrenergiceffects, which will cause hypotension and lowercoronary artery perfusion pressure. 81—84 If givenvia the trachea, the dose of adrenaline is 3 mgdiluted to at least 10 ml with sterile water. Dilutionwith water instead of 0.9% saline may achievebetter drug absorption. 85 The solutions in prefilledsyringes are acceptable for this purpose.Adrenaline. Despite the widespread use ofadrenaline during resuscitation, and severalstudies involving vasopressin, there is no placebocontrolledstudy that shows that the routine use ofany vasopressor at any stage during human cardiacarrest increases survival to hospital discharge. Currentevidence is insufficient to support or refutethe routine use of any particular drug or sequenceof drugs. Despite the lack of human data, the useof adrenaline is still recommended, based largelyon animal data. The alpha-adrenergic actions ofadrenaline cause vasoconstriction, which increasesmyocardial and cerebral perfusion pressure. Thehigher coronary blood flow increases the frequencyof the VF waveform and should improve the chanceof restoring a circulation when defibrillation isattempted. 86—88 The optimal duration of CPR andnumber of shocks that should be given beforegiving drugs is unknown. On the basis of expertconsensus, if VF/VT persists after two shocks,give adrenaline and repeat every 3—5 min duringcardiac arrest. Do not interrupt CPR to give drugs.Anti-arrhythmic drugs. There is no evidence thatgiving any anti-arrhythmic drug routinely duringhuman cardiac arrest increases survival tohospital discharge. In comparison with placebo 89and lidocaine, 90 the use of amiodarone in shock-

S48refractory VF improves the short-term outcome ofsurvival to hospital admission. In these studies,the anti-arrhythmic therapy was given if VF/VTpersisted after at least three shocks; however,these were delivered using the conventional threestackedshocks strategy. There are no data on theuse of amiodarone for shock-refractory VF/VT whensingle shocks are used. On the basis of expert consensus,if VF/VT persists after three shocks, give300 mg amiodarone by bolus injection. A furtherdose of 150 mg may be given for recurrent or refractoryVF/VT, followed by an infusion of 900 mg over24. Lidocaine 1 mg kg −1 may be used as an alternativeif amiodarone is not available, but do not givelidocaine if amiodarone has been given already.Magnesium. Although the routine use of magnesiumin cardiac arrest does not increasesurvival, 91—95 give magnesium (8 mmol=4ml 50%magnesium sulphate or 2 g) for refractory VF ifthere is any suspicion of hypomagnesaemia (e.g.,patients on potassium-losing diuretics).Bicarbonate. Administering sodium bicarbonateroutinely during cardiac arrest and CPR (especiallyin out-of-hospital cardiac arrests) or after return ofspontaneous circulation is not recommended. Givesodium bicarbonate (50 mmol) if cardiac arrest isassociated with hyperkalaemia or tricyclic antidepressantoverdose; repeat the dose according to theclinical condition and result of repeated blood gasanalysis. Some experts give bicarbonate if the arterialpH is less than 7.1, but this is controversial.During cardiac arrest, arterial blood gas values donot reflect the acid—base state of the tissues 96 ; thetissue pH will be lower than that in arterial blood.Mixed venous blood values give a more accurateestimate of the pH in the tissues, 96 but it is rarefor a pulmonary artery catheter to be in situ at thetime of cardiac arrest. If a central venous catheteris in situ, central venous blood gas analysis will providea closer estimate of tissue acid/base state thanthat provided by arterial blood.Persistent ventricular fibrillationIn VF persists, consider changing the position ofthe paddles (Section 3). Review all potentiallyreversible causes (see below) and treat any thatare identified.The duration of any individual resuscitationattempt is a matter of clinical judgement, takinginto consideration the circumstances and the perceivedprospect of a successful outcome. If it wasconsidered appropriate to start resuscitation, it isusually considered worthwhile continuing as long asthe patient remains in VF/VT.J.P. Nolan et al.Non-shockable rhythms (PEA and asystole)Pulseless electrical activity (PEA) is defined ascardiac electrical activity in the absence of anypalpable pulses. These patients often have somemechanical myocardial contractions, but these aretoo weak to produce a detectable pulse or bloodpressure. PEA is often caused by reversible conditions,and can be treated if those conditions areidentified and corrected (see below). Survival followingcardiac arrest with asystole or PEA is unlikelyunless a reversible cause can be found and treatedeffectively.If the initial monitored rhythm is PEA or asystole,start CPR 30:2 and give adrenaline 1 mg assoon as intravascular access is achieved. If asystoleis displayed, check without stopping CPR that theleads are attached correctly. Asystole is a conditionthat could be exacerbated or precipitated byexcessive vagal tone and, theoretically, this couldbe reversed by a vagolytic drug; therefore, despitethe lack of evidence that routine atropine for asystoliccardiac arrest increases survival, give atropine3 mg (the dose that will provide maximum vagalblockade) if there is asystole or the rhythm is slowPEA (rate

European Resuscitation Council Guidelines for Resuscitation 2005S49the algorithm. Otherwise, continue CPR and giveadrenaline every 3—5 min (every other loop of thealgorithm).Potentially reversible causesPotential causes or aggravating factors for whichspecific treatment exists must be considered duringany cardiac arrest. For ease of memory, these aredivided into two groups of four based upon theirinitial letter: either H or T. More details on many ofthese conditions are covered in Section 7.The four HsMinimise the risk of hypoxia by ensuring that thepatient’s lungs are ventilated adequately with 100%oxygen. Make sure there is adequate chest riseand bilateral breath sounds. Using the techniquesdescribed in Section 4d, check carefully that thetracheal tube is not misplaced in a bronchus or theoesophagus.Pulseless electrical activity caused by hypovolaemiais due usually to severe haemorrhage.This may be precipitated by trauma (Section 7i),gastrointestinal bleeding or rupture of an aorticaneurysm. Intravascular volume should be restoredrapidly with fluid, coupled with urgent surgery tostop the haemorrhage.Hyperkalaemia, hypokalaemia, hypocalcaemia,acidaemia and other metabolic disorders aredetected by biochemical tests or suggested by thepatient’s medical history, e.g. renal failure (Section7a). A 12-lead ECG may be diagnostic. Intravenouscalcium chloride is indicated in the presenceof hyperkalaemia, hypocalcaemia and calciumchannel-blocker overdose.Suspect hypothermia in any drowning incident(Sections 7c and d); use a low-reading thermometer.The four TsA tension pneumothorax may be the primary causeof PEA and may follow attempts at central venouscatheter insertion. The diagnosis is made clinically.Decompress rapidly by needle thoracocentesis, andthen insert a chest drain.Cardiac tamponade is difficult to diagnosebecause the typical signs of distended neck veinsand hypotension are usually obscured by thearrest itself. Cardiac arrest after penetrating chesttrauma is highly suggestive of tamponade and is anindication for needle pericardiocentesis or resuscitativethoracotomy (see Section 7i).In the absence of a specific history, the accidentalor deliberate ingestion of therapeutic ortoxic substances may be revealed only by laboratoryinvestigations (Section 7b). Where available,the appropriate antidotes should be used, but mostoften treatment is supportive.The commonest cause of thromboembolic ormechanical circulatory obstruction is massive pulmonaryembolus. If cardiac arrest is thought to becaused by pulmonary embolism, consider giving athrombolytic drug immediately (Section 4e). 974d. Airway management and ventilationIntroductionPatients requiring resuscitation often have anobstructed airway, usually secondary to loss of consciousness,but occasionally it may be the primarycause of cardiorespiratory arrest. Prompt assessment,with control of the airway and ventilation ofthe lungs, is essential. This will help to prevent secondaryhypoxic damage to the brain and other vitalorgans. Without adequate oxygenation it may beimpossible to restore a spontaneous cardiac output.These principles may not apply to the witnessed primarycardiac arrest in the vicinity of a defibrillator;in this case, the priority is immediate attempteddefibrillation.Airway obstructionCauses of airway obstructionObstruction of the airway may be partial or complete.It may occur at any level, from the noseand mouth down to the trachea (Figure 4.3). Inthe unconscious patient, the commonest site ofairway obstruction is at the level of the pharynx.Until recently this obstruction had been attributedto posterior displacement of the tongue caused bydecreased muscle tone; with the tongue ultimatelytouching the posterior pharyngeal wall. The precisecause of airway obstruction in the unconsciousstate has been identified by studying patients undergeneral anaesthesia. 98,99 These studies of anaesthetisedpatients have shown that the site of airwayobstruction is at the soft palate and epiglottisand not the tongue. Obstruction may be causedalso by vomit or blood (regurgitation of gastriccontents or trauma), or by foreign bodies. Laryngealobstruction may be caused by oedema fromburns, inflammation or anaphylaxis. Upper airwaystimulation may cause laryngeal spasm. Obstructionof the airway below the larynx is less com-

S50J.P. Nolan et al.In a patient who is making respiratory efforts,complete airway obstruction causes paradoxicalchest and abdominal movement, often describedas ‘see-saw breathing’. As the patient attempts tobreathe in, the chest is drawn in and the abdomenexpands; the opposite occurs during expiration.This is in contrast to the normal breathing patternof synchronous movement upwards and outwardsof the abdomen (pushed down by the diaphragm)with the lifting of the chest wall. During airwayobstruction, other accessory muscles of respirationare used, with the neck and the shoulder musclescontracting to assist movement of the thoraciccage. Full examination of the neck, chest andabdomen is required to differentiate the paradoxicalmovements that may mimic normal respiration.The examination must include listening forthe absence of breath sounds in order to diagnosecomplete airway obstruction reliably; any noisybreathing indicates partial airway obstruction. Duringapnoea, when spontaneous breathing movementsare absent, complete airway obstruction isrecognised by failure to inflate the lungs duringattempted positive pressure ventilation. Unless airwaypatency can be re-established to enable adequatelung ventilation within a period of a very fewminutes, neurological and other vital organ injurymay occur, leading to cardiac arrest.Figure 4.3Causes of airway obstruction.mon, but may arise from excessive bronchial secretions,mucosal oedema, bronchospasm, pulmonaryoedema or aspiration of gastric contents.Recognition of airway obstructionAirway obstruction can be subtle and is often missedby healthcare professionals, let alone by lay people.The ‘look, listen and feel’ approach is a simple,systematic method of detecting airway obstruction.• Look for chest and abdominal movements.• Listen and feel for airflow at the mouth and nose.In partial airway obstruction, air entry is diminishedand usually noisy. Inspiratory stridor is causedby obstruction at the laryngeal level or above. Expiratorywheeze implies obstruction of the lower airways,which tend to collapse and obstruct duringexpiration. Other characteristic sounds include thefollowing:• Gurgling is caused by liquid or semisolid foreignmaterial in the main airways.• Snoring arises when the pharynx is partiallyoccluded by the soft palate or epiglottis.• Crowing is the sound of laryngeal spasm.Basic airway managementOnce any degree of obstruction is recognised,immediate measures must be taken to create andmaintain a clear airway. There are three manoeuvresthat may improve the patency of an airwayobstructed by the tongue or other upper airwaystructures: head tilt, chin lift, and jaw thrust.Head tilt and chin liftThe rescuer’s hand is placed on the patient’s foreheadand the head gently tilted back; the fingertipsof the other hand are placed under the point of thepatient’s chin, which is gently lifted to stretch theanterior neck structures (Figure 4.4). 100—105Jaw thrustJaw thrust is an alternative manoeuvre for bringingthe mandible forward and relieving obstruction bythe soft palate and epiglottis. The rescuer’s indexand other fingers are placed behind the angle ofthe mandible, and pressure is applied upwards andforwards. Using the thumbs, the mouth is openedslightly by downward displacement of the chin(Figure 4.5).

European Resuscitation Council Guidelines for Resuscitation 2005S51Airway management in patients with suspectedcervical spine injuryIf spinal injury is suspected (e.g., if the victim hasfallen, been struck on the head or neck, or has beenrescued after diving into shallow water), maintainthe head, neck, chest and lumbar region in the neutralposition during resuscitation. Excessive headtilt could aggravate the injury and damage the cervicalspinal cord 106—110 ; however, this complicationhas not been documented and the relative risk isunknown. When there is a risk of cervical spineinjury, establish a clear upper airway by using jawthrust or chin lift in combination with manual inlinestabilisation (MILS) of the head and neck by anassistant. 111,112 If life-threatening airway obstructionpersists despite effective application of jawthrust or chin lift, add head tilt a small amountat a time until the airway is open; establishing apatent airway takes priority over concerns about apotential cervical spine injury.Adjuncts to basic airway techniquesFigure 4.4 Head tilt and chin lift. © 2005 EuropeanResuscitation Council.These simple positional methods are successfulin most cases where airway obstruction results fromrelaxation of the soft tissues. If a clear airway cannotbe achieved, look for other causes of airwayobstruction. Use a finger sweep to remove any solidforeign body seen in the mouth. Remove broken ordisplaced dentures, but leave well-fitting denturesas they help to maintain the contours of the mouth,facilitating a good seal for ventilation.Simple airway adjuncts are often helpful, andsometimes essential, to maintain an open airway,particularly when resuscitation is prolonged. Theposition of the head and neck must be maintainedto keep the airway aligned. Oropharyngeal andnasopharyngeal airways overcome backward displacementof the soft palate and tongue in anunconscious patient, but head tilt and jaw thrustmay also be required.Oropharyngeal airways. Oropharyngeal airwaysare available in sizes suitable for the newbornto large adults. An estimate of the size requiredis obtained by selecting an airway with a lengthcorresponding to the vertical distance betweenFigure 4.5Jaw thrust. © 2005 European Resuscitation Council.

S52J.P. Nolan et al.Figure 4.6Insertion of oropharyngeal airway. © 2005 European Resuscitation Council.the patient’s incisors and the angle of the jaw(Figure 4.6). The most common sizes are 2, 3 and 4for small, medium and large adults, respectively.If the glossopharyngeal and laryngeal reflexesare present, vomiting or laryngospasm may becaused by inserting an oropharyngeal airway; thus,insertion should be attempted only in comatosepatients. The oropharyngeal airway can becomeobstructed at three possible sites: 113 part of thetongue can occlude the end of the airway; the airwaycan lodge in the vallecula; and the airway canbe obstructed by the epiglottis.OxygenGive oxygen whenever it is available. A standardoxygen mask will deliver up to 50% oxygenconcentration, providing the flow of oxygenis high enough. A mask with a reservoir bag (nonrebreathingmask), can deliver an inspired oxygenconcentration of 85% at flows of 10—15 l min −1 . Initially,give the highest possible oxygen concentration,which can then be titrated to the oxygen saturationby pulse oximeter (SpO 2 ) or arterial bloodgases.Nasopharyngeal airways. In patients who are notdeeply unconscious, a nasopharyngeal airway istolerated better than an oropharyngeal airway.The nasopharyngeal airway may be life saving inpatients with clenched jaws, trismus or maxillofacialinjuries, when insertion of an oral airway isimpossible. Inadvertent insertion of a nasopharyngealairway through a fracture of the skull baseand into the cranial vault is possible, but extremelyrare. 114,115 In the presence of a known or suspectedbasal skull fracture an oral airway is preferred but,if this is not possible and the airway is obstructed,gentle insertion of a nasopharyngeal airway may belife saving (i.e., the benefits may far outweigh therisks).The tubes are sized in millimetres according totheir internal diameter, and the length increaseswith diameter. The traditional methods of sizinga nasopharyngeal airway (measurement againstthe patient’s little finger or anterior nares) donot correlate with the airway anatomy and areunreliable. 116 Sizes of 6—7 mm are suitable foradults. Insertion can cause damage to the mucosallining of the nasal airway, with bleeding in up to30% of cases. 117 If the tube is too long it may stimulatethe laryngeal or glossopharyngeal reflexes toproduce laryngospasm or vomiting.SuctionUse a wide-bore rigid sucker (Yankauer) to removeliquid (blood, saliva and gastric contents) fromthe upper airway. Use the sucker cautiously if thepatient has an intact gag reflex; the sucker can provokevomiting.VentilationProvide artificial ventilation as soon as possiblefor any patient in whom spontaneous ventilationis inadequate or absent. Expired air ventilation(rescue breathing) is effective, but the rescuer’sexpired oxygen concentration is only 16—17%, soit must be replaced as soon as possible by ventilationwith oxygen-enriched air. Although mouthto-mouthventilation has the benefit of not requiringany equipment, the technique is aestheticallyunpleasant, particularly when vomit or bloodis present, and rescuers may be reluctant toplace themselves in intimate contact with a victimwho may be unknown to them. 118—121 Thereare only isolated reports of individuals acquiringinfections after providing CPR, e.g. tuberculosis 122and severe acute respiratory distress syndrome(SARS). 123 Transmission of human immunodefi-

European Resuscitation Council Guidelines for Resuscitation 2005S53an adequate volume, minimising the risk of gastricinflation, and allowing adequate time for chestcompressions. During CPR with an unprotected airway,give two ventilations after each sequence of30 chest compressions.Self-inflating bagFigure 4.7 Mouth-to-mask ventilation. © 2005 EuropeanResuscitation Council.ciency virus (HIV) during provision of CPR hasnever been reported. Simple adjuncts are availableto enable direct person-to-person contact tobe avoided; some of these devices may reduce therisk of cross-infection between patient and rescuer,although they are unlikely to offer significantprotection from SARS. 123 The pocket resuscitationmask is used widely. It is similar to an anaestheticfacemask, and enables mouth-to-mask ventilation.It has a unidirectional valve, which directs thepatient’s expired air away from the rescuer. Themask is transparent so that vomit or blood from thepatient can be seen. Some masks have a connectorfor the addition of oxygen. When using maskswithout a connector, supplemental oxygen can begiven by placing the tubing underneath one side andensuring an adequate seal. Use a two-hand techniqueto maximise the seal with the patient’s face(Figure 4.7).High airway pressures can be generated if thetidal volumes or inspiratory flows are excessive,predisposing to gastric inflation and subsequent riskof regurgitation and pulmonary aspiration. The possibilityof gastric inflation is increased by• malalignment of the head and neck, and anobstructed airway• an incompetent oesophageal sphincter (presentin all patients with cardiac arrest)• a high inflation pressureConversely, if inspiratory flow is too low, inspiratorytime will be prolonged and the time availableto give chest compressions is reduced. Delivereach breath over approximately 1 s and transfera volume that corresponds to normal chest movement;this represents a compromise between givingThe self-inflating bag can be connected to a facemask,tracheal tube or alternative airway devicesuch as the LMA or Combitube. Without supplementaloxygen, the self-inflating bag ventilatesthe patient’s lungs with ambient air (21% oxygen).This can be increased to about 45% by attachingoxygen directly to the bag. If a reservoir systemis attached and the oxygen flow is increased toapproximately 10 l min −1 , an inspired oxygen concentrationof approximately 85% can be achieved.Although the bag-mask device enables ventilationwith high concentrations of oxygen, its use by asingle person requires considerable skill. When usedwith a face mask, it is often difficult to achieve agas-tight seal between the mask and the patient’sface, and to maintain a patent airway with one handwhile squeezing the bag with the other. 124 Any significantleak will cause hypoventilation and, if theairway is not patent, gas may be forced into thestomach. 125,126 This will reduce ventilation furtherand greatly increase the risk of regurgitation andaspiration. 127 Cricoid pressure can reduce this riskbut requires the presence of a trained assistant.Poorly applied cricoid pressure may make it moredifficult to ventilate the patient’s lungs. 128The two-person technique for bag-mask ventilationis preferable (Figure 4.8). One person holdsthe facemask in place using a jaw thrust with bothFigure 4.8 The two-person technique for bag-mask ventilation.© 2005 European Resuscitation Council.

S54hands, and an assistant squeezes the bag. In thisway, a better seal can be achieved and the patient’slungs can be ventilated more effectively and safely.Once a tracheal tube, Combitube or supraglotticairway device has been inserted, ventilate the lungsat a rate of 10 breaths min −1 and continue chestcompressions without pausing during ventilations.The seal of the LMA around the larynx is unlikelyto be good enough to prevent at least some gasleaking when inspiration coincides with chest compressions.Moderate gas leakage is acceptable, particularlyas most of this gas will pass up through thepatient’s mouth; if excessive gas leakage results ininadequate ventilation of the patient’s lungs, chestcompressions will have to be interrupted to enableventilation, using a compression—ventilation ratioof 30:2.Automatic ventilatorsVery few studies address specific aspects of ventilationduring advanced life support. There are somedata indicating that the ventilation rates deliveredby healthcare personnel during cardiac arrest areexcessive. 61,129 Automatic ventilators or resuscitatorsprovide a constant flow of gas to the patientduring inspiration; the volume delivered is dependenton the inspiratory time (a longer time providesa greater tidal volume). Because pressure in the airwayrises during inspiration, these devices are oftenpressure limited to protect the lungs against barotrauma.An automatic ventilator can be used witheither a facemask or other airway device (e.g., trachealtube, LMA).An automatic resuscitator should be set initiallyto deliver a tidal volume of 6—7 ml kg −1 at10 breaths min −1 . Some ventilators have coordinatedmarkings on the controls to facilitate easyand rapid adjustment for patients of different sizes,and others are capable of sophisticated variation inrespiratory pattern. In the presence of a spontaneouscirculation, the correct setting will be determinedby analysis of the patient’s arterial bloodgases.Automatic resuscitators provide many advantagesover alternative methods of ventilation.• In unintubated patients, the rescuer has bothhands free for mask and airway alignment.• Cricoid pressure can be applied with one handwhile the other seals the mask on the face.• In intubated patients they free the rescuer forother tasks.• Once set, they provide a constant tidal volume,respiratory rate and minute ventilation; thus,they may help to avoid excessive ventilation.J.P. Nolan et al.A manikin study of simulated cardiac arrest anda study involving fire-fighters ventilating the lungsof anaesthetised patients both showed a significantdecrease in gastric inflation with manuallytriggeredflow-limited oxygen-powered resuscitatorsand mask compared with a bag-mask. 130,131However, the effect of automatic resuscitators ongastric inflation in humans in cardiac arrest has notbeen studied, and there are no data demonstratingclear benefit over bag-valve-mask devices.Alternative airway devicesThe tracheal tube has generally been consideredthe optimal method of managing the airway duringcardiac arrest. There is evidence that, withoutadequate training and experience, the incidence ofcomplications, such as unrecognised oesophagealintubation (6—14% in some studies) 132—135 anddislodgement, is unacceptably high. 136 Prolongedattempts at tracheal intubation are harmful; thecessation of chest compressions during this timewill compromise coronary and cerebral perfusion.Several alternative airway devices have been consideredfor airway management during CPR. TheCombitube, the LMA, and the Laryngeal Tube(LT) are the only alternative devices to be studiedduring CPR, but none of these studies havebeen powered adequately to enable survival tobe studied as a primary endpoint; instead, mostresearchers have studied insertion and ventilationsuccess rates. There are no data supporting theroutine use of any specific approach to airwaymanagement during cardiac arrest. The best techniqueis dependent on the precise circumstancesof the cardiac arrest and the competence of therescuer.Laryngeal mask airway (LMA)The laryngeal mask airway comprises a wide-boretube with an elliptical inflated cuff designed to sealaround the laryngeal opening (Figure 4.9). It is easierto insert than a tracheal tube. 137—143 The LMAhas been studied during CPR, but none of thesestudies has compared it directly with the trachealtube. During CPR, successful ventilation is achievedwith the LMA in 72—98% of cases. 144—150Ventilation using the LMA is more efficient andeasier than with a bag-mask. 124 When an LMA can beinserted without delay it is preferable to avoid bagmaskventilation altogether. When used for intermittentpositive pressure ventilation, provided highinflation pressures (>20 cm H 2 O) are avoided, gastricinflation can be minimised. In comparison withbag-mask ventilation, use of a self-inflating bag and

European Resuscitation Council Guidelines for Resuscitation 2005S55Figure 4.9Insertion of a laryngeal mask airway. © 2005 European Resuscitation Council.LMA during cardiac arrest reduces the incidence ofregurgitation. 127In comparison with tracheal intubation, the perceiveddisadvantages of the LMA are the increasedrisk of aspiration and inability to provide adequateventilation in patients with low lung and/or chestwallcompliance. There are no data demonstratingwhether or not it is possible to provide adequateventilation via an LMA without interruption of chestcompressions. The ability to ventilate the lungsadequately while continuing to compress the chestmay be one of the main benefits of a tracheal tube.There are remarkably few cases of pulmonary aspirationreported in the studies of the LMA duringCPR.The CombitubeThe Combitube is a double-lumen tube introducedblindly over the tongue, and provides aroute for ventilation whether the tube has passedinto the oesophagus (Figure 4.10a) or the tra-Figure 4.10 (a) Combitube in the oesophageal position. (b) Combitube in the tracheal position. © 2005 EuropeanResuscitation Council.

S56chea (Figure 4.10b). There are many studies ofthe Combitube in CPR and successful ventilationwas achieved in 79—98% of patients. 146,151—157 Allexcept one 151 of these studies involved out-ofhospitalcardiac arrest, which reflects the infrequencywith which the Combitube is used in hospitals.On the basis of these studies, the Combitubeappears as safe and effective as tracheal intubationfor airway management during cardiac arrest; however,there are inadequate survival data to be ableto comment with certainty on the impact on outcome.It is possible to attempt to ventilate the lungsthrough the wrong port of the Combitube (2.2% inone study) 152 : This is equivalent to unrecognisedoesophageal intubation with a standard trachealtube.Other airway devicesLaryngeal Tube. The LT is a relatively new airwaydevice; its function in anaesthetised patientshas been reported in several studies. The performanceof the LT is favourable in comparisonwith the classic LMA and LMA, 158,159 and successfulinsertion rates have been reported even instudies of paramedics. 160 There are sporadic casereports relating to use of the laryngeal tube duringCPR. 161,162 In a recent study, the LT was placed in30 patients in cardiac arrest out of hospital by minimallytrained nurses. 163 LT insertion was successfulwithin two attempts in 90% of patients, and ventilationwas adequate in 80% of cases. No regurgitationoccurred in any patient.ProSeal LMA. The ProSeal LMA has been studiedextensively in anaesthetised patients, but there areno studies of its function and performance duringCPR. It has several attributes that, in theory, makeit more suitable than the classic LMA for use duringCPR: improved seal with the larynx enablingventilation at higher airway pressures, 164,165 theinclusion of a gastric drain tube enabling venting ofliquid regurgitated gastric contents from the upperoesophagus and passage of a gastric tube to drainliquid gastric contents, and the inclusion of a biteblock. The Proseal LMA has potential weaknesses asan airway device for CPR: it is slightly more difficultto insert than a classic LMA, it is not available in disposableform and is relatively expensive, and solidregurgitated gastric contents will block the gastricdrainage tube. Data are awaited on its performanceduring CPR.Airway management device. In anaesthetisedpatients, the airway management device (AMD)performed poorly in one study, 166 but a modifiedJ.P. Nolan et al.version appeared to function slightly better. 167 Thepharyngeal airway express (PAX) also performedpoorly in one study of anaesthetised patients. 168There are no data on the use of either of thesedevices during CPR.Intubating LMA. The intubating LMA (ILMA) isvaluable for managing the difficult airway duringanaesthesia, but it has not been studied duringCPR. Although it is relatively easy to insert theILMA, 169,170 reliable, blind insertion of a trachealtube requires considerable training 171 and, for thisreason, it is not an ideal technique for the inexperiencedprovider.Tracheal intubationThere is insufficient evidence to support or refutethe use of any specific technique to maintain anairway and provide ventilation in adults with cardiopulmonaryarrest. Despite this, tracheal intubationis perceived as the optimal method of providingand maintaining a clear and secure airway. It shouldbe used only when trained personnel are availableto carry out the procedure with a high level of skilland confidence. The only randomised controlledtrial comparing tracheal intubation with bag-maskventilation was undertaken in children requiringairway management out-of-hospital. 172 In thisinvestigation there was no difference in survival todischarge, but it is unclear how applicable this paediatricstudy is to adult resuscitation. Two reportscompared outcomes from out-of-hospital cardiacarrest in adults when treated by either emergencymedical technicians or paramedics. 173,174The skills provided by the paramedics, includingintubation and intravenous cannulation and drugadministration, 174 made no difference to survivalto hospital discharge.The perceived advantages of tracheal intubationover bag-mask ventilation include: maintenance ofa patent airway, which is protected from aspirationof gastric contents or blood from the oropharynx;ability to provide an adequate tidal volume reliablyeven when chest compressions are uninterrupted;the potential to free the rescuer’s hands for othertasks; the ability to suction airway secretions; andthe provision of a route for giving drugs. Use of thebag-mask is more likely to cause gastric distensionwhich, theoretically, is more likely to cause regurgitationwith risk of aspiration. However, there areno reliable data to indicate that the incidence ofaspiration is any more in cardiac arrest patientsventilated with bag-mask versus those that are ventilatedvia tracheal tube.

European Resuscitation Council Guidelines for Resuscitation 2005S57The perceived disadvantages of tracheal intubationover bag-mask ventilation include: the riskof an unrecognised misplaced tracheal tube, whichin patients with out-of-hospital cardiac arrest insome studies ranges from 6% 132—134 to 14% 135 ;aprolonged period without chest compressions whileintubation is attempted; and a comparatively highfailure rate. Intubation success rates correlate withthe intubation experience attained by individualparamedics. 175 Rates for failure to intubate areas high as 50% in prehospital systems with a lowpatient volume and providers who do not performintubation frequently. 134 The cost of training prehospitalstaff to undertake intubation should alsobe considered. Healthcare personnel who undertakeprehospital intubation should do so only withina structured, monitored programme, which shouldinclude comprehensive competency-based trainingand regular opportunities to refresh skills.In some cases, laryngoscopy and attemptedintubation may prove impossible or cause lifethreateningdeterioration in the patient’s condition.Such circumstances include acute epiglottalconditions, pharyngeal pathology, head injury(where straining may occur further rise in intracranialpressure) or cervical spine injury. In thesecircumstances, specialist skills such as the use ofanaesthetic drugs or fibreoptic laryngoscopy maybe required. These techniques require a high levelof skill and training.Rescuers must weigh the risks and benefits ofintubation against the need to provide effectivechest compressions. The intubation attempt willrequire interruption of chest compressions but,once an advanced airway is in place, ventilationwill not require interruption of chest compressions.Personnel skilled in advanced airway managementshould be able to undertake laryngoscopy withoutstopping chest compressions; a brief pause inchest compressions will be required only as thetube is passed through the vocal cords. Alternatively,to avoid any interruptions in chest compressions,the intubation attempt may be deferred untilreturn of spontaneous circulation. No intubationattempt should take longer than 30 s; if intubationhas not been achieved after this time, recommencebag-mask ventilation. After intubation, tube placementmust be confirmed and the tube secured adequately.Confirmation of correct placement of thetracheal tubeUnrecognised oesophageal intubation is the mostserious complication of attempted tracheal intubation.Routine use of primary and secondary techniquesto confirm correct placement of the trachealtube should reduce this risk. Primary assessmentincludes observation of chest expansion bilaterally,auscultation over the lung fields bilaterallyin the axillae (breath sounds should be equaland adequate) and over the epigastrium (breathsounds should not be heard). Clinical signs of correcttube placement (condensation in the tube,chest rise, breath sounds on auscultation of lungs,and inability to hear gas entering the stomach) arenot completely reliable. Secondary confirmation oftracheal tube placement by an exhaled carbon dioxideor oesophageal detection device should reducethe risk of unrecognised oesophageal intubation. Ifthere is doubt about correct tube placement, usethe laryngoscope and look directly to see if the tubepasses through the vocal cords.None of the secondary confirmation techniqueswill differentiate between a tube placed in a mainbronchus and one placed correctly in the trachea.There are inadequate data to identify the optimalmethod of confirming tube placement during cardiacarrest, and all devices should be consideredas adjuncts to other confirmatory techniques. 176There are no data quantifying their ability to monitortube position after initial placement.The oesophageal detector device creates a suctionforce at the tracheal end of the trachealtube, either by pulling back the plunger on a largesyringe or releasing a compressed flexible bulb. Airis aspirated easily from the lower airways througha tracheal tube placed in the cartilage-supportedrigid trachea. When the tube is in the oesophagus,air cannot be aspirated because the oesophaguscollapses when aspiration is attempted. Theoesophageal detector device is generally reliable inpatients with both a perfusing and a non-perfusingrhythm, but it may be misleading in patients withmorbid obesity, late pregnancy or severe asthmaor when there are copious tracheal secretions; inthese conditions the trachea may collapse whenaspiration is attempted. 133,177—180Carbon dioxide detector devices measure theconcentration of exhaled carbon dioxide from thelungs. The persistence of exhaled carbon dioxideafter six ventilations indicates placement of thetracheal tube in the trachea or a main bronchus. 181Confirmation of correct placement above the carinawill require auscultation of the chest bilaterally inthe mid-axillary lines. In patients with a spontaneouscirculation, a lack of exhaled carbon dioxideindicates that the tube is in the oesophagus. Duringcardiac arrest, pulmonary blood flow may be solow that there is insufficient exhaled carbon dioxide,so the detector does not identify a correctlyplaced tracheal tube. When exhaled carbon dioxide

S58is detected in cardiac arrest, it indicates reliablythat the tube is in the trachea or main bronchus but,when it is absent, tracheal tube placement is bestconfirmed with an oesophageal detector device. Avariety of electronic as well as simple, inexpensive,colorimetric carbon dioxide detectors are availablefor both in-hospital and out-of-hospital use.Cricoid pressureDuring bag-mask ventilation and attempted intubation,cricoid pressure applied by a trained assistantshould prevent passive regurgitation of gastriccontents and the consequent risk of pulmonaryaspiration. If the technique is applied impreciselyor with excessive force, ventilation and intubationcan be made more difficult. 128 If ventilation of thepatient’s lungs is not possible, reduce the pressureapplied to the cricoid cartilage or remove it completely.If the patient vomits, release the cricoidimmediately.Securing the tracheal tubeAccidental dislodgement of a tracheal tube canoccur at any time, but may be more likely duringresuscitation and during transport. The most effectivemethod for securing the tracheal tube has yetto be determined; use either conventional tapes orties, or purpose-made tracheal tube holders.CricothyroidotomyOccasionally, it will be impossible to ventilate anapnoeic patient with a bag-mask, or to pass a trachealtube or alternative airway device. This mayoccur in patients with extensive facial trauma orlaryngeal obstruction due to oedema or foreignmaterial. In these circumstances, delivery of oxygenthrough a needle or surgical cricothyroidotomymay be life-saving. A tracheostomy is contraindicatedin an emergency, as it is time consuming,hazardous and requires considerable surgical skilland equipment.Surgical cricothyroidotomy provides a definitiveairway that can be used to ventilate thepatient’s lungs until semi-elective intubation or tracheostomyis performed. Needle cricothyroidotomyis a much more temporary procedure providingonly short-term oxygenation. It requires a widebore,non-kinking cannula, a high-pressure oxygensource, runs the risk of barotrauma and can be particularlyineffective in patients with chest trauma.It is also prone to failure because of kinking of thecannula, and is unsuitable for patient transfer.4e. Assisting the circulationDrugs and fluids for cardiac arrestJ.P. Nolan et al.This topic is divided into: drugs used during themanagement of a cardiac arrest; anti-arrhythmicdrugs used in the peri-arrest period; other drugsused in the peri-arrest period; fluids; and routesfor drug delivery. Every effort has been made toprovide accurate information on the drugs in theseguidelines, but literature from the relevant pharmaceuticalcompanies will provide the most up-todatedata.Drugs used during the treatment of cardiacarrestOnly a few drugs are indicated during the immediatemanagement of a cardiac arrest, and thereis limited scientific evidence supporting their use.Drugs should be considered only after initial shockshave been delivered (if indicated) and chest compressionsand ventilation have been started.There are three groups of drugs relevant to themanagement of cardiac arrest that were reviewedduring the 2005 Consensus Conference: vasopressors,anti-arrhythmics and other drugs. Routes ofdrug delivery other than the optimal intravenousroute were also reviewed and are discussed.VasopressorsThere are currently no placebo-controlled studiesshowing that the routine use of any vasopressor atany stage during human cardiac arrest increasessurvival to hospital discharge. The primary goalof cardiopulmonary resuscitation is to re-establishblood flow to vital organs until the restoration ofspontaneous circulation. Despite the lack of datafrom cardiac arrest in humans, vasopressors continueto be recommended as a means of increasingcerebral and coronary perfusion during CPR.Adrenaline (epinephrine) versus vasopressin.Adrenaline has been the primary sympathomimeticagent for the management of cardiac arrest for40 years. 182 Its primary efficacy is due to itsalpha-adrenergic, vasoconstrictive effects causingsystemic vasoconstriction, which increasescoronary and cerebral perfusion pressures. Thebeta-adrenergic actions of adrenaline (inotropic,chronotropic) may increase coronary and cerebralblood flow, but concomitant increases in myocardialoxygen consumption, ectopic ventriculararrhythmias (particularly when the myocardiumis acidotic) and transient hypoxaemia due to

European Resuscitation Council Guidelines for Resuscitation 2005S59pulmonary arteriovenous shunting may offset thesebenefits.The potentially deleterious beta-effects ofadrenaline have led to exploration of alternativevasopressors. Vasopressin is a naturally occurringantidiuretic hormone. In very high doses it is apowerful vasoconstrictor that acts by stimulationof smooth muscle V1 receptors. The importance ofvasopressin in cardiac arrest was first recognised instudies of out-of-hospital cardiac arrest patients,where vasopressin levels were found to be higher insuccessfully resuscitated patients. 183,184 Althoughclinical 185,186 and animal 187—189 studies demonstratedimproved haemodynamic variables whenusing vasopressin as an alternative to adrenalineduring resuscitation from cardiac arrest, some, 186but not all, demonstrated improved survival. 190,191The first clinical use of vasopressin during cardiacarrest was reported in 1996 and appearedpromising. In a study of cardiac arrest patientsrefractory to standard therapy with adrenaline,vasopressin restored a spontaneous circulation inall eight patients, three of whom were dischargedneurologically intact. 186 The following year, thesame group published a small randomised trialof out-of-hospital ventricular fibrillation, in whichthe rates of successful resuscitation and survivalfor 24 h were significantly higher in patientstreated with vasopressin than in those treated withadrenaline. 192 Following these two studies, theAmerican Heart Association (AHA) recommendedthat vasopressin could be used as an alternativeto adrenaline for the treatment of adult shockrefractoryVF. 182 The success of these small studiesled to two large randomised studies comparingvasopressin with adrenaline for in-hospital 193and out-of-hospital 194 cardiac arrest. Both studiesrandomised patients to receive vasopressin oradrenaline initially, and used adrenaline as a rescuetreatment in patients refractory to the initialdrug. Both studies were unable to demonstrate anoverall increase in the rates of ROSC or survivalfor vasopressin 40 U, 193 with the dose repeatedin one study, 194 when compared with adrenaline(1 mg, repeated), as the initial vasopressor. In thelarge out-of-hospital cardiac arrest study, 194 posthocanalysis suggested that the subset of patientswith asystole had significant improvement in survivalto discharge, but survival neurologically intactwas no different.A recent meta-analysis of five randomisedtrials 195 showed no statistically significant differencebetween vasopressin and adrenaline for ROSC,death within 24 h or death before hospital discharge.The subgroup analysis based on initial cardiacrhythm did not show any statistically significantdifference in the rate of death before hospitaldischarge. 195Participants at the 2005 Consensus Conferencedebated in depth the treatment recommendationsthat should follow from this evidence. Despite theabsence of placebo-controlled trials, adrenalinehas been the standard vasopressor in cardiac arrest.It was agreed that there is currently insufficientevidence to support or refute the use of vasopressinas an alternative to, or in combination with,adrenaline in any cardiac arrest rhythm. Currentpractice still supports adrenaline as the primaryvasopressor for the treatment of cardiac arrest ofall rhythms.AdrenalineIndications• Adrenaline is the first drug used in cardiac arrestof any aetiology: it is included in the ALS algorithmfor use every 3—5 min of CPR.• Adrenaline is preferred in the treatment of anaphylaxis(Section 7g).• Adrenaline is second-line treatment for cardiogenicshock.Dose. During cardiac arrest, the initial intravenousdose of adrenaline is 1 mg. When intravascular(intravenous or intra-osseous) access is delayedor cannot be achieved, give 2—3 mg, diluted to10 ml with sterile water, via the tracheal tube.Absorption via the tracheal route is highly variable.There is no evidence supporting the use of higherdoses of adrenaline for patients in refractory cardiacarrest. In some cases, an adrenaline infusion isrequired in the post-resuscitation period.Following return of spontaneous circulation,excessive (≥1 mg) doses of adrenaline may inducetachycardia, myocardial ischaemia, VT and VF.Once a perfusing rhythm is established, if furtheradrenaline is deemed necessary, titrate the dosecarefully to achieve an appropriate blood pressure.Intravenous doses of 50—100 mcg are usually sufficientfor most hypotensive patients. Use adrenalinecautiously in patients with cardiac arrest associatedwith cocaine or other sympathomimetic drugs.Use. Adrenaline is available most commonly intwo dilutions:• 1 in 10,000 (10 ml of this solution contains 1 mgof adrenaline)• 1 in 1000 (1 ml of this solution contains 1 mg ofadrenaline)Both these dilutions are used routinely in Europeancountries.

S60Various other pressor drugs (e.g.,noradrenaline) 196 have been used experimentallyas an alternative to adrenaline for thetreatment of cardiac arrest.Anti-arrhythmicsAs with vasopressors, the evidence that antiarrhythmicdrugs are of benefit in cardiac arrestis limited. No anti-arrhythmic drug given duringhuman cardiac arrest has been shown to increasesurvival to hospital discharge, although amiodaronehas been shown to increase survival to hospitaladmission. 89,90 Despite the lack of human long-termoutcome data, the balance of evidence is in favourof the use anti-arrhythmic drugs for the managementof arrhythmias in cardiac arrest.Amiodarone. Amiodarone is a membranestabilisinganti-arrhythmic drug that increases theduration of the action potential and refractoryperiod in atrial and ventricular myocardium. Atrioventricularconduction is slowed, and a similareffect is seen with accessory pathways. Amiodaronehas a mild negative inotropic action and causesperipheral vasodilation through non-competitivealpha-blocking effects. The hypotension thatoccurs with intravenous amiodarone is related tothe rate of delivery and is due more to the solvent(Polysorbate 80), which causes histamine release,rather than the drug itself. 197 The use of anaqueous amiodarone preparation that is relativelyfree from these side effects is encouraged but isnot yet widely available 198,199 .Following three initial shocks, amiodarone inshock-refractory VF improves the short-term outcomeof survival to hospital admission comparedwith placebo 89 or lignocaine. 90 Amiodaronealso appears to improve the response todefibrillation when given to humans or animalswith VF or haemodynamically unstable ventriculartachycardia. 198—202 There is no evidence to indicatethe time at which amiodarone should be givenwhen using a single shock strategy. In the clinicalstudies to date, the amiodarone was given ifVF/VT persisted after at least three shocks. For thisreason, and in the absence of any other data, amiodarone300 mg is recommended if VF/VT persistsafter three shocks.Indications. Amiodarone is indicated in• refractory VF/VT• haemodynamically stable ventricular tachycardia(VT) and other resistant tachyarrhythmias (Section4f)Dose. Consider an initial intravenous dose of300 mg amiodarone, diluted in 5% dextrose to aJ.P. Nolan et al.volume of 20 ml (or from a pre-filled syringe), ifVF/VT persists after the third shock. Amiodaronecan cause thrombophlebitis when injected into aperipheral vein; use a central venous catheter ifone is in situ but,if not, use a large peripheral veinand a generous flush. Details about the use of amiodaronefor the treatment of other arrhythmias aregiven in Section 4f.Clinical aspects of use. Amiodarone may paradoxicallybe arrhythmogenic, especially if givenconcurrently with drugs that prolong the QTinterval. However, it has a lower incidence ofpro-arrhythmic effects than other anti-arrhythmicdrugs under similar circumstances. The major acuteadverse effects from amiodarone are hypotensionand bradycardia, which can be prevented by slowingthe rate of drug infusion, or can be treated withfluids and/or inotropic drugs. The side effects associatedwith prolonged oral use (abnormalities ofthyroid function, corneal microdeposits, peripheralneuropathy, and pulmonary/hepatic infiltrates) arenot relevant in the acute setting.Lidocaine. Until the publication of the 2000 ILCORguidelines, lidocaine was the antiarrhythmic drugof choice. Comparative studies with amiodarone 90have displaced it from this position, and lidocaineis now recommended only when amiodarone isunavailable. Amiodarone should be available at allhospital arrests and to all out-of-hospital arrestsattended by ambulance crew.Lidocaine is a membrane-stabilising antiarrhythmicdrug that acts by increasing themyocyte refractory period. It decreases ventricularautomaticity, and its local anaesthetic actionsuppresses ventricular ectopic activity. Lidocainesuppresses activity of depolarised, arrhythmogenictissues while interfering minimally with the electricalactivity of normal tissues. Therefore, it iseffective in suppressing arrhythmias associatedwith depolarisation (e.g. ischaemia, digitalis toxicity)but is relatively ineffective against arrhythmiasoccurring in normally polarised cells (e.g., atrialfibrillation/flutter). Lidocaine raises the thresholdfor ventricular fibrillation.Lidocaine toxicity causes paraesthesia, drowsiness,confusion and muscular twitching progressingto convulsions. It is considered generally that a safedose of lidocaine must not exceed 3 mg kg −1 overthe first hour. If there are signs of toxicity, stop theinfusion immediately; treat seizures if they occur.Lidocaine depresses myocardial function, but to amuch lesser extent than amiodarone. The myocardialdepression is usually transient and can betreated with intravenous fluids or vasopressors.

European Resuscitation Council Guidelines for Resuscitation 2005S61Indications. Lidocaine is indicated in refractoryVF/VT (when amiodarone is unavailable).Dose. When amiodarone is unavailable, consideran initial dose of 100 mg (1—1.5 mg kg −1 )oflidocaine for VF/pulseless VT refractory to threeshocks. Give an additional bolus of 50 mg if necessary.The total dose should not exceed 3 mg kg −1during the first hour.Clinical aspects of use. Lidocaine is metabolisedby the liver, and its half-life is prolonged if thehepatic blood flow is reduced, e.g. in the presenceof reduced cardiac output, liver diseaseor in the elderly. During cardiac arrest normalclearance mechanisms do not function, thus highplasma concentrations may be achieved after asingle dose. After 24 h of continuous infusion, theplasma half-life increases significantly. Reduce thedose in these circumstances, and regularly reviewthe indication for continued therapy. Lidocaine isless effective in the presence of hypokalaemiaand hypomagnesaemia, which should be correctedimmediately.Magnesium sulphate. Magnesium is an importantconstituent of many enzyme systems, especiallythose involved with ATP generation in muscle.It plays a major role in neurochemical transmission,where it decreases acetylcholine release andreduces the sensitivity of the motor endplate.Magnesium also improves the contractile responseof the stunned myocardium, and limits infarctsize by a mechanism that has yet to be fullyelucidated. 203 The normal plasma range of magnesiumis 0.8—1.0 mmol l −1 .Hypomagnesaemia is often associated withhypokalaemia, and may contribute to arrhythmiasand cardiac arrest. Hypomagnesaemia increasesmyocardial digoxin uptake and decreases cellularNa + /K + -ATP-ase activity. Patients with hypomagnesaemia,hypokalaemia, or both may become cardiotoxiceven with therapeutic digitalis levels. Magnesiumdeficiency is not uncommon in hospitalisedpatients and frequently coexists with other electrolytedisturbances, particularly hypokalaemia,hypophosphataemia, hyponatraemia and hypocalcaemia.Although the benefits of giving magnesium inknown hypomagnesaemic states are recognised, thebenefit of giving magnesium routinely during cardiacarrest is unproven. Studies in adults in and outof hospital 91—95,204 have failed to demonstrate anyincrease in the rate of ROSC when magnesium isgiven routinely during CPR. There is some evidencethat magnesium may be beneficial in refractoryVF. 205Indications. Magnesium sulphate is indicated in• shock-refractory VF in the presence of possiblehypomagnesaemia• ventricular tachyarrhythmias in the presence ofpossible hypomagnesaemia• torsades de pointes• digoxin toxicityDose. In shock-refractory VF, give an initial intravenousdose of 2 g (4 ml (8 mmol)) of 50% magnesiumsulphate) peripherally over 1—2 min; it maybe repeated after 10—15 min. Preparations of magnesiumsulphate solutions differ among Europeancountries.Clinical aspects of use. Hypokalaemic patientsare often hypomagnesaemic. If ventricular tachyarrhythmiasarise, intravenous magnesium is asafe, effective treatment. The role of magnesiumin acute myocardial infarction is still in doubt. Magnesiumis excreted by the kidneys, but side effectsassociated with hypermagnesaemia are rare, evenin renal failure. Magnesium inhibits smooth musclecontraction, causing vasodilation and a doserelatedhypotension, which is usually transient andresponds to intravenous fluids and vasopressors.Other drugsThe evidence for the benefits of other drugs, includingatropine, aminophylline and calcium, givenroutinely during human cardiac arrest, is limited.Recommendations for the use of these drugs arebased on our understanding of their pharmacodynamicproperties and the pathophysiology of cardiacarrest.Atropine. Atropine antagonises the action of theparasympathetic neurotransmitter acetylcholine atmuscarinic receptors. Therefore, it blocks theeffect of the vagus nerve on both the sinoatrial (SA)node and the atrioventricular (AV) node, increasingsinus automaticity and facilitating AV node conduction.Side effects of atropine are dose-related(blurred vision, dry mouth and urinary retention);they are not relevant during a cardiac arrest.Acute confusional states may occur after intravenousinjection, particularly in elderly patients.After cardiac arrest, dilated pupils should not beattributed solely to atropine.Atropine is indicated in:• asystole• pulseless electrical activity (PEA) with a rate

S62The recommended adult dose of atropine forasystole or PEA with a rate

European Resuscitation Council Guidelines for Resuscitation 2005S63of-hospital cardiac arrests) or after return of spontaneouscirculation is not recommended. Considersodium bicarbonate for life-threatening hyperkalaemiaor cardiac arrest associated with hyperkalaemia,severe metabolic acidosis, or tricyclicoverdose. Give 50 mmol (50 ml of an 8.4% solution)of sodium bicarbonate intravenously. Repeatthe dose as necessary, but use acid/base analysis(either arterial or central venous) to guide therapy.Severe tissue damage may be caused by subcutaneousextravasation of concentrated sodium bicarbonate.The solution is incompatible with calciumsalts as it causes the precipitation of calcium carbonate.Thrombolysis during CPR. Adult cardiac arrestis usually caused by acute myocardial ischaemiafollowing coronary artery occlusion by thrombus.There are several reports on the successful useof thrombolytics during cardiac arrest, particularlywhen the arrest was caused by pulmonaryembolism. The use of thrombolytic drugs to breakdown coronary artery and pulmonary artery thrombushas been the subject of several studies. Thrombolyticshave also been demonstrated in animalstudies to have beneficial effects on cerebral bloodflow during cardiopulmonary resuscitation, 223,224and a clinical study has reported less anoxicencephalopathy after thrombolytic therapy duringCPR. 225Several studies have examined the use of thrombolytictherapy given during non-traumatic cardiacarrest refractory to standard therapy. Two studieshave shown an increase in ROSC with nonsignificantimprovements in survival to hospitaldischarge, 97,226 and a further study demonstratedgreater ICU survival. 225 A small series of casereports has also reported survival to discharge inthree cases refractory to standard therapy with VFor PEA treated with thrombolytics 227 ; conversely,one large clinical trial 228 failed to show any significantbenefit for thrombolytics in cases of undifferentiatedPEA out-of-hospital cardiac arrest unresponsiveto initial interventions.When given to cardiac arrest patients withsuspected or proven pulmonary embolus, twostudies have demonstrated possible benefits 229,230 ;one found an improvement in 24-h survival. 229Several clinical studies 97,226,229,231 and caseseries 227,230,232—234 have not demonstrated anyincrease in bleeding complications with thrombolysisduring CPR in non-traumatic cardiac arrest.There are insufficient clinical data to recommendthe routine use of thrombolysis during nontraumaticcardiac arrest. Consider thrombolytictherapy when cardiac arrest is thought to be dueto proven or suspected acute pulmonary embolus.Thrombolysis may be considered in adult cardiacarrest on a case by case basis following initial failureof standard resuscitation in patients in whoman acute thrombotic aetiology for the arrest is suspected.Ongoing CPR is not a contraindication tothrombolysis.Following thrombolysis during CPR for acute pulmonaryembolism, survival and good neurologicaloutcome have been reported in cases requiring inexcess of 60 min of CPR. If a thrombolytic drug isgiven in these circumstances, consider performingCPR for at least 60—90 min before termination ofresuscitation attempts. 235,236Intravenous fluidsHypovolaemia is a potentially reversible cause ofcardiac arrest. Infuse fluids rapidly if hypovolaemiais suspected. In the initial stages of resuscitationthere are no clear advantages to using colloid, souse saline or Hartmann’s solution. Avoid dextrose,which is redistributed away from the intravascularspace rapidly and causes hyperglycaemia, whichmay worsen neurological outcome after cardiacarrest. 237—244Whether fluids should be infused routinely duringcardiac arrest is controversial. There are no publishedhuman studies of routine fluid use comparedto no fluids during normovolaemic cardiac arrest.Four animal studies 245—248 of experimental ventricularfibrillation neither support nor refute the useof intravenous fluids routinely. In the absence ofhypovolaemia, infusion of an excessive volume offluid is likely to be harmful. Use intravenous fluidto flush peripherally injected drugs into the centralcirculation.Alternative routes for drug deliveryIntraosseous routeIf intravenous access cannot be established,intraosseous delivery of resuscitation drugs willachieve adequate plasma concentrations. Severalstudies indicate that intraosseous access is safeand effective for fluid resuscitation, drug deliveryand laboratory evaluation. 78,249—255 Traditionally,the intraosseous route is used mainly for children,but it is also effective in adults.Drugs given via the tracheal tubeResuscitation drugs can also be given via the trachealtube, but the plasma concentrations achievedusing this route are variable and substantially

S64lower than those achieved by the intravenous orintraosseous routes.Doses of adrenaline 3—10 times higher than whengiven intravenously are required to achieve similarplasma concentrations. 79,80 During CPR, lungperfusion is only 10—30% of the normal value,resulting in a pulmonary adrenaline depot. Whencardiac output is restored after a high dose ofendobronchial adrenaline, prolonged reabsorptionof adrenaline from the lungs into the pulmonarycirculation may occur, causing arterial hypertension,malignant arrhythmias and recurrence of VF. 80Lidocaine and atropine can also be given via a trachealtube, but the plasma concentrations achievedare also variable. 256—258 If intravenous access isdelayed or cannot be achieved, consider obtainingintraosseous access. Give drugs via the trachealtube if intravascular (intravenous or intraosseous)access is delayed or cannot be achieved. There areno benefits from endobronchial injection comparedwith injection of the drug directly into the trachealtube. 256 Dilution with water instead of 0.9% salinemay achieve better drug absorption and cause lessreduction in PaO 2 . 85,259CPR techniques and devicesAt best, standard manual CPR produces coronaryand cerebral perfusion that is just 30% of normal. 260Several CPR techniques and devices may improvehaemodynamics or short-term survival when usedby well-trained providers in selected cases. To date,no adjunct has consistently been shown to be superiorto conventional manual CPR. CPR techniquesinclude the following.High-frequency chest compressions (HFCC)High-frequency (>100 compressions min −1 ) manualor mechanical chest compressions improve haemodynamicsbut have not been shown to improve longtermoutcome. 261—265Open-chest CPROpen-chest CPR produces better coronary perfusioncoronary pressure than standard CPR 266 and maybe indicated for patients with cardiac arrest due totrauma (see Section 7i), in the early postoperativephase after cardiothoracic surgery 267,268 (see Section7h) or when the chest or abdomen is alreadyopen (transdiaphragmatic approach), for example,in trauma surgery.J.P. Nolan et al.Interposed abdominal compression (IAC-CPR)The IAC-CPR technique involves compression ofthe abdomen during the relaxation phase ofchest compression. 269,270 This enhances venousreturn during CPR 271,272 and improves ROSCand short-term survival. 273,274 One study showedimproved survival to hospital discharge with IAC-CPR compared with standard CPR for out-ofhospitalcardiac arrest, 274 but another showed nosurvival advantage. 275 CPR devices include thefollowing.Active compression-decompression CPR(ACD-CPR)ACD-CPR is achieved with a hand-held deviceequipped with a suction cup to lift the anteriorchest actively during decompression. Decreasingintrathoracic pressure during the decompressionphase increases venous return to the heartand increases cardiac output and subsequent coronaryand cerebral perfusion pressures during thecompression phase. 276—279 Results of ACD-CPR havebeen mixed. In some clinical studies ACD-CPRimproved haemodynamics compared with standardCPR, 173,277,279,280 but in another study itdid not. 281 In three randomised studies, 280,282,283ACD-CPR improved long-term survival after out-ofhospitalcardiac arrest; however, in five other randomisedstudies, ACD-CPR made no difference tooutcome. 284—288 The efficacy of ACD-CPR may behighly dependent on the quality and duration oftraining. 289A meta-analysis of 10 trials of out-of-hospitalcardiac arrest and two of in-hospital cardiac arrestshowed no early or late survival benefit to ACD-CPRover conventional CPR. 290 Two post-mortem studieshave shown more rib and sternal fractures afterACD-CPR compared with conventional CPR, 291,292but another found no difference. 293Impedance threshold device (ITD)The impedance threshold device (ITD) is a valvethat limits air entry into the lungs during chestrecoil between chest compressions; this decreasesintrathoracic pressure and increases venous returnto the heart. When used with a cuffed trachealtube and active compression-decompression(ACD), 294—296 the ITD is thought to act synergisticallyto enhance venous return during activedecompression. The ITD has also been used duringconventional CPR with a tracheal tube orfacemask. 297 If rescuers can maintain a tight facemaskseal, the ITD may create the same negative

European Resuscitation Council Guidelines for Resuscitation 2005S65intrathoracic pressure as when used with a trachealtube. 297In two randomised studies of out-of-hospitalcardiac arrest, ACD-CPR plus the ITD improvedROSC and 24-h survival compared with standardCPR alone. 296,298 When used during standard CPR,the ITD increased 24-h survival after PEA out-ofhospitalcardiac arrest. 297Mechanical piston CPRMechanical piston devices depress the sternumby means of a compressed gas-powered plungermounted on a backboard. In several studies inanimals, 299,300 mechanical piston CPR improvedend-tidal carbon dioxide, cardiac output, cerebralblood flow, MAP and short-term neurological outcome.Studies in humans also document improvementin end-tidal carbon dioxide and mean arterialpressure when using mechanical piston CPR comparedwith conventional CPR. 301—303Lund University cardiac arrest system (LUCAS)CPRThe Lund University cardiac arrest system (LUCAS)is a gas-driven sternal compression device thatincorporates a suction cup for active decompression.There are no published randomised humanstudies comparing LUCAS-CPR with standard CPR.A study of pigs with VF showed that LUCAS-CPRimproves haemodynamic and short-term survivalcompared with standard CPR. 304 The LUCAS wasalso used in 20 patients, but incomplete outcomedata were reported. 304 In another pig study, in comparisonwith standard CPR, LUCAS-CPR increasedcerebral blood flow and cardiac output. 305 TheLUCAS enables delivery of continuous compressionsduring transport and defibrillation.Mechanical piston CPR or LUCAS CPR may be particularlyuseful when prolonged CPR is required;this might include during transport to hospital orafter cardiac arrest following hypothermia 306 orpoisoning.Load-distributing band CPR or vest CPRThe load distributing band (LDB) is a circumferentialchest compression device comprisinga pneumatically actuated constricting bandand backboard. The use of LDB CPR improveshaemodynamics. 307—309 A case—control study documentedimprovement in survival to the emergencydepartment when LDB-CPR was delivered after outof-hospitalcardiac arrest. 310Phased thoracic—abdominalcompression—decompression CPR (PTACD-CPR)Phased thoracic—abdominal compression—decompressionCPR combines the concepts of IAC-CPRand ACD-CPR. It comprises a hand-held devicethat alternates chest compression and abdominaldecompression with chest decompression andabdominal compression. One randomised study ofadults in cardiac arrest documented no improvementin survival from use of PTACD-CPR. 311Minimally invasive direct cardiac massageMinimally invasive direct cardiac massage (MIDCM)is accomplished by insertion of a small plunger-likedevice through a 2—4-cm incision in the chest wall.In one clinical study the MIDCM generated improvedblood pressure over standard CPR, but the devicecaused cardiac rupture in one postoperative cardiovascularsurgical patient. 312 The plunger device isno longer manufactured.4f. Peri-arrest arrhythmiasIntroductionA successful strategy to reduce the mortalityand morbidity of cardiac arrest includes measuresto prevent other potentially serious arrhythmias,and optimal treatment should they occur. Cardiacarrhythmias are well recognised complications ofmyocardial infarction. They may precede ventricularfibrillation or follow successful defibrillation.The treatment algorithms described in this sectionhave been designed to enable the non-specialistALS provider to treat the patient effectively andsafely in an emergency; for this reason, they havebeen kept as simple as possible. If patients arenot acutely ill there may be several other treatmentoptions, including the use of drugs (oral orparenteral), that will be less familiar to the nonexpert.In this situation there will be time to seekadvice from cardiologists or other doctors with theappropriate expertise.More comprehensive information on themanagement of arrhythmias can be found atwww.escardio.org.Principles of treatmentIn all cases, give oxygen and insert an intravenouscannula while the arrhythmia is assessed. Wheneverpossible, record a 12-lead ECG; this will help determinethe precise rhythm, either before treatment

S66or retrospectively, if necessary with the help of anexpert. Correct any electrolyte abnormalities (e.g.,K + ,Mg 2+ ,Ca 2+ ) (Section 7a).The assessment and treatment of all arrhythmiasaddresses two factors: the condition of thepatient (stable versus unstable), and the nature ofthe arrhythmia.Adverse signsThe presence or absence of adverse signs or symptomswill dictate the appropriate treatment formost arrhythmias. The following adverse factorsindicate a patient who is unstable because of thearrhythmia.1. Clinical evidence of low cardiac output. Thisis seen as pallor, sweating, cold and clammyextremities (increased sympathetic activity),impaired consciousness (reduced cerebral bloodflow), and hypotension (e.g., systolic blood pressure150 min −1 ) reduce diastolecritically, decreasing coronary blood flow andcausing myocardial ischaemia. Broad, complextachycardias are tolerated less well by the heartthan narrow, complex tachycardias.3. Excessive bradycardia. This is defined as aheart rate of

European Resuscitation Council Guidelines for Resuscitation 2005S67Figure 4.11Bradycardia algorithm.• Möbitz type II AV block• complete (third-degree) heart block (especiallywith broad QRS or initial heart rate0.20 s), and is usually benign. SeconddegreeAV block is divided into Möbitz types I and II.In Möbitz type I, the block is at the AV node, is oftentransient and may be asymptomatic. In Möbitz typeII, the block is most often below the AV node atthe bundle of His or at the bundle branches, and isoften symptomatic, with the potential to progressto complete AV block. Third-degree heart block isdefined by AV dissociation which may be permanentor transient, depending on the underlying cause.Pacing is likely to be required if there is a riskof asystole, or if the patient is unstable and hasfailed to respond satisfactorily to atropine. Underthese circumstances, the definitive treatment istransvenous pacing. One or more of the followinginterventions can be used to improve the patient’scondition while waiting for the appropriate personneland facilities:

S68• transcutaneous pacing• adrenaline infusion in the range of2—10 mcg min −1 titrated to responseOther drugs that can be given for symptomaticbradycardia include dopamine, isoprenaline andtheophylline. Consider giving intravenous glucagonif beta-blockers or calcium channel blockers area potential cause of the bradycardia. Do not giveatropine to patients with cardiac transplants—–paradoxically, it can cause a high-degree AV blockor even sinus arrest. 315Complete heart block with a narrow QRS is notan absolute indication for pacing, because AV junctionalectopic pacemakers (with a narrow QRS) mayprovide a reasonable and stable heart rate.PacingTranscutaneous pacing. Initiate transcutaneouspacing immediately if there is no response toatropine, if atropine is unlikely to be effective or ifthe patient is severely symptomatic, particularly ifthere is high-degree block (Möbitz Type II second- orJ.P. Nolan et al.third-degree block). Transcutaneous pacing can bepainful and may fail to produce effective mechanicalcapture. Verify mechanical capture and reassessthe patient’s condition. Use analgesia and sedationto control pain, and attempt to identify the causeof the bradyarrhythmia.Fist pacing. If atropine is ineffective and transcutaneouspacing is not immediately available, fistpacing can be attempted while waiting for pacingequipment 316—318 : give serial rhythmic blows withthe closed fist over the left lower edge of the sternumto pace the heart at a physiological rate of50—70 beats min −1 .TachycardiasPrevious ERC guidelines have included three separatetachycardia algorithms: broad-complex tachycardia,narrow-complex tachycardia and atrial fibrillation.In the peri-arrest setting, many treatmentprinciples are common to all the tachycardias; forthis reason, they have been combined into a singletachycardia algorithm (Figure 4.12).Figure 4.12Tachycardia algorithm.

European Resuscitation Council Guidelines for Resuscitation 2005S69If the patient is unstable and deteriorating,with signs and symptoms caused by the tachycardia(e.g., impaired conscious level, chest pain,heart failure, hypotension or other signs of shock),attempt synchronised cardioversion immediately.In patients with otherwise normal hearts, serioussigns and symptoms are uncommon if the ventricularrate is 0.12 s and are usually ventricular in origin.Although broad-complex tachycardias may becaused by supraventricular rhythms with aberrantconduction, in the unstable patient in the periarrestcontext assume they are ventricular in origin.In the stable patient with broad-complex tachycardia,the next step is to determine if the rhythm isregular or irregular.Regular broad complex tachycardia. A regularbroad-complex tachycardia is likely to be ventriculartachycardia or SVT with bundle branch block.Stable ventricular tachycardia can be treated withamiodarone 300 mg intravenously over 20—60 minfollowed by an infusion of 900 mg over 24 h. If thebroad-complex regular tachycardia is thought to beSVT with bundle branch block, give adenosine, usingthe strategy indicated for narrow-complex tachycardia(below).Irregular broad complex tachycardia. Irregularbroad complex tachycardia is most likely tobe AF with bundle branch block, but carefulexamination of a 12-lead ECG (if necessary byan expert) may enable confident identificationof the rhythm. Another possible cause is AFwith ventricular pre-excitation (in patients withWolff—Parkinson—White (WPW) syndrome). Thereis more variation in the appearance and width of theQRS complexes than in AF with bundle branch block.A third possible cause is polymorphic VT (e.g., torsadede pointes), but polymorphic VT is relativelyunlikely to be present without adverse features.Seek expert help with the assessment and treatmentof irregular broad-complex tachyarrhythmia.If treating AF with bundle branch block, treat as forAF (see below). If pre-excited AF (or atrial flutter) issuspected, avoid adenosine, digoxin, verapamil anddiltiazem. These drugs block the AV node and causea relative increase in pre-excitation. Electrical cardioversionis usually the safest treatment option.Treat torsades de pointes VT immediately bystopping all drugs known to prolong QT interval.Correct electrolyte abnormalities, especiallyhypokalaemia. Give magnesium sulphate, 2 g, intravenouslyover 10 min. 319,320 Obtain expert help, asother treatment (e.g., overdrive pacing) may beindicated to prevent relapse once the arrhythmiahas been corrected. If adverse features develop(which is usual), arrange immediate synchronisedcardioversion. If the patient becomes pulseless,attempt defibrillation immediately (cardiac arrestalgorithm).

S70Narrow-complex tachycardiaRegular narrow-complex tachycardias include:• sinus tachycardia• AV nodal re-entry tachycardia (AVNRT, the commonesttype of SVT)• AV re-entry tachycardia (AVRT (due to WPW syndrome))• atrial flutter with regular AV conduction (usually2:1)Irregular narrow-complex tachycardia is mostcommonly AF or sometimes atrial flutter with variableAV conduction (‘variable block’).Regular narrow-complex tachycardiaSinus tachycardia. Sinus tachycardia is a commonphysiological response to a stimulus such asexercise or anxiety. In a sick patient it may be seenin response to many stimuli, such as pain, fever,anaemia, blood loss and heart failure. Treatmentis almost always directed at the underlying cause;trying to slow sinus tachycardia that has occurredin response to most of these situations will makethe situation worse.AVNRT and AVRT (paroxysmal SVT). AVNRT is thecommonest type of paroxysmal SVT, often seen inpeople without any other form of heart diseaseand is relatively uncommon in a peri-arrest setting.It causes a regular narrow-complex tachycardia,often with no clearly visible atrial activity on theECG, with heart rates usually well above the typicalrange of sinus rates at rest (60—120 beats min −1 ).It is usually benign, unless there is additional coincidentalstructural heart disease or coronary disease,but may cause symptoms that the patientfinds frightening.AV re-entry tachycardia (AVRT) is seen in patientswith the WPW syndrome and is also usually benignunless there happens to be additional structuralheart disease. The common type of AVRT is a regularnarrow-complex tachycardia, also often havingno visible atrial activity on the ECG.Atrial flutter with regular AV conduction (often2:1 block). Atrial flutter with regular AV conduction(often 2:1 block) produces a regular narrowcomplextachycardia in which it may be difficultto see atrial activity and identify flutter waveswith confidence, so it may be indistinguishable initiallyfrom AVNRT and AVRT. When atrial flutterwith 2:1 block or even 1:1 conduction is accompaniedby bundle branch block, it produces a regularbroad-complex tachycardia that will usually be verydifficult to distinguish from VT; treatment of thisrhythm as if it were VT will usually be effective,J.P. Nolan et al.or will slow the ventricular response enabling identificationof the rhythm. Most typical atrial flutterhas an atrial rate of about 300 beats min −1 , so atrialflutter with 2:1 block tends to produce a tachycardiaof about 150 beats min −1 . Much faster rates(170 beats min −1 or more) are unlikely to be due toatrial flutter with 2:1 block.Treatment of regular narrow complex tachycardia.If the patient is unstable with adverse featurescaused by the arrhythmia, attempt synchronisedelectrical cardioversion. It is reasonable togive adenosine to an unstable patient with a regularnarrow-complex tachycardia while preparationsare made for synchronised cardioversion; however,do not delay electrical cardioversion if the adenosinefails to restore sinus rhythm. In the absence ofadverse features, proceed as follows.• Start with vagal manoeuvres. Carotid sinus massageor the Valsalva manoeuvre will terminateup to a quarter of episodes of paroxysmal SVT.A Valsalva manoeuvre (forced expiration againsta closed glottis) in the supine position may bethe most effective technique. A practical wayof achieving this without protracted explanationis to ask the patient to blow into a 20-ml syringe with enough force to push back theplunger. Avoid carotid massage if a carotid bruitis present; rupture of an atheromatous plaquecould cause cerebral embolism and stroke. In thecontext of acute ischaemia or digitalis toxicity,sudden bradycardia may trigger VF. Record anECG (preferably multi-lead) during each manoeuvre.If the rhythm is atrial flutter, slowing of theventricular response will often occur and demonstrateflutter waves.• If the arrhythmia persists and is not atrial flutter,use adenosine. Give 6 mg as a rapid intravenousbolus. Record an ECG (preferably multi-lead) duringeach injection. If the ventricular rate slowstransiently but the arrhythmia then persists, lookfor atrial activity such as atrial flutter or otheratrial tachycardia and treat accordingly. If thereis no response to adenosine 6 mg, give a 12-mgbolus; if there is no response, give one further12 mg-bolus.• Successful termination of a tachyarrhythmia byvagal manoeuvres or adenosine indicates thatit was almost certainly AVNRT or AVRT. Monitorthe patients for further rhythm abnormalities.Treat recurrence either with further adenosine orwith a longer-acting drug with AV nodal-blockingaction (e.g., diltiazem or beta-blocker).• Vagal manoeuvres or adenosine will terminatealmost all AVNRT or AVRT within seconds. Failureto terminate a regular narrow-complex tachycar-

European Resuscitation Council Guidelines for Resuscitation 2005S71dia with adenosine suggests an atrial tachycardiasuch as atrial flutter.• If adenosine is contraindicated or fails to terminatea regular narrow-complex tachycardiawithout demonstrating that it is atrial flutter,give a calcium channel blocker (e.g., verapamil2.5—5 mg intravenously over 2 min).Irregular narrow-complex tachycardiaAn irregular narrow-complex tachycardia is mostlikely to be AF with an uncontrolled ventricularresponse or, less commonly, atrial flutter with variableAV block. Record a 12-lead ECG to identifythe rhythm. If the patient is unstable with adversefeatures caused by the arrhythmia, attempt synchronisedelectrical cardioversion.If there are no adverse features, treatmentoptions include:• rate control by drug therapy• rhythm control using drugs to encourage chemicalcardioversion• rhythm control by electrical cardioversion• treatment to prevent complications (e.g., anticoagulation)Obtain expert help to determine the most appropriatetreatment for the individual patient. Thelonger a patient remains in AF, the greater isthe likelihood of atrial clot developing. In general,patients who have been in AF for more than48 h should not be treated by cardioversion (electricalor chemical) until they have received fullanticoagulation or absence of atrial clot has beenshown by transoesophageal echocardiography. Ifthe aim is to control heart rate, options includea beta-blocker, 321,322 digoxin, diltiazem, 323,324magnesium 325,326 or combinations of these.If the duration of AF is less than 48 h and rhythmcontrol is considered appropriate, this may beattempted using amiodarone (300 mg intravenouslyover 20—60 min followed by 900 mg over 24 h). Ibutilideor flecainide can also be given for rhythm control,but expert advice should be obtained beforeusing these drugs for this purpose. Electrical cardioversionremains an option in this setting and willrestore sinus rhythm in more patients than chemicalcardioversion.Seek expert help if any patient with AF is knownor found to have ventricular pre-excitation (WPWsyndrome). Avoid using adenosine, diltiazem, verapamilor digoxin to patients with pre-excited AF oratrial flutter, as these drugs block the AV node andcause a relative increase in pre-excitation.Antiarrhythmic drugsAdenosineAdenosine is a naturally occurring purinenucleotide. It slows transmission across theAV node but has little effect on other myocardialcells or conduction pathways. It is highly effectivefor terminating paroxysmal SVT with re-entrantcircuits that include the AV node (AVNRT). Inother narrow-complex tachycardias, adenosine willreveal the underlying atrial rhythms by slowing theventricular response. It has an extremely short halflifeof 10—15 s and, therefore, is given as a rapidbolus into a fast running intravenous infusion or followedby a saline flush. The smallest dose likely tobe effective is 6 mg (which is outside some currentlicences for an initial dose) and, if unsuccessfulthis can be followed with up to two doses each of12 mg every 1—2 min. Patients should be warnedof transient unpleasant side effects, in particularnausea, flushing, and chest discomfort. 327 Adenosineis not available in some European countries,but adenosine triphosphate (ATP) is an alternative.In a few European countries neither preparationmay be available; verapamil is probably the nextbest choice. Theophylline and related compoundsblock the effect of adenosine. Patients receivingdipyridamole or carbamazepine, or with denervated(transplanted) hearts, display a markedlyexaggerated effect that may be hazardous. Inthese patients, or if injected into a central vein,reduce the initial dose of adenosine to 3 mg. In thepresence of WPW syndrome, blockage of conductionacross the AV node by adenosine may promoteconduction across an accessory pathway. In thepresence of supraventricular arrhythmias this maycause a dangerously rapid ventricular response. Inthe presence of WPW syndrome, rarely, adenosinemay precipitate atrial fibrillation associated with adangerously rapid ventricular response.AmiodaroneIntravenous amiodarone has effects on sodium,potassium and calcium channels as well as alphaandbeta-adrenergic blocking properties. Indicationsfor intravenous amiodarone include:• control of haemodynamically stable VT, polymorphicVT and wide-complex tachycardia of uncertainorigin• paroxysmal SVT uncontrolled by adenosine, vagalmanoeuvres or AV nodal blockade• to control rapid ventricular rate due to accessorypathway conduction in pre-excited atrial arrhythmias

S72Give amiodarone, 300 mg intravenously, over10—60 min depending on the circumstances andhaemodynamic stability of the patient. This loadingdose is followed by an infusion of 900 mg over24 h. Additional infusions of 150 mg can be repeatedas necessary for recurrent or resistant arrhythmiasto a maximum manufacturer-recommendedtotal daily dose of 2 g (this maximum licensed dosevaries between countries). In patients known tohave severely impaired heart function, intravenousamiodarone is preferable to other anti-arrhythmicdrugs for atrial and ventricular arrhythmias. Majoradverse effects from amiodarone are hypotensionand bradycardia, which can be prevented by slowingthe rate of drug infusion. The hypotension associatedwith amiodarone is caused by vasoactive solvents(Polysorbate 80 and benzyl alcohol). A newaqueous formulation of amiodarone does not containthese solvents and causes no more hypotensionthan lidocaine. 198 Whenever possible, intravenousamiodarone should be given via a central venouscatheter; it causes thrombophlebitis when infusedinto a peripheral vein. In an emergency it should beinjected into a large peripheral vein.Calcium channel blockers: verapamil anddiltiazemVerapamil and diltiazem are calcium channel blockingdrugs that slow conduction and increase refractorinessin the AV node. Intravenous diltiazem isnot available in some countries. These actions mayterminate re-entrant arrhythmias and control ventricularresponse rate in patients with a variety ofatrial tachycardias. Indications include:• stable regular narrow-complex tachycardiasuncontrolled or unconverted by adenosine orvagal manoeuvres• to control ventricular rate in patients with AF oratrial flutter and preserved ventricular functionwhen the duration of the arrhythmia is less than48 hThe initial dose of verapamil is 2.5—5 mg intravenouslygiven over 2 min. In the absence of a therapeuticresponse or drug-induced adverse event,give repeated doses of 5—10 mg every 15—30 minto a maximum of 20 mg. Verapamil should be givenonly to patients with narrow-complex paroxysmalSVT or arrhythmias known with certainty to be ofsupraventricular origin.Diltiazem at a dose of 250 mcg kg −1 , followed bya second dose of 350 mcg kg −1 , is as effective asverapamil. Verapamil and, to a lesser extent, diltiazemmay decrease myocardial contractility andcritically reduce cardiac output in patients withJ.P. Nolan et al.severe LV dysfunction. For the reasons stated underadenosine (above), calcium channel blockers areconsidered harmful when given to patients withAF or atrial flutter associated with known preexcitation(WPW) syndrome.Beta-adrenergic blockersBeta-blocking drugs (atenolol, metoprolol,labetalol (alpha- and beta-blocking effects),propranolol, esmolol) reduce the effects of circulatingcatecholamines and decrease heart rateand blood pressure. They also have cardioprotectiveeffects for patients with acute coronarysyndromes. Beta-blockers are indicated for thefollowing tachycardias:• narrow-complex regular tachycardias uncontrolledby vagal manoeuvres and adenosine in thepatient with preserved ventricular function• to control rate in AF and atrial flutter when ventricularfunction is preservedThe intravenous dose of atenolol (beta 1 ) is5 mg given over 5 min, repeated if necessary after10 min. Metoprolol (beta 1 ) is given in doses of2—5 mg at 5-min intervals to a total of 15 mg. Propranolol(beta 1 and beta 2 effects), 100 mcg kg −1 ,isgiven slowly in three equal doses at 2—3-min intervals.Intravenous esmolol is a short-acting (halflifeof 2—9 min) beta 1 -selective beta-blocker. Itis given as an intravenous loading dose of500 mcg kg −1 over 1 min, followed by an infusion of50—200 mcg kg −1 min −1 .Side effects of beta-blockade include bradycardias,AV conduction delays and hypotension. Contraindicationsto the use of beta-adrenergic blockingagents include second- or third-degree heartblock, hypotension, severe congestive heart failureand lung disease associated with bronchospasm.MagnesiumMagnesium can be given for control of ventricularrate in atrial fibrillation. 326,328—330 Give magnesiumsulphate 2 g (8 mmol) over 10 min. This can berepeated once if necessary.4g. Post-resuscitation careIntroductionROSC is the just the first step toward the goalof complete recovery from cardiac arrest. Interventionsin the post-resuscitation period are likely

European Resuscitation Council Guidelines for Resuscitation 2005S73to influence the final outcome significantly, 237,331yet there are relatively few data relating to thisphase. Of 22,105 patients admitted to intensivecare units in the UK after cardiac arrest, 9974 (45%)survived to leave intensive care and 6353 (30%)survived to hospital discharge (data from IntensiveCare National Audit and Research Centre (ICNARC),London, December 1995 to October 2004). To returnthe patient to a state of normal cerebral functionwith no neurological deficit, a stable cardiacrhythm and normal haemodynamic function, furtherresuscitation tailored to each patient’s individualneeds is required. The post-resuscitation phasestarts at the location where ROSC is achieved but,once stabilised, the patient is transferred to themost appropriate high-care area (e.g., intensivecare unit, coronary care unit) for continued monitoringand treatment.Airway and breathingPatients who have had a brief period of cardiacarrest responding immediately to appropriatetreatment may achieve an immediate returnof normal cerebral function. These patients donot require tracheal intubation and ventilation butshould be given oxygen via a facemask. Hypoxiaand hypercarbia both increase the likelihood of afurther cardiac arrest and may contribute to secondarybrain injury. Consider tracheal intubation,sedation and controlled ventilation in any patientwith obtunded cerebral function. Ensure the trachealtube is positioned correctly well above thecarina. Hypocarbia causes cerebral vasoconstrictionand a decreased cerebral blood flow. 332 Aftercardiac arrest, hypocapnia induced by hyperventilationcauses cerebral ischaemia. 333—336 There areno data to support the targeting of a specific arterialPCO 2 after resuscitation from cardiac arrest,but it is reasonable to adjust ventilation to achievenormocarbia and to monitor this using the endtidalPCO 2 and arterial blood gas values. Adjustthe inspired oxygen concentrations to achieve adequatearterial oxygen saturation.Insert a gastric tube to decompress the stomach;gastric distension caused by mouth-to-mouthor bag-mask-valve ventilation will splint thediaphragm and impair ventilation. Avoid coughing;this will increase intracranial pressure and maycause transient hypoxaemia. Give adequate dosesof sedative and, if absolutely necessary, give a neuromuscularblocking drug. Obtain a chest radiographto check the position of the tracheal tubeand central venous lines, etc., assess for pulmonaryoedema and to detect complications from CPR suchas a pneumothorax associated with rib fractures.CirculationIf there is evidence of coronary occlusion, considerthe need for immediate revascularisation by thrombolysisor percutaneous coronary intervention (seeacute coronary syndromes).Haemodynamic instability is common after cardiacarrest and manifests as hypotension, lowcardiac index and arrhythmias. 337 This postresuscitationmyocardial dysfunction (or myocardialstunning) is usually transient and often reverseswithin 24—48 h. 338 The post-resuscitation periodis associated with marked elevations in plasmacytokine concentrations, manifesting as a sepsislikesyndrome and multiple organ dysfunction. 339Infusion of fluids may be required to increaseright heart filling pressures or, conversely, diureticsand vasodilators may be needed to treat left ventricularfailure. In the ICU an arterial line for continuousblood pressure monitoring is essential, and theuse of a non-invasive or invasive (pulmonary arterycatheter) cardiac output monitor may be helpful.There are very few randomised trials evaluating therole of blood pressure on the outcome after cardiacarrest. One randomised study demonstratedno difference in the neurological outcome amongpatients randomised to a mean arterial blood pressureof >100 mmHg versus ≤100 mmHg 5 min afterROSC; however, good functional recovery was associatedwith a higher blood pressure during the first2 h after ROSC. 340 In the absence of definitive data,target the mean arterial blood pressure to achievean adequate urine output, taking into considerationthe patient’s normal blood pressure.Immediately after a cardiac arrest there istypically a period of hyperkalaemia. Subsequentendogenous catecholamine release promotesintracellular transportation of potassium, causinghypokalaemia. Hypokalaemia may predispose toventricular arrhythmias. Give potassium to maintainthe serum potassium concentration between4.0 and 4.5 mmol l −1 .Disability (optimising neurological recovery)Cerebral perfusionImmediately after ROSC there is a period of cerebralhyperaemia. 341 After 15—30 min of reperfusion,however, global cerebral blood flow decreasesand there is generalised hypoperfusion. Normalcerebral autoregulation is lost, leaving cerebralperfusion dependent on mean arterial pressure.Under these circumstances, hypotension will compromisecerebral blood flow severely and will compoundany neurological injury. Thus, after ROSC,

S74maintain mean arterial pressure at the patient’snormal level.SedationAlthough it has been common practice to sedateand ventilate patients for up to 24 h after ROSC,there are no data to support a defined period ofventilation, sedation and neuromuscular blockadeafter cardiac arrest. The duration of sedation andventilation may be influenced by the use of therapeutichypothermia (see below). There are no datato indicate whether or not the choice of sedationinfluences outcome, but short-acting drugs (e.g.,propofol, alfentanil, remifentanil) will enable earlierneurological assessment. There is an increasedincidence of pneumonia when sedation is prolongedbeyond 48 h after prehospital or in-hospital cardiacarrest. 342Control of seizuresSeizures and/or myoclonus occur in 5—15% ofadult patients who achieve ROSC, and in approximately40% of those who remain comatose. 343Seizures increase cerebral metabolism by up tofour-fold. Prolonged seizure activity may causecerebral injury, and should be controlled with benzodiazepines,phenytoin, propofol or a barbiturate.Each of these drugs can cause hypotension, andthis must be treated appropriately. Seizures andmyoclonus per se are not related significantly tooutcome, but status epilepticus and, in particular,status myoclonus are associated with a pooroutcome. 343,344Temperature controlTreatment of hyperpyrexia. A period of hyperthermia(hyperpyrexia) is common in the first 48 hafter cardiac arrest. 345—347 The risk of a poor neurologicaloutcome increases for each degree of bodytemperature >37 ◦ C. 348 Antipyretics and/or physicalcooling methods decrease infarct volumes inanimal models of global ischaemia. 349,350 Treat anyhyperthermia occurring in the first 72 h after cardiacarrest with antipyretics or active cooling.Therapeutic hypothermia. Mild therapeutichypothermia is thought to suppress many ofthe chemical reactions associated with reperfusioninjury. These reactions include free-radicalproduction, excitatory amino acid release, andcalcium shifts, which can in turn lead to mitochondrialdamage and apoptosis (programmedcell death). 351—353 Two randomised clinical trialsJ.P. Nolan et al.showed improved outcome in adults remainingcomatose after initial resuscitation from outof-hospitalVF cardiac arrest, who were cooledwithin minutes to hours after ROSC. 354,355 Thesubjects were cooled to 32—34 ◦ C for 12—24 h. Onestudy documented improved metabolic endpoints(lactate and O 2 extraction) when comatose adultpatients were cooled after ROSC from out-ofhospitalcardiac arrest in which the initial rhythmwas PEA/asystole. 356 A small study showed benefitafter therapeutic hypothermia in comatosesurvivors of non-VF arrest. 357External and/or internal cooling techniques canbe used to initiate cooling. 354—356,358—361 An infusionof 30 mg kg −1 of 4 ◦ C-saline decreases coretemperature by 1.5 ◦ C. 358,359,361,362 Intravascularcooling enables more precise control of core temperaturethan external methods, but it is unknownwhether this improves outcome. 360,363—365Complications of mild therapeutic hypothermiainclude increased infection, cardiovascularinstability, coagulopathy, hyperglycaemia and electrolyteabnormalities such as hypophosphataemiaand hypomagnesaemia. 366,367Unconscious adult patients with spontaneous circulationafter out-of-hospital VF cardiac arrestshould be cooled to 32—34 ◦ C. Cooling should bestarted as soon as possible and continued for atleast 12—24 h. 368—374 Induced hypothermia mightalso benefit unconscious adult patients with spontaneouscirculation after out-of-hospital cardiacarrest from a non-shockable rhythm, or cardiacarrest in hospital. Treat shivering by ensuring adequatesedation and giving neuromuscular blockingdrugs. Bolus doses of neuromuscular blockersare usually adequate, but infusions are necessaryoccasionally. Rewarm the patient slowly(0.25—0.5 ◦ Ch −1 ) and avoid hyperthermia. Theoptimum target temperature, rate of cooling, durationof hypothermia and rate of rewarming have yetto be determined; further studies are essential.Blood glucose controlThere is a strong association between high bloodglucose after resuscitation from cardiac arrestand poor neurological outcome. 237—244 Persistenthyperglycaemia after stroke is also associatedwith a worse neurological outcome. 375—378 Tightcontrol of blood glucose (4.4—6.1 mmol l −1 or80—110 mg dl −1 ) using insulin reduces hospital mortalityin critically ill adults, 379,380 but this has notbeen demonstrated in post-cardiac arrest patientsspecifically. The benefit is thought to result fromthe strict glycaemic control rather than the doseof insulin infused. 381 One rat study has shown

European Resuscitation Council Guidelines for Resuscitation 2005S75that glucose plus insulin improves cerebral outcomeafter asphyxial cardiac arrest. 382 There areno randomised controlled human trials of glucosecontrol after cardiac arrest. The optimal blood glucosetarget in critically ill patients has not beendetermined. Comatose patients are at particularrisk from unrecognised hypoglycaemia, and the riskof this complication occurring increases as the targetblood glucose concentration is lowered.In common with all critically ill patients, patientsadmitted to a critical care environment after cardiacarrest should have their blood glucose monitoredfrequently and hyperglycaemia treated withan insulin infusion. The blood glucose concentrationthat triggers insulin therapy, and the target rangeof blood glucose concentrations, should be determinedby local policy. There is a need for studies ofglucose control after cardiac arrest.PrognosticationOnce a heart has been resuscitated to a stablerhythm and cardiac output, the organ that influencesan individual’s survival most significantly isthe brain. Two thirds of those dying after admissionto ICU following out-of-hospital cardiac arrest diefrom neurological injury. 383 A quarter of those dyingafter admission to ICU following in-hospital cardiacarrest die from neurological injury. A means of predictingneurological outcome that can be appliedto individual patients immediately after ROSC isrequired. Such a test of prognosis must have 100%specificity.Clinical testsThere are no neurological signs that can predictoutcome in the first hours after ROSC. By 3 daysafter the onset of coma relating to cardiac arrest,50% of patients with no chance of ultimate recoveryhave died. In the remaining patients, the absenceof pupil light reflexes on day 3 and an absent motorresponse to pain on day 3 are both independentlypredictive of a poor outcome (death or vegetativestate) with very high specificity. 384—386Biochemical testsMeasurement of serum neuron-specific enolase(NSE) and protein S-100b may be usefulin determining the outcome of a cardiacarrest. 237,243,244,387—399 However, the 95% confidenceinterval (CI) in the trials undertaken todate is wide, and in many of the studies returnto consciousness (without comment on level offunction) was considered a ‘‘good’’ outcome. Theonly meta-analysis to look at this topic estimatedthat to obtain 95% CI with 5% false-positive ratewould require a study population of approximately600 patients. 400 No study this large has beenconducted, and these biochemical tests remainunreliable for predicting outcome in individualcases.Electrophysiological testsMedian nerve somatosensory evoked potentials innormothermic patients, comatose for at least 72 hafter cardiac arrest, predict poor outcome with100% specificity. 384 Bilateral absence of the N20component of the evoked potentials in comatosepatients with coma of hypoxic-anoxic origin is uniformlyfatal. When recorded at least 24—48 h afterROSC, the electroencephalogram (EEG), provideslimited prognostic information. 401—413 A normal orgrossly abnormal EEG predicts outcome reliably, butan EEG between these extremes is unreliable forprognostication.References1. Gwinnutt CL, Columb M, Harris R. Outcome after cardiacarrest in adults in UK hospitals: effect of the 1997 guidelines.Resuscitation 2000;47:125—35.2. Peberdy MA, Kaye W, Ornato JP, et al. Cardiopulmonaryresuscitation of adults in the hospital: a report of 14720cardiac arrests from the National Registry of CardiopulmonaryResuscitation. Resuscitation 2003;58:297—308.3. Hodgetts TJ, Kenward G, Vlackonikolis I, et al. Incidence,location and reasons for avoidable in-hospital cardiacarrest in a district general hospital. Resuscitation2002;54:115—23.4. Kause J, Smith G, Prytherch D, Parr M, Flabouris A, HillmanK. A comparison of antecedents to cardiac arrests,deaths and emergency intensive care admissions in Australiaand New Zealand, and the United Kingdom—–theACADEMIA study. Resuscitation 2004;62:275—82.5. Herlitz J, Bang A, Aune S, Ekstrom L, Lundstrom G, HolmbergS. Characteristics and outcome among patients sufferingin-hospital cardiac arrest in monitored and nonmonitoredareas. Resuscitation 2001;48:125—35.6. Franklin C, Mathew J. Developing strategies to preventinhospital cardiac arrest: analyzing responses of physiciansand nurses in the hours before the event. Crit Care Med1994;22:244—7.7. McQuillan P, Pilkington S, Allan A, et al. Confidential inquiryinto quality of care before admission to intensive care. BMJ1998;316:1853—8.8. National Confidential Enquiry into Patient Outcome andDeath. An Acute Problem? London, National ConfidentialEnquiry into Patient Outcome and Death, 2005.9. Cashman JN. In-hospital cardiac arrest: what happens tothe false arrests? Resuscitation 2002;53:271—6.10. Smith GB, Poplett N. Knowledge of aspects of acute carein trainee doctors. Postgrad Med J 2002;78:335—8.11. Meek T. New house officers’ knowledge of resuscitation,fluid balance and analgesia. Anaesthesia 2000;55:1128—9.

S76J.P. Nolan et al.12. Gould TH, Upton PM, Collins P. A survey of the intendedmanagement of acute postoperative pain by newly qualifieddoctors in the south west region of England in August1992. Anaesthesia 1994;49:807—10.13. Jackson E, Warner J. How much do doctors know aboutconsent and capacity? J R Soc Med 2002;95:601—3.14. Kruger PS, Longden PJ. A study of a hospital staff’sknowledge of pulse oximetry. Anaesth Intensive Care1997;25:38—41.15. Wheeler DW, Remoundos DD, Whittlestone KD, et al.Doctors’ confusion over ratios and percentages in drugsolutions: the case for standard labelling. J R Soc Med2004;97:380—3.16. Perkins GD, Stephenson B, Hulme J, Monsieurs KG. Birminghamassessment of breathing study (BABS). Resuscitation2005;64:109—13.17. Goldacre MJ, Lambert T, Evans J, Turner G. Preregistrationhouse officers’ views on whether their experience atmedical school prepared them well for their jobs: nationalquestionnaire survey. BMJ 2003;326:1011—2.18. Thwaites BC, Shankar S, Niblett D, Saunders J. Can consultantsresuscitate? J R Coll Physicians Lond 1992;26:265—7.19. Saravanan P, Soar J. A survey of resuscitation training needsof senior anaesthetists. Resuscitation 2005;64:93—6.20. Featherstone P, Smith GB, Linnell M, Easton S, Osgood VM.Impact of a one-day inter-professional course (ALERT TM )on attitudes and confidence in managing critically ill adultpatients. Resuscitation 2005;65:329—36.21. Harrison GA, Jacques TC, Kilborn G, McLaws ML. The prevalenceof recordings of the signs of critical conditions andemergency responses in hospital wards—–the SOCCER study.Resuscitation 2005;65:149—57.22. Buist M, Bernard S, Nguyen TV, Moore G, Anderson J. Associationbetween clinically abnormal observations and subsequentin-hospital mortality: a prospective study. Resuscitation2004;62:137—41.23. Goldhill DR, Worthington L, Mulcahy A, Tarling M, SumnerA. The patient-at-risk team: identifying and managing seriouslyill ward patients. Anaesthesia 1999;54:853—60.24. Hodgetts TJ, Kenward G, Vlachonikolis IG, Payne S, CastleN. The identification of risk factors for cardiac arrest andformulation of activation criteria to alert a medical emergencyteam. Resuscitation 2002;54:125—31.25. Subbe CP, Davies RG, Williams E, Rutherford P, Gemmell L.Effect of introducing the Modified Early Warning score onclinical outcomes, cardio-pulmonary arrests and intensivecare utilisation in acute medical admissions. Anaesthesia2003;58:797—802.26. Lee A, Bishop G, Hillman KM, Daffurn K. The Medical EmergencyTeam. Anaesth Intensive Care 1995;23:183—6.27. Cuthbertson BH. Outreach critical care—–cash for no questions?Br J Anaesth 2003;90:4—6.28. Parr M. Critical care outreach: some answers, more questions.Intensive Care Med 2004;30:1261—2.29. Goldhill DR, McNarry AF. Physiological abnormalities inearly warning scores are related to mortality in adult inpatients.Br J Anaesth 2004;92:882—4.30. Subbe CP, Williams EM, Gemmell LW. Are medical emergencyteams picking up enough patients with increasedrespiratory rate? Crit Care Med 2004;32:1983—4.31. McBride J, Knight D, Piper J, Smith GB. Long-term effectof introducing an early warning score on respiratory ratecharting on general wards. Resuscitation 2005;65:41—4.32. Carberry M. Implementing the modified early warning system:our experiences. Nurs Crit Care 2002;7:220—6.33. Sandroni C, Ferro G, Santangelo S, et al. In-hospital cardiacarrest: survival depends mainly on the effectivenessof the emergency response. Resuscitation 2004;62:291—7.34. Soar J, McKay U. A revised role for the hospital cardiacarrest team? Resuscitation 1998;38:145—9.35. Bellomo R, Goldsmith D, Uchino S, et al. A prospectivebefore-and-after trial of a medical emergency team. MedJ Aust 2003;179:283—7.36. Buist MD, Moore GE, Bernard SA, Waxman BP, AndersonJN, Nguyen TV. Effects of a medical emergency teamon reduction of incidence of and mortality from unexpectedcardiac arrests in hospital: preliminary study. BMJ2002;324:387—90.37. Parr MJ, Hadfield JH, Flabouris A, Bishop G, Hillman K. TheMedical Emergency Team: 12 month analysis of reasons foractivation, immediate outcome and not-for-resuscitationorders. Resuscitation 2001;50:39—44.38. Bellomo R, Goldsmith D, Uchino S, et al. Prospective controlledtrial of effect of medical emergency team on postoperativemorbidity and mortality rates. Crit Care Med2004;32:916—21.39. Kenward G, Castle N, Hodgetts T, Shaikh L. Evaluation of amedical emergency team one year after implementation.Resuscitation 2004;61:257—63.40. Jones D, Bates S, Warrillow S, et al. Circadian pattern ofactivation of the medical emergency team in a teachinghospital. Crit Care 2005;9:R303—6.41. The MERIT study investigators. Introduction of the medicalemergency team (MET) system: a cluster-randomisedcontrolled trial. Lancet 2005;365:2091—7.42. Critical care outreach 2003: progress in developing services.The National Outreach Report 2003. London, Departmentof Health and National Health Service ModernisationAgency; 2003.43. Ball C, Kirkby M, Williams S. Effect of the critical care outreachteam on patient survival to discharge from hospitaland readmission to critical care: non-randomised populationbased study. BMJ 2003;327:1014.44. Priestley G, Watson W, Rashidian A, et al. Introducing CriticalCare Outreach: a ward-randomised trial of phasedintroduction in a general hospital. Intensive Care Med2004;30:1398—404.45. Story DA, Shelton AC, Poustie SJ, Colin-Thome NJ, McNicolPL. The effect of critical care outreach on postoperativeserious adverse events. Anaesthesia 2004;59:762—6.46. Szalados JE. Critical care teams managing floor patients:the continuing evolution of hospitals into intensive careunits? Crit Care Med 2004;32:1071—2.47. Cooke MW, Higgins J, Kidd P. Use of emergency observationand assessment wards: a systematic literature review.Emerg Med J 2003;20:138—42.48. Rivers E, Nguyen B, Havstad S, et al. Early goal-directedtherapy in the treatment of severe sepsis and septic shock.N Engl J Med 2001;345:1368—77.49. Leeson-Payne CG, Aitkenhead AR. A prospective study toassess the demand for a high dependency unit. Anaesthesia1995;50:383—7.50. Guidelines for the utilisation of intensive care units. EuropeanSociety of Intensive Care Medicine. Intensive CareMed 1994;20:163—4.51. Haupt MT, Bekes CE, Brilli RJ, et al. Guidelines on criticalcare services and personnel: recommendations based on asystem of categorization of three levels of care. Crit CareMed 2003;31:2677—83.52. Hillson SD, Rich EC, Dowd B, Luxenberg MG. Call nightsand patients care: effects on inpatients at one teachinghospital. J Gen Intern Med 1992;7:405—10.

European Resuscitation Council Guidelines for Resuscitation 2005S7753. Bell CM, Redelmeier DA. Mortality among patients admittedto hospitals on weekends as compared with weekdays. NEngl J Med 2001;345:663—8.54. Beck DH, McQuillan P, Smith GB. Waiting for the break ofdawn? The effects of discharge time, discharge TISS scoresand discharge facility on hospital mortality after intensivecare. Intensive Care Med 2002;28:1287—93.55. Needleman J, Buerhaus P, Mattke S, Stewart M, ZelevinskyK. Nurse-staffing levels and the quality of care in hospitals.N Engl J Med 2002;346:1715—22.56. Baskett PJ, Lim A. The varying ethical attitudes towardsresuscitation in Europe. Resuscitation 2004;62:267—73.57. Gabbott D, Smith G, Mitchell S, et al. Cardiopulmonaryresuscitation standards for clinical practice and training inthe UK. Resuscitation 2005;64:13—9.58. Bristow PJ, Hillman KM, Chey T, et al. Rates of in-hospitalarrests, deaths and intensive care admissions: the effect ofa medical emergency team. Med J Aust 2000;173:236—40.59. Eberle B, Dick WF, Schneider T, Wisser G, Doetsch S,Tzanova I. Checking the carotid pulse check: diagnosticaccuracy of first responders in patients with and withouta pulse. Resuscitation 1996;33:107—16.60. Ruppert M, Reith MW, Widmann JH, et al. Checkingfor breathing: evaluation of the diagnostic capability ofemergency medical services personnel, physicians, medicalstudents, and medical laypersons. Ann Emerg Med1999;34:720—9.61. Abella BS, Alvarado JP, Myklebust H, et al. Quality ofcardiopulmonary resuscitation during in-hospital cardiacarrest. JAMA 2005;293:305—10.62. Abella BS, Sandbo N, Vassilatos P, et al. Chest compressionrates during cardiopulmonary resuscitation are suboptimal:a prospective study during in-hospital cardiac arrest. Circulation2005;111:428—34.63. Perkins GD, Roberts C, Gao F. Delays in defibrillation: influenceof different monitoring techniques. Br J Anaesth2002;89:405—8.64. Soar J, Perkins GD, Harris S, Nolan JP. The immediate lifesupport course. Resuscitation 2003;57:21—6.65. Nolan J. Advanced life support training. Resuscitation2001;50:9—11.66. Perkins G, Lockey A. The advanced life support providercourse. BMJ 2002;325:S81.67. Bayes de Luna A, Coumel P, Leclercq JF. Ambulatory suddencardiac death: mechanisms of production of fatal arrhythmiaon the basis of data from 157 cases. Am Heart J1989;117:151—9.68. Rea TD, Shah S, Kudenchuk PJ, Copass MK, Cobb LA. Automatedexternal defibrillators: to what extent does the algorithmdelay CPR? Ann Emerg Med 2005;46:132—41.69. van Alem AP, Sanou BT, Koster RW. Interruption of cardiopulmonaryresuscitation with the use of the automatedexternal defibrillator in out-of-hospital cardiac arrest. AnnEmerg Med 2003;42:449—57.70. Hess EP, White RD. Ventricular fibrillation is not provokedby chest compression during post-shock organizedrhythms in out-of-hospital cardiac arrest. Resuscitation2005;66:7—11.71. Eftestol T, Wik L, Sunde K, Steen PA. Effects of cardiopulmonaryresuscitation on predictors of ventricular fibrillationdefibrillation success during out-of-hospital cardiacarrest. Circulation 2004;110:10—5.72. Eftestol T, Sunde K, Aase SO, Husoy JH, Steen PA. Predictingoutcome of defibrillation by spectral characterizationand nonparametric classification of ventricular fibrillationin patients with out-of-hospital cardiac arrest. Circulation2000;102:1523—9.73. Eftestol T, Sunde K, Steen PA. Effects of interrupting precordialcompressions on the calculated probability of defibrillationsuccess during out-of-hospital cardiac arrest. Circulation2002;105:2270—3.74. Caldwell G, Millar G, Quinn E. Simple mechanical methodsfor cardioversion: defence of the precordial thump andcough version. Br Med J 1985;291:627—30.75. Kohl P, King AM, Boulin C. Antiarrhythmic effects of acutemechanical stiumulation. In: Kohl P, Sachs F, Franz MR, editors.Cardiac mechano-electric feedback and arrhythmias:form pipette to patient. Philadelphia: Elsevier Saunders;2005. p. 304—14.76. Krijne R. Rate acceleration of ventricular tachycardia aftera precordial chest thump. Am J Cardiol 1984;53:964—5.77. Emerman CL, Pinchak AC, Hancock D, Hagen JF. Effect ofinjection site on circulation times during cardiac arrest.Crit Care Med 1988;16:1138—41.78. Glaeser PW, Hellmich TR, Szewczuga D, Losek JD, Smith DS.Five-year experience in prehospital intraosseous infusionsin children and adults. Ann Emerg Med 1993;22:1119—24.79. Schuttler J, Bartsch A, Ebeling BJ, et al. Endobronchialadministration of adrenaline in preclinical cardiopulmonaryresuscitation. Anasth Intensivther Notfallmed1987;22:63—8.80. Hornchen U, Schuttler J, Stoeckel H, Eichelkraut W,Hahn N. Endobronchial instillation of epinephrineduring cardiopulmonary resuscitation. Crit Care Med1987;15:1037—9.81. Vaknin Z, Manisterski Y, Ben-Abraham R, et al. Is endotrachealadrenaline deleterious because of the beta adrenergiceffect? Anesth Analg 2001;92:1408—12.82. Manisterski Y, Vaknin Z, Ben-Abraham R, et al. Endotrachealepinephrine: a call for larger doses. Anesth Analg2002;95:1037—41 [table of contents].83. Efrati O, Ben-Abraham R, Barak A, et al. Endobronchialadrenaline: should it be reconsidered? Doseresponse and haemodynamic effect in dogs. Resuscitation2003;59:117—22.84. Elizur A, Ben-Abraham R, Manisterski Y, et al. Trachealepinephrine or norepinephrine preceded by beta blockadein a dog model. Can beta blockade bestow any benefits?Resuscitation 2003;59:271—6.85. Naganobu K, Hasebe Y, Uchiyama Y, Hagio M, Ogawa H. Acomparison of distilled water and normal saline as diluentsfor endobronchial administration of epinephrine in the dog.Anesth Analg 2000;91:317—21.86. Eftestol T, Wik L, Sunde K, Steen PA. Effects of cardiopulmonaryresuscitation on predictors of ventricular fibrillationdefibrillation success during out-of-hospital cardiacarrest. Circulation 2004;110:10—5.87. Berg RA, Hilwig RW, Kern KB, Ewy GA. Precountershockcardiopulmonary resuscitation improves ventricular fibrillationmedian frequency and myocardial readiness for successfuldefibrillation from prolonged ventricular fibrillation:a randomized, controlled swine study. Ann Emerg Med2002;40:563—70.88. Achleitner U, Wenzel V, Strohmenger HU, et al. The beneficialeffect of basic life support on ventricular fibrillationmean frequency and coronary perfusion pressure. Resuscitation2001;51:151—8.89. Kudenchuk PJ, Cobb LA, Copass MK, et al. Amiodarone forresuscitation after out-of-hospital cardiac arrest due toventricular fibrillation. N Engl J Med 1999;341:871—8.90. Dorian P, Cass D, Schwartz B, Cooper R, GelaznikasR, Barr A. Amiodarone as compared with lidocaine forshock-resistant ventricular fibrillation. N Engl J Med2002;346:884—90.

S7891. Thel MC, Armstrong AL, McNulty SE, Califf RM, O’ConnorCM. Randomised trial of magnesium in in-hospital cardiacarrest. Lancet 1997;350:1272—6.92. Allegra J, Lavery R, Cody R, et al. Magnesium sulfate inthe treatment of refractory ventricular fibrillation in theprehospital setting. Resuscitation 2001;49:245—9.93. Fatovich D, Prentice D, Dobb G. Magnesium in in-hospitalcardiac arrest. Lancet 1998;351:446.94. Hassan TB, Jagger C, Barnett DB. A randomised trial toinvestigate the efficacy of magnesium sulphate for refractoryventricular fibrillation. Emerg Med J 2002;19:57—62.95. Miller B, Craddock L, Hoffenberg S, et al. Pilot study ofintravenous magnesium sulfate in refractory cardiac arrest:safety data and recommendations for future studies. Resuscitation1995;30:3—14.96. Weil MH, Rackow EC, Trevino R, Grundler W, Falk JL, GriffelMI. Difference in acid—base state between venous andarterial blood during cardiopulmonary resuscitation. N EnglJ Med 1986;315:153—6.97. Bottiger BW, Bode C, Kern S, et al. Efficacy and safety ofthrombolytic therapy after initially unsuccessful cardiopulmonaryresuscitation: a prospective clinical trial. Lancet2001;357:1583—5.98. Boidin MP. Airway patency in the unconscious patient. Br JAnaesth 1985;57:306—10.99. Nandi PR, Charlesworth CH, Taylor SJ, Nunn JF, Dore CJ.Effect of general anaesthesia on the pharynx. Br J Anaesth1991;66:157—62.100. Guildner CW. Resuscitation: opening the airway. A comparativestudy of techniques for opening an airway obstructedby the tongue. JACEP 1976;5:588—90.101. Safar P, Aguto-Escarraga L. Compliance in apneic anesthetizedadults. Anesthesiology 1959;20:283—9.102. Greene DG, Elam JO, Dobkin AB, Studley CL. Cinefluorographicstudy of hyperextension of the neck and upperairway patency. Jama 1961;176:570—3.103. Morikawa S, Safar P, Decarlo J. Influence of the headjawposition upon upper airway patency. Anesthesiology1961;22:265—70.104. Ruben HM, Elam JO, Ruben AM, Greene DG. Investigation ofupper airway problems in resuscitation. 1. Studies of pharyngealX-rays and performance by laymen. Anesthesiology1961;22:271—9.105. Elam JO, Greene DG, Schneider MA, et al. Head-tilt methodof oral resuscitation. JAMA 1960;172:812—5.106. Aprahamian C, Thompson BM, Finger WA, Darin JC. Experimentalcervical spine injury model: evaluation of airwaymanagement and splinting techniques. Ann Emerg Med1984;13:584—7.107. Donaldson 3rd WF, Heil BV, Donaldson VP, Silvaggio VJ. Theeffect of airway maneuvers on the unstable C1-C2 segment.A cadaver study. Spine 1997;22:1215—8.108. Donaldson 3rd WF, Towers JD, Doctor A, Brand A, DonaldsonVP. A methodology to evaluate motion of the unstable spineduring intubation techniques. Spine 1993;18:2020—3.109. Hauswald M, Sklar DP, Tandberg D, Garcia JF. Cervicalspine movement during airway management: cinefluoroscopicappraisal in human cadavers. Am J Emerg Med1991;9:535—8.110. Brimacombe J, Keller C, Kunzel KH, Gaber O, Boehler M,Puhringer F. Cervical spine motion during airway management:a cinefluoroscopic study of the posteriorly destabilizedthird cervical vertebrae in human cadavers. AnesthAnalg 2000;91:1274—8.111. Majernick TG, Bieniek R, Houston JB, Hughes HG. Cervicalspine movement during orotracheal intubation. Ann EmergMed 1986;15:417—20.J.P. Nolan et al.112. Lennarson PJ, Smith DW, Sawin PD, Todd MM, Sato Y,Traynelis VC. Cervical spinal motion during intubation: efficacyof stabilization maneuvers in the setting of completesegmental instability. J Neurosurg Spine 2001;94:265—70.113. Marsh AM, Nunn JF, Taylor SJ, Charlesworth CH. Airwayobstruction associated with the use of the Guedel airway.Br J Anaesth 1991;67:517—23.114. Schade K, Borzotta A, Michaels A. Intracranial malpositionof nasopharyngeal airway. J Trauma 2000;49:967—8.115. Muzzi DA, Losasso TJ, Cucchiara RF. Complication from anasopharyngeal airway in a patient with a basilar skull fracture.Anesthesiology 1991;74:366—8.116. Roberts K, Porter K. How do you size a nasopharyngeal airway.Resuscitation 2003;56:19—23.117. Stoneham MD. The nasopharyngeal airway. Assessmentof position by fibreoptic laryngoscopy. Anaesthesia1993;48:575—80.118. Moser DK, Dracup K, Doering LV. Effect of cardiopulmonaryresuscitation training for parents of high-risk neonateson perceived anxiety, control, and burden. Heart Lung1999;28:326—33.119. Kandakai T, King K. Perceived self-efficacy in performinglifesaving skills: an assessment of the American RedCross’s Responding to Emergencies course. J Health Educ1999;30:235—41.120. Lester CA, Donnelly PD, Assar D. Lay CPR trainees: retraining,confidence and willingness to attempt resuscitation 4years after training. Resuscitation 2000;45:77—82.121. Pane GA, Salness KA. A survey of participants in a mass CPRtraining course. Ann Emerg Med 1987;16:1112—6.122. Heilman KM, Muschenheim C. Primary cutaneous tuberculosisresulting from mouth-to-mouth respiration. N Engl JMed 1965;273:1035—6.123. Christian MD, Loutfy M, McDonald LC, et al. Possible SARScoronavirus transmission during cardiopulmonary resuscitation.Emerg Infect Dis 2004;10:287—93.124. Alexander R, Hodgson P, Lomax D, Bullen C. A comparisonof the laryngeal mask airway and Guedel airway, bag andface mask for manual ventilation following formal training.Anaesthesia 1993;48:231—4.125. Dorges V, Sauer C, Ocker H, Wenzel V, Schmucker P.Smaller tidal volumes during cardiopulmonary resuscitation:comparison of adult and paediatric self-inflatablebags with three different ventilatory devices. Resuscitation1999;43:31—7.126. Ocker H, Wenzel V, Schmucker P, Dorges V. Effectivenessof various airway management techniques in a benchmodel simulating a cardiac arrest patient. J Emerg Med2001;20:7—12.127. Stone BJ, Chantler PJ, Baskett PJ. The incidence of regurgitationduring cardiopulmonary resuscitation: a comparisonbetween the bag valve mask and laryngeal mask airway.Resuscitation 1998;38:3—6.128. Hartsilver EL, Vanner RG. Airway obstruction with cricoidpressure. Anaesthesia 2000;55:208—11.129. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al.Hyperventilation-induced hypotension during cardiopulmonaryresuscitation. Circulation 2004;109:1960—5.130. Stallinger A, Wenzel V, Wagner-Berger H, et al. Effects ofdecreasing inspiratory flow rate during simulated basic lifesupport ventilation of a cardiac arrest patient on lung andstomach tidal volumes. Resuscitation 2002;54:167—73.131. Noordergraaf GJ, van Dun PJ, Kramer BP, et al. Canfirst responders achieve and maintain normocapnia whensequentially ventilating with a bag-valve device and twooxygen-driven resuscitators? A controlled clinical trial in104 patients. Eur J Anaesthesiol 2004;21:367—72.

European Resuscitation Council Guidelines for Resuscitation 2005S79132. Jones JH, Murphy MP, Dickson RL, Somerville GG, BrizendineEJ. Emergency physician-verified out-of-hospital intubation:miss rates by paramedics. Acad Emerg Med2004;11:707—9.133. Pelucio M, Halligan L, Dhindsa H. Out-of-hospital experiencewith the syringe esophageal detector device. AcadEmerg Med 1997;4:563—8.134. Sayre MR, Sakles JC, Mistler AF, Evans JL, Kramer AT, PancioliAM. Field trial of endotracheal intubation by basic EMTs.Ann Emerg Med 1998;31:228—33.135. Katz SH, Falk JL. Misplaced endotracheal tubes byparamedics in an urban emergency medical services system.Ann Emerg Med 2001;37:32—7.136. Nolan JP, Prehospital. resuscitative airway care: shouldthe gold standard be reassessed? Curr Opin Crit Care2001;7:413—21.137. Davies PR, Tighe SQ, Greenslade GL, Evans GH. Laryngealmask airway and tracheal tube insertion by unskilled personnel.Lancet 1990;336:977—9.138. Flaishon R, Sotman A, Ben-Abraham R, Rudick V, Varssano D,Weinbroum AA. Antichemical protective gear prolongs timeto successful airway management: a randomized, crossoverstudy in humans. Anesthesiology 2004;100:260—6.139. Ho BY, Skinner HJ, Mahajan RP. Gastro-oesophageal refluxduring day case gynaecological laparoscopy under positivepressure ventilation: laryngeal mask vs. tracheal intubation.Anaesthesia 1998;53:921—4.140. Reinhart DJ, Simmons G. Comparison of placement ofthe laryngeal mask airway with endotracheal tube byparamedics and respiratory therapists. Ann Emerg Med1994;24:260—3.141. Rewari W, Kaul HL. Regurgitation and aspiration duringgynaecological laparoscopy: comparison between laryngealmask airway and tracheal intubation. J Anaesth Clin Pharmacol1999;15:67—70.142. Pennant JH, Walker MB. Comparison of the endotrachealtube and laryngeal mask in airway management byparamedical personnel. Anesth Analg 1992;74:531—4.143. Maltby JR, Beriault MT, Watson NC, Liepert DJ, Fick GH.LMA-Classic and LMA-ProSeal are effective alternatives toendotracheal intubation for gynecologic laparoscopy. CanJ Anaesth 2003;50:71—7.144. Rumball CJ, MacDonald D, The PTL. Combitube, laryngealmask, and oral airway: a randomized prehospital comparativestudy of ventilatory device effectiveness and costeffectivenessin 470 cases of cardiorespiratory arrest. PrehospEmerg Care 1997;1:1—10.145. Verghese C, Prior-Willeard PF, Baskett PJ. Immediate managementof the airway during cardiopulmonary resuscitationin a hospital without a resident anaesthesiologist. EurJ Emerg Med 1994;1:123—5.146. Tanigawa K, Shigematsu A. Choice of airway devices for12,020 cases of nontraumatic cardiac arrest in Japan. PrehospEmerg Care 1998;2:96—100.147. The use of the laryngeal mask airway by nurses during cardiopulmonaryresuscitation: results of a multicentre trial.Anaesthesia 1994;49:3—7.148. Grantham H, Phillips G, Gilligan JE. The laryngeal mask inprehospital emergency care. Emerg Med 1994;6:193—7.149. Kokkinis K. The use of the laryngeal mask airway in CPR.Resuscitation 1994;27:9—12.150. Leach A, Alexander CA, Stone B. The laryngeal mask in cardiopulmonaryresuscitation in a district general hospital: apreliminary communication. Resuscitation 1993;25:245—8.151. Staudinger T, Brugger S, Watschinger B, et al. Emergencyintubation with the Combitube: comparison with the endotrachealairway. Ann Emerg Med 1993;22:1573—5.152. Lefrancois DP, Dufour DG. Use of the esophageal trachealcombitube by basic emergency medical technicians. Resuscitation2002;52:77—83.153. Ochs M, Vilke GM, Chan TC, Moats T, Buchanan J. Successfulprehospital airway management by EMT-Ds using the combitube.Prehosp Emerg Care 2000;4:333—7.154. Vezina D, Lessard MR, Bussieres J, Topping C, TrepanierCA. Complications associated with the use of theesophageal—tracheal Combitube. Can J Anaesth1998;45:76—80.155. Richards CF. Piriform sinus perforation duringesophageal—tracheal Combitube placement. J EmergMed 1998;16:37—9.156. Rumball C, Macdonald D, Barber P, Wong H, Smecher C.Endotracheal intubation and esophageal tracheal Combitubeinsertion by regular ambulance attendants: a comparativetrial. Prehosp Emerg Care 2004;8:15—22.157. Rabitsch W, Schellongowski P, Staudinger T, et al. Comparisonof a conventional tracheal airway with the Combitubein an urban emergency medical services system run byphysicians. Resuscitation 2003;57:27—32.158. Cook TM, McCormick B, Asai T. Randomized comparisonof laryngeal tube with classic laryngeal mask airwayfor anaesthesia with controlled ventilation. Br J Anaesth2003;91:373—8.159. Cook TM, McKinstry C, Hardy R, Twigg S. Randomizedcrossover comparison of the ProSeal laryngeal mask airwaywith the laryngeal tube during anaesthesia with controlledventilation. Br J Anaesth 2003;91:678—83.160. Asai T, Kawachi S. Use of the laryngeal tube by paramedicstaff. Anaesthesia 2004;59:408—9.161. Asai T, Moriyama S, Nishita Y, Kawachi S. Use of thelaryngeal tube during cardiopulmonary resuscitation byparamedical staff. Anaesthesia 2003;58:393—4.162. Genzwuerker HV, Dhonau S, Ellinger K. Use of the laryngealtube for out-of-hospital resuscitation. Resuscitation2002;52:221—4.163. Kette F, Reffo I, Giordani G, et al. The use of laryngealtube by nurses in out-of-hospital emergencies: preliminaryexperience. Resuscitation 2005;66:21—5.164. Cook TM, Nolan JP, Verghese C, et al. Randomized crossovercomparison of the proseal with the classic laryngeal maskairway in unparalysed anaesthetized patients. Br J Anaesth2002;88:527—33.165. Cook TM, Lee G, Nolan JP. The ProSealTM laryngeal maskairway: a review of the literature [Le masque laryngeProSealTM: un examen des publications]. Can J Anaesth2005;52:739—60.166. Cook TM, Gupta K, Gabbott DA, Nolan JP. An evaluationof the airway management device. Anaesthesia2001;56:660—4.167. Chiu CL, Wang CY. An evaluation of the modifiedairway management device. Anaesth Intensive Care2004;32:77—80.168. Cook TM, McCormick B, Gupta K, Hersch P, Simpson T. Anevaluation of the PA(Xpress) pharyngeal airway—–a new singleuse airway device. Resuscitation 2003;58:139—43.169. Burgoyne L, Cyna A. Laryngeal mask vs intubating laryngealmask: insertion and ventilation by inexperienced resuscitators.Anaesth Intensive Care 2001;29:604—8.170. Choyce A, Avidan MS, Shariff A, Del Aguila M, RadcliffeJJ, Chan T. A comparison of the intubating and standardlaryngeal mask airways for airway management by inexperiencedpersonnel. Anaesthesia 2001;56:357—60.171. Baskett PJ, Parr MJ, Nolan JP. The intubating laryngealmask. Results of a multicentre trial with experience of 500cases. Anaesthesia 1998;53:1174—9.

S80172. Gausche M, Lewis RJ, Stratton SJ, et al. Effect of outof-hospitalpediatric endotracheal intubation on survivaland neurological outcome: a controlled clinical trial. JAMA2000;283:783—970.173. Guly UM, Mitchell RG, Cook R, Steedman DJ, RobertsonCE. Paramedics and technicians are equally successfulat managing cardiac arrest outside hospital. BMJ1995;310:1091—4.174. Stiell IG, Wells GA, Field B, et al. Advanced cardiac lifesupport in out-of-hospital cardiac arrest. N Engl J Med2004;351:647—56.175. Garza AG, Gratton MC, Coontz D, Noble E, Ma OJ. Effectof paramedic experience on orotracheal intubation successrates. J Emerg Med 2003;25:251—6.176. Li J. Capnography alone is imperfect for endotracheal tubeplacement confirmation during emergency intubation. JEmerg Med 2001;20:223—9.177. Tanigawa K, Takeda T, Goto E, Tanaka K. Accuracy and reliabilityof the self-inflating bulb to verify tracheal intubationin out-of-hospital cardiac arrest patients. Anesthesiology2000;93:1432—6.178. Takeda T, Tanigawa K, Tanaka H, Hayashi Y, Goto E, TanakaK. The assessment of three methods to verify trachealtube placement in the emergency setting. Resuscitation2003;56:153—7.179. Baraka A, Khoury PJ, Siddik SS, Salem MR, Joseph NJ. Efficacyof the self-inflating bulb in differentiating esophagealfrom tracheal intubation in the parturient undergoingcesarean section. Anesth Analg 1997;84:533—7.180. Davis DP, Stephen KA, Vilke GM. Inaccuracy in endotrachealtube verification using a Toomey syringe. J EmergMed 1999;17:35—8.181. Grmec S. Comparison of three different methods to confirmtracheal tube placement in emergency intubation. IntensiveCare Med 2002;28:701—4.182. American Heart Association in collaboration with InternationalLiaison Committee on Resuscitation. Guidelines 2000for Cardiopulmonary Resuscitation and Emergency CardiovascularCare: International Consensus on Science. Part 6.Advanced Cardiovascular Life Support: Section 6. PharmacologyII: Agents to Optimize Cardiac Output and BloodPressure. Circulation 2000;102(Suppl. I):I129—35.183. Lindner KH, Strohmenger HU, Ensinger H, Hetzel WD, AhnefeldFW, Georgieff M. Stress hormone response duringand after cardiopulmonary resuscitation. Anesthesiology1992;77:662—8.184. Lindner KH, Haak T, Keller A, Bothner U, Lurie KG. Releaseof endogenous vasopressors during and after cardiopulmonaryresuscitation. Heart 1996;75:145—50.185. Morris DC, Dereczyk BE, Grzybowski M, et al. Vasopressincan increase coronary perfusion pressure duringhuman cardiopulmonary resuscitation. Acad Emerg Med1997;4:878—83.186. Lindner KH, Prengel AW, Brinkmann A, Strohmenger HU,Lindner IM, Lurie KG. Vasopressin administration in refractorycardiac arrest. Ann Intern Med 1996;124:1061—4.187. Lindner KH, Brinkmann A, Pfenninger EG, Lurie KG, GoertzA, Lindner IM. Effect of vasopressin on hemodynamicvariables, organ blood flow, and acid—base status in apig model of cardiopulmonary resuscitation. Anesth Analg1993;77:427—35.188. Lindner KH, Prengel AW, Pfenninger EG, et al. Vasopressinimproves vital organ blood flow during closedchestcardiopulmonary resuscitation in pigs. Circulation1995;91:215—21.189. Wenzel V, Lindner KH, Prengel AW, et al. Vasopressinimproves vital organ blood flow after prolonged cardiacJ.P. Nolan et al.arrest with postcountershock pulseless electrical activityin pigs. Crit Care Med 1999;27:486—92.190. Voelckel WG, Lurie KG, McKnite S, et al. Comparison ofepinephrine and vasopressin in a pediatric porcine model ofasphyxial cardiac arrest. Crit Care Med 2000;28:3777—83.191. Babar SI, Berg RA, Hilwig RW, Kern KB, Ewy GA. Vasopressinversus epinephrine during cardiopulmonary resuscitation:a randomized swine outcome study. Resuscitation1999;41:185—92.192. Lindner KH, Dirks B, Strohmenger HU, Prengel AW, LindnerIM, Lurie KG. Randomised comparison of epinephrine andvasopressin in patients with out-of-hospital ventricular fibrillation.Lancet 1997;349:535—7.193. Stiell IG, Hebert PC, Wells GA, et al. Vasopressin versusepinephrine for inhospital cardiac arrest: a randomisedcontrolled trial. Lancet 2001;358:105—9.194. Wenzel V, Krismer AC, Arntz HR, Sitter H, Stadlbauer KH,Lindner KH. A comparison of vasopressin and epinephrinefor out-of-hospital cardiopulmonary resuscitation. N Engl JMed 2004;350:105—13.195. Aung K, Htay T. Vasopressin for cardiac arrest: a systematicreview and meta-analysis. Arch Intern Med2005;165:17—24.196. Callaham M, Madsen C, Barton C, Saunders C, DaleyM, Pointer J. A randomized clinical trial of highdoseepinephrine and norepinephrine versus standarddoseepinephrine in prehospital cardiac arrest. JAMA1992;268:2667—72.197. Masini E, Planchenault J, Pezziardi F, Gautier P, Gagnol JP.Histamine-releasing properties of Polysorbate 80 in vitroand in vivo: correlation with its hypotensive action in thedog. Agents Actions 1985;16:470—7.198. Somberg JC, Bailin SJ, Haffajee CI, et al. Intravenous lidocaineversus intravenous amiodarone (in a new aqueousformulation) for incessant ventricular tachycardia. Am JCardiol 2002;90:853—9.199. Somberg JC, Timar S, Bailin SJ, et al. Lack of a hypotensiveeffect with rapid administration of a new aqueousformulation of intravenous amiodarone. Am J Cardiol2004;93:576—81.200. Skrifvars MB, Kuisma M, Boyd J, et al. The use of undilutedamiodarone in the management of out-of-hospital cardiacarrest. Acta Anaesthesiol Scand 2004;48:582—7.201. Petrovic T, Adnet F, Lapandry C. Successful resuscitationof ventricular fibrillation after low-dose amiodarone. AnnEmerg Med 1998;32:518—9.202. Levine JH, Massumi A, Scheinman MM, et al. Intravenousamiodarone for recurrent sustained hypotensive ventriculartachyarrhythmias. Intravenous Amiodarone MulticenterTrial Group. J Am Coll Cardiol 1996;27:67—75.203. Matsusaka T, Hasebe N, Jin YT, Kawabe J, Kikuchi K.Magnesium reduces myocardial infarct size via enhancementof adenosine mechanism in rabbits. Cardiovasc Res2002;54:568—75.204. Longstreth Jr WT, Fahrenbruch CE, Olsufka M, Walsh TR,Copass MK, Cobb LA. Randomized clinical trial of magnesium,diazepam, or both after out-of-hospital cardiacarrest. Neurology 2002;59:506—14.205. Baraka A, Ayoub C, Kawkabani N. Magnesium therapyfor refractory ventricular fibrillation. J Cardiothorac VascAnesth 2000;14:196—9.206. Stiell IG, Wells GA, Hebert PC, Laupacis A, Weitzman BN.Association of drug therapy with survival in cardiac arrest:limited role of advanced cardiac life support drugs. AcadEmerg Med 1995;2:264—73.207. Engdahl J, Bang A, Lindqvist J, Herlitz J. Can we definepatients with no and those with some chance of sur-

European Resuscitation Council Guidelines for Resuscitation 2005S81vival when found in asystole out of hospital? Am J Cardiol2000;86:610—4.208. Engdahl J, Bang A, Lindqvist J, Herlitz J. Factors affectingshort- and long-term prognosis among 1069 patientswith out-of-hospital cardiac arrest and pulseless electricalactivity. Resuscitation 2001;51:17—25.209. Dumot JA, Burval DJ, Sprung J, et al. Outcome of adultcardiopulmonary resuscitations at a tertiary referral centerincluding results of ‘‘limited’’ resuscitations. Arch InternMed 2001;161:1751—8.210. Tortolani AJ, Risucci DA, Powell SR, Dixon R. In-hospitalcardiopulmonary resuscitation during asystole. Therapeuticfactors associated with 24-hour survival. Chest1989;96:622—6.211. Viskin S, Belhassen B, Roth A, et al. Aminophylline forbradyasystolic cardiac arrest refractory to atropine andepinephrine. Ann Intern Med 1993;118:279—81.212. Mader TJ, Gibson P. Adenosine receptor antagonism inrefractory asystolic cardiac arrest: results of a human pilotstudy. Resuscitation 1997;35:3—7.213. Mader TJ, Smithline HA, Gibson P. Aminophylline in undifferentiatedout-of-hospital asystolic cardiac arrest. Resuscitation1999;41:39—45.214. Mader TJ, Smithline HA, Durkin L, Scriver G. A randomizedcontrolled trial of intravenous aminophylline foratropine-resistant out-of-hospital asystolic cardiac arrest.Acad Emerg Med 2003;10:192—7.215. Dybvik T, Strand T, Steen PA. Buffer therapy during outof-hospitalcardiopulmonary resuscitation. Resuscitation1995;29:89—95.216. Aufderheide TP, Martin DR, Olson DW, et al. Prehospitalbicarbonate use in cardiac arrest: a 3-year experience. AmJ Emerg Med 1992;10:4—7.217. Delooz H, Lewi PJ. Are inter-center differences inEMS-management and sodium-bicarbonate administrationimportant for the outcome of CPR? The CerebralResuscitation Study Group. Resuscitation 1989;17(Suppl.):S199—206.218. Roberts D, Landolfo K, Light R, Dobson K. Early predictorsof mortality for hospitalized patients suffering cardiopulmonaryarrest. Chest 1990;97:413—9.219. Suljaga-Pechtel K, Goldberg E, Strickon P, Berger M,Skovron ML. Cardiopulmonary resuscitation in a hospitalizedpopulation: prospective study of factors associatedwith outcome. Resuscitation 1984;12:77—95.220. Weil MH, Trevino RP, Rackow EC. Sodium bicarbonate duringCPR. Does it help or hinder? Chest 1985;88:487.221. Bar-Joseph G, Abramson NS, Kelsey SF, Mashiach T, CraigMT, Safar P. Improved resuscitation outcome in emergencymedical systems with increased usage of sodium bicarbonateduring cardiopulmonary resuscitation. Acta AnaesthesiolScand 2005;49:6—15.222. Sandeman DJ, Alahakoon TI, Bentley SC. Tricyclicpoisoning—–successful management of ventricular fibrillationfollowing massive overdose of imipramine. AnaesthIntensive Care 1997;25:542—5.223. Lin SR. The effect of dextran and streptokinase on cerebralfunction and blood flow after cardiac arrest. An experimentalstudy on the dog. Neuroradiology 1978;16:340—2.224. Fischer M, Bottiger BW, Popov-Cenic S, Hossmann KA.Thrombolysis using plasminogen activator and heparinreduces cerebral no-reflow after resuscitation from cardiacarrest: an experimental study in the cat. Intensive CareMed 1996;22:1214—23.225. Ruiz-Bailen M, Aguayo de Hoyos E, Serrano-Corcoles MC,Diaz-Castellanos MA, Ramos-Cuadra JA, Reina-Toral A. Efficacyof thrombolysis in patients with acute myocardialinfarction requiring cardiopulmonary resuscitation. IntensiveCare Med 2001;27:1050—7.226. Lederer W, Lichtenberger C, Pechlaner C, Kroesen G,Baubin M. Recombinant tissue plasminogen activator duringcardiopulmonary resuscitation in 108 patients with out-ofhospitalcardiac arrest. Resuscitation 2001;50:71—6.227. Tiffany PA, Schultz M, Stueven H. Bolus thrombolyticinfusions during CPR for patients with refractory arrestrhythms: outcome of a case series. Ann Emerg Med1998;31:124—6.228. Abu-Laban RB, Christenson JM, Innes GD, et al. Tissue plasminogenactivator in cardiac arrest with pulseless electricalactivity. N Engl J Med 2002;346:1522—8.229. Janata K, Holzer M, Kurkciyan I, et al. Major bleeding complicationsin cardiopulmonary resuscitation: the place ofthrombolytic therapy in cardiac arrest due to massive pulmonaryembolism. Resuscitation 2003;57:49—55.230. Scholz KH, Hilmer T, Schuster S, Wojcik J, Kreuzer H, TebbeU. Thrombolysis in resuscitated patients with pulmonaryembolism. Dtsch Med Wochenschr 1990;115:930—5.231. Lederer W, Lichtenberger C, Pechlaner C, Kinzl J, KroesenG, Baubin M. Long-term survival and neurological outcomeof patients who received recombinant tissue plasminogenactivator during out-of-hospital cardiac arrest. Resuscitation2004;61:123—9.232. Gramann J, Lange-Braun P, Bodemann T, Hochrein H. DerEinsatz von Thrombolytika in der Reanimation als Ultimaratio zur Überwindung des Herztodes. Intensiv- und Notfallbehandlung1991;16:134—7.233. Klefisch F, et al. Praklinische ultima-ratio thrombolyse beitherapierefraktarer kardiopulmonaler reanimation. Intensivmedizin1995;32:155—62.234. Ruiz-Bailen M, Aguayo-de-Hoyos E, Serrano-Corcoles MC,et al. Thrombolysis with recombinant tissue plasminogenactivator during cardiopulmonary resuscitation in fulminantpulmonary embolism. A case series. Resuscitation2001;51:97—101.235. Böttiger BW, Martin E. Thrombolytic therapy during cardiopulmonaryresuscitation and the role of coagulationactivation after cardiac arrest. Curr Opin Crit Care2001;7:176—83.236. Spöhr F, Böttiger BW. Safety of thrombolysis duringcardiopulmonary resuscitation. Drug Saf 2003;26:367—79.237. Langhelle A, Tyvold SS, Lexow K, Hapnes SA, Sunde K, SteenPA. In-hospital factors associated with improved outcomeafter out-of-hospital cardiac arrest. A comparison betweenfour regions in Norway. Resuscitation 2003;56:247—63.238. Calle PA, Buylaert WA, Vanhaute OA. Glycemia in thepost-resuscitation period. The Cerebral Resuscitation StudyGroup. Resuscitation 1989;17(Suppl.):S181—8.239. Longstreth Jr WT, Diehr P, Inui TS. Prediction of awakeningafter out-of-hospital cardiac arrest. N Engl J Med1983;308:1378—82.240. Longstreth Jr WT, Inui TS. High blood glucose level on hospitaladmission and poor neurological recovery after cardiacarrest. Ann Neurol 1984;15:59—63.241. Longstreth Jr WT, Copass MK, Dennis LK, Rauch-MatthewsME, Stark MS, Cobb LA. Intravenous glucose after out-ofhospitalcardiopulmonary arrest: a community-based randomizedtrial. Neurology 1993;43:2534—41.242. Mackenzie CF. A review of 100 cases of cardiac arrest andthe relation of potassium, glucose, and haemoglobin levelsto survival. West Indian Med J 1975;24:39—45.243. Mullner M, Sterz F, Binder M, Schreiber W, Deimel A,Laggner AN. Blood glucose concentration after cardiopulmonaryresuscitation influences functional neurological

S82recovery in human cardiac arrest survivors. J Cereb BloodFlow Metab 1997;17:430—6.244. Skrifvars MB, Pettila V, Rosenberg PH, Castren M. A multiplelogistic regression analysis of in-hospital factorsrelated to survival at six months in patients resuscitatedfrom out-of-hospital ventricular fibrillation. Resuscitation2003;59:319—28.245. Ditchey RV, Lindenfeld J. Potential adverse effects of volumeloading on perfusion of vital organs during closedchestresuscitation. Circulation 1984;69:181—9.246. Gentile NT, Martin GB, Appleton TJ, Moeggenberg J, ParadisNA, Nowak RM. Effects of arterial and venous volumeinfusion on coronary perfusion pressures during canine CPR.Resuscitation 1991;22:55—63.247. Jameson SJ, Mateer JR, DeBehnke DJ. Early volume expansionduring cardiopulmonary resuscitation. Resuscitation1993;26:243—50.248. Voorhees WD, Ralston SH, Kougias C, Schmitz PM. Fluidloading with whole blood or Ringer’s lactate solution duringCPR in dogs. Resuscitation 1987;15:113—23.249. Banerjee S, Singhi SC, Singh S, Singh M. The intraosseousroute is a suitable alternative to intravenous route for fluidresuscitation in severely dehydrated children. Indian Pediatr1994;31:1511—20.250. Brickman KR, Krupp K, Rega P, Alexander J, Guinness M.Typing and screening of blood from intraosseous access.Ann Emerg Med 1992;21:414—7.251. Fiser RT, Walker WM, Seibert JJ, McCarthy R, Fiser DH. Tibiallength following intraosseous infusion: a prospective,radiographic analysis. Pediatr Emerg Care 1997;13:186—8.252. Ummenhofer W, Frei FJ, Urwyler A, Drewe J. Are laboratoryvalues in bone marrow aspirate predictable for venousblood in paediatric patients? Resuscitation 1994;27:123—8.253. Guy J, Haley K, Zuspan SJ. Use of intraosseous infusionin the pediatric trauma patient. J Pediatr Surg1993;28:158—61.254. Macnab A, Christenson J, Findlay J, et al. A new system forsternal intraosseous infusion in adults. Prehosp Emerg Care2000;4:173—7.255. Ellemunter H, Simma B, Trawoger R, Maurer H. Intraosseouslines in preterm and full term neonates. Arch Dis Child FetalNeonatal Ed 1999;80:F74—5.256. Prengel AW, Lindner KH, Hahnel JH, Georgieff M. Pharmacokineticsand technique of endotracheal and deependobronchial lidocaine administration. Anesth Analg1993;77:985—9.257. Prengel AW, Rembecki M, Wenzel V, Steinbach G. A comparisonof the endotracheal tube and the laryngeal maskairway as a route for endobronchial lidocaine administration.Anesth Analg 2001;92:1505—9.258. Steinfath M, Scholz J, Schulte am Esch J, Laer S, ReymannA, Scholz H. The technique of endobronchial lidocaineadministration does not influence plasma concentrationprofiles and pharmacokinetic parameters in humans. Resuscitation1995;29:55—62.259. Hahnel JH, Lindner KH, Schurmann C, Prengel A, AhnefeldFW. Plasma lidocaine levels and PaO2 with endobronchialadministration: dilution with normal saline ordistilled water? Ann Emerg Med 1990;19:1314—7.260. Del Guercio LRM, Feins NR, Cohn JD, Coumaraswamy RP,Wollmann SB, State D. Comparison of blood flow duringexternal and internal cardiac massage in man. Circulation1965;31(Suppl. 1):I171—80.261. Feneley MP, Maier GW, Kern KB, et al. Influence of compressionrate on initial success of resuscitation and 24 hoursurvival after prolonged manual cardiopulmonary resuscitationin dogs. Circulation 1988;77:240—50.J.P. Nolan et al.262. Halperin HR, Tsitlik JE, Guerci AD, et al. Determinants ofblood flow to vital organs during cardiopulmonary resuscitationin dogs. Circulation 1986;73:539—50.263. Kern KB, Sanders AB, Raife J, Milander MM, Otto CW,Ewy GA. A study of chest compression rates during cardiopulmonaryresuscitation in humans: the importanceof rate-directed chest compressions. Arch Intern Med1992;152:145—9.264. Ornato JP, Gonzalez ER, Garnett AR, Levine RL, McClungBK. Effect of cardiopulmonary resuscitation compressionrate on end-tidal carbon dioxide concentration and arterialpressure in man. Crit Care Med 1988;16:241—5.265. Swenson RD, Weaver WD, Niskanen RA, Martin J, DahlbergS. Hemodynamics in humans during conventional andexperimental methods of cardiopulmonary resuscitation.Circulation 1988;78:630—9.266. Boczar ME, Howard MA, Rivers EP, et al. A technique revisited:hemodynamic comparison of closed- and open-chestcardiac massage during human cardiopulmonary resuscitation.Crit Care Med 1995;23:498—503.267. Anthi A, Tzelepis GE, Alivizatos P, Michalis A, PalatianosGM, Geroulanos S. Unexpected cardiac arrest after cardiacsurgery: incidence, predisposing causes, and outcomeof open chest cardiopulmonary resuscitation. Chest1998;113:15—9.268. Pottle A, Bullock I, Thomas J, Scott L. Survival to dischargefollowing Open Chest Cardiac Compression (OCCC).A 4-year retrospective audit in a cardiothoracic specialistcentre—–Royal Brompton and Harefield NHS Trust, UnitedKingdom. Resuscitation 2002;52:269—72.269. Babbs CF. Interposed abdominal compression CPR: acomprehensive evidence based review. Resuscitation2003;59:71—82.270. Babbs CF, Nadkarni V. Optimizing chest compression to rescueventilation ratios during one-rescuer CPR by professionalsand lay persons: children are not just little adults.Resuscitation 2004;61:173—81.271. Beyar R, Kishon Y, Kimmel E, Neufeld H, Dinnar U. Intrathoracicand abdominal pressure variations as an efficientmethod for cardiopulmonary resuscitation: studies in dogscompared with computer model results. Cardiovasc Res1985;19:335—42.272. Voorhees WD, Niebauer MJ, Babbs CF. Improved oxygendelivery during cardiopulmonary resuscitation withinterposed abdominal compressions. Ann Emerg Med1983;12:128—35.273. Sack JB, Kesselbrenner MB, Jarrad A. Interposed abdominalcompression-cardiopulmonary resuscitation and resuscitationoutcome during asystole and electromechanical dissociation.Circulation 1992;86:1692—700.274. Sack JB, Kesselbrenner MB, Bregman D. Survival from inhospitalcardiac arrest with interposed abdominal counterpulsationduring cardiopulmonary resuscitation. JAMA1992;267:379—85.275. Mateer JR, Stueven HA, Thompson BM, Aprahamian C,Darin JC. Pre-hospital IAC-CPR versus standard CPR:paramedic resuscitation of cardiac arrests. Am J Emerg Med1985;3:143—6.276. Lindner KH, Pfenninger EG, Lurie KG, SchurmannW, Lindner IM, Ahnefeld FW. Effects of activecompression—decompression resuscitation on myocardialand cerebral blood flow in pigs. Circulation1993;88:1254—63.277. Shultz JJ, Coffeen P, Sweeney M, et al. Evaluation of standardand active compression—decompression CPR in anacute human model of ventricular fibrillation. Circulation1994;89:684—93.

European Resuscitation Council Guidelines for Resuscitation 2005S83278. Chang MW, Coffeen P, Lurie KG, Shultz J, Bache RJ, WhiteCW. Active compression—decompression CPR improvesvital organ perfusion in a dog model of ventricular fibrillation.Chest 1994;106:1250—9.279. Orliaguet GA, Carli PA, Rozenberg A, Janniere D, SauvalP, Delpech P. End-tidal carbon dioxide during out-ofhospitalcardiac arrest resuscitation: comparison of activecompression—decompression and standard CPR. Ann EmergMed 1995;25:48—51.280. Tucker KJ, Galli F, Savitt MA, Kahsai D, Bresnahan L, RedbergRF. Active compression—decompression resuscitation:effect on resuscitation success after in-hospital cardiacarrest. J Am Coll Cardiol 1994;24:201—9.281. Malzer R, Zeiner A, Binder M, et al. Hemodynamic effects ofactive compression—decompression after prolonged CPR.Resuscitation 1996;31:243—53.282. Lurie KG, Shultz JJ, Callaham ML, et al. Evaluation ofactive compression—decompression CPR in victims of outof-hospitalcardiac arrest. JAMA 1994;271:1405—11.283. Cohen TJ, Goldner BG, Maccaro PC, et al. A comparisonof active compression—decompression cardiopulmonaryresuscitation with standard cardiopulmonary resuscitationfor cardiac arrests occurring in the hospital. N Engl J Med1993;329:1918—21.284. Schwab TM, Callaham ML, Madsen CD, Utecht TA. A randomizedclinical trial of active compression—decompressionCPR vs standard CPR in out-of-hospital cardiac arrest intwo cities. JAMA 1995;273:1261—8.285. Stiell I, H’ebert P, Well G, et al. Tne Ontario trial of activecompression—decompression cardiopulmonary resuscitationfor in-hospital and prehospital cardiac arrest. JAMA1996;275:1417—23.286. Mauer D, Schneider T, Dick W, Withelm A, Elich D, MauerM. Active compression—decompression resuscitation: aprospective, randomized study in a two-tiered EMS systemwith physicians in the field. Resuscitation 1996;33:125—34.287. Nolan J, Smith G, Evans R, et al. The United Kingdompre-hospital study of active compression—decompressionresuscitation. Resuscitation 1998;37:119—25.288. Luiz T, Ellinger K, Denz C. Activecompression—decompression cardiopulmonary resuscitationdoes not improve survival in patients withprehospital cardiac arrest in a physician-manned emergencymedical system. J Cardiothorac Vasc Anesth1996;10:178—86.289. Plaisance P, Lurie KG, Vicaut E, et al. A comparisonof standard cardiopulmonary resuscitation andactive compression—decompression resuscitationfor out-of-hospital cardiac arrest. French ActiveCompression—Decompression Cardiopulmonary ResuscitationStudy Group. N Engl J Med 1999;341:569—75.290. Lafuente-Lafuente C, Melero-Bascones M. Active chestcompression—decompression for cardiopulmonary resuscitation.Cochrane Database Syst Rev 2004:CD002751.291. Baubin M, Rabl W, Pfeiffer KP, Benzer A, Gilly H. Chestinjuries after active compression—decompression cardiopulmonaryresuscitation (ACD-CPR) in cadavers. Resuscitation1999;43:9—15.292. Rabl W, Baubin M, Broinger G, Scheithauer R. Serious complicationsfrom active compression—decompressioncardiopulmonary resuscitation. Int J Legal Med1996;109:84—9.293. Hoke RS, Chamberlain D. Skeletal chest injuries secondaryto cardiopulmonary resuscitation. Resuscitation2004;63:327—38.294. Plaisance P, Lurie KG, Payen D. Inspiratory impedance duringactive compression—decompression cardiopulmonaryresuscitation: a randomized evaluation in patients in cardiacarrest. Circulation 2000;101:989—94.295. Plaisance P, Soleil C, Lurie KG, Vicaut E, Ducros L, PayenD. Use of an inspiratory impedance threshold device ona facemask and endotracheal tube to reduce intrathoracicpressures during the decompression phase of activecompression—decompression cardiopulmonary resuscitation.Crit Care Med 2005;33:990—4.296. Wolcke BB, Mauer DK, Schoefmann MF, et al. Comparisonof standard cardiopulmonary resuscitation versus the combinationof active compression—decompression cardiopulmonaryresuscitation and an inspiratory impedance thresholddevice for out-of-hospital cardiac arrest. Circulation2003;108:2201—5.297. Aufderheide T, Pirrallo R, Provo T, Lurie K. Clinicalevaluation of an inspiratory impedance thresholddevice during standard cardiopulmonary resuscitation inpatients with out-of-hospital cardiac arrest. Crit Care Med2005;33:734—40.298. Plaisance P, Lurie KG, Vicaut E, et al. Evaluation of animpedance threshold device in patients receiving activecompression—decompression cardiopulmonary resuscitationfor out of hospital cardiac arrest. Resuscitation2004;61:265—71.299. Sunde K, Wik L, Steen PA. Quality of mechanical, manualstandard and active compression—decompression CPR onthe arrest site and during transport in a manikin model.Resuscitation 1997;34:235—42.300. Wik L, Bircher NG, Safar P. A comparison of prolongedmanual and mechanical external chest compression aftercardiac arrest in dogs. Resuscitation 1996;32:241—50.301. Dickinson ET, Verdile VP, Schneider RM, Salluzzo RF. Effectivenessof mechanical versus manual chest compressionsin out-of-hospital cardiac arrest resuscitation: a pilot study.Am J Emerg Med 1998;16:289—92.302. McDonald JL. Systolic and mean arterial pressures duringmanual and mechanical CPR in humans. Ann Emerg Med1982;11:292—5.303. Ward KR, Menegazzi JJ, Zelenak RR, Sullivan RJ, McSwain JrN. A comparison of chest compressions between mechanicaland manual CPR by monitoring end-tidal PCO 2 duringhuman cardiac arrest. Ann Emerg Med 1993;22:669—74.304. Steen S, Liao Q, Pierre L, Paskevicius A, Sjoberg T. Evaluationof LUCAS, a new device for automatic mechanicalcompression and active decompression resuscitation.Resuscitation 2002;55:285—99.305. Rubertsson S, Karlsten R. Increased cortical cerebral bloodflow with LUCAS; a new device for mechanical chest compressionscompared to standard external compressions duringexperimental cardiopulmonary resuscitation. Resuscitation2005;65:357—63.306. Nielsen N, Sandhall L, Schersten F, Friberg H, Olsson SE.Successful resuscitation with mechanical CPR, therapeutichypothermia and coronary intervention during manualCPR after out-of-hospital cardiac arrest. Resuscitation2005;65:111—3.307. Timerman S, Cardoso LF, Ramires JA, Halperin H. Improvedhemodynamic performance with a novel chest compressiondevice during treatment of in-hospital cardiac arrest.Resuscitation 2004;61:273—80.308. Halperin H, Berger R, Chandra N, et al. Cardiopulmonaryresuscitation with a hydraulic-pneumatic band. Crit CareMed 2000;28:N203—6.309. Halperin HR, Paradis N, Ornato JP, et al. Cardiopulmonaryresuscitation with a novel chest compression device in aporcine model of cardiac arrest: improved hemodynamicsand mechanisms. J Am Coll Cardiol 2004;44:2214—20.

S84310. Casner M, Anderson D, et al. Preliminary report of theimpact of a new CPR assist device on the rate of return ofspontaneous circulation in out of hospital cardiac arrest.Prehosp Emerg Med 2005;9:61—7.311. Arntz HR, Agrawal R, Richter H, et al. Phased chestand abdominal compression—decompression versus conventionalcardiopulmonary resuscitation in out-of-hospitalcardiac arrest. Circulation 2001;104:768—72.312. Rozenberg A, Incagnoli P, Delpech P, et al. Prehospital useof minimally invasive direct cardiac massage (MID-CM): apilot study. Resuscitation 2001;50:257—62.313. Dauchot P, Gravenstein JS. Effects of atropine on the electrocardiogramin different age groups. Clin Pharmacol Ther1971;12:274—80.314. Chamberlain DA, Turner P, Sneddon JM. Effects of atropineon heart-rate in healthy man. Lancet 1967;2:12—5.315. Bernheim A, Fatio R, Kiowski W, Weilenmann D, Rickli H,Rocca HP. Atropine often results in complete atrioventricularblock or sinus arrest after cardiac transplantation: anunpredictable and dose-independent phenomenon. Transplantation2004;77:1181—5.316. Klumbies A, Paliege R, Volkmann H. Mechanical emergencystimulation in asystole and extreme bradycardia. ZGesamte Inn Med 1988;43:348—52.317. Zeh E, Rahner E. The manual extrathoracal stimulation ofthe heart. Technique and effect of the precordial thump(author’s transl). Z Kardiol 1978;67:299—304.318. Chan L, Reid C, Taylor B. Effect of three emergency pacingmodalities on cardiac output in cardiac arrest due toventricular asystole. Resuscitation 2002;52:117—9.319. Manz M, Pfeiffer D, Jung W, Lueritz B. Intravenous treatmentwith magnesium in recurrent persistent ventriculartachycardia. New Trends Arrhythmias 1991;7:437—42.320. Tzivoni D, Banai S, Schuger C, et al. Treatment oftorsade de pointes with magnesium sulfate. Circulation1988;77:392—7.321. Sticherling C, Tada H, Hsu W, et al. Effects of diltiazemand esmolol on cycle length and spontaneous conversionof atrial fibrillation. J Cardiovasc Pharmacol Ther2002;7:81—8.322. Shettigar UR, Toole JG, Appunn DO. Combined use ofesmolol and digoxin in the acute treatment of atrial fibrillationor flutter. Am Heart J 1993;126:368—74.323. Demircan C, Cikriklar HI, Engindeniz Z, et al. Comparison ofthe effectiveness of intravenous diltiazem and metoprololin the management of rapid ventricular rate in atrial fibrillation.Emerg Med J 2005;22:411—4.324. Wattanasuwan N, Khan IA, Mehta NJ, et al. Acute ventricularrate control in atrial fibrillation: IV combinationof diltiazem and digoxin vs. IV diltiazem alone. Chest2001;119:502—6.325. Davey MJ, Teubner D. A randomized controlled trial of magnesiumsulfate, in addition to usual care, for rate controlin atrial fibrillation. Ann Emerg Med 2005;45:347—53.326. Chiladakis JA, Stathopoulos C, Davlouros P, Manolis AS.Intravenous magnesium sulfate versus diltiazem in paroxysmalatrial fibrillation. Int J Cardiol 2001;79:287—91.327. Camm AJ, Garratt CJ. Adenosine and supraventriculartachycardia. N Engl J Med 1991;325:1621—9.328. Wang HE, O’Connor RE, Megargel RE, et al. The use ofdiltiazem for treating rapid atrial fibrillation in the outof-hospitalsetting. Ann Emerg Med 2001;37:38—45.329. Martinez-Marcos FJ, Garcia-Garmendia JL, Ortega-CarpioA, Fernandez-Gomez JM, Santos JM, Camacho C. Comparisonof intravenous flecainide, propafenone, and amiodaronefor conversion of acute atrial fibrillation to sinusrhythm. Am J Cardiol 2000;86:950—3.J.P. Nolan et al.330. Kalus JS, Spencer AP, Tsikouris JP, et al. Impact of prophylactici.v. magnesium on the efficacy of ibutilide forconversion of atrial fibrillation or flutter. Am J Health SystPharm 2003;60:2308—12.331. Langhelle A, Nolan J, Herlitz J, et al. Recommended guidelinesfor reviewing, reporting, and conducting researchon post-resuscitation care: the Utstein style. Resuscitation2005;66:271—83.332. Menon DK, Coles JP, Gupta AK, et al. Diffusion limitedoxygen delivery following head injury. Crit Care Med2004;32:1384—90.333. Buunk G, van der Hoeven JG, Meinders AE. Cerebrovascularreactivity in comatose patients resuscitated from a cardiacarrest. Stroke 1997;28:1569—73.334. Buunk G, van der Hoeven JG, Meinders AE. A comparisonof near-infrared spectroscopy and jugular bulb oximetryin comatose patients resuscitated from a cardiac arrest.Anaesthesia 1998;53:13—9.335. Roine RO, Launes J, Nikkinen P, Lindroth L, Kaste M.Regional cerebral blood flow after human cardiac arrest. Ahexamethylpropyleneamine oxime single photon emissioncomputed tomographic study. Arch Neurol 1991;48:625—9.336. Beckstead JE, Tweed WA, Lee J, MacKeen WL. Cerebralblood flow and metabolism in man following cardiac arrest.Stroke 1978;9:569—73.337. Laurent I, Monchi M, Chiche JD, et al. Reversible myocardialdysfunction in survivors of out-of-hospital cardiacarrest. J Am Coll Cardiol 2002;40:2110—6.338. Kern KB, Hilwig RW, Rhee KH, Berg RA. Myocardial dysfunctionafter resuscitation from cardiac arrest: an exampleof global myocardial stunning. J Am Coll Cardiol1996;28:232—40.339. Adrie C, Adib-Conquy M, Laurent I, et al. Successfulcardiopulmonary resuscitation after cardiac arrest as a‘‘sepsis-like’’ syndrome. Circulation 2002;106:562—8.340. Mullner M, Sterz F, Binder M, et al. Arterial blood pressureafter human cardiac arrest and neurological recovery.Stroke 1996;27:59—62.341. Angelos MG, Ward KR, Hobson J, Beckley PD. Organ bloodflow following cardiac arrest in a swine low-flow cardiopulmonarybypass model. Resuscitation 1994;27:245—54.342. Rello J, Diaz E, Roque M, Valles J. Risk factors for developingpneumonia within 48 hours of intubation. Am J RespirCrit Care Med 1999;159:1742—6.343. Krumholz A, Stern BJ, Weiss HD. Outcome from coma aftercardiopulmonary resuscitation: relation to seizures andmyoclonus. Neurology 1988;38:401—5.344. Wijdicks EF, Parisi JE, Sharbrough FW. Prognostic value ofmyoclonus status in comatose survivors of cardiac arrest.Ann Neurol 1994;35:239—43.345. Takino M, Okada Y. Hyperthermia following cardiopulmonaryresuscitation. Intensive Care Med 1991;17:419—20.346. Hickey RW, Kochanek PM, Ferimer H, Alexander HL, GarmanRH, Graham SH. Induced hyperthermia exacerbatesneurologic neuronal histologic damage after asphyxial cardiacarrest in rats. Crit Care Med 2003;31:531—5.347. Takasu A, Saitoh D, Kaneko N, Sakamoto T, Okada Y. Hyperthermia:is it an ominous sign after cardiac arrest? Resuscitation2001;49:273—7.348. Zeiner A, Holzer M, Sterz F, et al. Hyperthermia after cardiacarrest is associated with an unfavorable neurologicoutcome. Arch Intern Med 2001;161:2007—12.349. Coimbra C, Boris-Moller F, Drake M, Wieloch T. Diminishedneuronal damage in the rat brain by late treatmentwith the antipyretic drug dipyrone or cooling followingcerebral ischemia. Acta Neuropathol (Berl) 1996;92:447—53.

European Resuscitation Council Guidelines for Resuscitation 2005S85350. Coimbra C, Drake M, Boris-Moller F, Wieloch T. Long-lastingneuroprotective effect of postischemic hypothermia andtreatment with an anti-inflammatory/antipyretic drug: evidencefor chronic encephalopathic processes followingischemia. Stroke 1996;27:1578—85.351. Colbourne F, Sutherland G, Corbett D. Postischemichypothermia. A critical appraisal with implications for clinicaltreatment. Mol Neurobiol 1997;14:171—201.352. Ginsberg MD, Sternau LL, Globus MY, Dietrich WD, BustoR. Therapeutic modulation of brain temperature: relevanceto ischemic brain injury. Cerebrovasc Brain MetabRev 1992;4:189—225.353. Safar PJ, Kochanek PM. Therapeutic hypothermia after cardiacarrest. N Engl J Med 2002;346:612—3.354. Hypothermia After Cardiac Arrest Study Group. Mild therapeutichypothermia to improve the neurologic outcomeafter cardiac arrest. N Engl J Med 2002;346:549—56.355. Bernard SA, Gray TW, Buist MD, et al. Treatment ofcomatose survivors of out-of-hospital cardiac arrest withinduced hypothermia. N Engl J Med 2002;346:557—63.356. Hachimi-Idrissi S, Corne L, Ebinger G, Michotte Y, HuyghensL. Mild hypothermia induced by a helmet device: a clinicalfeasibility study. Resuscitation 2001;51:275—81.357. Bernard SA, Jones BM, Horne MK. Clinical trial of inducedhypothermia in comatose survivors of out-of-hospital cardiacarrest. Ann Emerg Med 1997;30:146—53.358. Bernard S, Buist M, Monteiro O, Smith K. Induced hypothermiausing large volume, ice-cold intravenous fluid incomatose survivors of out-of-hospital cardiac arrest: a preliminaryreport. Resuscitation 2003;56:9—13.359. Virkkunen I, Yli-Hankala A, Silfvast T. Induction of therapeutichypothermia after cardiac arrest in prehospitalpatients using ice-cold Ringer’s solution: a pilot study.Resuscitation 2004;62:299—302.360. Al-Senani FM, Graffagnino C, Grotta JC, et al. A prospective,multicenter pilot study to evaluate the feasibility andsafety of using the CoolGard System and Icy catheter followingcardiac arrest. Resuscitation 2004;62:143—50.361. Kliegel A, Losert H, Sterz F, et al. Cold simple intravenousinfusions preceding special endovascular cooling for fasterinduction of mild hypothermia after cardiac arrest—–a feasibilitystudy. Resuscitation 2005;64:347—51.362. Kim F, Olsufka M, Carlbom D, et al. Pilot study of rapid infusionof 2 L of 4 degrees C normal saline for induction of mildhypothermia in hospitalized, comatose survivors of out-ofhospitalcardiac arrest. Circulation 2005;112:715—9.363. Schmutzhard E, Engelhardt K, Beer R, et al. Safety andefficacy of a novel intravascular cooling device to controlbody temperature in neurologic intensive care patients: aprospective pilot study. Crit Care Med 2002;30:2481—8.364. Diringer MN, Reaven NL, Funk SE, Uman GC. Elevatedbody temperature independently contributes to increasedlength of stay in neurologic intensive care unit patients.Crit Care Med 2004;32:1489—95.365. Keller E, Imhof HG, Gasser S, Terzic A, Yonekawa Y.Endovascular cooling with heat exchange catheters: a newmethod to induce and maintain hypothermia. IntensiveCare Med 2003;29:939—43.366. Polderman KH, Peerdeman SM, Girbes AR. Hypophosphatemiaand hypomagnesemia induced by coolingin patients with severe head injury. J Neurosurg2001;94:697—705.367. Polderman KH. Application of therapeutic hypothermiain the intensive care unit. Opportunities and pitfallsof a promising treatment modality—–Part 2. Practicalaspects and side effects. Intensive Care Med 2004;30:757—69.368. Agnew DM, Koehler RC, Guerguerian AM, et al. Hypothermiafor 24 hours after asphyxic cardiac arrest inpiglets provides striatal neuroprotection that is sustained10 days after rewarming. Pediatr Res 2003;54:253—62.369. Hicks SD, DeFranco DB, Callaway CW. Hypothermiaduring reperfusion after asphyxial cardiac arrest improvesfunctional recovery and selectively alters stressinducedprotein expression. J Cereb Blood Flow Metab2000;20:520—30.370. Sterz F, Safar P, Tisherman S, Radovsky A, Kuboyama K,Oku K. Mild hypothermic cardiopulmonary resuscitationimproves outcome after prolonged cardiac arrest in dogs.Crit Care Med 1991;19:379—89.371. Xiao F, Safar P, Radovsky A. Mild protective and resuscitativehypothermia for asphyxial cardiac arrest in rats. Am JEmerg Med 1998;16:17—25.372. Katz LM, Young A, Frank JE, Wang Y, Park K. Neurotensininducedhypothermia improves neurologic outcome afterhypoxic-ischemia. Crit Care Med 2004;32:806—10.373. Abella BS, Zhao D, Alvarado J, Hamann K, VandenHoek TL, Becker LB. Intra-arrest cooling improves outcomesin a murine cardiac arrest model. Circulation2004;109:2786—91.374. Nolan JP, Morley PT, Vanden Hoek TL, Hickey RW. Therapeutichypothermia after cardiac arrest. An advisory statementby the Advancement Life support Task Force of the InternationalLiaison committee on Resuscitation. Resuscitation2003;57:231—5.375. Baird TA, Parsons MW, Phanh T, et al. Persistent poststrokehyperglycemia is independently associated withinfarct expansion and worse clinical outcome. Stroke2003;34:2208—14.376. Capes SE, Hunt D, Malmberg K, Pathak P, Gerstein HC.Stress hyperglycemia and prognosis of stroke in nondiabeticand diabetic patients: a systematic overview. Stroke2001;32:2426—32.377. Scott JF, Robinson GM, French JM, O’Connell JE, AlbertiKG, Gray CS. Glucose potassium insulin infusions in thetreatment of acute stroke patients with mild to moderatehyperglycemia: the Glucose Insulin in Stroke Trial (GIST).Stroke 1999;30:793—9.378. Yip PK, He YY, Hsu CY, Garg N, Marangos P, Hogan EL. Effectof plasma glucose on infarct size in focal cerebral ischemiareperfusion.Neurology 1991;41:899—905.379. van den Berghe G, Wouters P, Weekers F, et al. Intensiveinsulin therapy in the critically ill patients. N Engl J Med2001;345:1359—67.380. Krinsley JS. Effect of an intensive glucose management protocolon the mortality of critically ill adult patients. MayoClin Proc 2004;79:992—1000.381. Van den Berghe G, Wouters PJ, Bouillon R, et al. Outcomebenefit of intensive insulin therapy in the criticallyill: insulin dose versus glycemic control. Crit Care Med2003;31:359—66.382. Katz LM, Wang Y, Ebmeyer U, Radovsky A, Safar P. Glucoseplus insulin infusion improves cerebral outcome afterasphyxial cardiac arrest. Neuroreport 1998;9:3363—7.383. Laver S, Farrow C, Turner D, Nolan J. Mode of death afteradmission to an intensive care unit following cardiac arrest.Intensive Care Med 2004;30:2126—8.384. Zandbergen EG, de Haan RJ, Stoutenbeek CP, KoelmanJH, Hijdra A. Systematic review of early predictionof poor outcome in anoxic-ischaemic coma. Lancet1998;352:1808—12.385. Booth CM, Boone RH, Tomlinson G, Detsky AS. Is this patientdead, vegetative, or severely neurologically impaired?

S86J.P. Nolan et al.Assessing outcome for comatose survivors of cardiac arrest.Jama 2004;291:870—9.386. Edgren E, Hedstrand U, Kelsey S, Sutton-Tyrrell K, SafarP. Assessment of neurological prognosis in comatose survivorsof cardiac arrest. BRCT I Study Group. Lancet1994;343:1055—9.387. Tiainen M, Roine RO, Pettila V, Takkunen O. Serumneuron-specific enolase and S-100B protein in cardiacarrest patients treated with hypothermia. Stroke2003;34:2881—6.388. Fogel W, Krieger D, Veith M, et al. Serum neuron-specificenolase as early predictor of outcome after cardiac arrest.Crit Care Med 1997;25:1133—8.389. Mussack T, Biberthaler P, Kanz KG, et al. Serum S-100Band interleukin-8 as predictive markers for comparativeneurologic outcome analysis of patients after cardiacarrest and severe traumatic brain injury. Crit Care Med2002;30:2669—74.390. Mussack T, Biberthaler P, Kanz KG, Wiedemann E, Gippner-Steppert C, Jochum M. S-100b, sE-selectin, and sP-selectinfor evaluation of hypoxic brain damage in patients aftercardiopulmonary resuscitation: pilot study. World J Surg2001;25:539—43 [discussion 44].391. Rosen H, Karlsson JE, Rosengren L. CSF levels of neurofilamentis a valuable predictor of long-term outcome aftercardiac arrest. J Neurol Sci 2004;221:19—24.392. Rosen H, Rosengren L, Herlitz J, Blomstrand C. Increasedserum levels of the S-100 protein are associated withhypoxic brain damage after cardiac arrest. Stroke1998;29:473—7.393. Meynaar IA, Straaten HM, van der Wetering J, et al. Serumneuron-specific enolase predicts outcome in post-anoxiccoma: a prospective cohort study. Intensive Care Med2003;29:189—95.394. Rosen H, Sunnerhagen KS, Herlitz J, Blomstrand C, RosengrenL. Serum levels of the brain-derived proteins S-100and NSE predict long-term outcome after cardiac arrest.Resuscitation 2001;49:183—91.395. Schreiber W, Herkner H, Koreny M, et al. Predictors of survivalin unselected patients with acute myocardial infarctionrequiring continuous catecholamine support. Resuscitation2002;55:269—76.396. Schoerkhuber W, Kittler H, Sterz F, et al. Time course ofserum neuron-specific enolase. A predictor of neurologicaloutcome in patients resuscitated from cardiac arrest.Stroke 1999;30:1598—603.397. Bottiger BW, Mobes S, Glatzer R, et al. Astroglial proteinS-100 is an early and sensitive marker of hypoxic braindamage and outcome after cardiac arrest in humans. Circulation2001;103:2694—8.398. Martens P, Raabe A, Johnsson P, Serum. S-100 and neuronspecificenolase for prediction of regaining consciousnessafter global cerebral ischemia. Stroke 1998;29:2363—6.399. Zingler VC, Krumm B, Bertsch T, Fassbender K, Pohlmann-Eden B. Early prediction of neurological outcome after cardiopulmonaryresuscitation: a multimodal approach combiningneurobiochemical and electrophysiological investigationsmay provide high prognostic certainty in patientsafter cardiac arrest. Eur Neurol 2003;49:79—84.400. Zandbergen EG, de Haan RJ, Hijdra A. Systematic review ofprediction of poor outcome in anoxic-ischaemic coma withbiochemical markers of brain damage. Intensive Care Med2001;27:1661—7.401. Synek VM. Validity of a revised EEG coma scale for predictingsurvival in anoxic encephalopathy. Clin Exp Neurol1989;26:119—27.402. Moller M, Holm B, Sindrup E, Nielsen BL. Electroencephalographicprediction of anoxic brain damage after resuscitationfrom cardiac arrest in patients with acute myocardialinfarction. Acta Med Scand 1978;203:31—7.403. Scollo-Lavizzari G, Bassetti C. Prognostic value of EEGin post-anoxic coma after cardiac arrest. Eur Neurol1987;26:161—70.404. Bassetti C, Karbowski K. Prognostic value of electroencephalographyin non-traumatic comas. Schweiz MedWochenschr 1990;120:1425—34.405. Bassetti C, Bomio F, Mathis J, Hess CW. Early prognosisin coma after cardiac arrest: a prospective clinical, electrophysiological,and biochemical study of 60 patients. JNeurol Neurosurg Psychiatry 1996;61:610—5.406. Rothstein TL. Recovery from near death following cerebralanoxia: a case report demonstrating superiority of mediansomatosensory evoked potentials over EEG in predictinga favorable outcome after cardiopulmonary resuscitation.Resuscitation 2004;60:335—41.407. Berkhoff M, Donati F, Bassetti C. Postanoxic alpha (theta)coma: a reappraisal of its prognostic significance. Clin Neurophysiol2000;111:297—304.408. Kaplan PW, Genoud D, Ho TW, Jallon P. Etiology, neurologiccorrelations, and prognosis in alpha coma. Clin Neurophysiol1999;110:205—13.409. Yamashita S, Morinaga T, Ohgo S, et al. Prognostic valueof electroencephalogram (EEG) in anoxic encephalopathyafter cardiopulmonary resuscitation: relationship amonganoxic period, EEG grading and outcome. Intern Med1995;34:71—6.410. Ajisaka H. Early electroencephalographic findings inpatients with anoxic encephalopathy after cardiopulmonaryarrest and successful resusitation. J Clin Neurosci2004;11:616—8.411. Rothstein TL, Thomas EM, Sumi SM. Predicting outcome inhypoxic-ischemic coma. A prospective clinical and electrophysiologicstudy. Electroencephalogr Clin Neurophysiol1991;79:101—7.412. Edgren E, Hedstrand U, Nordin M, Rydin E, Ronquist G.Prediction of outcome after cardiac arrest. Crit Care Med1987;15:820—5.413. Sorensen K, Thomassen A, Wernberg M. Prognostic significanceof alpha frequency EEG rhythm in coma after cardiacarrest. J Neurol Neurosurg Psychiatry 1978;41:840—2.

Resuscitation (2005) 67S1, S87—S96European Resuscitation Council Guidelines forResuscitation 2005Section 5. Initial management of acutecoronary syndromesHans-Richard Arntz, Leo Bossaert, Gerasimos S. FilippatosIntroductionThe incidence of acute myocardial infarction(AMI) is decreasing in many European countries. 1Although in-hospital mortality from AMI has beenreduced significantly by modern reperfusion therapyand improved secondary prophylaxis, 1 the overall28-day mortality is virtually unchanged becauseabout two thirds of those that die do so beforearrival at hospital. 2 Thus, the best chance ofimproving survival after AMI is by improving treatmentin the early, and particularly the out-of hospital,phase of the disease.The term acute coronary syndrome (ACS) encompassesthree different entities within the acutemanifestation of coronary heart disease: ST elevationmyocardial infarction (STEMI), non-ST elevationmyocardial infarction (NSTEMI) and unstableangina pectoris (UAP) (Figure 5.1). The commonpathophysiology of ACS is a ruptured or erodedatherosclerotic plaque. 3 Electrocardiographic characteristics(absence or presence of ST elevation)differentiate STEMI from the other forms of ACS.A NSTEMI or UAP may present with ST segmentdepression or non-specific ST segment wave abnormalities,or even a normal ECG. In the absence ofST elevation, an increase in the plasma concentrationof cardiac markers, particularly troponin T orI as the most specific markers of myocardial cellnecrosis, indicates NSTEMI.Acute coronary syndromes are the commonestcause of malignant arrhythmias leading to suddencardiac death. The therapeutic goals are to treatacute life-threatening conditions, such as ventricularfibrillation (VF) or extreme bradycardias, and topreserve left ventricular function and prevent heartfailure by minimising the extent of any myocardialinfarction. These guidelines address the firsthours after onset of symptoms. Out-of-hospitaltreatment and initial therapy in the emergencydepartment may vary according to local capabilities,resources and regulations. The data supportingout-of-hospital treatment are usually extrapolatedfrom studies of initial treatment early after hospitaladmission; there are only few high-quality out-ofhospitalstudies. Comprehensive guidelines for thediagnosis and treatment of ACS with and withoutST elevation have been published by the EuropeanSociety of Cardiology and the American College ofCardiology/American Heart Association. 4,5 The currentrecommendations are in line with these guidelines.Diagnostic tests in acute coronarysyndromesSince early treatment offers the greatest benefits,and myocardial ischaemia is the leading precipitantof sudden cardiac death, it is essential that the0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.doi:10.1016/j.resuscitation.2005.10.003

S88H.-R. Arntz et al.Figure 5.1Classification of acute coronary syndromes.public are aware of the typical symptoms associatedwith ACS. Patients at risk, and their families,should be able to recognise characteristic symptomssuch as chest pain, which may radiate intoother areas of the upper body, often accompaniedby other symptoms including dyspnoea, sweating,nausea or vomiting and syncope. They should understandthe importance of early activation of theemergency medical service (EMS) system and, ideally,should be trained in basic life support (BLS).EMS dispatchers must be trained to recognizeACS symptoms and to ask targeted questions. Whenan ACS is suspected, an EMS crew trained inadvanced life support (ALS) and capable of makingthe diagnosis and starting treatment shouldbe alerted. The sensitivity, specificity and clinicalimpact of various diagnostic strategies have beenevaluated for ACS/AMI. These include signs andsymptoms, the 12-lead electrocardiogram (ECG)and biochemical markers of cardiac risk.Signs and symptoms of ACS/AMIEven though typical symptoms such as radiatingchest pain, shortness of breath or sweating may bemore intense and generally last longer in patientswith AMI, they are not adequately specific for areliable diagnosis of AMI. A 12-lead ECG, cardiacbiomarkers and other diagnostic tests are requiredbefore ACS or AMI can be ruled out in the presenceof a typical history. Atypical symptoms or unusualpresentations may occur in the elderly, in females,and in people with diabetes. 6,712-lead ECGA 12-lead ECG is the key investigation for assessmentof an ACS. In case of STEMI, a 12-lead ECG canindicate the need for immediate reperfusion therapy(e.g., primary percutaneous coronary intervention(PCI) or prehospital thrombolysis). Recordingof a 12-lead ECG out-of-hospital enables advancednotification to the receiving facility and expeditestreatment decisions after hospital arrival;in many studies, the time from hospital admissionto initiating reperfusion therapy is reduced by10—60 min. 8—10 Recording and transmission of diagnosticquality ECGs to the hospital takes usuallyless than 5 min. Trained EMS personnel (emergencyphysicians, paramedics and nurses) can identifySTEMI, defined by ST elevation of ≥0.1 mV elevationin at least two adjacent limb leads or >0.2 mV intwo adjacent precordial leads, with high specificityand sensitivity comparable to diagnostic accuracyin the hospital. 11—13BiomarkersIn the presence of a suggestive history, the absenceof ST elevation on the ECG, and elevated concentrationsof biomarkers (troponin T and troponinI, CK, CK-MB, myoglobin) characterise non-STEMI

European Resuscitation Council Guidelines for Resuscitation 2005S89and distinguish it from STEMI and unstable angina,respectively. 3 Elevated concentrations of troponinare particularly helpful in identifying patients atincreased risk of adverse outcome. 14 However,the delay in release of biomarkers from damagedmyocardium prevents their use in diagnosingmyocardial infarction in the first 4—6 h after theonset of symptoms. 15Principles of acute treatment for ACSNitratesGlyceryl trinitrate is an effective treatment forischaemic chest pain (Figure 5.2) and has somebeneficial haemodynamic effects, e.g., dilation ofthe venous capacitance vessels, coronary arteriesand, to a minor degree, peripheral arteries. Glyceryltrinitrate may be considered if the systolicblood pressure is higher than 90 mmHg and thepatient has ongoing ischaemic chest pain. Glyceryltrinitrate can be useful in the treatment ofacute pulmonary congestion. Do not use nitrates inpatients with hypotension (systolic blood pressure≤90 mmHg), particularly if combined with bradycardia,nor in patients with inferior infarction andsuspected right ventricular involvement. Use ofnitrates under these circumstances may cause aprecipitous decrease in blood pressure and cardiacoutput.MorphineMorphine is the analgesic of choice for nitraterefractorypain. Being a dilator of venous capacitancevessels, it may have additional benefit inpatients with pulmonary congestion. Give morphinein initial doses of 3—5 mg intravenously and repeatevery few minutes until the patient is pain free.OxygenGive supplementary oxygen (4—8 l min −1 ) to allpatients with arterial oxygen saturation

S90Reperfusion therapyReperfusion therapy is the most important advancein the treatment of AMI in the last 20 years.Large clinical trials have proven that fibrinolytictherapy in ACS patients with STEMI or new orpresumed new LBBB, who present within 12 h ofonset of symptoms, reduces short- and long-termmortality. 17,21—23 The benefit achieved with fibrinolytictherapy is profoundly time dependent; itis particularly effective if given within the first 3 hof the onset of symptoms. 17,21,22,24 The efficacy ofprimary PCI is also time-sensitive but less so thanfibrinolysis. 25Out-of-hospital fibrinolysisA meta-analysis of six trials involving 6434 patientsdocumented a 17% decrease in the mortality amongpatients treated with out-of-hospital fibrinolysiscompared with in-hospital fibrinolysis. 26 The averagetime gained by out-of-hospital fibrinolysis was60 min, and the results were independent of theexperience of the provider. Thus, giving fibrinolyticsout-of-hospital to patients with STEMI or signsand symptoms of an ACS with presumed new LBBB isbeneficial. Fibrinolytic therapy can be given safelyby trained paramedics, nurses or physicians usingan established protocol. 27—29 The efficacy is greatestwithin the first 3 h of the onset of symptoms.An effective and safe system for out-of-hospitalthrombolytic therapy requires adequate facilitiesfor the diagnosis and treatment of STEMI and itscomplications. Ideally, there should be a capabilityto communicate with experienced hospital doctors(e.g., emergency physicians or cardiologists).Patients with symptoms of ACS and ECG evidenceof STEMI (or presumably new LBBB or true posteriorinfarction) presenting directly to the emergencydepartment should be given fibrinolytic therapy assoon as possible unless there is immediate accessto primary PCI within 90 min.Risks of fibrinolytic therapyHealthcare professionals who give fibrinolytictherapy must be aware of its contraindications(Table 5.1) and risks. Patients with large AMIs (e.g.,indicated by extensive ECG changes) are likely toderive the greatest benefit from fibrinolytic therapy.Benefits of fibrinolytic therapy are less impressivein inferior wall infarctions than in anteriorinfarctions. Older patients have an absolute higherrisk of death, but the absolute benefit of fibrinolytictherapy is similar to that of younger patients.Patients over 75 years of age have an increasedH.-R. Arntz et al.Table 5.1 Contraindications for thrombolysis a .Absolute contraindicationsHaemorrhagic stroke or stroke of unknown originat any timeIschaemic stroke in the preceding 6 monthsCentral nervous system damage or neoplasmsRecent major trauma/surgery/head injury (withinthe preceding 3 weeks)Gastro-intestinal bleeding within the last monthKnown bleeding disorderAortic dissectionRelative contraindicationsTransient ischaemic attack in preceding 6 monthsOral anticoagulant therapyPregnancy within 1 week post partumNon-compressible puncturesTraumatic resuscitationRefractory hypertension (systolic blood pressure>180 mmHgAdvanced liver diseaseInfective endocarditisActive peptic ulcera According to the guidelines of the European Society ofCardiology.risk of intracranial bleeding from fibrinolysis; thus,the absolute benefit of thrombolysis is reduced bythis complication. 30 The risk of intracranial bleedingin patients with a systolic blood pressure of over180 mmHg is increased; this degree of hypertensionis a relative contraindication to fibrinolytic therapy.The intracranial bleeding risk also depends in parton which fibrinolytic drug is used; the total mortalityis lower with the more fibrin-specific thrombolytics(alteplase, tenecteplase, reteplase), butthe intracranial bleeding risk is lower with streptokinase.The risk of intracranial bleeding is alsoincreased by the use of antithrombotic therapy,particularly heparin.Primary percutaneous interventionCoronary angioplasty with or without stent placementhas become the first-line treatment forpatients with STEMI, because it has been shownto be superior to fibrinolysis in the combined endpointsof death, stroke and reinfarction in severalstudies and meta-analyses. 31,32 This improvementwas found when primary PCI was undertakenby a skilled person in a high-volume centre (i.e.,>75 procedures per operator per year), with adelay of balloon inflation of not more than 90 minafter first contact. In the randomised studies comparingprimary PCI and fibrinolytic therapy, thetypical delay from decision to the beginning of

European Resuscitation Council Guidelines for Resuscitation 2005S91treatment with either primary PCI or fibrinolytictherapy was less than 60 min; however, in registriesthat reflect standard practice more realistically,the delay was often longer. One study 33 and onepost hoc analysis 34 comparing fibrinolytic therapywith primary PCI showed no difference in survivalif fibrinolytic therapy was initiated within 2 or 3 hof onset of symptoms.All patients presenting with STEMI and symptomsof ACS and presumably new LBBB presenting within12 h after onset of symptoms should be evaluatedfor reperfusion therapy (fibrinolytic therapy or PCI).Primary PCI is preferred in patients with symptomduration of over 3 h, if a skilled team can undertakeit within 90 min after first patient contact, andin all patients who have contraindications to fibrinolytictherapy. If the duration of symptoms is lessthan 3 h, treatment is more time-sensitive and thesuperiority of out-of-hospital fibrinolytic therapy,immediate in-hospital fibrinolytic therapy or transferfor primary PCI is not yet established clearly.Triage and interfacility transfer for primary PCI.The risk of death, reinfarction or stroke is reducedif patients with STEMI are transferred promptlyfrom community hospitals to tertiary care facilitiesfor primary PCI. 35 It is unclear whether immediatefibrinolytic therapy (in- or out-of-hospital) ortransfer for primary PCI is superior for patientspresenting with STEMI with a symptom duration of

S92serious bleeding is not increased. Early treatmentwith LMWH (enoxaparin) is the preferred therapyfor patients with NSTEMI/UAP in addition to ASA,whenever a non-interventional strategy is planned.Consider UFH if reperfusion is planned in thefirst 24—36 h after symptom onset. Optimal targetvalue of aPPT is 50—70 s. Avoid switching betweenUFH and LMWH, because it may increase bleedingcomplications. 43Unfractionated heparin versuslow-molecular-weight heparin in STEMITwo large randomised controlled thrombolysis studiescomparing LMWH with UFH demonstrated areduced frequency of ischaemic complicationswhen given to patients with STEMI within 6 h ofthe onset of symptoms. 44,45 This must be balancedagainst the increase in intracranial haemorrhage inpatients over 75 years of age who receive LMWH. 45There is no evidence to support giving LMWH topatients with STEMI proceeding to an invasive strategy.Thus, LMWH is an acceptable alternative toUFH as an ancillary therapy for patients youngerthan 75 years without significant renal dysfunctionwho are treated with fibrinolytic therapy. UFH isrecommended as an ancillary therapy to fibrinolytictherapy in elderly patients and any STEMI patientfor whom revascularisation is planned. The optimaltarget value of aPPT is 50—70 s. The use of heparin(preferably LMWH) depends partly on whichfibrinolytic drug is used. Heparin is needed aftershorter-acting drugs because of the rebound hypercoagulablestate that occurs after a few hours,but not after streptokinase because the fibrinolyticeffect of streptokinase lasts for about 48 h.Glycoprotein IIb/IIIa inhibitorsThe platelet glycoprotein (Gp) IIb/IIIa receptor isthe final common pathway to platelet aggregation.The synthetic substances eptifibatide and tirofibanmodulate this receptor activity reversibly, whereasthe receptor antibody abciximab blocks it irreversibly.H.-R. Arntz et al.Gp IIb/IIIa inhibitors in NSTEMI/unstable angina.The incidences of death and recurrent ischaemiaare reduced when Gp IIb/IIIa inhibitors are addedto standard therapy including ASA and heparinin high-risk patients with UAP/NSTEMI treatedwith mechanical reperfusion. 46 High-risk featuresinclude persistent pain, haemodynamic or rhythminstability, diabetes, acute or dynamic ECG changesand any elevation in cardiac troponins. Tirofibanor eptifibatide failed to reduce death or recurrentischaemia in patients with UA/NSTEMI withoutmechanical perfusion, but showed a reductionin 30-day mortality in a later meta-analysis. 46In patients with UA/NSTEMI, abciximab, given inaddition to standard therapy without mechanicalintervention, resulted in a trend towards a worseoutcome. 47 Therefore, in high-risk patients, giveGp IIb/IIIa inhibitors in addition to standard therapyin patients for whom revascularisation therapyis planned. If revascularisation therapy is notplanned, tirofiban and eptifibatide can be given tohigh-risk NSTEMI/UAP patients in conjunction withASA and LMWH. Do not give abciximab if PCI is notplanned.Gp IIb/IIIa inhibitors in STEMI. Gp IIb/IIIa receptorblockers in combination with a reduced dose of fibrinolyticsdo not reduce mortality in patients withSTEMI, but increase bleeding risk in patients over75 years of age. 44,48 Abciximab reduces mortalitywhen given to patients with STEMI and plannedprimary PCI, but is not beneficial in patients notproceeding to primary PCI. 46 Prehospital use ofabciximab may improve the patency of the infarctrelatedartery with regard to PCI. 49 There is nobenefit in giving tirofiban in addition to standardtherapy out of hospital or in the emergencydepartment. 50 Abciximab may be helpful in reducingshort-term mortality and short-term reinfarctionin patients treated with PCI without fibrinolytictherapy. Abciximab is not recommended in combinationwith fibrinolytics in patients with STEMI.ClopidogrelClopidogrel inhibits the platelet ADP receptor irreversibly,which further reduces platelet aggregationin addition to that produced by ASA. Comparedwith ASA, there is no increased risk of bleedingwith clopidogrel. 51 If given in addition to heparinand ASA within 4 h of presentation, clopidogrelimproves outcome in patients with highriskACS. 52,53 There is a significant reduction inadverse ischaemic events at 28 days after electivePCI when clopidogrel is given at least 6 h beforeintervention. 54 A recent trial documented a significantreduction in the composite endpoint of anoccluded infarct-related artery (TIMI flow grade 0or 1) on angiography or death or recurrent myocardialinfarction before angiography, when clopidogrel(300 mg loading dose, followed by 75 mg dailydose up to 8 days in hospital) is given to patients upto 75 years of age with STEMI who are treated withfibrinolytic therapy, ASA and heparin. 55Give a 300-mg oral loading dose of clopidogrelearly, as well as standard care, to patients withACS if they have an increase in serum cardiac

European Resuscitation Council Guidelines for Resuscitation 2005S93biomarkers and/or new ECG changes consistentwith ischaemia when a medical approach or PCI isplanned. Give clopidogrel to patients with STEMIup to 75 years of age receiving fibrinolytic therapy,ASA and heparin. Clopidogrel, 300 mg, can be giveninstead of ASA to patients with a suspected ACS whohave a true allergy to or gastrointestinal intoleranceof ASA.Primary and secondary preventioninterventionsStart preventive interventions, at the latest, at theinitial admission with a confirmed diagnosis of ACS.Give a beta-blocker as soon as possible unless contraindicatedor poorly tolerated. Treat all patientswith a statin (HRG co-enzyme A reductase inhibitor)unless contraindicated or poorly tolerated. Start anACE inhibitor in all patients with STEMI, all patientswith STEMI and left ventricular systolic impairment,and consider it in all other patients withSTEMI unless contraindicated or poorly tolerated.In patients unable to tolerate an ACE inhibitor, anangiotensin receptor blocker may be used as a substitutein those patients with left ventricular systolicimpairment.Beta-blockersSeveral studies, undertaken mainly in the prereperfusionera, indicate decreased mortality andincidence of reinfarction and cardiac rupture aswell as a lower incidence of VF and supraventriculararrhythmia in patients treated early with abeta-blocker. 56,57 Intravenous beta-blockade mayalso reduce mortality in patients undergoing primaryPCI who are not on oral beta-blockers. 58Haemodynamically stable patients presentingwith an ACS should be given intravenous betablockerspromptly, followed by regular oral therapyunless contraindicated or poorly tolerated. Contraindicationsto beta-blockers include hypotension,bradycardia, second- or third-degree AV block,moderate to severe congestive heart failure andsevere reactive airway disease. Give a beta-blockerirrespective of the need for early revascularisationtherapy.Anti-arrhythmicsApart from the use of a beta-blocker as recommendedabove, there is no evidence to supportthe use of anti-arrhythmic prophylaxis after ACS.VF accounts for most of the early deaths fromACS; the incidence of VF is highest in the firsthours after onset of symptoms. 59,60 This explainswhy numerous studies have been performed withthe aim of demonstrating the prophylactic effectof anti-arrhythmic therapy. The effects of antiarrhythmicdrugs (lidocaine, magnesium, disopyramide,mexiletine, verapamil) given prophylacticallyto patients with ACS have been studied. 61—63Prophylaxis with lidocaine reduces the incidenceof VF but may increase mortality. 58 Routine treatmentwith magnesium in patients with AMI doesnot improve mortality. 64 Arrhythmia prophylaxisusing disopyramide, mexiletine or verapamil, givenwithin the first hours of an ACS, does not improvemortality. 63 In contrast, intravenous beta-blockersreduced the incidence of VF when given to patientswith ACS. 56,57Angiotensin-converting enzyme inhibitorsand angiotensin-II receptor blockersOral angiotensin-converting inhibitors (ACE) inhibitorsreduce mortality when given to patients withacute myocardial infarction with or without earlyreperfusion therapy. 65,66 The beneficial effects aremost pronounced in patients presenting with anteriorinfarction, pulmonary congestion or left ventricularejection fraction

S94survival, event rates, and coronary heart disease mortalityacross the WHO MONICA Project populations. Lancet2000;355:688—700.2. Lowel H, Meisinger C, Heier M, et al. Sex specific trendsof sudden cardiac death and acute myocardial infarction:results of the population-based KORA/MONICA-Augsburg register1985 to 1998. Dtsch Med Wochenschr 2002;127:2311—6.3. European Society Cardiology. Myocardial infarctionredefined—–a consensus document of The Joint EuropeanSociety of Cardiology/American College of CardiologyCommittee for the redefinition of myocardial infarction. JAm Coll Cardiol 2000;36:959—69.4. Van de Werf F, Ardissino D, Betriu A, et al. Management ofacute myocardial infarction in patients presenting with STsegmentelevation. The Task Force on the Management ofAcute Myocardial Infarction of the European Society of Cardiology.Eur Heart J 2003;24:28—66.5. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelinesfor the management of patients with ST-elevationmyocardial infarction—executive summary: a report of theAmerican College of Cardiology/American Heart AssociationTask Force on Practice Guidelines (Writing Committeeto Revise the 1999 Guidelines for the Managementof Patients With Acute Myocardial Infarction). Circulation2004;110:588—636.6. Douglas PS, Ginsburg GS. The evaluation of chest pain inwomen. N Engl J Med 1996;334:1311—5.7. Solomon CG, Lee TH, Cook EF, et al. Comparison of clinicalpresentation of acute myocardial infarction in patients olderthan 65 years of age to younger patients: the MulticenterChest Pain Study experience. Am J Cardiol 1989;63:772—6.8. Kereiakes DJ, Gibler WB, Martin LH, Pieper KS, Anderson LC.Relative importance of emergency medical system transportand the prehospital electrocardiogram on reducing hospitaltime delay to therapy for acute myocardial infarction: a preliminaryreport from the Cincinnati Heart Project. Am HeartJ 1992;123(Pt 1):835—40.9. Canto JG, Rogers WJ, Bowlby LJ, French WJ, Pearce DJ,Weaver WD. The prehospital electrocardiogram in acutemyocardial infarction: is its full potential being realized?National Registry of Myocardial Infarction 2 Investigators. JAm Coll Cardiol 1997;29:498—505.10. Aufderheide TP, Hendley GE, Thakur RK, et al. The diagnosticimpact of prehospital 12-lead electrocardiography. AnnEmerg Med 1990;19:1280—7.11. Foster DB, Dufendach JH, Barkdoll CM, Mitchell BK. Prehospitalrecognition of AMI using independent nurse/paramedic12-lead ECG evaluation: impact on in-hospital times tothrombolysis in a rural community hospital. Am J Emerg Med1994;12:25—31.12. Millar-Craig MW, Joy AV, Adamowicz M, Furber R, Thomas B.Reduction in treatment delay by paramedic ECG diagnosisof myocardial infarction with direct CCU admission. Heart1997;78:456—61.13. Brinfield K. Identification of ST elevation AMI on prehospital12 lead ECG; accuracy of unaided paramedic interpretation.J Emerg Med 1998;16:22S.14. Antman EM, Tanasijevic MJ, Thompson B, et al. Cardiacspecifictroponin I levels to predict the risk of mortalityin patients with acute coronary syndromes. N Engl J Med1996;335:1342—9.15. Schuchert A, Hamm C, Scholz J, Klimmeck S, Goldmann B,Meinertz T. Prehospital testing for troponin T in patientswith suspected acute myocardial infarction. Am Heart J1999;138:45—8.16. Rawles JM, Kenmure AC. Controlled trial of oxygen in uncomplicatedmyocardial infarction. BMJ 1976;1:1121—3.H.-R. Arntz et al.17. Randomised trial of intravenous streptokinase, oral aspirin,both, or neither among 17,187 cases of suspected acutemyocardial infarction: ISIS-2. ISIS-2 (Second InternationalStudy of Infarct Survival) Collaborative Group. Lancet1988;2:349—60.18. Gurfinkel EP, Manos EJ, Mejail RI, et al. Low molecular weightheparin versus regular heparin or aspirin in the treatmentof unstable angina and silent ischemia. J Am Coll Cardiol1995;26:313—8.19. Freimark D, Matetzky S, Leor J, et al. Timing of aspirinadministration as a determinant of survival of patients withacute myocardial infarction treated with thrombolysis. AmJ Cardiol 2002;89:381—5.20. Husted SE, Kristensen SD, Vissinger H, Morn B, Schmidt EB,Nielsen HK. Intravenous acetylsalicylic acid—–dose-relatedeffects on platelet function and fibrinolysis in healthy males.Thromb Haemost 1992;68:226—9.21. Indications for fibrinolytic therapy in suspected acutemyocardial infarction: collaborative overview of early mortalityand major morbidity results from all randomised trialsof more than 1000 patients. Fibrinolytic Therapy Trialists’(FTT) Collaborative Group. Lancet 1994;343:311—22.22. Effectiveness of intravenous thrombolytic treatment inacute myocardial infarction. Gruppo Italiano per lo Studiodella Streptochinasi nell’Infarto Miocardico (GISSI). Lancet1986;1:397—402.23. The GUSTO investigators. An international randomized trialcomparing four thrombolytic strategies for acute myocardialinfarction. N Engl J Med 1993;329:673—82.24. Boersma E, Maas AC, Deckers JW, Simoons ML. Early thrombolytictreatment in acute myocardial infarction: reappraisalof the golden hour. Lancet 1996;348:771—5.25. De Luca G, van’t Hof AW, de Boer MJ, et al. Time-totreatmentsignificantly affects the extent of ST-segment resolutionand myocardial blush in patients with acute myocardialinfarction treated by primary angioplasty. Eur Heart J2004;25:1009—13.26. Morrison LJ, Verbeek PR, McDonald AC, Sawadsky BV, CookDJ. Mortality and prehospital thrombolysis for acute myocardialinfarction: a meta-analysis. JAMA 2000;283:2686—92.27. Welsh RC, Goldstein P, Adgey J, et al. Variations in prehospitalfibrinolysis process of care: insights from the Assessmentof the Safety and Efficacy of a New Thrombolytic 3 Plusinternational acute myocardial infarction pre-hospital caresurvey. Eur J Emerg Med 2004;11:134—40.28. Weaver W, Cerqueira M, Hallstrom A, et al. Prehospitalinitiatedvs hospital-initiated thrombolytic therapy: theMyocardial Infacrtion Triage and Intervention Trial (MITI).JAMA 1993;270:1203—10.29. European Myocardial Infarction Project Group (EMIP). Prehospitalthrombolytic therapy in patients with suspectedacute myocardial infarction. The European MyocardialInfarction Project Group. N Engl J Med 1993;329:383—9.30. White HD. Debate: should the elderly receive thrombolytictherapy, or primary angioplasty? Current Control Trials CardiovascMed 2000;1:150—4.31. Weaver WD, Simes RJ, Betriu A, et al. Comparison of primarycoronary angioplasty and intravenous thrombolytic therapyfor acute myocardial infarction: a quantitative review. JAMA1997;278:2093—8.32. Keeley EC, Boura JA, Grines CL. Primary angioplasty versusintravenous thrombolytic therapy for acute myocardialinfarction: a quantitative review of 23 randomised trials.Lancet 2003;361:13—20.33. Widimsky P, Budesinsky T, Vorac D, et al. Long distancetransport for primary angioplasty vs immediate thrombolysisin acute myocardial infarction. Final results of the ran-

European Resuscitation Council Guidelines for Resuscitation 2005S95domized national multicentre trial—PRAGUE-2. Eur Heart J2003;24:94—104.34. Steg PG, Bonnefoy E, Chabaud S, et al. Impact of time totreatment on mortality after prehospital fibrinolysis or primaryangioplasty: data from the CAPTIM randomized clinicaltrial. Circulation 2003;108:2851—6.35. Dalby M, Bouzamondo A, Lechat P, Montalescot G. Transferfor primary angioplasty versus immediate thrombolysisin acute myocardial infarction: a meta-analysis. Circulation2003;108:1809—14.36. Scheller B, Hennen B, Hammer B, et al. Beneficial effects ofimmediate stenting after thrombolysis in acute myocardialinfarction. J Am Coll Cardiol 2003;42:634—41.37. Fernandez-Aviles F, Alonso JJ, Castro-Beiras A, et al. Routineinvasive strategy within 24 h of thrombolysis versusischaemia-guided conservative approach for acute myocardialinfarction with ST-segment elevation (GRACIA-1): a randomisedcontrolled trial. Lancet 2004;364:1045—53.38. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularizationin acute myocardial infarction complicated by cardiogenicshock. SHOCK Investigators. Should we emergentlyrevascularize occluded coronaries for cardiogenic shock. NEngl J Med 1999;341:625—34.39. Hochman JS, Sleeper LA, White HD, et al. One-year survivalfollowing early revascularization for cardiogenic shock.JAMA 2001;285:190—2.40. Antman EM, McCabe CH, Gurfinkel EP, et al. Enoxaparinprevents death and cardiac ischemic events in unstableangina/non-Q-wave myocardial infarction. Results of thethrombolysis in myocardial infarction (TIMI) 11B trial. Circulation1999;100:1593—601.41. Cohen M, Demers C, Gurfinkel EP, et al. A comparison of lowmolecular-weightheparin with unfractionated heparin forunstable coronary artery disease. Efficacy and Safety of SubcutaneousEnoxaparin in Non-Q-Wave Coronary Events StudyGroup. N Engl J Med 1997;337:447—52.42. Petersen JL, Mahaffey KW, Hasselblad V, et al. Efficacyand bleeding complications among patients randomized toenoxaparin or unfractionated heparin for antithrombin therapyin non-ST-Segment elevation acute coronary syndromes:a systematic overview. JAMA 2004;292:89—96.43. Ferguson JJ, Califf RM, Antman EM, et al. Enoxaparin vsunfractionated heparin in high-risk patients with non-STsegmentelevation acute coronary syndromes managed withan intended early invasive strategy: primary results of theSYNERGY randomized trial. JAMA 2004;292:45—54.44. Van de Werf FJ, Armstrong PW, Granger C, Wallentin L. Efficacyand safety of tenecteplase in combination with enoxaparin,abciximab, or unfractionated heparin: the ASSENT-3 randomised trial in acute myocardial infarction. Lancet2001;358:605—13.45. Wallentin L, Goldstein P, Armstrong PW, et al. Efficacyand safety of tenecteplase in combination with the lowmolecular-weightheparin enoxaparin or unfractionated heparinin the prehospital setting: the Assessment of the Safetyand Efficacy of a New Thrombolytic Regimen (ASSENT)-3PLUS randomized trial in acute myocardial infarction. Circulation2003;108:135—42.46. Boersma E, Harrington RA, Moliterno DJ, et al. Platelet glycoproteinIIb/IIIa inhibitors in acute coronary syndromes:a meta-analysis of all major randomised clinical trials.Lancet 2002;359:189—98 [erratum appears in Lancet 2002Jun 15;359(9323):2120].47. Simoons ML. Effect of glycoprotein IIb/IIIa receptor blockerabciximab on outcome in patients with acute coronary syndromeswithout early coronary revascularisation: the GUSTOIV-ACS randomised trial. Lancet 2001;357:1915—24.48. Topol EJ. Reperfusion therapy for acute myocardial infarctionwith fibrinolytic therapy or combination reduced fibrinolytictherapy and platelet glycoprotein IIb/IIIa inhibition:the GUSTO V randomised trial. Lancet 2001;357:1905—14.49. Montalescot G, Borentain M, Payot L, Collet JP, Thomas D.Early vs late administration of glycoprotein IIb/IIIa inhibitorsin primary percutaneous coronary intervention of acute STsegmentelevation myocardial infarction: a meta-analysis.JAMA 2004;292:362—6.50. van’t Hof AW, Ernst N, de Boer MJ, et al. Facilitation ofprimary coronary angioplasty by early start of a glycoprotein2b/3a inhibitor: results of the ongoing tirofiban inmyocardial infarction evaluation (On-TIME) trial. Eur HeartJ 2004;25:837—46.51. A randomised, blinded, trial of clopidogrel versus aspirin inpatients at risk of ischaemic events (CAPRIE). CAPRIE SteeringCommittee. Lancet 1996;348:1329—39.52. Yusuf S, Zhao F, Mehta SR, Chrolavicius S, Tognoni G, Fox KK.Effects of clopidogrel in addition to aspirin in patients withacute coronary syndromes without ST-segment elevation. NEngl J Med 2001;345:494—502.53. Mehta SR, Yusuf S, Peters RJ, et al. Effects of pretreatmentwith clopidogrel and aspirin followed by long-term therapyin patients undergoing percutaneous coronary intervention:the PCI-CURE study. Lancet 2001;358:527—33.54. Steinhubl SR, Berger PB, Mann IIIrd JT, et al. Early and sustaineddual oral antiplatelet therapy following percutaneouscoronary intervention: a randomized controlled trial. JAMA2002;288:2411—20.55. Sabatine MS, Cannon CP, Gibson CM, et al. Addition ofclopidogrel to aspirin and fibrinolytic therapy for myocardialinfarction with ST-segment elevation. N Engl J Med2005;352:1179—89.56. The MIAMI Trial Research Group. Metoprolol in acute myocardialinfarction (MIAMI): a randomised placebo-controlledinternational trial. Eur Heart J 1985;6:199—226.57. Randomised trial of intravenous atenolol among 16 027cases of suspected acute myocardial infarction: ISIS-1. FirstInternational Study of Infarct Survival Collaborative Group.Lancet 1986;2:57—66.58. Halkin A, Grines CL, Cox DA, et al. Impact of intravenousbeta-blockade before primary angioplasty on survivalin patients undergoing mechanical reperfusion therapyfor acute myocardial infarction. J Am Coll Cardiol2004;43:1780—7.59. Campbell RW, Murray A, Julian DG. Ventricular arrhythmiasin first 12 h of acute myocardial infarction: natural historystudy. Br Heart J 1981;46:351—7.60. O’Doherty M, Tayler DI, Quinn E, Vincent R, Chamberlain DA.Five hundred patients with myocardial infarction monitoredwithin one hour of symptoms. BMJ 1983;286:1405—8.61. Teo KK, Yusuf S, Furberg CD. Effects of prophylactic antiarrhythmicdrug therapy in acute myocardial infarction. Anoverview of results from randomized controlled trials. JAMA1993;270:1589—95.62. Sadowski ZP, Alexander JH, Skrabucha B, et al. Multicenterrandomized trial and a systematic overview of lidocainein acute myocardial infarction. Am Heart J 1999;137:792—8.63. McAlister FA, Teo KK. Antiarrhythmic therapies for theprevention of sudden cardiac death. Drugs 1997;54:235—52.64. ISIS-4: a randomised factorial trial assessing early oral captopril,oral mononitrate, and intravenous magnesium sulphatein 58,050 patients with suspected acute myocardial infarction.ISIS-4 (Fourth International Study of Infarct Survival)Collaborative Group. Lancet 1995;345:669—85.

S9665. Teo KK, Yusuf S, Pfeffer M, et al. Effects of long-term treatmentwith angiotensin-converting-enzyme inhibitors in thepresence or absence of aspirin: a systematic review. Lancet2002;360:1037—43.66. ACE Inhibitor MI Collaborative Group. Indications forACE inhibitors in the early treatment of acute myocardialinfarction: systematic overview of individual datafrom 100,000 patients in randomized trials. ACE InhibitorMyocardial Infarction Collaborative Group. Circulation1998;97:2202—12.H.-R. Arntz et al.67. Swedberg K, Held P, Kjekshus J, Rasmussen K, Ryden L,Wedel H. Effects of the early administration of enalaprilon mortality in patients with acute myocardial infarction.Results of the Cooperative New Scandinavian Enalapril SurvivalStudy II (CONSENSUS II). N Engl J Med 1992;327:678—84.68. Heeschen C, Hamm CW, Laufs U, Snapinn S, Bohm M,White HD. Withdrawal of statins increases event ratesin patients with acute coronary syndromes. Circulation2002;105:1446—52.

Resuscitation (2005) 67S1, S97—S133European Resuscitation Council Guidelines forResuscitation 2005Section 6. Paediatric life supportDominique Biarent, Robert Bingham, Sam Richmond, Ian Maconochie,Jonathan Wyllie, Sheila Simpson, Antonio Rodriguez Nunez,David ZidemanIntroductionThe processThe European Resuscitation Council (ERC) issuedguidelines for paediatric life support (PLS) in 1994,1998 and 2000. 1—4 The last edition was based onthe International Consensus on Science publishedby the American Heart Association in collaborationwith the International Liaison Committee on Resuscitation(ILCOR), undertaking a series of evidencebasedevaluations of the science of resuscitationwhich culminated in the publication of the Guidelines2000 for Cardiopulmonary Resuscitation andEmergency Cardiovascular Care in August 2000. 5,6This process was repeated in 2004/2005, and theresulting Consensus on Science and Treatment Recommendationswere published simultaneously inResuscitation, Circulation and Pediatrics in November2005. 7,8 The PLS Working Party of the ERC hasconsidered this document and the supporting scientificliterature, and has recommended changesto the ERC PLS Guidelines. These are presented inthis paper.Guidelines changesThe approach to changes has been to alter theguidelines in response to convincing new scientificevidence and, where possible, to simplify them inorder to assist teaching and retention. As before,there remains a paucity of good-quality evidence onpaediatric resuscitation specifically and some conclusionshave had to be drawn from animal workand extrapolated adult data.The current guidelines have a strong focus onsimplification based on the knowledge that manychildren receive no resuscitation at all because rescuersfear doing harm. This fear is fuelled by theknowledge that resuscitation guidelines for childrenare different. Consequently, a major area ofstudy was the feasibility of applying the same guidancefor all adults and children. Bystander resuscitationimproves outcome significantly, 9,10 and thereis good evidence from paediatric animal modelsthat even doing chest compressions or expired airventilation alone may be better than doing nothingat all. 11 It follows that outcomes could beimproved if bystanders, who would otherwise donothing, were encouraged to begin resuscitation,even if they do not follow an algorithm targetedspecifically at children. There are, however, dis-0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.doi:10.1016/j.resuscitation.2005.10.010

S98tinct differences between the predominantly adultarrest of cardiac origin and asphyxial arrest, whichis most common in children, 12 so a separate paediatricalgorithm is justified for those with a duty torespond to paediatric emergencies (usually healthcareprofessionals), who are also in a position toreceive enhanced training.Compression:ventilation ratiosThe ILCOR treatment recommendation was thatthe compression:ventilation ratio should be basedon whether one or more than one rescuers werepresent. ILCOR recommends that lay rescuers,who usually learn only single rescuer techniques,should be taught to use a ratio of 30 compressionsto 2 ventilations, which is the same as theadult guidelines and enables anyone trained inBLS techniques to resuscitate children with minimaladditional information. Two or more rescuerswith a duty to respond should learn a differentratio (15:2), as this has been validated by animaland manikin studies. 13—17 This latter group, whowould normally be healthcare professionals, shouldreceive enhanced training targeted specifically atthe resuscitation of children. Although there areno data to support the superiority of any particularratio in children, ratios of between 5:1 and15:2 have been studied in manikins, and animaland mathematical models, and there is increasingevidence that the 5:1 ratio delivers an inadequatenumber of compressions. 14,18 There is certainly nojustification for having two separate ratios for childrenaged greater or less than 8 years, so a singleratio of 15:2 for multiple rescuers with a duty torespond is a logical simplification.It would certainly negate any benefit of simplicityif lay rescuers were taught a different ratio foruse if there were two of them, but those with a dutyto respond can use the 30:2 ratio if they are alone,particularly if they are not achieving an adequatenumber of compressions because of difficulty in thetransition between ventilation and compression.Age definitionsD. Biarent et al.The adoption of single compression:ventilationratios for children of all ages, together with thechange in advice on the lower age limit for theuse of automated external defibrillators (AEDs),renders the previous guideline division betweenchildren above and below 8 years of age unnecessary.The differences between adult and paediatricresuscitation are based largely on differing aetiology,as primary cardiac arrest is more commonin adults whereas children usually suffer from secondarycardiac arrest. The onset of puberty, whichis the physiological end of childhood, is the mostlogical landmark for the upper age limit for useof paediatric guidance. This has the advantage ofbeing simple to determine, in contrast to an agelimit in years, as age may be unknown at the start ofresuscitation. Clearly, it is inappropriate and unnecessaryto establish the onset of puberty formally; ifrescuers believe the victim to be a child they shoulduse the paediatric guidelines. If a misjudgement ismade and the victim turns out to be a young adult,little harm will accrue, as studies of aetiology haveshown that the paediatric pattern of arrest continuesinto early adulthood. 19 An infant is a child under1 year of age; a child is between 1 year and puberty.It is necessary to differentiate between infants andolder children, as there are some important differencesbetween these two groups.Chest compression techniqueThe modification to age definitions enables a simplificationof the advice on chest compression.Advice for determining the landmarks for infantcompression is now the same as for older children,as there is evidence that the previous recommendationcould result in compression over theupper abdomen. 20 Infant compression techniqueremains the same: two-finger compression for singlerescuers and two-thumb, encircling techniquefor two or more rescuers, 21—25 but for older childrenthere is no division between the one- or two-handtechnique. 26 The emphasis is on achieving an adequatedepth of compression with minimal interruptions,using one or two hands according to rescuerpreference.Automated external defibrillatorsCase reports published since International Guidelines2000 have reported safe and successful use ofAEDs in children less than 8 years of age. 27,28 Furthermore,recent studies have shown that AEDs arecapable of identifying arrhythmias in children accuratelyand that, in particular, they are extremelyunlikely to advise a shock inappropriately. 29,30 Consequently,advice on the use of AEDs has beenrevised to include all children aged greater than 1year. 31 Nevertheless, if there is any possibility thatan AED may need to be used in children, the purchasershould check that the performance of theparticular model has been tested against paediatricarrhythmias.Many manufacturers now supply purpose-madepaediatric pads or programmes, which typicallyattenuate the output of the machine to 50—75 J. 32

European Resuscitation Council Guidelines for Resuscitation 2005S99These devices are recommended for children aged1—8 years. 33,34 If no such system or manuallyadjustable machine is available, an unmodifiedadult AED may be used in children older than 1year. 35 There is currently insufficient evidence tosupport a recommendation for or against the use ofAEDs in children aged less than 1 year.Manual defibrillatorsThe 2005 Consensus Conference treatment recommendationfor paediatric ventricular fibrillation(VF) or paediatric pulseless ventricular tachycardia(VT) is to defibrillate promptly. In adult ALS,the recommendation is to give a single shock andthen resume CPR immediately without checking fora pulse or reassessing the rhythm (see Section 3). Asa consequence of this single-shock strategy, whenusing a monophasic defibrillator in adults a higherinitial energy dose than used previously is recommended(360 J versus 200 J) (see Section 3). Theideal energy dose for safe and effective defibrillationin children is unknown, but animal modelsand small paediatric series show that doses largerthan 4 J kg −1 defibrillate effectively with negligibleside effects. 27,34,36,37 Biphasic shocks are at leastas effective and produce less post-shock myocardialdysfunction than monophasic shocks. 33,34,37—40 Forsimplicity of sequence and consistency with adultBLS and ALS, we recommend a single-shock strategyusing a non-escalating dose of 4 J kg −1 (monophasicor biphasic) for defibrillation in children.Foreign-body airway obstruction sequenceThe guidance for managing foreign-body airwayobstruction (FBAO) in children has been simplifiedand brought into closer alignment to the adultsequence. These changes are discussed in detail atthe end of this section.In the following text the masculine includes thefeminine and ‘child’ refers to both infants and childrenunless noted otherwise.6a Paediatric basic life supportSequence of actionRescuers who have been taught adult BLS and haveno specific knowledge of paediatric resuscitationmay use the adult sequence, with the exceptionthat they should perform 5 initial breaths followedby approximately 1 min of CPR before they go forhelp (Figure 6.1; also see adult BLS guideline).Figure 6.1Paediatric basic life support algorithm.The following sequence is to be observed bythose with a duty to respond to paediatric emergencies(usually health professionals).1. Ensure the safety of rescuer and child.2. Check the child’s responsiveness.• Gently stimulate the child and ask loudly:‘‘Are you all right?’’• Do not shake infants or children with suspectedcervical spinal injuries.3a If the child responds by answering or moving• leave the child in the position in which youfind him (provided he is not in further danger)• check his condition and get help if needed• reassess him regularly3b If the child does not respond• shout for help;• open the child’s airway by tilting the head andlifting the chin, as follows:o initially with the child in the position inwhich you find him, place your hand on hisforehead and gently tilt his head back;o at the same time, with your fingertip(s)under the point of the child’s chin, lift thechin. Do not push on the soft tissues underthe chin as this may block the airway;o if you still have difficulty in opening the airway,try the jaw thrust method. Place thefirst two fingers of each hand behind eachside of the child’s mandible and push thejaw forward;o both methods may be easier if the child isturned carefully onto his back.

S100If you suspect that there may have been an injuryto the neck, try to open the airway using chin lift orjaw thrust alone. If this is unsuccessful, add headtilt a small amount at a time until the airway isopen.4. Keeping the airway open, look, listen and feelfor normal breathing by putting your face closeto the child’s face and looking along the chest.• Look for chest movements.• Listen at the child’s nose and mouth for breathsounds.• Feel for air movement on your cheek.Look, listen and feel for no more than 10 s beforedeciding.5a If the child is breathing normally• turn the child on his side into the recoveryposition (see below)• check for continued breathing5b If the child is not breathing or is making agonalgasps (infrequent, irregular breaths)• carefully remove any obvious airway obstruction;• give five initial rescue breaths;• while performing the rescue breaths, noteany gag or cough response to your action.These responses or their absence will formpart of your assessment of signs of a circulation,which will be described later.Rescue breaths for a child over 1 year are performedas follows (Figure 6.2).• Ensure head tilt and chin lift.D. Biarent et al.• Pinch the soft part of the nose closed with theindex finger and thumb of your hand on his forehead.• Open his mouth a little, but maintain the chinupwards.• Take a breath and place your lips around themouth, making sure that you have a good seal.• Blow steadily into the mouth over about 1—1.5 s,watching for chest rise.• Maintain head tilt and chin lift, take your mouthaway from the victim and watch for his chest tofall as air is expelled.• Take another breath and repeat this sequencefive times. Identify effectiveness by seeing thatthe child’s chest has risen and fallen in a similarfashion to the movement produced by a normalbreath.Rescue breaths for an infant are performed asfollows (Figure 6.3).• Ensure a neutral position of the head and a chinlift.• Take a breath and cover the mouth and nasalapertures of the infant with your mouth, makingsure you have a good seal. If the nose and mouthcannot be covered in the older infant, the rescuermay attempt to seal only the infant’s noseor mouth with his mouth (if the nose is used, closethe lips to prevent air escape).• Blow steadily into the infant’s mouth and noseover 1—1.5 s, sufficient to make the chest visiblyrise.• Maintain head tilt and chin lift, take your mouthaway from the victim and watch for his chest tofall as air is expelled.• Take another breath and repeat this sequencefive times.Figure 6.2 Mouth-to-mouth ventilation— child. © 2005ERC.Figure 6.3 Mouth-to-mouth and nose ventilation—infant. © 2005 ERC.

European Resuscitation Council Guidelines for Resuscitation 2005S101If you have difficulty achieving an effective breath,the airway may be obstructed.• Open the child’s mouth and remove any visibleobstruction. Do not perform a blind finger sweep.• Ensure that there is adequate head tilt and chinlift but also that the neck is not over-extended.• If head tilt and chin lift have not opened the airway,try the jaw thrust method.• Make up to five attempts to achieve effectivebreaths; if still unsuccessful, move on to chestcompressions.6. Assess the child’s circulation. Take no more than10 s to• look for signs of a circulation. This includesany movement, coughing or normal breathing(not agonal gasps, which are infrequent, irregularbreaths);• check the pulse (if you are a health careprovider) but ensure you take no more than10 s.If the child is aged over 1 year, feel for thecarotid pulse in the neck.In an infant, feel for the brachial pulse on theinner aspect of the upper arm.7a If you are confident that you can detect signs ofa circulation within 10 s• continue rescue breathing, if necessary, untilthe child starts breathing effectively on hisown• turn the child onto his side (into the recoveryposition) if he remains unconscious• re-assess the child frequently7b If there are no signs of a circulation, or no pulseor a slow pulse (less than 60 min −1 with poorperfusion), or you are not sure• start chest compressions• combine rescue breathing and chest compressionsChest compressions are performed as follows.For all children, compress the lower third of thesternum. To avoid compressing the upper abdomen,locate the xiphisternum by finding the angle wherethe lowest ribs join in the middle. Compress thesternum one finger’s breadth above this; the compressionshould be sufficient to depress the sternumby approximately one third of the depth ofthe chest. Release the pressure and repeat at arate of about 100 min −1 . After 15 compressions,tilt the head, lift the chin, and give two effectivebreaths. Continue compressions and breaths in aratio of 15:2. Lone rescuers may use a ratio of 30:2,particularly if having difficulty with the transitionbetween compression and ventilation. Although theFigure 6.4Chest compression — infant. © 2005 ERC.rate of compressions will be 100 min −1 , the actualnumber delivered per minute will be less than 100because of pauses to give breaths. The best methodfor compression varies slightly between infants andchildren.To perform chest compression in infants, the lonerescuer compresses the sternum with the tips oftwo fingers (Figure 6.4). If there are two or morerescuers, use the encircling technique. Place boththumbs flat side by side on the lower third of thesternum (as above) with the tips pointing towardsthe infant’s head. Spread the rest of both handswith the fingers together to encircle the lower partof the infant’s rib cage with the tips of the fingerssupporting the infant’s back. Press down on thelower sternum with the two thumbs to depress itapproximately one third of the depth of the infant’schest.To perform chest compression in children over1 year of age, place the heel of one handover the lower third of the sternum (as above)(Figures 6.5 and 6.6). Lift the fingers to ensure thatpressure is not applied over the child’s ribs. Positionyourself vertically above the victim’s chest and,with your arm straight, compress the sternum todepress it by approximately one third of the depthof the chest. In larger children or for small rescuers,this is achieved most easily by using both hands withthe fingers interlocked.8. Continue resuscitation until• the child shows signs of life (spontaneous respiration,pulse, movement)• qualified help arrives• you become exhaustedWhen to call for assistanceIt is vital for rescuers to get help as quickly as possiblewhen a child collapses.

S102• When more than one rescuer is available, onestarts resuscitation while another rescuer goesfor assistance.• If only one rescuer is present, undertake resuscitationfor about 1 min before going for assistance.To minimise interruption in CPR, it maybe possible to carry an infant or small child whilesummoning help.• The only exception to performing 1 min of CPRbefore going for help is in the case of a child witha witnessed, sudden collapse when the rescuer isalone. In this case cardiac arrest is likely to bearrhythmogenic in origin and the child will needdefibrillation. Seek help immediately if there isno one to go for you.Recovery positionAn unconscious child whose airway is clear, and whois breathing spontaneously, should be turned on hisside into the recovery position. There are severalFigure 6.5 Chest compression with one hand — child.© 2005 ERC.D. Biarent et al.recovery positions; each has its advocates. Thereare important principles to be followed.• Place the child in as near true lateral positionas possible, with his mouth dependent to enablefree drainage of fluid.• The position should be stable. In an infant thismay require the support of a small pillow ora rolled-up blanket placed behind the back tomaintain the position.• Avoid any pressure on the chest that impairsbreathing.• It should be possible to turn the child onto his sideand to return him back easily and safely, takinginto consideration the possibility of cervical spineinjury.• Ensure the airway can be observed and accessedeasily.• The adult recovery position is suitable for use inchildren.Foreign-body airway obstruction (FBAO)No new evidence on this subject was presented duringthe 2005 Consensus Conference. Back blows,chest thrusts and abdominal thrusts all increaseintrathoracic pressure and can expel foreign bodiesfrom the airway. In half of the episodes,more than one technique is needed to relieve theobstruction. 41 There are no data to indicate whichmeasure should be used first or in which order theyshould be applied. If one is unsuccessful, try theothers in rotation until the object is cleared.The International Guidelines 2000 algorithm isdifficult to teach and knowledge retention poor.The FBAO algorithm for children has been simplifiedand aligned with the adult version (Figure 6.7).This should improve skill retention and encouragepeople, who might otherwise have been reluctant,to perform FBAO manoeuvres on children.Figure 6.6 Chest compression with two hands — child.© 2005 ERC.Figure 6.7algorithm.Paediatric foreign body airway obstruction

European Resuscitation Council Guidelines for Resuscitation 2005S103The most significant difference from the adultalgorithm is that abdominal thrusts should not beused to treat choking infants. Although abdominalthrusts have caused injuries in all age groups, therisk is particularly high in infants and very youngchildren. This is because of the horizontal positionof the ribs, which leaves the upper abdominal visceramuch more exposed to trauma. For this reason,the guidelines for the treatment of FBAO are differentbetween infants and children.Recognition of FBAOWhen a foreign body enters the airway, the childreacts immediately by coughing in an attempt toexpel it. A spontaneous cough is likely to be moreeffective and safer than any manoeuvre a rescuermight perform. However, if coughing is absent orineffective and the object completely obstructs theairway, the child will rapidly become asphyxiated.Active interventions to relieve FBAO are thereforerequired only when coughing becomes ineffective,but they then need to be commenced rapidly andconfidently.The majority of choking events in infants andchildren occur during play or eating episodes whena carer is usually present; thus, the events are frequentlywitnessed and interventions are usually initiatedwhen the child is conscious.Foreign-body airway obstruction is characterizedby the sudden onset of respiratory distress associatedwith coughing, gagging or stridor. Similar signsand symptoms may be associated with other causesof airway obstruction, such as laryngitis or epiglottitis,which require different management. SuspectFBAO if the onset was very sudden and there are noother signs of illness and if there are clues to alertthe rescuer, e.g. a history of eating or playing withsmall items immediately before the onset of symptoms.treatment of the choking child.• If the child is coughing effectively, no externalmanoeuvre is necessary. Encourage the child tocough, and monitor continually.• If the child’s coughing is (or is becoming) ineffective,shout for help immediately and determinethe child’s conscious level.2. Conscious child with FBAO• If the child is still conscious but has absent orineffective coughing, give back blows.• If back blows do not relieve the FBAO, givechest thrusts to infants or abdominal thrusts tochildren. These manoeuvres create an ‘artificialcough’ to increase intrathoracic pressure and dislodgethe foreign body.Back blows. Back blows in the infant are performedas follows.• Support the infant in a head downwards, proneposition, to enable gravity to assist removal ofthe foreign body.• A seated or kneeling rescuer should be able tosupport the infant safely across their lap.• Support the infant’s head by placing the thumb ofone hand at the angle of the lower jaw, and oneor two fingers from the same hand at the samepoint on the other side of the jaw.• Do not compress the soft tissues under theinfant’s jaw, as this will exacerbate the airwayobstruction.• Deliver up to five sharp back blows with the heelof one hand in the middle of the back betweenthe shoulder blades.• The aim is to relieve the obstruction with eachblow rather than to give all five blows.Back blows in the child over 1 year of age areperformed as follows.Relief of FBAO1. Safety and summoning assistanceSafety is paramount: rescuers must not place themselvesin danger and should consider the safest• Back blows are more effective if the child is positionedhead down.• A small child may be placed across the rescuer’slap, as with the infant.• If this is not possible, support the child in aforward-leaning position and deliver the backblows from behind.If back blows fail to dislodge the object, andthe child is still conscious, use chest thrusts forinfants or abdominal thrusts for children. Do notuse abdominal thrusts (Heimlich manoeuvre) ininfants.

S104Chest thrusts for infants.• Turn the infant into a head-downwards supineposition. This is achieved safely by placing thefree arm along the infant’s back and encirclingthe occiput with the hand.• Support the infant down your arm, which isplaced down (or across) your thigh.• Identify the landmark for chest compressions(lower sternum approximately a finger’s breadthabove the xiphisternum).• Give five chest thrusts; these are similar to chestcompressions but sharper and delivered at aslower rate.Abdominal thrusts for children over 1 year.• Stand or kneel behind the child; place your armsunder the child’s arms and encircle his torso.• Clench your fist and place it between the umbilicusand xiphisternum.• Grasp this hand with the other hand and pullsharply inwards and upwards.• Repeat up to five times.• Ensure that pressure is not applied to the xiphoidprocess or the lower rib cage; this might causeabdominal trauma.Following the chest or abdominal thrusts,reassess the child. If the object has not beenexpelled and the victim is still conscious, continuethe sequence of back blows and chest (for infant) orabdominal (for children) thrusts. Call out, or send,for help if it is still not available. Do not leave thechild at this stage.If the object is expelled successfully, assessthe child’s clinical condition. It is possible thatpart of the object may remain in the respiratorytract and cause complications. If there isany doubt, seek medical assistance. Abdominalthrusts may cause internal injuries, and all victimsso treated should be examined by a medicalpractitioner. 423. Unconscious child with FBAOIf the child with FBAO is, or becomes, unconscious,place him on a firm, flat surface. Callout, or send, for help if it is still not available.Do not leave the child at this stage; proceed asfollows.• Open the mouth and look for any obvious object.If an object is seen, make an attempt to remove itwith a single finger sweep. Do not attempt blindor repeated finger sweeps; these can impact theD. Biarent et al.object more deeply into the pharynx and causeinjury.• Open the airway using a head tilt and/or chinlift and attempt five rescue breaths. Assess theeffectiveness of each breath; if a breath does notmake the chest rise, reposition the head beforemaking the next attempt.• Attempt five rescue breaths and, if there isno response (moving, coughing, spontaneousbreaths), proceed to chest compressions withoutfurther assessment of the circulation.• Follow the sequence for single-rescuer CPR (step7b above) for approximately 1 min before summoningthe EMS (if this has not already been doneby someone else).• When the airway is opened for attempted deliveryof rescue breaths, look to see if the foreignbody can be seen in the mouth.• If an object is seen, attempt to remove it with asingle finger sweep.• If it appears the obstruction has been relieved,open and check the airway as above; deliver rescuebreaths if the child is not breathing.• If the child regains consciousness and exhibitsspontaneous effective breathing, place him in asafe position lying on his side and monitor breathingand conscious level while awaiting the arrivalof the EMS.6b Paediatric advanced life supportPrevention of cardiopulmonary arrestIn children, secondary cardiopulmonary arrests,caused by either circulatory or respiratory failure,are more frequent than primary arrestscaused by arrhythmias. 9,12,43—46 So-called ‘asphyxialarrests’ or respiratory arrests are also morecommon in young adulthood (e.g., trauma, drowning,poisoning). 47,48 The outcome from cardiopulmonaryarrests in children is poor; identification ofthe antecedent stages of cardiac or respiratory failureis a priority, as effective early intervention maybe life saving.The order of assessment and intervention for anyseriously ill or injured child follows the ABC principles.• A indicates airway (Ac for airway and cervicalspine stabilisation for the injured child).• B indicates breathing.• C indicates circulation.Interventions are made at each step of theassessment as abnormalities are identified; the next

European Resuscitation Council Guidelines for Resuscitation 2005S105step of the assessment is not started until thepreceding abnormality has been managed and correctedif possible.Diagnosing respiratory failure: assessmentof A and BThe first steps in the assessment of the seriously illor injured child are the management of the airwayand breathing. Abnormalities in airway patency andbreathing lead to respiratory failure. Signs of respiratoryfailure are• respiratory rate outside the normal range for thechild’s age—–either too fast or too slow• initially increasing work of breathing whichmay progress to inadequate/decreased workof breathing, additional noises such as stridor,wheeze or grunting, or the loss of breath sounds• cyanosis (without/with supplemental oxygen)There may be associated signs in other organ systemsaffected by inadequate ventilation and oxygenation;these are detectable in the C steps ofassessment, such as• increasing tachycardia progressing to bradycardia(this latter sign being an ominous indicator ofthe loss of compensatory mechanisms)• alteration in the level of consciousnessDiagnosing circulatory failure: assessmentof CShock is characterised by a mismatch betweenmetabolic tissue demand and delivery of oxygenand nutrients by the circulation. 49 Physiologicalcompensatory mechanisms lead to changesin the heart rate, in the systemic vascular resistance(which commonly increases as an adaptiveresponse) and in tissue and organ perfusion. Signsof circulatory failure are• increased heart rate (bradycardia is an ominoussign, heralding physiological decompensation)• decreased systemic blood pressure• decreased peripheral perfusion (prolonged capillaryrefill time, decreased skin temperature, paleor mottled skin)• weak or absent peripheral pulses• decreased or increased preload• decreased urine output and metabolic acidosisOther systems may be affected, for example• respiratory rate may be increased initially, becomingbradypnoeic with decompensated shock• level of consciousness may decrease because ofpoor cerebral perfusionDiagnosing cardiopulmonary arrestSigns of cardiopulmonary arrest include• unresponsiveness• apnoea or gasping respiratory pattern• absent circulation• pallor or deep cyanosisIn the absence of ‘signs of life’, search for acentral pulse or cardiac sounds (by direct chest auscultation)for a maximum of 10 s, before startingCPR. If there is any doubt, start CPR. 50—53Management of respiratory andcirculatory failureA and BOpen the airway and ensure adequate ventilationand oxygenation.• Deliver high-flow oxygen.• Achieving adequate ventilation and oxygenationmay include the use of airway adjuncts, bag-maskventilation (BMV), use of a laryngeal mask airway(LMA), securing a definitive airway by trachealintubation and positive pressure ventilation.• In rare, extreme circumstances, a surgical airwaymay be required.CEstablish cardiac monitoring.• Secure vascular access to the circulation. Thismay be via peripheral or central intravenous (IV)or by intraosseous (IO) cannulation.• Give a fluid bolus and/or inotropes as required.Assess and re-assess the child continuously, eachtime commencing at Airway before Breathing,thereafter moving onto the CirculationAirwayOpen the airway using basic life support techniques.Oropharyngeal and nasopharyngeal airwaysadjuncts can help maintain the airway. Use theoropharyngeal airway only in the unconscious child,in whom there is no gag reflex. Use the appropriatesize, to avoid pushing the tongue backwardand obstructing the epiglottis, or directlycompressing the glottic area. The soft palate in

S106the child can be damaged by insertion of theoropharygneal airway; avoid this by inserting theoropharygneal airway under direct vision and passingit over a tongue depressor or laryngoscope.The nasopharyngeal airway is tolerated better inthe conscious child (who has an effective gagreflex), but should not be used if there is a basalskull fracture or a coagulopathy. These simpleairway adjuncts do not protect the airway fromaspiration of secretions, blood or stomach contents.Laryngeal mask airwayThe LMA is an acceptable initial airway device forproviders experienced in its use. It may be particularlyhelpful in airway obstruction caused by upperairway abnormalities. The LMA does not, however,protect the airway from aspiration of secretions,blood or stomach contents, and therefore closeobservation is required. LMA use is associated witha higher incidence of complications in small childrencompared with adults. 54Tracheal intubationTracheal intubation is the most secure and effectiveway to establish and maintain the airway, preventgastric distension, protect the lungs against pulmonaryaspiration, enable optimal control of theairway pressure and provide positive end expiratorypressure (PEEP). The oral route is preferable duringresuscitation. Oral intubation is usually quicker andis associated with fewer complications than nasalplacement. The judicious use of anaesthetics, sedativesand neuromuscular blocking drugs is indicatedin the conscious child to avoid multiple intubationattempts or intubation failure. 55—65 The anatomyof a child’s airway differs significantly from that ofan adult; hence, intubation of a child requires specialtraining and experience. Check that trachealtube placement is correct by clinical examinationand end-tidal capnography. The tracheal tube mustbe secured, and monitoring of the vital signs isessential. 66It is also essential to plan an alternative airwaymanagement technique in case the trachea cannotbe intubated.D. Biarent et al.Rapid sequence induction and intubation. Thechild who is in cardiopulmonary arrest and deepcoma does not require sedation or analgesia to beintubated; otherwise, intubation must be precededby oxygenation, rapid sedation, analgesia and theuse of neuromuscular blocking drugs to minimiseintubation complications and failure. 63 The intubatormust be experienced and familiar with rapidsequenceinduction drugs.Tracheal tube sizes. The tracheal tube internaldiameters (ID) for different ages are• for neonates, 2.5—3.5 mm according to the formula(gestational age in weeks 10)• for infants, 4 or 4.5 mm• for children older than 1 year, according to theformula [(age in years/4) + 4]Tracheal tube size estimation according thelength of the child’s body as measured by resuscitationtapes is more accurate than using the aboveformulae. 67Cuffed versus uncuffed tracheal tubes. In the prehospitalsetting, an uncuffed tracheal tube may bepreferable when using sizes of up to 5.5 mm ID (i.e.,for children up to 8 years). In hospital, a cuffed trachealtube may be useful in certain circumstances,e.g. in cases of poor lung compliance, high airwayresistance or large glottic air leak. 68—70 Thecorrectly sized cuffed tracheal tube is as safe asan uncuffed tube for infants and children (not forneonates), provided attention is paid to its placement,size and cuff inflation pressure; excessivecuff pressure can lead to ischaemic necrosis ofthe surrounding laryngeal tissue and stenosis. Maintainthe cuff inflation pressure below 20 cmH 2 O andcheck it regularly. 71Confirmation of correct tracheal tube placement.Displaced, misplaced or obstructed tubes occurfrequently in the intubated child and are associatedwith increased risk of death. 72,73 No singletechnique is 100% reliable for distinguishingoesophageal from tracheal intubation. 74—76 Assessmentof the correct tracheal tube position is madeby• observation of the tube passing beyond the vocalcords• observation of symmetrical chest wall movementduring positive pressure ventilation• observation of mist in the tube during the expiratoryphase of ventilation• absence of gastric distension• equal air entry heard on bilateral auscultation ofboth axillae and apices of the chest• absence of air entry into the stomach on auscultation• detection of end-tidal CO 2 if the child has a perfusingrhythm (this may be seen with effectiveCPR)• improvement or stabilisation of SpO 2 to theexpected range

European Resuscitation Council Guidelines for Resuscitation 2005S107• improvement of heart rate towards the ageexpectedvalue (or remaining within the normalrange)If the child is in cardiopulmonary arrest andexhaled CO 2 is not detected, or if there is anydoubt, confirm tracheal tube position by directlaryngoscopy. After correct placement and confirmation,secure the tracheal tube and reassess itsposition. Maintain the child’s head in neutral position;flexion of the head drives the tube further intothe trachea whereas extension may pull it out of theairway. 77 Confirm the position of the tracheal tubeat mid trachea by plain chest radiograph; the trachealtube tip should be at the level of the 2nd or3rd thoracic vertebra.DOPES is a useful acronym for the causes of suddendeterioration in an intubated child• D: displacement of the tracheal tube• O: obstruction of the tracheal tube• P: pneumothorax• E: equipment failure (source of gas, BMV, ventilator,etc.)• S: stomach (gastric distension may alter diaphragmmechanics)BreathingOxygenationUse oxygen at the highest concentration (i.e., 100%)during resuscitation. Once circulation is restored,give sufficient oxygen to maintain peripheral oxygensaturation at or above 95%. 78,79Studies in neonates suggest some advantages tousing room air during resuscitation, but the evidenceas yet is inconclusive (see Section 6c). 80—83In the older child, there is no evidence for any suchadvantages, so use 100% oxygen for resuscitation.VentilationHealthcare providers commonly provide excessiveventilation to victims of cardiopulmonary or respiratoryarrest, and this may be detrimental.Hyperventilation causes increased thoracic pressure,decreased cerebral and coronary perfusion,and poorer survival rates in animals and adults. 84—89The ideal tidal volume should achieve modest chestwall rise. Use a ratio of 15 chest compressions to 2ventilations (a lone rescuer may use 30:2); the correctcompression rate is 100 min −1 .Once the airway is protected by tracheal intubation,continue positive pressure ventilation at12—20 breaths min −1 without interrupting chestcompressions. Take care to ensure that lung inflationis adequate during chest compressions. Whencirculation is restored, or if the child still has a perfusingrhythm, ventilate at 12—20 breaths min −1 toachieve a normal pCO 2 . Hyperventilation is harmful.Bag-mask ventilation. BMV is effective and safefor a child requiring assisted ventilation for a shortperiod, i.e. in the prehospital setting or in an emergencydepartment. 73,90—92 Assess the effectivenessof BMV by observing adequate chest rise, monitoringheart rate, auscultating for breath sounds andmeasuring peripheral oxygen saturation (SpO 2 ). Anyhealthcare provider dealing with children must beable to deliver BMV effectively.Prolonged ventilation. If prolonged ventilation isrequired, the benefits of a secured airway probablyoutweigh the potential risks associated withtracheal intubation.Monitoring of breathing and ventilationEnd tidal CO 2 . Monitoring end-tidal CO 2 with acolorimetric detector or capnometer confirms trachealtube placement in the child weighing morethan 2 kg, and may be used in pre- and in-hospitalsettings, as well as during any transportation of thechild. 93—97 A colour change or the presence of acapnographic waveform indicates that the tube isin the tracheobronchial tree, both in the presenceof a perfusing rhythm and during cardiopulmonaryarrest. Capnography does not rule out intubationof the right mainstem bronchus. The absence ofexhaled CO 2 during cardiopulmonary arrest may notbe caused by tube misplacement, since a low orabsent end-tidal CO 2 may reflect low or absent pulmonaryblood flow. 98—101Oesophageal detector devices. The self-inflatingbulb or aspirating syringe (oesophageal detectordevice, ODD) may be used for the secondary confirmationof tracheal tube placement in children witha perfusing rhythm. 102,103 There are no studies onthe use of ODD in children who are in cardiopulmonaryarrest.Pulse oximetry. Clinical evaluation of the oxygenlevel is unreliable; therefore monitor the child’speripheral oxygen saturation continuously by pulseoximetry. Pulse oximetry can be unreliable undercertain conditions, e.g. if the child is in shock, incardiopulmonary arrest or has poor peripheral perfusion.Although pulse oximetry is relatively simple,it is a poor guide to tracheal tube displacement;capnography detects tracheal tube dislodgementmore rapidly than pulse oximetry. 104

S108D. Biarent et al.CirculationVascular accessVascular access is essential to give drugs and fluidsand obtain blood samples. Venous access can be difficultto establish during resuscitation of an infantor child. 105 Limit the maximum number of attemptsto obtain IV access to three; thereafter, insert an IOneedle. 106Intraosseous access. IO access is a rapid, safe,and effective route to give drugs, fluids and bloodproducts. 107—113 The onset of action and timeto achieve adequate plasma drug concentrationsare similar to those provided by central venousaccess. 114,115 Bone marrow samples can be used tocross-match for blood type or group, 116 for chemicalanalysis, 117,118 and for blood gas measurement(the values are comparable to central venousblood gases). 117,119,120 Flush each drug with a bolusof normal saline to ensure dispersal beyond themarrow cavity and to achieve faster distributionto the central circulation. Inject large boluses offluid using manual pressure. Intraosseous access canbe maintained until definitive IV access has beenestablished.Intravenous access. Peripheral IV access providesplasma concentrations of drugs and clinicalresponses equivalent to central or IO access. 121—125Central lines provide more secure long-termaccess 121,122,124,125 but offer no advantages duringresuscitation, compared with IO or peripheral IVaccess.Tracheal tube accessIV and IO access are better than the tracheal routefor giving drugs. 126 Lipid-soluble drugs, such aslidocaine, atropine, adrenaline and naloxone areabsorbed via the lower airway. 127—131 Optimal trachealtube drug doses are unknown because of thegreat variability of alveolar drug absorption, butthe following dosages have been recommended asguidance• adrenaline, 100 mcg kg −1• lidocaine, 2—3 mg kg −1• atropine, 30 mcg kg −1The optimal dose of naloxone is not known.Dilute the drug in 5 ml of normal saline and followadministration with five ventilations. 132—134 Donot give non-lipid soluble medications (e.g., glucose,bicarbonate, calcium) via the tracheal tubebecause they will damage the airway mucosa.Fluids and drugsVolume expansion is indicated when a child showssigns of shock in the absence of volume overload. 135If systemic perfusion is inadequate, give a bolusof 20 ml kg −1 of an isotonic crystalloid, even if thesystemic blood pressure is normal. Following everybolus, re-assess the child’s clinical state using ABC,to decide whether a further bolus or other treatmentis required.There are insufficient data to make recommendationsabout the use of hypertonic saline for shockassociated with head injuries or hypovolaemia. 136There are also insufficient data to recommenddelayed fluid resuscitation in the hypotensive childwith blunt trauma. 137 Avoid dextrose-containingsolutions unless there is hypoglycaemia. 138—141However, hypoglycaemia must actively be soughtand avoided, particularly in the small child orinfant.AdenosineAdenosine is an endogenous nucleotide whichcauses a brief atrioventricular (AV) block andimpairs accessory bundle re-entry at the level of theAV node. Adenosine is recommended for the treatmentof supraventricular tachycardia (SVT). 142 It issafe to use, as it has a short half-life (10 s); giveit intravenously via upper limb or central veins, tominimise the time taken to reach the heart. Giveadenosine rapidly, followed by a flush of 3—5 ml ofnormal saline. 143Adrenaline (epinephrine)Adrenaline is an endogenous catecholamine withpotent alpha, beta-1 and beta-1 adrenergic actions.It is the essential medication in cardiopulmonaryarrest, and is placed prominently in the treatmentalgorithms for non-shockable and shockablerhythms. Adrenaline induces vasoconstriction,increases diastolic pressure and thereby improvescoronary artery perfusion pressure, enhancesmyocardial contractility, stimulates spontaneouscontractions and increases the amplitude and frequencyof VF, so increasing the likelihood of successfuldefibrillation. The recommended IV/IO doseof adrenaline in children is 10 mcg kg −1 . The dose ofadrenaline given via the tracheal tube is ten timesthis (100 mcg kg −1 ). 127,144—146 If needed, give furtherdoses of adrenaline every 3—5 min. The use ofhigher doses of adrenaline via the IV or IO route isnot recommended routinely, as it does not improvesurvival or neurological outcome after cardiopulmonaryarrest. 147—150

European Resuscitation Council Guidelines for Resuscitation 2005S109Once spontaneous circulation is restored, a continuousinfusion of adrenaline may be required. Itshaemodynamic effects are dose related; there isalso considerable variability between children inresponse, therefore, titrate the infusion dose tothe desired effect. High infusion rates may causeexcessive vasoconstriction, compromising extremity,mesenteric, and renal blood flow. High-doseadrenaline may cause severe hypertension andtachyarrhythmias. 151To avoid tissue damage it is essential to giveadrenaline through a secure intravascular line (IV orIO). Adrenaline and other catecholamines are inactivatedby alkaline solutions and should never bemixed with sodium bicarbonate. 152AmiodaroneAmiodarone is a non-competitive inhibitor of adrenergicreceptors; it depresses conduction in myocardialtissue and therefore slows AV conduction andprolongs the QT interval and the refractory period.Except when given for the treatment of refractoryVF/pulseless VT, amiodarone must be injectedslowly (over 10—20 min) with systemic blood pressureand ECG monitoring to avoid fast-infusionrelatedhypotension. This side effect is less commonwith the aqueous solution. 153 Other rare but significantadverse effects are bradycardia and polymorphicVT. 154AtropineAtropine accelerates sinus and atrial pacemakersby blocking the parasympathetic response. It mayalso increase AV conduction. Small doses (

S110D. Biarent et al.or refute the use of vasopressin as an alternative to,or in combination with, adrenaline in any cardiacarrest rhythm in adults. Thus, there is currentlyinsufficient evidence to recommend the routine useof vasopressin in the child with cardiopulmonaryarrest. 178—180DefibrillatorsDefibrillators are either automatically (such as theAED) or manually operated, and may be capableof delivering either monophasic or biphasic shocks.Manual defibrillators capable of delivering the fullenergy requirements from neonates upwards mustbe available within hospitals and in other healthcarefacilities caring for children at risk of cardiopulmonaryarrest. Automated external defibrillatorsare preset for all variables, including theenergy dose.Pad/paddle size for defibrillation. The largestpossible available paddles should be chosen to providegood contact with the chest wall. The idealsize is unknown, but there should be good separationbetween the pads. 181,182 Recommended sizesare• 4.5 cm diameter for infants and children weighing10 kg (older than1 year)To decrease skin and thoracic impedance,an electrically conducting interface is requiredbetween the skin and the paddles. Preformed gelpads or self-adhesive defibrillation electrodes areeffective. Do not use ultrasound gel, saline-soakedgauze, alcohol-soaked gauze/pads or ultrasoundgel.Position of the paddles. Apply the paddles firmlyto the bare chest in the anterolateral position, onepaddle placed below the right clavicle and the otherin the left axilla (Figure 6.8). If the paddles are toolarge, and there is a danger of charge arcing acrossthe paddles, one should be placed on the upperback, below the left scapula, and the other on thefront, to the left of the sternum. This is known asthe anteroposterior position.Optimal paddle force. To decrease transthoracicimpedance during defibrillation, apply a force of3 kg for children weighing

European Resuscitation Council Guidelines for Resuscitation 2005S111Figure 6.9Paediatric advanced life support algorithm.tion in the ratio of 15:2 (lone rescuer may use30:2).• Avoid rescuer fatigue by changing the rescuerperforming chest compressions frequently.• Establish cardiac monitoring.CAssess cardiac rhythm and signs of circulation(±check for a central pulse for no more than 10 s).Asystole, pulseless electrical activity(PEA)—–non-shockable• Give adrenaline, 10 mcg kg −1 IV or IO, and repeatevery 3—5 min.• If no vascular access is available and a trachealtube is in situ, give adrenaline, 100 mcg kg −1 , viathis route until IV/IO access is obtained.• Identify and treat any reversible causes (4Hs &4Ts).VF/pulseless VT—–shockable• Attempt defibrillation immediately (4 J kg −1 forall shocks).• Resume CPR as soon as possible.• After 2 min, check the cardiac rhythm on themonitor.• Give second shock if still in VF/pulselessVT.

S112• Immediately resume CPR for 2 min and checkmonitor; if no change, give adrenaline followedimmediately by a 3rd shock.• CPR for 2 min.• Give amiodarone if still in VF/pulseless VT followedimmediately by a 4th shock.• Give adrenaline every 3—5 min during CPR.• If the child remains in VF/pulseless VT, continueto alternate shocks with 2 min of CPR.• If signs of life become evident, check the monitorfor an organised rhythm; if this is present, checkfor a central pulse.• Identify and treat any reversible causes (4Hs &4Ts).• If defibrillation was successful but VF/pulselessVT recurs, resume CPR, give amiodarone anddefibrillate again at the dose that was effectivepreviously. Start a continuous infusion of amiodarone.Reversible causes of cardiac arrest (4 Hsand 4 Ts)• Hypoxia• Hypovolaemia• Hyper/hypokalaemia• Hypothermia• Tension pneumothorax• Tamponade (coronary or pulmonary)• Toxic/therapeutic disturbances• Thrombosis (coronary or pulmonary)Sequence of events in cardiopulmonaryarrest• When a child becomes unresponsive, withoutsigns of life (no breathing, cough or anydetectable movement), start CPR immediately.• Provide BMV with 100% oxygen.• Commence monitoring. Send for a manual orautomatic external defibrillator (AED) to identifyand treat shockable rhythms as quickly as possible.In the less common circumstance of a witnessedsudden collapse, early activation of emergency servicesand getting an AED may be more appropriate;start CPR as soon as possible.Rescuers must perform CPR with minimal interruptionuntil attempted defibrillation.Cardiac monitoringD. Biarent et al.Position the cardiac monitor leads or defibrillationpaddles as soon as possible, to enable differentiationbetween a shockable and a non-shockable cardiacrhythm. Invasive monitoring of systemic bloodpressure may help to improve effectiveness of chestcompression, 186 but must not delay the provision ofbasic or advanced resuscitation.Shockable rhythms comprise pulseless VT andVF. These rhythms are more likely in the childwho presents with sudden collapse. Non-shockablerhythms comprise PEA, bradycardia (50% survival. However,the success of defibrillation decreases dramaticallyas the time to defibrillation increases; for everyminute delay in defibrillation (without any CPR),survival decreases by 7—10%. Survival after morethan 12 min of VF in adult victims is

European Resuscitation Council Guidelines for Resuscitation 2005S113VF/pulseless VT. Experimental and clinical experiencewith amiodarone in children is scarce; evidencefrom adult studies 169,196,197 demonstratesincreased survival to hospital admission, but notto hospital discharge. One paediatric case seriesdemonstrates the effectiveness of amiodarone forlife-threatening ventricular arrhythmias. 198 Therefore,IV amiodarone has a role in the treatment ofdefibrillation refractory or recurrent VF/pulselessVT in children.ArrhythmiasUnstable arrhythmiasCheck the central pulse of any child with anarrhythmia; if the pulse is absent, proceed totreating the child as being in cardiopulmonaryarrest. If the child has a central pulse, evaluatehis haemodynamic status. Whenever the haemodynamicstatus is compromised, the first steps are asfollows.• Open the airway.• Assist ventilation and give oxygen.• Attach ECG monitor or defibrillator and assess thecardiac rhythm.• Evaluate if the rhythm is slow or fast for thechild’s age.• Evaluate if the rhythm is regular or irregular.• Measure QRS complex (narrow complexes, 0.08 s).• The treatment options are dependent on thechild’s haemodynamic stability.BradycardiaBradycardia is caused commonly by hypoxia, acidosisand severe hypotension; it may progress to cardiopulmonaryarrest. Give 100% oxygen, and positivepressure ventilation if required, to any childpresenting with bradyarrhythmia and circulatoryfailure.If a poorly perfused child has a heart rate

S114child’s clinical history, presentation and ECG diagnosis,a child with stable, wide-QRS-complex tachycardiamay be treated for SVT and be given vagalmanoeuvres or adenosine. Otherwise, consideramiodarone as a treatment option; similarly, consideramiodarone if the diagnosis of VT is confirmedby ECG. Procainamide may also be considered instable SVT refractory to vagal manoeuvres andadenosine 210—212 as well as in stable VT. 172,213,214Do not give procainamide with amiodarone.D. Biarent et al.Fever is common following cardiopulmonaryresuscitation; it is associated with a poor neurologicaloutcome, 230—232 the risk of which increaseswith each degree of body temperature greaterthan 37 ◦ C. 230 There are limited experimentaldata suggesting that the treatment of fever withantipyretics and/or physical cooling reduces neuronaldamage. 233,234 Antipyretics and accepteddrugs to treat fever are safe; therefore, use themto treat fever aggressively.Post-arrest managementMyocardial dysfunction is common after cardiopulmonaryresuscitation. 215,216 Vasoactive drugs mayimprove the child’s post-arrest haemodynamic values,but the drugs must be titrated according to theclinical condition. They must be given continuouslythrough an IV line.Temperature control and managementHypothermia is common in the child following cardiopulmonaryresuscitation. 217 Central hypothermia(32—34 ◦ C) may be beneficial, whereas fevermay be detrimental to the injured brain of survivors.Although there are no paediatric studies,mild hypothermia has an acceptable safety profilein adults 218,219 and neonates; 220—224 it couldincrease the number of neurologically intact survivors.A child who regains a spontaneous circulationbut remains comatose after cardiopulmonary arrestmay benefit from being cooled to a core temperatureof 32—34 ◦ C for 12—24 h. The successfullyresuscitated child with hypothermia and ROSCshould not be actively rewarmed unless the coretemperature is below 32 ◦ C. Following a periodof mild hypothermia, rewarm the child slowly at0.25—0.5 ◦ Ch −1 .There are several methods to induce, monitorand maintain body temperature in children.External and/or internal cooling techniques canbe used to initiate cooling. 225—227 Shivering canbe prevented by deep sedation and neuromuscularblockade. Complications can occur and include anincreased risk of infection, cardiovascular instability,coagulopathy, hyperglycaemia and electrolyteabnormalities. 228,229The optimum target temperature, rate of cooling,duration of hypothermia and rate of rewarmingafter deliberate cooling have yet to bedetermined; currently, no specific protocol for childrencan be recommended.Prognosis of cardiopulmonary arrestThere are no simple guidelines to determine whenresuscitative efforts become futile. After 20 minof resuscitation, the team leader of the resuscitationteam should consider whether or notto stop. 187,235—239 The relevant considerations inthe decision to continue the resuscitation includethe cause of arrest, 45,240 pre-existing conditions,whether the arrest was witnessed, the durationof untreated cardiopulmonary arrest (‘‘no flow’’),the effectiveness and duration of CPR (‘‘lowflow’’), the promptness of extracorporeal life supportfor a reversible disease process 241—243 andassociated special circumstances (e.g, icy waterdrowning, 9,244 exposure to toxic drugs).Parental presenceThe majority of parents would like to be presentduring resuscitation and when any procedure is carriedout on their child. 245—255 . Parents witnessingtheir child’s resuscitation can see that everythingpossible has been attempted. 256—260 Furthermore,they may have the opportunity to say goodbye totheir child; allowing parents to be at the side oftheir child has been shown to help them gain arealistic view of the attempted resuscitation andthe child’s death. 261 Families who were present attheir child’s death showed less anxiety and depression,better adjustment and had an improved grievingprocess when assessed several months later. 260Parental presence in the resuscitation room mayhelp healthcare providers maintain their professionalbehaviour while also helping them to see thechild as a human being and a family member. 261Family presence guidelinesA dedicated member of the resuscitation teamshould be present with the parents to explain theprocess in an empathetic manner, ensuring that

European Resuscitation Council Guidelines for Resuscitation 2005S115the parents do not interfere with or distract theresuscitation. If the presence of the parents isimpeding the progress of the resuscitation, theyshould be sensitively asked to leave. When appropriate,physical contact with the child should beallowed and, wherever possible, the parents shouldbe allowed to be with their dying child at the finalmoment. 256,261—264The leader of the resuscitation team, not theparents, will decide when to stop the resuscitation;this should be expressed with sensitivity andunderstanding. After the event the team should bedebriefed, to enable any concerns to be expressedand for the team to reflect on their clinical practicein a supportive environment.6c Resuscitation of babies at birthIntroductionThe following guidelines for resuscitation at birthhave been developed during the process that culminatedin the 2005 International Consensus Conferenceon Emergency Cardiovascular Care (ECC)and Cardiopulmonary Resuscitation (CPR) Sciencewith Treatment Recommendations. 265 They are anextension of the guidelines already published bythe ERC, 2 and take into account recommendationsmade by other national 266 and internationalorganisations. 267The guidelines that follow do not define the onlyway that resuscitation at birth should be achieved;they merely represent a widely accepted view ofhow resuscitation at birth can be carried out bothsafely and effectively.PreparationRelatively few babies need any resuscitation atbirth. Of those that do need help, the overwhelmingmajority will require only assisted lung aeration.A small minority may need a brief period ofchest compressions in addition to lung aeration.Of 100,000 babies born in Sweden in 1 year, only10 per 1000 (1%) babies weighing 2.5 kg or moreappeared to need resuscitation at delivery. 268 Ofthose babies receiving resuscitation, 8 per 1000responded to mask inflation and only 2 per 1000appeared to need intubation. 268 The same studytried to assess the unexpected need for resuscitationat birth, and found that for low-risk babies, i.e.those born after 32 weeks’ gestation and followingan apparently normal labour, about 2 per 1000(0.2%) appeared to need resuscitation at delivery.Of these, 90% responded to mask inflation alone,whereas the remaining 10% appeared not to respondto mask inflation and therefore were intubated atbirth.Resuscitation or specialist help at birth is morelikely to be needed by babies with intrapartum evidenceof significant fetal compromise, babies deliveringbefore 35 weeks’ gestation, babies deliveringvaginally by the breech and multiple pregnancies.Although it is often possible to predict the needfor resuscitation before a baby is born, this is notalways the case. Therefore, personnel trained innewborn life support should be easily available atevery delivery and, should there be any need forresuscitation, the care of the baby should be theirsole responsibility. One person experienced in trachealintubation of the newborn should also beeasily available for normal low-risk deliveries and,ideally, in attendance for deliveries associated witha high risk for neonatal resuscitation. Local guidelinesindicating who should attend deliveries shouldbe developed based on current practice and clinicalaudit.An organised programme educating in the standardsand skills required for resuscitation of thenewborn is therefore essential for any institutionin which deliveries occur.Planned home deliveriesThe recommendations for those who should attenda planned home delivery vary from country to country,but the decision to undergo a planned homedelivery, once agreed by the medical and midwiferystaff, should not compromise the standard of initialresuscitation at birth. There will inevitablybe some limitations to resuscitation of a newbornbaby in the home because of the distance fromfurther assistance, and this must be made clearto the mother at the time plans for home deliveryare made. Ideally, two trained professionals shouldbe present at all home deliveries; 269 one of thesemust be fully trained and experienced in providingmask ventilation and chest compressions in thenewborn.Equipment and environmentResuscitation at birth is often a predictable event.It is therefore simpler to prepare the environmentand the equipment before delivery of the babythan is the case in adult resuscitation. Resuscitationshould ideally take place in a warm, well-lit,draught-free area with a flat resuscitation surfaceplaced below a radiant heater and other resusci-

S116tation equipment immediately available. All equipmentmust be checked daily.When a birth takes place in a non-designateddelivery area, the recommended minimum set ofequipment includes a device for safe, assisted lungaeration of an appropriate size for the newborn,warm dry towels and blankets, a clean (sterile)instrument for cutting the umbilical cord and cleangloves for the attendant. It may also be helpful tohave a suction device with a suitably sized suctioncatheter and a tongue depressor (or laryngoscope),to enable the oropharynx to be examined.Temperature controlNaked, wet, newborn babies cannot maintain theirbody temperature in a room that feels comfortablywarm for adults. Compromised babies are particularlyvulnerable. 270 Exposure of the newborn tocold stress will lower arterial oxygen tension 271 andincrease metabolic acidosis. 272 Prevent heat loss by• protecting the baby from draughts• keeping the delivery room warm• drying the term baby immediately after delivery.Cover the head and body of the baby, apart fromthe face, with a warm towel to prevent furtherheat loss. Alternatively, place the baby skin toskin with the mother and cover both with a towel• placing the baby on a warm surface under a preheatedradiant warmer if resuscitation is neededIn very preterm babies (especially below 28weeks’ gestation), drying and wrapping may not besufficiently effective. A more effective method ofkeeping these babies warm is to cover the head andbody of the baby (apart from the face) with plasticwrapping, without drying the baby beforehand,and then to place the baby so covered under radiantheat.Initial assessmentThe Apgar scoring system was not designed to identifyprospectively babies needing resuscitation. 273Several studies have also suggested that it ishighly subjective. 274 However, components of thescore, namely respiratory rate, heart rate andcolour, if assessed rapidly, can identify babies needingresuscitation. 275 Furthermore, repeated assessmentof these components can indicate whether thebaby is responding or whether further efforts areneeded.Respiratory activityD. Biarent et al.Check whether the baby is breathing. If so, evaluatethe rate, depth and symmetry of respiration,together with any abnormal breathing pattern suchas gasping or grunting.Heart rateThis is best evaluated by listening to the apex beatwith a stethoscope. Feeling the pulse in the baseof the umbilical cord is often effective but can bemisleading; cord pulsation is only reliable if foundto be more than 100 beats min −1 . 276ColourA healthy baby is born blue but becomes pink within30 s of the onset of effective breathing. Observewhether the baby is centrally pink, cyanosed orpale. Peripheral cyanosis is common and does not,by itself, indicate hypoxaemia.ToneA very floppy baby is likely to be unconscious and islikely to need respiratory support.Tactile stimulationDrying the baby usually produces enough stimulationto induce effective respiration. Avoid morevigorous methods of stimulation. If the baby failsto establish spontaneous and effective respirationsfollowing a brief period of stimulation, further supportwill be required.Classification according to initial assessmentOn the basis of the initial assessment, the babiescan usually be divided into four groups.Group 1: vigorous breathing or cryinggood tonerapidly becoming pinkheart rate higher than 100 beats min −1This baby requires no intervention other thandrying, wrapping in a warm towel and, whereappropriate, handing to the mother. The baby willremain warm through skin-to-skin contact withmother under a cover, and may be put to the breastat this stage.

European Resuscitation Council Guidelines for Resuscitation 2005S117Group 2:breathing inadequately or apnoeicremaining centrally bluenormal or reduced toneheart rate less than 100 beats min −1This baby may respond to tactile stimulationand/or facial oxygen, but may need mask inflation.Group 3:breathing inadequately or apnoeicblue or palefloppyheart rate less than 100 beats min −1This baby may improve with mask inflation butmay also require chest compressions.Group 4:breathing inadequately or apnoeicpalefloppyno detectable heart rateThis baby will require immediate airway control,lung inflation and ventilation. Once this has beensuccessfully accomplished, the baby may also needchest compressions and perhaps drugs.There remains a very rare group of babies who,though breathing adequately and with a good heartrate, remain blue. This group includes a range ofpossible diagnoses such as diaphragmatic hernia,surfactant deficiency, congenital pneumonia, pneumothoraxor cyanotic congenital heart disease.Newborn life supportCommence newborn life support (Figure 6.10) ifassessment demonstrates that the baby has failedto establish adequate regular normal breathing, orhas a heart rate of less than 100 beats min −1 . Openingthe airway and aerating the lungs is usuallyall that is necessary. Furthermore, more complexinterventions will be futile unless these two firststeps have been successfully completed.AirwayThe baby should be on his or her back with thehead in a neutral position (Figure 6.11). A 2-cmthickness of the blanket or towel placed underthe baby’s shoulder may be helpful in maintainingproper head position. In floppy babies, applicationof jaw thrust or the use of an appropriately sizedoropharyngeal airway may be helpful in opening theairway.Suction is needed only if there is particulate matteror blood obstructing the airway. Aggressive pharyngealsuction can delay the onset of spontaneousbreathing and cause laryngeal spasm and vagalbradycardia. 277 The presence of thick meconium ina non-vigorous baby is the only indication for consideringimmediate suction. If suction is required,it is best done under direct vision. Connect a 12—14FG suction catheter, or a Yankauer sucker, to a suctionsource not exceeding −100 mmHg.BreathingThere is currently insufficient evidence to specifythe concentration of oxygen to be used when startingresuscitation. After initial steps at birth, if respiratoryefforts are absent or inadequate, lung aerationis the priority (Figure 6.12). The primary measureof adequate initial lung inflation is a promptimprovement in heart rate; assess chest wall movementif the heart rate does not improve.For the first few breaths maintain the initialinflation pressure for 2—3 s. This will help lungexpansion. Most babies needing resuscitation atbirth will respond with a rapid increase in heartrate within 30 s of lung inflation. If the heart rateincreases but the baby is not breathing adequately,continue ventilation at a rate of about 30 breathsmin −1 , allowing approximately 1 s for each inflation,until there is adequate spontaneous breathing.Adequate passive ventilation is usually indicatedby either a rapidly increasing heart rate or a heartrate that is maintained faster than 100 beats min −1 .If the baby does not respond in this way, themost likely reason is inadequate airway control orventilation. Look for passive chest movement intime with inflation efforts; if these are present,then lung aeration has been achieved. If theseare absent, then airway control and lung aerationhave not been confirmed. Without adequate lungaeration chest compressions will be ineffective;therefore, confirm lung aeration before progressingto circulatory support. Some practitioners willensure lung aeration by tracheal intubation, butthis requires training and experience to be achievedeffectively. If this skill is not available and the heartrate is decreasing, re-evaluate airway position anddeliver aeration breaths while summoning a colleaguewith intubation skills.Continue ventilatory support until the baby hasestablished normal regular breathing.Circulatory supportCirculatory support with chest compressions iseffective only if the lungs have first been successfullyinflated. Give chest compressions if the heartrate is less than 60 beats min −1 despite adequateventilation. The optimal technique is to place the

S118D. Biarent et al.Figure 6.10Newborn life support algorithm.two thumbs side by side over the lower third ofthe sternum, with the fingers encircling the torsoand supporting the back (Figure 6.13). 21,22,25,278,279The lower third of the sternum is compressed to aFigure 6.11 Newborn head in neutral position. © 2005Resuscitation Council (UK).depth of approximately one third of the anteriorposteriordiameter of the chest. A compression torelaxation ratio with a slightly shorter compressionthan relaxation phase offers theoretical advantagesfor blood flow in the very young infant. 280Do not lift the thumbs off the sternum duringthe relaxation phase, but allow the chest wall toreturn to its relaxed position between compressions.Use a 3:1 ratio of compressions to ventilations,aiming to achieve approximately 120 eventsmin −1 , i.e. approximately 90 compressions and 30breaths. However, the quality of the compressionsand breaths are more important than the rate. 281Check the heart rate after about 30 s and periodicallythereafter. Discontinue chest compressionswhen the spontaneous heart rate is faster then 60beats min −1 .

European Resuscitation Council Guidelines for Resuscitation 2005S119Figure 6.12 Airway and ventilation — newborn. © 2005Resuscitation Council (UK).DrugsDrugs are rarely indicated in resuscitation of thenewborn infant. Bradycardia in the newborn infantis usually caused by inadequate lung inflation orprofound hypoxia, and establishing adequate ventilationis the most important step to correct it.However, if the heart rate remains less than 60beats min −1 despite adequate ventilation and chestcompressions, drugs may be needed. These drugsare presumed to exert their effect by their actionon the heart and are being given because cardiacfunction is inadequate. It is therefore necessary togive them as close to the heart as possible, ideallyvia a rapidly inserted umbilical venous catheter(Figure 6.14).AdrenalineDespite the lack of human data, it is reasonable tocontinue to use adrenaline when adequate ventilationand chest compressions have failed to increasethe heart rate above 60 beats min −1 . Use the IVroute as soon as venous access is established. Therecommended IV dose is 10—30 mcg kg −1 . The trachealroute is not recommended (see below) but, ifFigure 6.14 Newborn umbilical cord showing the arteriesand veins. © 2005 Resuscitation Council (UK).it is used, it is highly likely that doses of 30 mcg kg −1or less are ineffective. Try a higher dose (up to100 mcg kg −1 ). The safety of these higher trachealdoses has not been studied. Do not give high IVdoses.BicarbonateIf effective spontaneous cardiac output is notrestored despite adequate ventilation and adequatechest compressions, reversing intracardiacacidosis may improve myocardial functionand achieve a spontaneous circulation. Give1—2 mmol kg −1 IV.FluidsConsider volume expansion when there has beensuspected blood loss or the infant appears to bein shock (pale, poor perfusion, weak pulse) andhas not responded adequately to other resuscitativemeasures. In the absence of suitable blood(i.e., irradiated and leucocyte-depleted group ORh-negative blood) isotonic crystalloid rather thanalbumin is the solution of choice for restoringintravascular volume in the delivery room. Give abolus of 10—20 ml kg −1 .Stopping resuscitationFigure 6.13 Ventilation and chest compression — newborn.© 2005 Resuscitation Council (UK).Local and national committees will determine theindications for stopping resuscitation. However,data from infants without signs of life from birthlasting at least 10 min or longer show either highmortality or severe neurodevelopmental disability.After 10 min of continuous and adequate resuscitationefforts, discontinuation of resuscitation maybe justified if there are no signs of life.

S120D. Biarent et al.Communication with the parentsIt is vitally important that the team caring forthe newborn baby informs the parents of thebaby’s progress. At delivery adhere to the routinelocal plan and, if possible, hand the baby to themother at the earliest opportunity. If resuscitationis required, inform the parents of the proceduresbeing undertaken and why they are required.Decisions to discontinue resuscitation ideallyshould involve senior paediatric staff. Wheneverpossible, the decision to attempt resuscitation ofan extremely preterm baby should be taken in closeconsultation with the parents and senior paediatricand obstetric staff. Where a difficulty has beenforeseen, for example in the case of severe congenitalmalformation, the options and prognosisshould be discussed with the parents, midwives,obstetricians and birth attendants before delivery.All discussions and decisions should be carefullyrecorded in the mother’s notes before delivery andalso in the baby’s records after birth.Specific questions addressed at the2005 Consensus ConferenceMaintaining normal temperature in preterminfantsSignificantly, preterm babies are likely to becomehypothermic despite careful application of the traditionaltechniques for keeping them warm (drying,wrapping and placing under radiant heat). 282Several randomised controlled trials and observationalstudies have shown that placing pretermbabies under radiant heat and then covering thebabies with food-grade plastic wrapping, withoutdrying them, significantly improves temperature onadmission to intensive care compared with traditionaltechniques. 283—285 The baby’s temperaturemust be monitored closely because of thesmall but described risk of hyperthermia with thistechnique. 286 All resuscitation procedures, includingintubation, chest compression and insertion oflines, can be achieved with the plastic cover inplace.Infants born to febrile mothers have beenreported to have a higher incidence of perinatalrespiratory depression, neonatal seizures, earlymortality and cerebral palsy. 286—288 Animal studiesindicate that hyperthermia during or followingischaemia is associated with a progression of cerebralinjury. 233,289 Hyperthermia should be avoided.MeconiumFive years ago, a large randomised controlled studyshowed that attempting to intubate and aspirateinhaled meconium from the tracheas of vigorousinfants at birth was not beneficial. 290 A more recentlarge multicentre randomised controlled study hasnow shown that suctioning meconium from thebaby’s nose and mouth before delivery of the baby’schest (intrapartum suctioning) does not reducethe incidence or severity of meconium aspirationsyndrome. 291 Intrapartum suctioning is thereforeno longer recommended. Intubation and suction ofmeconium from the trachea of non-vigorous infantsborn through meconium-stained liquor is still recommended.Air or 100% oxygenSeveral studies in recent years have raised concernsabout the potential adverse effects of 100% oxygenon respiratory physiology and cerebral circulation,and the potential tissue damage from oxygen freeradicals. There are also concerns about tissue damagefrom oxygen deprivation during and followingasphyxia. Studies examining blood pressure, cerebralperfusion, and various biochemical measuresof cell damage in asphyxiated animals resuscitatedwith 100% versus 21% oxygen, have shown conflictingresults. 292—296 One study of preterm infants(below 33 weeks’ gestation) exposed to 80% oxygenfound lower cerebral blood flow when comparedwith those stabilised with 21% oxygen. 297Some animal data indicate the opposite effect,i.e. reduced blood pressure and cerebral perfusionwith air versus 100% oxygen. 292 Meta-analysisof four human studies demonstrated a reductionin mortality and no evidence of harm in infantsresuscitated with air versus those resuscitated with100% oxygen. However, there are several significantconcerns about the methodology of these studies,and these results should be interpreted withcaution. 80,298At present, the standard approach to resuscitationis to use 100% oxygen. Some clinicians mayelect to start resuscitation with an oxygen concentrationless than 100%, including some whomay start with air. Evidence suggests that thisapproach may be reasonable. However, where possible,ensure supplemental oxygen is availablefor use if there is no rapid improvement followingsuccessful lung aeration. If supplemental oxygenis not readily available, ventilate the lungswith air. Supplemental oxygen is recommendedfor babies who are breathing but have centralcyanosis.

European Resuscitation Council Guidelines for Resuscitation 2005S121Monitoring the oxygen saturation of babiesundergoing resuscitation may be useful, but studieshave shown that term healthy newborns maytake more than 10 min to achieve a preductal oxygensaturation above 95% and nearly an hour toachieve this post-ductally. 299—301 Giving a variableconcentration of oxygen guided by pulse oximetrymay improve the ability to achieve ‘normal’ oxygensaturation values while more quickly avoiding‘hyperoxia’, but the definition of these two termsin the baby at birth are undetermined. Oxygen is adrug, and oxidant injury is theoretically more likelyin preterm infants.Initial breaths and assisted ventilationIn term infants, spontaneous or assisted initialinflations create a functional residual capacity(FRC). 302—309 The optimum pressure, inflation timeand flow required to establish an effective FRC havenot been determined. Average initial peak inflatingpressures of 30—40 cmH 2 O (inflation time undefined)usually ventilate unresponsive term infantssuccessfully. 305—307,309 Assisted ventilation rates of30—60 breaths min −1 are used commonly, but therelative efficacy of various rates has not been investigated.The primary measure of adequate initial ventilationis prompt increase in heart rate; assesspassive chest wall movement if the heart ratedoes not increase. The initial peak inflating pressuresneeded are variable and unpredictable, andshould be individualised to achieve an increase inheart rate or movement of the chest with eachbreath. Where pressure is being monitored, an initialinflation pressure of 20 cmH 2 O may be effective,but 30—40 cmH 2 O or higher may be requiredin some term babies. If pressure is not being monitoredbut merely limited by a non-adjustable ‘blowoff’valve, use the minimum inflation required toachieve an increase in heart rate. There is insufficientevidence to recommend an optimum inflationtime. In summary, provide artificial ventilation at30—60 breaths min −1 to achieve or maintain a heartrate higher than 100 beats min −1 promptly.Assisted ventilation of preterm infantsAnimal studies show that preterm lungs are easilydamaged by large volume inflations immediatelyafter birth, 310 and that maintaining a positive endexpiratorypressure (PEEP) immediately after birthprotects against lung damage. PEEP also improveslung compliance and gas exchange. 311,312 Humancase series show that most apnoeic preterm infantscan be ventilated with an initial inflation pressureof 20—25 cmH 2 O, though some infants appear torequire a higher pressure. 313,314When ventilating preterm infants, very obviouspassive chest wall movement may indicate excessivetidal volumes and should be avoided. Monitoringof pressure may help to provide consistent inflationsand avoid high pressures. If positive-pressureventilation is required, an initial inflation pressureof 20—25 cmH 2 O is adequate for most preterminfants. If a prompt increase in heart rate or chestmovement is not obtained, higher pressures maybe needed. If continued positive-pressure ventilationis required, PEEP may be beneficial. Continuouspositive airway pressure (CPAP) in spontaneouslybreathing preterm infants following resuscitationmay also be beneficial. 314DevicesEffective ventilation can be achieved with eithera flow-inflating or self-inflating bag or with aT-piece mechanical device designed to regulatepressure. 315—317 The blow-off valves of selfinflatingbags are flow dependent, and pressuresgenerated may exceed the value specified by themanufacturer. 318 Target inflation pressures and longinspiratory times are achieved more consistently inmechanical models when using T-piece devices thanwhen using bags, 319 although the clinical implicationsare not clear. More training is required toprovide an appropriate pressure using flow-inflatingbags compared with self-inflating bags. 320 A selfinflatingbag, a flow-inflating bag or a T-piecemechanical device, all designed to regulate pressureor limit pressure applied to the airway, can beused to ventilate a newborn.Laryngeal mask airways (LMAs) are effectivefor ventilating newborn near-term and full-terminfants. 321,322 There are few data on the use ofthese devices in small preterm infants. 323,324 Threecase series show that the LMA can provide effectiveventilation in a time frame consistent with currentresuscitation guidelines, although the babies beingstudied were not being resuscitated. 322,325,326 Arandomised controlled trial found no clinicallysignificant difference between the LMA and trachealintubation when bag-mask ventilation wasunsuccessful. 321 It is unclear whether the conclusionsof this study can be generalized, since theLMA was inserted by experienced providers. Casereports suggest that when bag-mask ventilation hasbeen unsuccessful and tracheal intubation is unfeasibleor unsuccessful, the LMA may provide effectiveventilation. 327—329 There is insufficient evidenceto support the routine use of the LMA as theprimary airway device for resuscitation at birth.

S122D. Biarent et al.Table 6.1Calculation of tracheal tube size and depth of insertion aChild’s weight (kg) Gestation (weeks) Tube size (mm ID) Depth of insertion (cm) a38 3.5/4.0 >9a Depth of insertion from the upper lip can be estimated as insertion depth at lip (cm) = weight in kg+6cm.There are also reservations concerning its effectivenessin the following situations• when chest compressions are required• for very low birth weight (VLBW) babies• when the amniotic fluid is meconium stainedConfirming tracheal tube placementTracheal intubation may be considered at severalpoints during neonatal resuscitation• when suctioning to remove meconium or othertracheal blockage is required• if bag-mask ventilation is ineffective or prolonged• when chest compressions are performed• in special circumstances (e.g., congenitaldiaphragmatic hernia or birth weight below1000 g)The use and timing of tracheal intubation willdepend on the skill and experience of the availableresuscitators.Following tracheal intubation and intermittentpositive pressure, a prompt increase in heart rateis the best indicator that the tube is in the tracheobronchialtree. 330 Exhaled CO 2 detection is effectivefor confirmation of tracheal tube placementin infants, including VLBW infants. 331—334 Detectionof exhaled CO 2 in patients with adequate cardiacoutput confirms placement of the tube within thetrachea, whereas failure to detect exhaled CO 2strongly suggests oesophageal intubation. 331,333Poor or absent pulmonary blood flow or trachealobstruction may prevent detection of exhaled CO 2despite correct tracheal tube placement. Trachealtube placement is identified correctly in nearly allpatients who are not in cardiac arrest 99 ; however, incritically ill infants with poor cardiac output, inabilityto detect exhaled CO 2 despite correct placementmay lead to unnecessary extubation. Otherclinical indicators of correct tracheal tube placementinclude evaluation of condensed humidifiedgas during exhalation and presence or absence ofchest movement, but these have not been evaluatedsystematically in newborn babies.Tracheal tube placement (Table 6.1) must beassessed visually during intubation and, in mostcases, will be confirmed by a rapid increase in heartrate on ventilating via the tracheal tube. If theheart rate remains slow, incorrect tube placementis the most likely cause. Check tube placementeither visually or by detection of exhaledCO 2 .Route and dose of adrenalineThere are no placebo-controlled studies that haveevaluated the use of adrenaline at any stagein human neonatal resuscitation. A paediatricstudy 148 and newborn animal studies 335,336 showedno benefit and a trend toward reduced survivaland worse neurological status after highdoseIV adrenaline (100 mcg kg −1 ) during resuscitation.Animal and adult human studies demonstratethat, when given via the trachea, considerablyhigher doses of adrenaline than currentlyrecommended are required to achieve adequateplasma concentrations. 337—339 One neonatal animalstudy using the currently recommended doseof tracheal adrenaline (10 mcg kg −1 ) showed nobenefit. 126 One neonatal cohort study of ninepreterm babies requiring resuscitation showedthat tracheal adrenaline was absorbed, but theseworkers used 7—25 times the dose recommendedcurrently. 340Post-resuscitation careBabies who have required resuscitation may deteriorate.Once adequate ventilation and circulationare established, the infant should be maintainedin or transferred to an environment in which closemonitoring and anticipatory care can be provided.GlucoseHypoglycaemia was associated with adverse neurologicaloutcome in a neonatal animal modelof asphyxia and resuscitation. 341 Newborn animalswhich were hypoglycaemic at the time of

European Resuscitation Council Guidelines for Resuscitation 2005S123an anoxic or hypoxic-ischaemic insult had largerareas of cerebral infarction and/or decreased survivalcompared with controls. 342,343 One clinicalstudy demonstrated an association between hypoglycaemiaand poor neurological outcome followingperinatal asphyxia. 344 No clinical neonatal studieshave investigated the relationship between hyperglycaemiaand neurological outcome, although inadults hyperglycaemia is associated with a worseoutcome. 345 The range of blood glucose concentrationthat is associated with the least brain injuryfollowing asphyxia and resuscitation cannot bedefined on available evidence. Infants who requiresignificant resuscitation should be monitored andtreated to maintain blood glucose within the normalrange.Induced hypothermiaIn a multicentre trial involving newborns withsuspected asphyxia (indicated by need for resuscitationat birth, metabolic acidosis and earlyencephalopathy), selective head cooling (34.5 ◦ C)was associated with a non-significant reduction inthe number of survivors with severe disability at18 months, but a significant benefit in the subgroupwith moderate encephalopathy as judgedby amplitude-integrated electroencephalogram. 220Infants with severe electroencephalographic suppressionand seizures did not benefit fromtreatment. 346 A second, small, controlled pilotstudy in asphyxiated infants with early inducedsystemic hypothermia resulted in fewer deathsand disabilities at 12 months. Modest hypothermiais associated with bradycardia and elevatedblood pressure that do not usually requiretreatment, but a rapid increase in body temperaturemay cause hypotension. 347 Profoundhypothermia (core temperature below 33 ◦ C) maycause arrhythmia, bleeding, thrombosis and sepsis,but studies so far have not reported thesecomplications in infants treated with modesthypothermia. 220,348There are insufficient data to recommend routineuse of modest systemic or selective cerebralhypothermia following resuscitation of infantswith suspected asphyxia. Further clinical trials areneeded to determine which infants benefit mostand which method of cooling is most effective.Withholding or discontinuing resuscitationMortality and morbidity for newborns varies accordingto region and to availability of resources. 349Social science studies indicate that parents desirea larger role in decisions to resuscitate and tocontinue life support in severely compromisedbabies. 350 There is considerable variability amongproviders about the benefits and disadvantages ofaggressive therapies in such babies. 351,352Withholding resuscitationIt is possible to identify conditions associated withhigh mortality and poor outcome, where withholdingresuscitation may be considered reasonable,particularly when there has been the opportunityfor discussion with parents. 282,353 A consistent andcoordinated approach to individual cases by theobstetric and neonatal teams and the parents is animportant goal. Withholding resuscitation and discontinuationof life-sustaining treatment during orfollowing resuscitation are considered by many tobe ethically equivalent, and clinicians should notbe hesitant to withdraw support when the possibilityof functional survival is highly unlikely. Thefollowing guidelines must be interpreted accordingto current regional outcomes.• Where gestation, birth weight and/or congenitalanomalies are associated with almost certainearly death, and unacceptably high morbidity islikely among the rare survivors, resuscitation isnot indicated. Examples from the published literatureinclude extreme prematurity (gestationalage

S124References1. Zideman D, Bingham R, Beattie T, et al. Guidelines forpaediatric life support: a Statement by the Paediatric LifeSupport Working Party of the European Resuscitation Council.Resuscitation 1994;27:91—105.2. European Resuscitation Council. Paediatric life support:(including the recommendations for resuscitation of babiesat birth). Resuscitation 1998;37:95—6.3. Phillips B, Zideman D, Garcia-Castrillo L, Felix M, Shwarz-Schwierin U. European Resuscitation Council Guidelines2000 for Basic Paediatric Life Support. A statement fromthe Paediatric Life Support Working Group and approvedby the Executive Committee of the European ResuscitationCouncil. Resuscitation 2001;48:223—9.4. Phillips B, Zideman D, Garcia-Castrillo L, Felix M, Shwarz-Schwierin V. European Resuscitation Council Guidelines2000 for Advanced Paediatric Life Support. A statementfrom Paediatric Life Support Working Group and approvedby the Executive Committee of the European ResuscitationCouncil. Resuscitation 2001;48:231—4.5. American Heart Association in collaboration with InternationalLiaison Committee on Resuscitation. Guidelines forCardiopulmonary Resuscitation and Emergency CardiovascularCare—–an international consensus on science. Resuscitation2000;46:3—430.6. American Heart Association in collaboration with InternationalLiaison Committee on Resuscitation. Guidelines 2000for Cardiopulmonary Resuscitation and Emergency CardiovascularCare: International Consensus on Science. Circulation2000;102(Suppl. I):I-1—I-370.7. International Liaison Committee on Resuscitation. 2005International Consensus on Cardiopulmonary Resuscitationand Emergency Cardiovascular Care Science with TreatmentRecommendations. Resuscitation 2005;67:157—341.8. International Liaison Committee on Resuscitation. 2005International Consensus on Cardiopulmonary Resuscitationand Emergency Cardiovascular Care Science with TreatmentRecommendations. Circulation, in press.9. Kuisma M, Suominen P, Korpela R. Paediatric out-of-hospitalcardiac arrests: epidemiology and outcome. Resuscitation1995;30:141—50.10. Kyriacou DN, Arcinue EL, Peek C, Kraus JF. Effect of immediateresuscitation on children with submersion injury.Pediatrics 1994;94:137—42.11. Berg RA, Hilwig RW, Kern KB, Ewy GA. Bystander’’chest compressions and assisted ventilation independentlyimprove outcome from piglet asphyxial pulseless ‘‘cardiacarrest’’. Circulation 2000;101:1743—8.12. Young KD, Seidel JS. Pediatric cardiopulmonary resuscitation:a collective review. Ann Emerg Med 1999;33:195—205.13. Berg RA, Hilwig RW, Kern KB, Babar I, Ewy GA. Simulatedmouth-to-mouth ventilation and chest compressions(bystander cardiopulmonary resuscitation) improves outcomein a swine model of prehospital pediatric asphyxialcardiac arrest. Crit Care Med 1999;27:1893—9.14. Dorph E, Wik L, Steen PA. Effectiveness of ventilationcompressionratios 1:5 and 2:15 in simulated single rescuerpaediatric resuscitation. Resuscitation 2002;54:259—64.15. Turner I, Turner S, Armstrong V. Does the compression toventilation ratio affect the quality of CPR: a simulationstudy. Resuscitation 2002;52:55—62.16. Babbs CF, Kern KB. Optimum compression to ventilationratios in CPR under realistic, practical conditions:D. Biarent et al.a physiological and mathematical analysis. Resuscitation2002;54:147—57.17. Babbs CF, Nadkarni V. Optimizing chest compression to rescueventilation ratios during one-rescuer CPR by professionalsand lay persons: children are not just little adults.Resuscitation 2004;61:173—81.18. Whyte SD, Wyllie JP. Paediatric basic life support: a practicalassessment. Resuscitation 1999;41:153—217.19. Safranek DJ, Eisenberg MS, Larsen MP. The epidemiologyof cardiac arrest in young adults. Ann Emerg Med1992;21:1102—6.20. Clements F, McGowan J. Finger position for chest compressionsin cardiac arrest in infants. Resuscitation2000;44:43—6.21. Houri PK, Frank LR, Menegazzi JJ, Taylor R. A randomized,controlled trial of two-thumb vs two-finger chest compressionin a swine infant model of cardiac arrest. PrehospEmerg Care 1997;1:65—7.22. David R. Closed chest cardiac massage in the newborninfant. Pediatrics 1988;81:552—4.23. Dorfsman ML, Menegazzi JJ, Wadas RJ, Auble TE. Twothumbvs two-finger chest compression in an infant modelof prolonged cardiopulmonary resuscitation. Acad EmergMed 2000;7:1077—82.24. Whitelaw CC, Slywka B, Goldsmith LJ. Comparison of a twofingerversus two-thumb method for chest compressions byhealthcare providers in an infant mechanical model. Resuscitation2000;43:213—6.25. Menegazzi JJ, Auble TE, Nicklas KA, Hosack GM, Rack L,Goode JS. Two-thumb versus two-finger chest compressionduring CRP in a swine infant model of cardiac arrest. AnnEmerg Med 1993;22:240—3.26. Stevenson AG, McGowan J, Evans AL, Graham CA. CPR forchildren: one hand or two? Resuscitation 2005;64:205—8.27. Gurnett CA, Atkins DL. Successful use of a biphasic waveformautomated external defibrillator in a high-risk child.Am J Cardiol 2000;86:1051—3.28. Konig B, Benger J, Goldsworthy L. Automatic externaldefibrillation in a 6 year old. Arch Dis Child 2005;90:310—1.29. Atkinson E, Mikysa B, Conway JA, et al. Specificity and sensitivityof automated external defibrillator rhythm analysisin infants and children. Ann Emerg Med 2003;42:185—96.30. Cecchin F, Jorgenson DB, Berul CI, et al. Is arrhythmiadetection by automatic external defibrillator accurate forchildren? Sensitivity and specificity of an automatic externaldefibrillator algorithm in 696 pediatric arrhythmias.Circulation 2001;103:2483—8.31. Samson R, Berg R, Bingham R. Pediatric Advanced Life SupportTask Force ILCoR. Use of automated external defibrillatorsfor children: an update. An advisory statement fromthe Pediatric Advanced Life Support Task Force of the InternationalLiaison Committee on Resuscitation. Resuscitation2003;57:237—43.32. Jorgenson D, Morgan C, Snyder D, et al. Energy attenuatorfor pediatric application of an automated external defibrillator.Crit Care Med 2002;30:S145—7.33. Tang W, Weil MH, Jorgenson D, et al. Fixed-energy biphasicwaveform defibrillation in a pediatric model of cardiacarrest and resuscitation. Crit Care Med 2002;30:2736—41.34. Berg RA, Chapman FW, Berg MD, et al. Attenuated adultbiphasic shocks compared with weight-based monophasicshocks in a swine model of prolonged pediatric ventricularfibrillation. Resuscitation 2004;61:189—97.35. Berg RA, Samson RA, Berg MD, et al. Better outcome afterpediatric defibrillation dosage than adult dosage in a swinemodel of pediatric ventricular fibrillation. J Am Coll Cardiol2005;45:786—9.

European Resuscitation Council Guidelines for Resuscitation 2005S12536. Rossano JQ, Schiff L, Kenney MA, Atkins DL. Survivalis not correlated with defibrillation dosing in pediatricout-of-hospital ventricular fibrillation. Circulation2003;108:320—1.37. Clark CB, Zhang Y, Davies LR, Karlsson G, Kerber RE. Pediatrictransthoracic defibrillation: biphasic versus monophasicwaveforms in an experimental model. Resuscitation2001;51:159—63.38. Schneider T, Martens PR, Paschen H, et al. Multicenter,randomized, controlled trial of 150-J biphasic shocks comparedwith 200- to 360-J monophasic shocks in the resuscitationof out-of-hospital cardiac arrest victims. OptimizedResponse to Cardiac Arrest (ORCA) Investigators. Circulation2000;102:1780—7.39. Faddy SC, Powell J, Craig JC. Biphasic and monophasicshocks for transthoracic defibrillation: a meta analysis ofrandomised controlled trials. Resuscitation 2003;58:9—16.40. van Alem AP, Chapman FW, Lank P, Hart AA, KosterRW. A prospective, randomised and blinded comparisonof first shock success of monophasic and biphasicwaveforms in out-of-hospital cardiac arrest. Resuscitation2003;58:17—24.41. Redding JS. The choking controversy: critique of evidenceon the Heimlich maneuver. Crit Care Med 1979;7:475—9.42. International Liaison Committee on Resuscitation. Part 2.Adult Basic Life Support. 2005 International Consensuson Cardiopulmonary Resuscitation and Emergency CardiovascularCare Science with Treatment Recommendations.Resuscitation 2005;67:187—200.43. Sirbaugh PE, Pepe PE, Shook JE, et al. A prospective,population-based study of the demographics, epidemiology,management, and outcome of out-of-hospitalpediatric cardiopulmonary arrest. Ann Emerg Med1999;33:174—84.44. Hickey RW, Cohen DM, Strausbaugh S, Dietrich AM. Pediatricpatients requiring CPR in the prehospital setting. AnnEmerg Med 1995;25:495—501.45. Reis AG, Nadkarni V, Perondi MB, Grisi S, Berg RA. Aprospective investigation into the epidemiology of inhospitalpediatric cardiopulmonary resuscitation usingthe international Utstein reporting style. Pediatrics2002;109:200—9.46. Young KD, Gausche-Hill M, McClung CD, Lewis RJ. Aprospective, population-based study of the epidemiologyand outcome of out-of-hospital pediatric cardiopulmonaryarrest. Pediatrics 2004;114:157—64.47. Richman PB, Nashed AH. The etiology of cardiac arrest inchildren and young adults: special considerations for EDmanagement. Am J Emerg Med 1999;17:264—70.48. Engdahl J, Bang A, Karlson BW, Lindqvist J, Herlitz J. Characteristicsand outcome among patients suffering from outof hospital cardiac arrest of non-cardiac aetiology. Resuscitation2003;57:33—41.49. Carcillo JA. Pediatric septic shock and multiple organ failure.Crit Care Clin 2003;19:413—40, viii.50. Eberle B, Dick WF, Schneider T, Wisser G, Doetsch S,Tzanova I. Checking the carotid pulse check: diagnosticaccuracy of first responders in patients with and withouta pulse. Resuscitation 1996;33:107—16.51. Moule P. Checking the carotid pulse: diagnostic accuracyin students of the healthcare professions. Resuscitation2000;44:195—201.52. Lapostolle F, Le Toumelin P, Agostinucci JM, Catineau J,Adnet F. Basic cardiac life support providers checking thecarotid pulse: performance, degree of conviction, andinfluencing factors. Acad Emerg Med 2004;11:878—80.53. Frederick K, Bixby E, Orzel MN, Stewart-Brown S, WillettK. Will changing the emphasis from ‘pulseless’ to ‘no signsof circulation’ improve the recall scores for effective lifesupport skills in children? Resuscitation 2002;55:255—61.54. Park C, Bahk JH, Ahn WS, Do SH, Lee KH. The laryngealmask airway in infants and children. Can J Anaesth2001;48:413—7.55. Hedges JR, Dronen SC, Feero S, Hawkins S, Syverud SA,Shultz B. Succinylcholine-assisted intubations in prehospitalcare. Ann Emerg Med 1988;17:469—72.56. Murphy-Macabobby M, Marshall WJ, Schneider C, Dries D.Neuromuscular blockade in aeromedical airway management.Ann Emerg Med 1992;21:664—8.57. Sayre M, Weisgerber I. The use of neuromuscular blockingagents by air medical services. J Air Med Transp1992;11:7—11.58. Rose W, Anderson L, Edmond S. Analysis of intubations.Before and after establishment of a rapid sequence intubationprotocol for air medical use. Air Med J 1994;13:475—8.59. Sing RF, Reilly PM, Rotondo MF, Lynch MJ, McCans JP,Schwab CW. Out-of-hospital rapid-sequence induction forintubation of the pediatric patient. Acad Emerg Med1996;3:41—5.60. Ma OJ, Atchley RB, Hatley T, Green M, Young J, Brady W.Intubation success rates improve for an air medical programafter implementing the use of neuromuscular blockingagents. Am J Emerg Med 1998;16:125—7.61. Tayal V, Riggs R, Marx J, Tomaszewski C, Schneider R. Rapidsequenceintubation at an emergency medicine residency:success rate and adverse events during a two-year period.Acad Emerg Med 1999;6:31—7.62. Wang HE, Sweeney TA, O’Connor RE, Rubinstein H.Failed prehospital intubations: an analysis of emergencydepartment courses and outcomes. Prehosp Emerg Care2001;5:134—41.63. Sagarin MJ, Chiang V, Sakles JC, et al. Rapid sequenceintubation for pediatric emergency airway management.Pediatr Emerg Care 2002;18:417—43.64. Kaye K, Frascone RJ, Held T. Prehospital rapid-sequenceintubation: a pilot training program. Prehosp Emerg Care2003;7:235—40.65. Wang HE, Kupas DF, Paris PM, Bates RR, Costantino JP, YealyDM. Multivariate predictors of failed prehospital endotrachealintubation. Acad Emerg Med 2003;10:717—24.66. Pepe P, Zachariah B, Chandra N. Invasive airway techniquein resuscitation. Ann Emerg Med 1991;22:393—403.67. Luten RC, Wears RL, Broselow J, et al. Length-based endotrachealtube and emergency equipment in pediatrics. AnnEmerg Med 1992;21:900—4.68. Deakers TW, Reynolds G, Stretton M, Newth CJ. Cuffedendotracheal tubes in pediatric intensive care. J Pediatr1994;125:57—62.69. Khine HH, Corddry DH, Kettrick RG, et al. Comparisonof cuffed and uncuffed endotracheal tubes inyoung children during general anesthesia. Anesthesiology1997;86:627—31.70. Newth CJ, Rachman B, Patel N, Hammer J. The use ofcuffed versus uncuffed endotracheal tubes in pediatricintensive care. J Pediatr 2004;144:333—7.71. Mhanna MJ, Zamel YB, Tichy CM, Super DM. The ‘‘air leak’’test around the endotracheal tube, as a predictor of postextubationstridor, is age dependent in children. Crit CareMed 2002;30:2639—43.72. Katz SH, Falk JL. Misplaced endotracheal tubes byparamedics in an urban emergency medical services system.Ann Emerg Med 2001;37:32—7.

S12673. Gausche M, Lewis RJ, Stratton SJ, et al. Effect of outof-hospitalpediatric endotracheal intubation on survivaland neurological outcome: a controlled clinical trial. JAMA2000;283:783—90.74. Kelly JJ, Eynon CA, Kaplan JL, de Garavilla L, Dalsey WC.Use of tube condensation as an indicator of endotrachealtube placement. Ann Emerg Med 1998;31:575—8.75. Andersen KH, Hald A. Assessing the position of the trachealtube: the reliability of different methods. Anaesthesia1989;44:984—5.76. Andersen KH, Schultz-Lebahn T. Oesophageal intubationcan be undetected by auscultation of the chest. ActaAnaesthesiol Scand 1994;38:580—2.77. Hartrey R, Kestin IG. Movement of oral and nasal trachealtubes as a result of changes in head and neck position.Anaesthesia 1995;50:682—7.78. Van de Louw A, Cracco C, Cerf C, et al. Accuracy of pulseoximetry in the intensive care unit. Intensive Care Med2001;27:1606—13.79. Seguin P, Le Rouzo A, Tanguy M, Guillou YM, Feuillu A,Malledant Y. Evidence for the need of bedside accuracyof pulse oximetry in an intensive care unit. Crit Care Med2000;28:703—6.80. Tan A, Schulze A, O’Donnell CP, Davis PG. Air versus oxygenfor resuscitation of infants at birth. Cochrane Database SystRev 2004:CD002273.81. Ramji S, Rasaily R, Mishra PK, et al. Resuscitation of asphyxiatednewborns with room air or 100% oxygen at birth: amulticentric clinical trial. Indian Pediatr 2003;40:510—7.82. Vento M, Asensi M, Sastre J, Garcia-Sala F, Pallardo FV,Vina J. Resuscitation with room air instead of 100% oxygenprevents oxidative stress in moderately asphyxiated termneonates. Pediatrics 2001;107:642—7.83. Saugstad OD. Resuscitation of newborn infants with roomair or oxygen. Semin Neonatol 2001;6:233—9.84. Aufderheide TP, Lurie KG. Death by hyperventilation: acommon and life-threatening problem during cardiopulmonaryresuscitation. Crit Care Med 2004;32:S345—51.85. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al.Hyperventilation-induced hypotension during cardiopulmonaryresuscitation. Circulation 2004;109:1960—5.86. Wik L, Kramer-Johansen J, Myklebust H, et al. Quality ofcardiopulmonary resuscitation during out-of-hospital cardiacarrest. JAMA 2005;293:299—304.87. Abella BS, Alvarado JP, Myklebust H, et al. Quality ofcardiopulmonary resuscitation during in-hospital cardiacarrest. AMA 2005;293:305—10.88. Abella BS, Sandbo N, Vassilatos P, et al. Chest compressionrates during cardiopulmonary resuscitation are suboptimal:a prospective study during in-hospital cardiac arrest. Circulation2005;111:428—34.89. Borke WB, Munkeby BH, Morkrid L, Thaulow E, SaugstadOD. Resuscitation with 100% O(2) does not protect themyocardium in hypoxic newborn piglets. Arch Dis ChildFetal Neonatal Ed 2004;89:F156—60.90. Stockinger ZT, McSwain Jr NE. Prehospital endotrachealintubation for trauma does not improve survival over bagvalve-maskventilation. J Trauma 2004;56:531—6.91. Pitetti R, Glustein JZ, Bhende MS. Prehospital care and outcomeof pediatric out-of-hospital cardiac arrest. PrehospEmerg Care 2002;6:283—90.92. Cooper A, DiScala C, Foltin G, Tunik M, Markenson D,Welborn C. Prehospital endotracheal intubation for severehead injury in children: a reappraisal. Semin Pediatr Surg2001;10:3—6.93. Bhende MS, Thompson AE, Cook DR, Saville AL. Validity of adisposable end-tidal CO 2 detector in verifying endotrachealD. Biarent et al.tube placement in infants and children. Ann Emerg Med1992;21:142—5.94. Bhende MS, Thompson AE, Orr RA. Utility of an end-tidalcarbon dioxide detector during stabilization and transportof critically ill children. Pediatrics 1992;89(pt 1):1042—4.95. Bhende MS, LaCovey DC. End-tidal carbon dioxide monitoringin the prehospital setting. Prehosp Emerg Care2001;5:208—13.96. Ornato JP, Shipley JB, Racht EM, et al. Multicenter study ofa portable, hand-size, colorimetric end-tidal carbon dioxidedetection device. Ann Emerg Med 1992;21:518—23.97. Gonzalez del Rey JA, Poirier MP, Digiulio GA. Evaluationof an ambu-bag valve with a self-contained, colorimetricend-tidal CO 2 system in the detection of airway mishaps:an animal trial. Pediatr Emerg Care 2000;16:121—3.98. Bhende MS, Thompson AE. Evaluation of an end-tidal CO 2detector during pediatric cardiopulmonary resuscitation.Pediatrics 1995;95:395—9.99. Bhende MS, Karasic DG, Karasic RB. End-tidal carbon dioxidechanges during cardiopulmonary resuscitation afterexperimental asphyxial cardiac arrest. Am J Emerg Med1996;14:349—50.100. DeBehnke DJ, Hilander SJ, Dobler DW, Wickman LL, SwartGL. The hemodynamic and arterial blood gas response toasphyxiation: a canine model of pulseless electrical activity.Resuscitation 1995;30:169—75.101. Ornato JP, Garnett AR, Glauser FL. Relationship betweencardiac output and the end-tidal carbon dioxide tension.Ann Emerg Med 1990;19:1104—6.102. Sharieff GQ, Rodarte A, Wilton N, Silva PD, Bleyle D. Theself-inflating bulb as an esophageal detector device in childrenweighing more than twenty kilograms: a comparisonof two techniques. Ann Emerg Med 2003;41:623—9.103. Sharieff GQ, Rodarte A, Wilton N, Bleyle D. The selfinflatingbulb as an airway adjunct: is it reliable in childrenweighing less than 20 kilograms? Acad Emerg Med2003;10:303—8.104. Poirier MP, Gonzalez Del-Rey JA, McAneney CM, DiGiulio GA.Utility of monitoring capnography, pulse oximetry, and vitalsigns in the detection of airway mishaps: a hyperoxemicanimal model. Am J Emerg Med 1998;16:350—2.105. Lillis KA, Jaffe DM. Prehospital intravenous access in children.Ann Emerg Med 1992;21:1430—4.106. Kanter RK, Zimmerman JJ, Strauss RH, Stoeckel KA. Pediatricemergency intravenous access. Evaluation of a protocol.Am J Dis Child 1986;140:132—4.107. Banerjee S, Singhi SC, Singh S, Singh M. The intraosseousroute is a suitable alternative to intravenous route for fluidresuscitation in severely dehydrated children. Indian Pediatr1994;31:1511—20.108. Glaeser PW, Hellmich TR, Szewczuga D, Losek JD, Smith DS.Five-year experience in prehospital intraosseous infusionsin children and adults. Ann Emerg Med 1993;22:1119—24.109. Guy J, Haley K, Zuspan SJ. Use of intraosseous infusionin the pediatric trauma patient. J Pediatr Surg1993;28:158—61.110. Orlowski JP, Julius CJ, Petras RE, Porembka DT, GallagherJM. The safety of intraosseous infusions: risks offat and bone marrow emboli to the lungs. Ann Emerg Med1989;18:1062—7.111. Orlowski JP, Porembka DT, Gallagher JM, Lockrem JD, Van-Lente F. Comparison study of intraosseous, central intravenous,and peripheral intravenous infusions of emergencydrugs. Am J Dis Child 1990;144:112—7.112. Abe KK, Blum GT, Yamamoto LG. Intraosseous is fasterand easier than umbilical venous catheterization in new-

European Resuscitation Council Guidelines for Resuscitation 2005S127born emergency vascular access models. Am J Emerg Med2000;18:126—9.113. Ellemunter H, Simma B, Trawoger R, Maurer H. Intraosseouslines in preterm and full term neonates. Arch Dis Child FetalNeonatal Ed 1999;80:F74—5.114. Cameron JL, Fontanarosa PB, Passalaqua AM. A comparativestudy of peripheral to central circulation deliverytimes between intraosseous and intravenous injection usinga radionuclide technique in normovolemic and hypovolemiccanines. J Emerg Med 1989;7:123—7.115. Warren DW, Kissoon N, Sommerauer JF, Rieder MJ. Comparisonof fluid infusion rates among peripheral intravenous andhumerus, femur, malleolus, and tibial intraosseous sitesin normovolemic and hypovolemic piglets. Ann Emerg Med1993;22:183—6.116. Brickman KR, Krupp K, Rega P, Alexander J, Guinness M.Typing and screening of blood from intraosseous access.Ann Emerg Med 1992;21:414—7.117. Johnson L, Kissoon N, Fiallos M, Abdelmoneim T, MurphyS. Use of intraosseous blood to assess blood chemistriesand hemoglobin during cardiopulmonary resuscitation withdrug infusions. Crit Care Med 1999;27:1147—52.118. Ummenhofer W, Frei FJ, Urwyler A, Drewe J. Are laboratoryvalues in bone marrow aspirate predictable for venousblood in paediatric patients? Resuscitation 1994;27:123—8.119. Kissoon N, Idris A, Wenzel V, Murphy S, Rush W. Intraosseousand central venous blood acid—base relationship duringcardiopulmonary resuscitation. Pediatr Emerg Care1997;13:250—3.120. Abdelmoneim T, Kissoon N, Johnson L, Fiallos M, MurphyS. Acid-base status of blood from intraosseous andmixed venous sites during prolonged cardiopulmonaryresuscitation and drug infusions. Crit Care Med 1999;27:1923—8.121. Venkataraman ST, Orr RA, Thompson AE. Percutaneous infraclavicularsubclavian vein catheterization in critically illinfants and children. J Pediatr 1988;113:480—5.122. Fleisher G, Caputo G, Baskin M. Comparison of externaljugular and peripheral venous administration of sodiumbicarbonate in puppies. Crit Care Med 1989;17:251—4.123. Hedges JR, Barsan WB, Doan LA, et al. Central versusperipheral intravenous routes in cardiopulmonary resuscitation.Am J Emerg Med 1984;2:385—90.124. Neufeld JD, Marx JA, Moore EE, Light AI. Comparison ofintraosseous, central, and peripheral routes of crystalloidinfusion for resuscitation of hemorrhagic shock in a swinemodel. J Trauma 1993;34:422—8.125. Stenzel JP, Green TP, Fuhrman BP, Carlson PE, MarchessaultRP. Percutaneous femoral venous catheterizations:a prospective study of complications. J Pediatr1989;114:411—5.126. Kleinman ME, Oh W, Stonestreet BS. Comparison of intravenousand endotracheal epinephrine during cardiopulmonaryresuscitation in newborn piglets. Crit Care Med1999;27:2748—54.127. Efrati O, Ben-Abraham R, Barak A, et al. Endobronchialadrenaline: should it be reconsidered? Doseresponse and haemodynamic effect in dogs. Resuscitation2003;59:117—22.128. Howard RF, Bingham RM. Endotracheal compared withintravenous administration of atropine. Arch Dis Child1990;65:449—50.129. Prengel AW, Lindner KH, Hahnel J, Ahnefeld FW. Endotrachealand endobronchial lidocaine administration: effectson plasma lidocaine concentration and blood gases. CritCare Med 1991;19:911—5.130. Crespo SG, Schoffstall JM, Fuhs LR, Spivey WH. Comparisonof two doses of endotracheal epinephrine in a cardiacarrest model. Ann Emerg Med 1991;20:230—4.131. Lee PL, Chung YT, Lee BY, Yeh CY, Lin SY, Chao CC. Theoptimal dose of atropine via the endotracheal route. MaZui Xue Za Zhi 1989;27:35—8.132. Hahnel JH, Lindner KH, Schurmann C, Prengel A, AhnefeldFW. Plasma lidocaine levels and PaO 2 with endobronchialadministration: dilution with normal saline or distilledwater? Ann Emerg Med 1990;19:1314—7.133. Jasani MS, Nadkarni VM, Finkelstein MS, Mandell GA,Salzman SK, Norman ME. Effects of different techniquesof endotracheal epinephrine administration in pediatricporcine hypoxic-hypercarbic cardiopulmonary arrest. CritCare Med 1994;22:1174—80.134. Steinfath M, Scholz J, Schulte am Esch J, Laer S, ReymannA, Scholz H. The technique of endobronchial lidocaineadministration does not influence plasma concentrationprofiles and pharmacokinetic parameters in humans. Resuscitation1995;29:55—62.135. Carcillo JA, Fields AI. Clinical practice parameters forhemodynamic support of pediatric and neonatal patientsin septic shock. Crit Care Med 2002;30:1365—78.136. Simma B, Burger R, Falk M, Sacher P, Fanconi S. A prospective,randomized, and controlled study of fluid managementin children with severe head injury: lactatedRinger’s solution versus hypertonic saline. Crit Care Med1998;26:1265—70.137. Rocha e Silva M. Hypertonic saline resuscitation. Medicina(B Aries) 1998; 58:393-402.138. Katz LM, Wang Y, Ebmeyer U, Radovsky A, Safar P. Glucoseplus insulin infusion improves cerebral outcome afterasphyxial cardiac arrest. Neuroreport 1998;9:3363—7.139. Longstreth Jr WT, Copass MK, Dennis LK, Rauch-MatthewsME, Stark MS, Cobb LA. Intravenous glucose after out-ofhospitalcardiopulmonary arrest: a community-based randomizedtrial. Neurology 1993;43:2534—41.140. Chang YS, Park WS, Ko SY, et al. Effects of fastingand insulin-induced hypoglycemia on brain cell membranefunction and energy metabolism during hypoxia-ischemiain newborn piglets. Brain Res 1999;844:135—42.141. Cherian L, Goodman JC, Robertson CS. Hyperglycemiaincreases brain injury caused by secondary ischemiaafter cortical impact injury in rats. Crit Care Med1997;25:1378—83.142. Paul T, Bertram H, Bokenkamp R, Hausdorf G. Supraventriculartachycardia in infants, children and adolescents:diagnosis, and pharmacological and interventional therapy.Paediatr Drugs 2000;2:171—81.143. Losek JD, Endom E, Dietrich A, Stewart G, Zempsky W,Smith K. Adenosine and pediatric supraventricular tachycardiain the emergency department: multicenter studyand review. Ann Emerg Med 1999;33:185—91.144. Roberts JR, Greenburg MI, Knaub M, Baskin SI. Comparisonof the pharmacological effects of epinephrine administeredby the intravenous and endotracheal routes. JACEP1978;7:260—4.145. Zaritsky A. Pediatric resuscitation pharmacology. Membersof the Medications in Pediatric Resuscitation Panel. AnnEmerg Med 1993;22(pt 2):445—55.146. Manisterski Y, Vaknin Z, Ben-Abraham R, et al. Endotrachealepinephrine: a call for larger doses. Anesth Analg2002;95:1037—41 [table of contents].147. Patterson MD, Boenning DA, Klein BL, et al. The use ofhigh-dose epinephrine for patients with out-of-hospitalcardiopulmonary arrest refractory to prehospital interventions.Pediatr Emerg Care 2005;21:227—37.

S128148. Perondi MB, Reis AG, Paiva EF, Nadkarni VM, Berg RA. Acomparison of high-dose and standard-dose epinephrinein children with cardiac arrest. N Engl J Med 2004;350:1722—30.149. Carpenter TC, Stenmark KR. High-dose epinephrineis not superior to standard-dose epinephrine in pediatricin-hospital cardiopulmonary arrest. Pediatrics1997;99:403—8.150. Dieckmann R, Vardis R. High-dose epinephrine in pediatricout-of-hospital cardiopulmonary arrest. Pediatrics1995;95:901—13.151. Berg RA, Otto CW, Kern KB, et al. High-dose epinephrineresults in greater early mortality after resuscitation fromprolonged cardiac arrest in pigs: a prospective, randomizedstudy. Crit Care Med 1994;22:282—90.152. Rubertsson S, Wiklund L. Hemodynamic effects ofepinephrine in combination with different alkaline buffersduring experimental, open-chest, cardiopulmonary resuscitation.Crit Care Med 1993;21:1051—7.153. Somberg JC, Timar S, Bailin SJ, et al. Lack of a hypotensiveeffect with rapid administration of a new aqueousformulation of intravenous amiodarone. Am J Cardiol2004;93:576—81.154. Yap S-C, Hoomtje T, Sreeram N. Polymorphic ventriculartachycardia after use of intravenous amiodarone forpostoperative junctional ectopic tachycardia. Int J Cardiol2000;76:245—7.155. Dauchot P, Gravenstein JS. Effects of atropine on the electrocardiogramin different age groups. Clin Pharmacol Ther1971;12:274—80.156. Stulz PM, Scheidegger D, Drop LJ, Lowenstein E, Laver MB.Ventricular pump performance during hypocalcemia: clinicaland experimental studies. J Thorac Cardiovasc Surg1979;78:185—94.157. van Walraven C, Stiell IG, Wells GA, Hebert PC, VandemheenK, The OTAC Study Group. Do advanced cardiaclife support drugs increase resuscitation rates from inhospitalcardiac arrest? Ann Emerg Med 1998;32:544—53.158. Paraskos JA. Cardiovascular pharmacology III: atropine,calcium, calcium blockers, and (beta)-blockers. Circulation1986;74:IV-86—9.159. Stueven HA, Thompson B, Aprahamian C, Tonsfeldt DJ,Kastenson EH. The effectiveness of calcium chloride inrefractory electromechanical dissociation. Ann Emerg Med1985;14:626—9.160. Stueven HA, Thompson B, Aprahamian C, Tonsfeldt DJ, KastensonEH. Lack of effectiveness of calcium chloride inrefractory asystole. Ann Emerg Med 1985;14:630—2.161. Srinivasan V, Spinella PC, Drott HR, Roth CL, Helfaer MA,Nadkarni V. Association of timing, duration, and intensityof hyperglycemia with intensive care unit mortality in criticallyill children. Pediatr Crit Care Med 2004;5:329—36.162. Krinsley JS. Effect of an intensive glucose management protocolon the mortality of critically ill adult patients. MayoClin Proc 2004;79:992—1000.163. Losek JD. Hypoglycemia and the ABC’S (sugar) of pediatricresuscitation. Ann Emerg Med 2000;35:43—6.164. Finney SJ, Zekveld C, Elia A, Evans TW. Glucose control andmortality in critically ill patients. Jama 2003;290:2041—7.165. Allegra J, Lavery R, Cody R, et al. Magnesium sulfate inthe treatment of refractory ventricular fibrillation in theprehospital setting. Resuscitation 2001;49:245—9.166. Tzivoni D, Banai S, Schuger C, et al. Treatment oftorsade de pointes with magnesium sulfate. Circulation1988;77:392—7.167. Lokesh L, Kumar P, Murki S, Narang A. A randomizedcontrolled trial of sodium bicarbonate in neonatalD. Biarent et al.resuscitation-effect on immediate outcome. Resuscitation2004;60:219—23.168. Bar-Joseph G, Abramson NS, Kelsey SF, Mashiach T, CraigMT, Safar P. Improved resuscitation outcome in emergencymedical systems with increased usage of sodium bicarbonateduring cardiopulmonary resuscitation. Acta AnaesthesiolScand 2005;49:6—15.169. Dorian P, Cass D, Schwartz B, Cooper R, GelaznikasR, Barr A. Amiodarone as compared with lidocaine forshock-resistant ventricular fibrillation. N Engl J Med2002;346:884—90.170. Walsh EP, Saul JP, Sholler GF, et al. Evaluation of a stagedtreatment protocol for rapid automatic junctional tachycardiaafter operation for congenital heart disease. J AmColl Cardiol 1997;29:1046—53.171. Wang L. Congenital long QT syndrome: 50 years of electrophysiologicalresearch from cell to bedside. Acta Cardiologica2003;58:133—8.172. Singh BN, Kehoe R, Woosley RL, Scheinman M, QuartB, Sotalol Multicenter Study Group. Multicenter trial ofsotalol compared with procainamide in the suppression ofinducible ventricular tachycardia: a double-blind, randomizedparallel evaluation. Am Heart J 1995;129:87—97.173. Luedtke SA, Kuhn RJ, McCaffrey FM. Pharmacologic managementof supraventricular tachycardias in children, part2: atrial flutter, atrial fibrillation, and junctional and atrialectopic tachycardia. Ann Pharmacother 1997;31:1347—59.174. Luedtke SA, Kuhn RJ, McCaffrey FM. Pharmacologic managementof supraventricular tachycardias in children. Part1: Wolff-Parkinson-White and atrioventricular nodal reentry.Ann Pharmacother 1997;31:1227—43.175. Mandapati R, Byrum CJ, Kavey RE, et al. Procainamide forrate control of postsurgical junctional tachycardia. PediatrCardiol 2000;21:123—8.176. Wang JN, Wu JM, Tsai YC, Lin CS. Ectopic atrial tachycardiain children. J Formos Med Assoc 2000;99:766—70.177. Holmes CL, Landry DW, Granton JT. Science review: Vasopressinand the cardiovascular system part 1—–receptorphysiology. Crit Care 2003;7:427—34.178. Voelckel WG, Lurie KG, McKnite S, et al. Effects ofepinephrine and vasopressin in a piglet model of prolongedventricular fibrillation and cardiopulmonary resuscitation.Crit Care Med 2002;30:957—62.179. Voelckel WG, Lurie KG, McKnite S, et al. Comparison ofepinephrine and vasopressin in a pediatric porcine modelof asphyxial cardiac arrest. Crit Care Med 2000;28:3777—83.180. Mann K, Berg RA, Nadkarni V. Beneficial effects of vasopressinin prolonged pediatric cardiac arrest: a case series.Resuscitation 2002;52:149—56.181. Atkins DL, Kerber RE. Pediatric defibrillation: current flowis improved by using ‘‘adult’’ electrode paddles. Pediatrics1994;94:90—3.182. Atkins DL, Sirna S, Kieso R, Charbonnier F, Kerber RE. Pediatricdefibrillation: importance of paddle size in determiningtransthoracic impedance. Pediatrics 1988;82:914—8.183. Bennetts SH, Deakin CD, Petley GW, Clewlow F. Is optimalpaddle force applied during paediatric external defibrillation?Resuscitation 2004;60:29—32.184. Deakin C, Bennetts S, Petley G, Clewlow F. What is the optimalpaddle force for paediatric defibrillation? Resuscitation2002;55:59.185. Atkins DL, Hartley LL, York DK. Accurate recognition andeffective treatment of ventricular fibrillation by automatedexternal defibrillators in adolescents. Pediatrics1998;101(pt 1):393—7.

European Resuscitation Council Guidelines for Resuscitation 2005S129186. Pierpont GL, Kruse JA, Nelson DH. Intra-arterial monitoringduring cardiopulmonary resuscitation. Cathet CardiovascDiagn 1985;11:513—20.187. Zaritsky A, Nadkarni V, Getson P, Kuehl K. CPR in children.Ann Emerg Med 1987;16:1107—11.188. Mogayzel C, Quan L, Graves JR, Tiedeman D, FahrenbruchC, Herndon P. Out-of-hospital ventricular fibrillation in childrenand adolescents: causes and outcomes. Ann EmergMed 1995;25:484—91.189. Herlitz J, Engdahl J, Svensson L, Young M, Angquist KA,Holmberg S. Characteristics and outcome among childrensuffering from out of hospital cardiac arrest in Sweden.Resuscitation 2005;64:37—40.190. Berg RA. Role of mouth-to-mouth rescue breathing inbystander cardiopulmonary resuscitation for asphyxial cardiacarrest. Crit Care Med 2000;28(Suppl.):N193—5.191. Appleton GO, Cummins RO, Larson MP, Graves JR. CPRand the single rescuer: at what age should you ‘‘callfirst’’ rather than ‘‘call fast’’? Ann Emerg Med 1995;25:492—4.192. Larsen MP, Eisenberg MS, Cummins RO, Hallstrom AP.Predicting survival from out-of-hospital cardiac arrest: agraphic model. Ann Emerg Med 1993;22:1652—8.193. Cobb LA, Fahrenbruch CE, Walsh TR, et al. Influenceof cardiopulmonary resuscitation prior to defibrillation inpatients with out-of-hospital ventricular fibrillation. JAMA1999;281:1182—8.194. Wik L, Hansen TB, Fylling F, et al. Delaying defibrillation togive basic cardiopulmonary resuscitation to patients without-of-hospital ventricular fibrillation: a randomized trial.JAMA 2003;289:1389—95.195. Jacobs IG, Finn JC, Oxer HF, Jelinek GA. CPR before defibrillationin out-of-hospital cardiac arrest: a randomized trial.Emerg Med Australas 2005;17:39—45.196. Somberg JC, Bailin SJ, Haffajee CI, et al. Intravenous lidocaineversus intravenous amiodarone (in a new aqueousformulation) for incessant ventricular tachycardia. Am JCardiol 2002;90:853—9.197. Kudenchuk PJ, Cobb LA, Copass MK, et al. Amiodaronefor resuscitation after out-of-hospital cardiac arrest dueto ventricular fibrillation. N Engl J Med 1999;341:871—8.198. Perry JC, Fenrich AL, Hulse JE, Triedman JK, Friedman RA,Lamberti JJ. Pediatric use of intravenous amiodarone: efficacyand safety in critically ill patients from a multicenterprotocol. J Am Coll Cardiol 1996;27:1246—50.199. Cummins RO, Graves JR, Larsen MP, et al. Out-of-hospitaltranscutaneous pacing by emergency medical techniciansin patients with asystolic cardiac arrest. N Engl J Med1993;328:1377—82.200. Sreeram N, Wren C. Supraventricular tachycardia ininfants: response to initial treatment. Arch Dis Child1990;65:127—9.201. Bianconi L, Castro AMD, Dinelli M, et al. Comparison ofintravenously administered dofetilide versus amiodaronein the acute termination of atrial fibrillation and flutter.A multicentre, randomized, double-blind, placebocontrolledstudy. Eur Heart J 2000;21:1265—73.202. Burri S, Hug MI, Bauersfeld U. Efficacy and safety of intravenousamiodarone for incessant tachycardias in infants.Eur J Pediatr 2003;162:880—4.203. Celiker A, Ceviz N, Ozme S. Effectiveness and safety ofintravenous amiodarone in drug-resistant tachyarrhythmiasof children. Acta Paediatrica Japonica 1998;40:567—72.204. Dodge-Khatami A, Miller O, Anderson R, Gil-Jaurena J,Goldman A, de Leval M. Impact of junctional ectopictachycardia on postoperative morbidity following repairof congenital heart defects. Eur J Cardio-Thoracic Surg2002;21:255—9.205. Figa FH, Gow RM, Hamilton RM, Freedom RM. Clinical efficacyand safety of intravenous Amiodarone in infants andchildren. Am J Cardiol 1994;74:573—7.206. Hoffman TM, Bush DM, Wernovsky G, et al. Postoperativejunctional ectopic tachycardia in children: incidence,risk factors, and treatment. Ann Thorac Surg 2002;74:1607—11.207. Soult JA, Munoz M, Lopez JD, Romero A, Santos J, TovaruelaA. Efficacy and safety of intravenous amiodarone for shorttermtreatment of paroxysmal supraventricular tachycardiain children. Pediatr Cardiol 1995;16:16—9.208. Benson Jr D, Smith W, Dunnigan A, Sterba R, Gallagher J.Mechanisms of regular wide QRS tachycardia in infants andchildren. Am J Cardiol 1982;49:1778—88.209. Drago F, Mazza A, Guccione P, Mafrici A, Di Liso G, RagoneseP. Amiodarone used alone or in combination with propranolol:a very effective therapy for tachyarrhythmias ininfants and children. Pediatr Cardiol 1998;19:445—9.210. Benson DJ, Dunnigan A, Green T, Benditt D, Schneider S.Periodic procainamide for paroxysmal tachycardia. Circulation1985;72:147—52.211. Komatsu C, Ishinaga T, Tateishi O, Tokuhisa Y, YoshimuraS. Effects of four antiarrhythmic drugs on the inductionand termination of paroxysmal supraventricular tachycardia.Jpn Circ J 1986;50:961—72.212. Mandel WJ, Laks MM, Obayashi K, Hayakawa H, DaleyW. The Wolff-Parkinson-White syndrome: pharmacologiceffects of procaine amide. Am Heart J 1975;90:744—54.213. Meldon SW, Brady WJ, Berger S, Mannenbach M. Pediatricventricular tachycardia: a review with three illustrativecases. Pediatr Emerg Care 1994;10:294—300.214. Shih JY, Gillette PC, Kugler JD, et al. The electrophysiologiceffects of procainamide in the immature heart. PediatrPharmacol (New York) 1982;2:65—73.215. Hildebrand CA, Hartmann AG, Arcinue EL, Gomez RJ, BingRJ. Cardiac performance in pediatric near-drowning. CritCare Med 1988;16:331—5.216. Checchia PA, Sehra R, Moynihan J, Daher N, Tang W, WeilMH. Myocardial injury in children following resuscitationafter cardiac arrest. Resuscitation 2003;57:131—7.217. Hickey RW, Ferimer H, Alexander HL, et al. Delayed,spontaneous hypothermia reduces neuronal damageafter asphyxial cardiac arrest in rats. Crit Care Med2000;28:3511—6.218. Hypothermia After Cardiac Arrest Study Aroup. Mild therapeutichypothermia to improve the neurologic outcomeafter cardiac arrest. N Engl J Med 2002;346:549—56.219. Bernard SA, Gray TW, Buist MD, et al. Treatment ofcomatose survivors of out-of-hospital cardiac arrest withinduced hypothermia. N Engl J Med 2002;346:557—63.220. Gluckman PD, Wyatt JS, Azzopardi D, et al. Selectivehead cooling with mild systemic hypothermia after neonatalencephalopathy: multicentre randomised trial. Lancet2005;365:663—70.221. Battin MR, Penrice J, Gunn TR, Gunn AJ. Treatment ofterm infants with head cooling and mild systemic hypothermia(35.0 degrees C and 34.5 degrees C) after perinatalasphyxia. Pediatrics 2003;111:244—51.222. Compagnoni G, Pogliani L, Lista G, Castoldi F, FontanaP, Mosca F. Hypothermia reduces neurological damagein asphyxiated newborn infants. Biol Neonate 2002;82:222—7.223. Gunn AJ, Gluckman PD, Gunn TR. Selective head coolingin newborn infants after perinatal asphyxia: a safety study.Pediatrics 1998;102:885—92.

S130224. Debillon T, Daoud P, Durand P, et al. Whole-body coolingafter perinatal asphyxia: a pilot study in term neonates.Dev Med Child Neurol 2003;45:17—23.225. Hachimi-Idrissi S, Corne L, Ebinger G, Michotte Y, HuyghensL. Mild hypothermia induced by a helmet device: a clinicalfeasibility study. Resuscitation 2001;51:275—81.226. Bernard S, Buist M, Monteiro O, Smith K. Induced hypothermiausing large volume, ice-cold intravenous fluid incomatose survivors of out-of-hospital cardiac arrest: a preliminaryreport. Resuscitation 2003;56:9—13.227. Kliegel A, Losert H, Sterz F, et al. Cold simple intravenousinfusions preceding special endovascular cooling for fasterinduction of mild hypothermia after cardiac arrest—–a feasibilitystudy. Resuscitation 2005;64:347—51.228. Polderman KH, Peerdeman SM, Girbes AR. Hypophosphatemiaand hypomagnesemia induced by coolingin patients with severe head injury. J Neurosurg2001;94:697—705.229. Polderman KH. Application of therapeutic hypothermia inthe intensive care unit. Opportunities and pitfalls of apromising treatment modality—–Part 2. Practical aspectsand side effects. Intensive Care Med 2004;30:757—69.230. Zeiner A, Holzer M, Sterz F, et al. Hyperthermia after cardiacarrest is associated with an unfavorable neurologicoutcome. Arch Intern Med 2001;161:2007—12.231. Takino M, Okada Y. Hyperthermia following cardiopulmonaryresuscitation. Intensive Care Med 1991;17:419—20.232. Takasu A, Saitoh D, Kaneko N, Sakamoto T, Okada Y. Hyperthermia:is it an ominous sign after cardiac arrest? Resuscitation2001;49:273—7.233. Coimbra C, Boris-Moller F, Drake M, Wieloch T. Diminishedneuronal damage in the rat brain by late treatment withthe antipyretic drug dipyrone or cooling following cerebralischemia. Acta Neuropathol (Berl) 1996;92:447—53.234. Coimbra C, Drake M, Boris-Moller F, Wieloch T. Long-lastingneuroprotective effect of postischemic hypothermia andtreatment with an anti-inflammatory/antipyretic drug: evidencefor chronic encephalopathic processes followingischemia. Stroke 1996;27:1578—85.235. Gillis J, Dickson D, Rieder M, Steward D, Edmonds J.Results of inpatient pediatric resuscitation. Crit Care Med1986;14:469—71.236. Schindler MB, Bohn D, Cox PN, et al. Outcome of out-ofhospitalcardiac or respiratory arrest in children. N Engl JMed 1996;335:1473—9.237. Suominen P, Korpela R, Kuisma M, Silfvast T, Olkkola KT.Paediatric cardiac arrest and resuscitation provided byphysician-staffed emergency care units. Acta AnaesthesiolScand 1997;41:260—5.238. Lopez-Herce J, Garcia C, Rodriguez-Nunez A, et al. Longtermoutcome of paediatric cardiorespiratory arrest inSpain. Resuscitation 2005;64:79—85.239. Lopez-Herce J, Garcia C, Dominguez P, et al. Characteristicsand outcome of cardiorespiratory arrest in children.Resuscitation 2004;63:311—20.240. Hazinski MF, Chahine AA, Holcomb III GW, Morris Jr JA. Outcomeof cardiovascular collapse in pediatric blunt trauma.Ann Emerg Med 1994;23:1229—35.241. Morris MC, Wernovsky G, Nadkarni VM. Survival outcomesafter extracorporeal cardiopulmonary resuscitation institutedduring active chest compressions following refractoryin-hospital pediatric cardiac arrest. Pediatr Crit Care Med2004;5:440—6.242. Duncan BW, Ibrahim AE, Hraska V, et al. Use of rapiddeploymentextracorporeal membrane oxygenation for theresuscitation of pediatric patients with heart disease aftercardiac arrest. J Thorac Cardiovasc Surg 1998;116:305—11.D. Biarent et al.243. Parra DA, Totapally BR, Zahn E, et al. Outcome of cardiopulmonaryresuscitation in a pediatric cardiac intensive careunit. Crit Care Med 2000;28:3296—300.244. Idris AH, Berg RA, Bierens J, et al. Recommended guidelinesfor uniform reporting of data from drowning: the ‘‘Utsteinstyle’’. Resuscitation 2003;59:45—57.245. Bauchner H, Waring C, Vinci R. Parental presence duringprocedures in an emergency room: results from 50 observations.Pediatrics 1991;87:544—8.246. Bauchner H, Vinci R, Waring C. Pediatric procedures: doparents want to watch? Pediatrics 1989;84:907—9 [comment].247. Bauchner H, Zuckerman B. Cocaine, sudden infantdeath syndrome, and home monitoring. J Pediatr1990;117:904—6.248. Haimi-Cohen Y, Amir J, Harel L, Straussberg R, VarsanoY. Parental presence during lumbar puncture: anxietyand attitude toward the procedure. Clin Pediatr (Phila)1996;35:2—4.249. Sacchetti A, Lichenstein R, Carraccio CA, Harris RH. Familymember presence during pediatric emergency departmentprocedures. Pediatr Emerg Care 1996;12:268—71.250. Boie ET, Moore GP, Brummett C, Nelson DR. Do parentswant to be present during invasive procedures performedon their children in the emergency department? A surveyof 400 parents. Ann Emerg Med 1999;34:70—4.251. Taylor N, Bonilla L, Silver P, Sagy M. Pediatric procedure: doparents want to be present? Crit Care Med 1996;24:A131.252. Powers KS, Rubenstein JS. Family presence during invasiveprocedures in the pediatric intensive care unit: a prospectivestudy. Arch Pediatr Adolesc Med 1999;153:955—8.253. Cameron JA, Bond MJ, Pointer SC. Reducing the anxietyof children undergoing surgery: parental presenceduring anaesthetic induction. J Paediatr Child Health1996;32:51—6.254. Merritt KA, Sargent JR, Osborn LM. Attitudes regardingparental presence during medical procedures. Am J DisChild 1990;144:270—1.255. Wolfram RW, Turner ED. Effects of parental presence duringchildren’s venipuncture. Acad Emerg Med 1996;3:58—64.256. Jarvis AS. Parental presence during resuscitation: attitudesof staff on a paediatric intensive care unit. Intensive CritCare Nurs 1998;14:3—7.257. Meyers TA, Eichhorn DJ, Guzzetta CE. Do families want tobe present during CPR? A retrospective survey. J Emerg Nurs1998;24:400—5.258. Doyle CJ, Post H, Burney RE, Maino J, Keefe M, Rhee KJ.Family participation during resuscitation: an option. AnnEmerg Med 1987;16:673—5.259. Hanson C, Strawser D. Family presence during cardiopulmonaryresuscitation: Foote Hospital emergencydepartment’s nine-year perspective. J Emerg Nurs1992;18:104—6.260. Robinson SM, Mackenzie-Ross S, Campbell Hewson GL, EglestonCV, Prevost AT. Psychological effect of witnessed resuscitationon bereaved relatives. Lancet 1998;352:614—7.261. Meyers TA, Eichhorn DJ, Guzzetta CE, et al. Family presenceduring invasive procedures and resuscitation. Am JNurs 2000;100:32—42 [quiz 3].262. Beckman AW, Sloan BK, Moore GP, et al. Should parentsbe present during emergency department procedures onchildren, and who should make that decision? A survey ofemergency physician and nurse attitudes. Acad Emerg Med2002;9:154—8.263. Eppich WJ, Arnold LD. Family member presence inthe pediatric emergency department. Curr Opin Pediatr2003;15:294—8.

European Resuscitation Council Guidelines for Resuscitation 2005S131264. Eichhorn DJ, Meyers TA, Mitchell TG, Guzzetta CE. Openingthe doors: family presence during resuscitation. J CardiovascNurs 1996;10:59—70.265. International Liaison Committee on Resuscitation. Part7. Neonatal Life Support. 2005 International Consensuson Cardiopulmonary Resuscitation and Emergency CardiovascularCare Science with Treatment Recommendations.Resuscitation 2005;67:293—303.266. Resuscitation Council (UK). Resuscitation at birth. Newbornlife support course provider manual. London, ResuscitationCouncil (UK); 2001.267. Niermeyer S, Kattwinkel J, Van Reempts P, et al. InternationalGuidelines for Neonatal Resuscitation: an excerptfrom the Guidelines 2000 for Cardiopulmonary Resuscitationand Emergency Cardiovascular Care: InternationalConsensus on Science. Contributors and Reviewersfor the Neonatal Resuscitation Guidelines. PediatricsE2000;106:29.268. Palme-Kilander C. Methods of resuscitation in low-Apgarscorenewborn infants—–a national survey. Acta Paediatr1992;81:739—44.269. British Paediatric Association Working Party. NeonatalResuscitation. London: British Paediatric Association; 1993.270. Dahm LS, James LS. Newborn temperature and calculatedheat loss in the delivery room. Pediatrics 1972;49:504—13.271. Stephenson J, Du J, Tk O. The effect if cooling on blood gastensions in newborn infants. J Pediatr 1970;76:848—52.272. Gandy GM, Adamsons Jr K, Cunningham N, Silverman WA,James LS. Thermal environment and acid—base homeostasisin human infants during the first few hours of life. J ClinInvest 1964;43:751—8.273. Apgar V. A proposal for a new method of evaluation of thenewborn infant. Curr Res Anesth Analg 1953:32.274. Anonymous. Is the Apgar score outmoded? Lancet1989;i:591—2.275. Chamberlain G, Banks J. Assessment of the Apgar score.Lancet 1974;2:1225—8.276. Owen CJ, Wyllie JP. Determination of heart rate in the babyat birth. Resuscitation 2004;60:213—7.277. Cordero Jr L, Hon EH. Neonatal bradycardia followingnasopharyngeal stimulation. J Pediatr 1971;78:441—7.278. Thaler MM, Stobie GH. An improved technique of externalcaridac compression in infants and young children. N EnglJ Med 1963;269:606—10.279. Todres ID, Rogers MC. Methods of external cardiac massagein the newborn infant. J Pediatr 1975;86:781—2.280. Dean JM, Koehler RC, Schleien CL, et al. Improved bloodflow during prolonged cardiopulmonary resuscitation with30% duty cycle in infant pigs. Circulation 1991;84:896—904.281. Whyte SD, Sinha AK, Wyllie JP. Neonatal resuscitation: apractical assessment. Resuscitation 1999;40:21—5.282. Costeloe K, Hennessy E, Gibson AT, Marlow N, WilkinsonAR. The EPICure study: outcomes to discharge from hospitalfor infants born at the threshold of viability. Pediatrics2000;106:659—71.283. Vohra S, Frent G, Campbell V, Abbott M, Whyte R. Effect ofpolyethylene occlusive skin wrapping on heat loss in verylow birth weight infants at delivery: a randomized trial. JPediatr 1999;134:547—51.284. Lenclen R, Mazraani M, Jugie M, et al. Use of a polyethylenebag: a way to improve the thermal environment ofthe premature newborn at the delivery room. Arch Pediatr2002;9:238—44.285. Bjorklund LJ, Hellstrom-Westas L. Reducing heat loss atbirth in very preterm infants. J Pediatr 2000;137:739—40.286. Vohra S, Roberts RS, Zhang B, Janes M, Schmidt B. Heatloss prevention (HeLP) in the delivery room: a randomizedcontrolled trial of polyethylene occlusive skin wrapping invery preterm infants. J Pediatr 2004;145:750—3.287. Lieberman E, Eichenwald E, Mathur G, Richardson D,Heffner L, Cohen A. Intrapartum fever and unexplainedseizures in term infants. Pediatrics 2000;106:983—8.288. Grether JK, Nelson KB. Maternal infection and cerebralpalsy in infants of normal birth weight. JAMA1997;278:207—11.289. Dietrich WD, Alonso O, Halley M, Busto R. Delayed posttraumaticbrain hyperthermia worsens outcome after fluid percussionbrain injury: a light and electron microscopic studyin rats. Neurosurgery 1996;38:533—41 [discussion 41].290. Wiswell TE, Gannon CM, Jacob J, et al. Delivery roommanagement of the apparently vigorous meconium-stainedneonate: results of the multicenter, international collaborativetrial. Pediatrics 2000;105:1—7.291. Vain NE, Szyld EG, Prudent LM, Wiswell TE, Aguilar AM,Vivas NI. Oropharyngeal and nasopharyngeal suctioning ofmeconium-stained neonates before delivery of their shoulders:multicentre, randomised controlled trial. Lancet2004;364:597—602.292. Solas AB, Kutzsche S, Vinje M, Saugstad OD. Cerebralhypoxemia-ischemia and reoxygenation with 21% or 100%oxygen in newborn piglets: effects on extracellular levelsof excitatory amino acids and microcirculation. Pediatr CritCare Med 2001;2:340—5.293. Solas AB, Kalous P, Saugstad OD. Reoxygenationwith 100 or 21% oxygen after cerebral hypoxemiaischemia-hypercapniain newborn piglets. Biol Neonate2004;85:105—11.294. Solas AB, Munkeby BH, Saugstad OD. Comparison ofshort- and long-duration oxygen treatment after cerebralasphyxia in newborn piglets. Pediatr Res 2004;56:125—31.295. Huang CC, Yonetani M, Lajevardi N, Delivoria-PapadopoulosM, Wilson DF, Pastuszko A. Comparison of postasphyxialresuscitation with 100% and 21% oxygen on cortical oxygenpressure and striatal dopamine metabolism in newbornpiglets. J Neurochem 1995;64:292—8.296. Kutzsche S, Ilves P, Kirkeby OJ, Saugstad OD. Hydrogen peroxideproduction in leukocytes during cerebral hypoxia andreoxygenation with 100% or 21% oxygen in newborn piglets.Pediatr Res 2001;49:834—42.297. Lundstrom KE, Pryds O, Greisen G. Oxygen at birth and prolongedcerebral vasoconstriction in preterm infants. ArchDis Child Fetal Neonatal Ed 1995;73:F81—6.298. Davis PG, Tan A, O’Donnell CP, Schulze A. Resuscitationof newborn infants with 100% oxygen or air: a systematicreview and meta-analysis. Lancet 2004;364:1329—33.299. Harris AP, Sendak MJ, Donham RT. Changes in arterialoxygen saturation immediately after birth in the humanneonate. J Pediatr 1986;109:117—9.300. Reddy VK, Holzman IR, Wedgwood JF. Pulse oximetry saturationsin the first 6 hours of life in normal term infants.Clin Pediatr (Phila) 1999;38:87—92.301. Toth B, Becker A, Seelbach-Gobel B. Oxygen saturation inhealthy newborn infants immediately after birth measuredby pulse oximetry. Arch Gynecol Obstet 2002;266:105—7.302. Karlberg P, Koch G. Respiratory studies in newborn infants.III. Development of mechanics of breathing during thefirst week of life. A longitudinal study Acta Paediatr1962;(Suppl. 135):121—9.303. Vyas H, Milner AD, Hopkins IE. Intrathoracic pressure andvolume changes during the spontaneous onset of respirationin babies born by cesarean section and by vaginaldelivery. J Pediatr 1981;99:787—91.

S132304. Mortola JP, Fisher JT, Smith JB, Fox GS, Weeks S, WillisD. Onset of respiration in infants delivered by cesareansection. J Appl Physiol 1982;52:716—24.305. Hull D. Lung expansion and ventilation during resuscitationof asphyxiated newborn infants. J Pediatr 1969;75:47—58.306. Upton CJ, Milner AD. Endotracheal resuscitation ofneonates using a rebreathing bag. Arch Dis Child1991;66:39—42.307. Vyas H, Milner AD, Hopkin IE, Boon AW. Physiologicresponses to prolonged and slow-rise inflation in the resuscitationof the asphyxiated newborn infant. J Pediatr1981;99:635—9.308. Vyas H, Field D, Milner AD, Hopkin IE. Determinants of thefirst inspiratory volume and functional residual capacity atbirth. Pediatr Pulmonol 1986;2:189—93.309. Boon AW, Milner AD, Hopkin IE. Lung expansion, tidalexchange, and formation of the functional residual capacityduring resuscitation of asphyxiated neonates. J Pediatr1979;95:1031—6.310. Ingimarsson J, Bjorklund LJ, Curstedt T, et al. Incompleteprotection by prophylactic surfactant against the adverseeffects of large lung inflations at birth in immature lambs.Intensive Care Med 2004;30:1446—53.311. Nilsson R, Grossmann G, Robertson B. Bronchiolar epitheliallesions induced in the premature rabbit neonate by shortperiods of artificial ventilation. Acta Pathol Microbiol Scand[A] 1980;88:359—67.312. Probyn ME, Hooper SB, Dargaville PA, et al. Positiveend expiratory pressure during resuscitation of prematurelambs rapidly improves blood gases without adverselyaffecting arterial pressure. Pediatr Res 2004;56:198—204.313. Hird MF, Greenough A, Gamsu HR. Inflating pressures foreffective resuscitation of preterm infants. Early Hum Dev1991;26:69—72.314. Lindner W, Vossbeck S, Hummler H, Pohlandt F. Deliveryroom management of extremely low birth weightinfants: spontaneous breathing or intubation? Pediatrics1999;103:961—7.315. Allwood AC, Madar RJ, Baumer JH, Readdy L, Wright D.Changes in resuscitation practice at birth. Arch Dis ChildFetal Neonatal Ed 2003;88:F375—9.316. Cole AF, Rolbin SH, Hew EM, Pynn S. An improved ventilatorsystem for delivery-room management of the newborn.Anesthesiology 1979;51:356—8.317. Hoskyns EW, Milner AD, Hopkin IE. A simple method of facemask resuscitation at birth. Arch Dis Child 1987;62:376—8.318. Ganga-Zandzou PS, Diependaele JF, Storme L, et al. Is Ambuventilation of newborn infants a simple question of fingertouch?Arch Pediatr 1996;3:1270—2.319. Finer NN, Rich W, Craft A, Henderson C. Comparison ofmethods of bag and mask ventilation for neonatal resuscitation.Resuscitation 2001;49:299—305.320. Kanter RK. Evaluation of mask-bag ventilation in resuscitationof infants. Am J Dis Child 1987;141:761—3.321. Esmail N, Saleh M, et al. Laryngeal mask airway versusendotracheal intubation for Apgar score improvementin neonatal resuscitation. Egypt J Anesthesiol2002;18:115—21.322. Gandini D, Brimacombe JR. Neonatal resuscitation withthe laryngeal mask airway in normal and low birth weightinfants. Anesth Analg 1999;89:642—3.323. Brimacombe J, Gandini D. Airway rescue and drug deliveryin an 800 g neonate with the laryngeal mask airway. PaediatrAnaesth 1999;9:178.324. Lonnqvist PA. Successful use of laryngeal mask airway inlow-weight expremature infants with bronchopulmonaryD. Biarent et al.dysplasia undergoing cryotherapy for retinopathy of thepremature. Anesthesiology 1995;83:422—4.325. Paterson SJ, Byrne PJ, Molesky MG, Seal RF, Finucane BT.Neonatal resuscitation using the laryngeal mask airway.Anesthesiology 1994;80:1248—53.326. Trevisanuto D, Ferrarese P, Zanardo V, Chiandetti L. Laryngealmask airway in neonatal resuscitation: a survey ofcurrent practice and perceived role by anaesthesiologistsand paediatricians. Resuscitation 2004;60:291—6.327. Hansen TG, Joensen H, Henneberg SW, Hole P. Laryngealmask airway guided tracheal intubation in a neonatewith the Pierre Robin syndrome. Acta Anaesthesiol Scand1995;39:129—31.328. Osses H, Poblete M, Asenjo F. Laryngeal mask for difficultintubation in children. Paediatr Anaesth 1999;9:399—401.329. Stocks RM, Egerman R, Thompson JW, Peery M. Airwaymanagement of the severely retrognathic child: use of thelaryngeal mask airway. Ear Nose Throat J 2002;81:223—6.330. Palme-Kilander C, Tunell R, Chiwei Y. Pulmonary gasexchange immediately after birth in spontaneously breathinginfants. Arch Dis Child 1993;68:6—10.331. Aziz HF, Martin JB, Moore JJ. The pediatric disposable endtidalcarbon dioxide detector role in endotracheal intubationin newborns. J Perinatol 1999;19:110—3.332. Bhende MS, LaCovey D. A note of caution about the continuoususe of colorimetric end-tidal CO 2 detectors in children.Pediatrics 1995;95:800—1.333. Repetto JE, Donohue P-CP, Baker SF, Kelly L, Nogee LM.Use of capnography in the delivery room for assessment ofendotracheal tube placement. J Perinatol 2001;21:284—7.334. Roberts WA, Maniscalco WM, Cohen AR, Litman RS,Chhibber A. The use of capnography for recognition ofesophageal intubation in the neonatal intensive care unit.Pediatr Pulmonol 1995;19:262—8.335. Berg RA, Otto CW, Kern KB, et al. A randomized,blinded trial of high-dose epinephrine versus standard-doseepinephrine in a swine model of pediatric asphyxial cardiacarrest. Crit Care Med 1996;24:1695—700.336. Burchfield DJ, Preziosi MP, Lucas VW, Fan J. Effects ofgraded doses of epinephrine during asphxia-induced bradycardiain newborn lambs. Resuscitation 1993;25:235—44.337. Ralston SH, Voorhees WD, Babbs CF. Intrapulmonaryepinephrine during prolonged cardiopulmonary resuscitation:improved regional blood flow and resuscitation indogs. Ann Emerg Med 1984;13:79—86.338. Ralston SH, Tacker WA, Showen L, Carter A, Babbs CF.Endotracheal versus intravenous epinephrine during electromechanicaldissociation with CPR in dogs. Ann EmergMed 1985;14:1044—8.339. Redding JS, Asuncion JS, Pearson JW. Effective routes ofdrug administration during cardiac arrest. Anesth Analg1967;46:253—8.340. Schwab KO, von Stockhausen HB. Plasma catecholaminesafter endotracheal administration of adrenaline duringpostnatal resuscitation. Arch Dis Child Fetal Neonatal Ed1994;70:F213—7.341. Brambrink AM, Ichord RN, Martin LJ, Koehler RC, TraystmanRJ. Poor outcome after hypoxia-ischemia in newbornsis associated with physiological abnormalities during earlyrecovery. Possible relevance to secondary brain injury afterhead trauma in infants. Exp Toxicol Pathol 1999;51:151—62.342. Vannucci RC, Vannucci SJ. Cerebral carbohydratemetabolism during hypoglycemia and anoxia in newbornrats. Ann Neurol 1978;4:73—9.343. Yager JY, Heitjan DF, Towfighi J, Vannucci RC. Effectof insulin-induced and fasting hypoglycemia on peri-

European Resuscitation Council Guidelines for Resuscitation 2005S133natal hypoxic-ischemic brain damage. Pediatr Res1992;31:138—42.344. Salhab WA, Wyckoff MH, Laptook AR, Perlman JM. Initialhypoglycemia and neonatal brain injury in term infants withsevere fetal acidemia. Pediatrics 2004;114:361—6.345. Kent TA, Soukup VM, Fabian RH. Heterogeneity affectingoutcome from acute stroke therapy: making reperfusionworse. Stroke 2001;32:2318—27.346. Eicher DJ, Wagner CL, Katikaneni LP, et al. Moderatehypothermia in neonatal encephalopathy: efficacy outcomes.Pediatr Neurol 2005;32:11—7.347. Thoresen M, Whitelaw A. Cardiovascular changes duringmild therapeutic hypothermia and rewarming ininfants with hypoxic-ischemic encephalopathy. Pediatrics2000;106:92—9.348. Shankaran S, Laptook A, Wright LL, et al. Whole-bodyhypothermia for neonatal encephalopathy: animal observationsas a basis for a randomized, controlled pilot studyin term infants. Pediatrics 2002;110:377—85.349. De Leeuw R, Cuttini M, Nadai M, et al. Treatment choicesfor extremely preterm infants: an international perspective.J Pediatr 2000;137:608—16.350. Lee SK, Penner PL, Cox M. Comparison of the attitudesof health care professionals and parents toward activetreatment of very low birth weight infants. Pediatrics1991;88:110—4.351. Kopelman LM, Irons TG, Kopelman AE. Neonatologistsjudge the ‘‘Baby Doe’’ regulations. N Engl J Med1988;318:677—83.352. Sanders MR, Donohue PK, Oberdorf MA, Rosenkrantz TS,Allen MC. Perceptions of the limit of viability: neonatologists’attitudes toward extremely preterm infants. J Perinatol1995;15:494—502.353. Draper ES, Manktelow B, Field DJ, James D. Tables forpredicting survival for preterm births are updated. BMJ2003;327:872.354. Jain L, Ferre C, Vidyasagar D, Nath S, Sheftel D. Cardiopulmonaryresuscitation of apparently stillborn infants:survival and long-term outcome. J Pediatr 1991;118:778—82.355. Haddad B, Mercer BM, Livingston JC, Talati A, Sibai BM.Outcome after successful resuscitation of babies born withapgar scores of 0 at both 1 and 5 minutes. Am J ObstetGynecol 2000;182:1210—4.

Resuscitation (2005) 67S1, S135—S170European Resuscitation Council Guidelines forResuscitation 2005Section 7. Cardiac arrest in special circumstancesJasmeet Soar, Charles D. Deakin, Jerry P. Nolan, Gamal Abbas,Annette Alfonzo, Anthony J. Handley, David Lockey,Gavin D. Perkins, Karl Thies7a. Life-threatening electrolytedisorders• Treat life-threatening electrolyte abnormalitiesbefore cardiac arrest occurs.• After initial treatment, remove any precipitatingfactors (e.g., drugs) and monitor electrolyte levelsto prevent recurrence of the abnormality.• Monitor renal function in patients at risk of electrolytedisorders.• In haemodialysis patients, review the dialysisprescription regularly to avoid inappropriateelectrolyte shifts during treatment.Prevention of electrolyte disordersOverviewElectrolyte abnormalities can cause cardiacarrhythmias or cardiopulmonary arrest. Lifethreateningarrhythmias are associated commonlywith potassium disorders, particularly hyperkalaemia,and less commonly with disorders ofserum calcium and magnesium. In some casestherapy for life-threatening electrolyte disordersshould start before the laboratory results becomeavailable.Potassium disordersThe electrolyte values for definitions have beenchosen as a guide to clinical decision-making. Potassium homeostasisThe precise values that trigger treatment decisionswill depend on the patient’s clinical conditionand the rate of change of the electrolytevalues.There is little or no evidence base for the treatmentof electrolyte abnormalities during cardiacarrest. Guidance during cardiac arrest is basedon the strategies used in the non-arrest patient.There are no major changes in the treatment ofthese disorders since the International Guidelines2000. 1Extracellular potassium concentration is regulatedtightly between 3.5—5.0 mmol l −1 . A large concentrationgradient normally exists between theintracellular and extracellular fluid compartments.This potassium gradient across the cell membranescontributes to the excitability of nerve and musclecells, including the myocardium. Evaluationof serum potassium must take into considerationthe effects of changes in serum pH. When serumpH decreases, serum potassium increases because0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.doi:10.1016/j.resuscitation.2005.10.004

S136potassium shifts from the cellular to the vascularspace. When serum pH increases, serum potassiumdecreases because potassium shifts intracellularly.We therefore anticipate the effects of pH changeson serum potassium during the therapy for hyperkalaemiaor hypokalaemia.HyperkalaemiaThis is the most common electrolyte disorder associatedwith cardiopulmonary arrest. It is usuallycaused by increased potassium release from thecells or impaired excretion by the kidneys.Definition. There is no universal definition,although we have defined hyperkalaemia as a serumpotassium concentration higher than 5.5 mmol l −1 ;in practice, hyperkalaemia is a continuum. Asthe potassium concentration increases above thisvalue, the risk of adverse events increases and theneed for urgent treatment increases. Severe hyperkalaemiahas been defined as a serum potassiumconcentration higher than 6.5 mmol l −1 .Causes. There are several potential causes ofhyperkalaemia, including renal failure, drugs(angiotensin converting enzyme inhibitors (ACEI),angiotensin II receptor blockers (ARB), potassiumsparingdiuretics, non-steroidal anti-inflammatorydrugs (NSAIDs), beta-blockers, trimethoprim, tissuebreakdown (rhabdomyolysis, tumour lysis,haemolysis), metabolic acidosis, endocrine disorders(Addison’s disease), hyperkalaemic periodicparalysis, or diet, which may be the sole causein patients with established renal failure. Abnormalerythrocytes or thrombocytosis may cause aspuriously high potassium concentration. The riskof hyperkalaemia is even greater when there isa combination of factors, such as the concomitantuse of ACEI and NSAIDs or potassium-sparingdiuretics.Recognition of hyperkalaemia. Exclude hyperkalaemiain patients with an arrhythmia or cardiacarrest. 2 Patients may present with weaknessprogressing to flaccid paralysis, paraesthesia ordepressed deep tendon reflexes. The first indicatorof hyperkalaemia may also be the presence ofECG abnormalities, arrhythmias, cardiopulmonaryarrest or sudden death. The effect of hyperkalaemiaon the ECG depends on the absolute serumpotassium as well as the rate of increase. Mostpatients will have ECG abnormalities at a serumpotassium concentration higher than 6.7 mmol l −1 . 3The ECG manifestations of hyperkalaemia are usuallyprogressive and include:J. Soar et al.• first-degree heart block (prolonged PR interval)>0.2 s;• flattened or absent P waves;• tall, peaked (tented) T waves, larger than R wavein more than one lead;• ST segment depression;• S and T waves merging;• widened QRS >0.12 s;• ventricular tachycardia (VT);• bradycardia;• cardiac arrest, i.e., pulseless electrical activity(PEA), ventricular fibrillation (VF), asystole.Treatment of hyperkalaemia.in treating hyperkalaemia are:The five key steps1. cardiac protection by antagonising the effects ofhyperkalaemia;2. shifting potassium into cells;3. removing potassium from the body;4. monitoring serum potassium for rebound hyperkalaemia;5. prevention of recurrence of hyperkalaemia.When hyperkalaemia is strongly suspected, e.g.,in the presence of ECG changes, start life-savingtreatment even before laboratory results are available.The management of hyperkalaemia is the subjectof a recent Cochrane review. 4Patient not in cardiac arrest. If the patientis not in cardiac arrest, assess fluid status;if hypovolaemic, give fluid to enhance urinarypotassium excretion. The values for classificationare an approximate guide. For mild elevation(5.5—6 mmol l −1 ), remove potassium from the bodywith:• potassium exchange resins, i.e., calcium resonium15—30 g or sodium polystyrene sulfonate(Kayexalate ® )15—30gin50—100 ml of 20% sorbitol,given either orally or by retention enema(onset in 1—3 h, maximal effect at 6 h);• diuretics, i.e., furosemide 1 mg kg −1 IV slowly(onset with the diuresis);• dialysis; haemodialysis is more efficient thanperitoneal dialysis at removing potassium (immediateonset, 25—30 mmol potassium h −1 removedwith haemodialysis).For moderate elevation (6—6.5 mmol l −1 ) withoutECG changes, shift potassium into cells with:• dextrose/insulin: 10 units short-acting insulinand 50 g glucose IV over 15—30 min (onset in15—30 min, maximal effect at 30—60 min; monitorblood glucose). Use in addition to removalstrategies above.

European Resuscitation Council Guidelines for Resuscitation 2005S137For severe elevation (≥6.5 mmol l −1 ) withoutECG changes, shift potassium into cells with:• salbutamol, 5 mg nebulised. Several doses maybe required (onset in 15—30 min);• sodium bicarbonate, 50 mmol IV over 5 min ifmetabolic acidosis present (onset in 15—30 min).Bicarbonate alone is less effective than glucoseplus insulin or nebulised salbutamol; it is bestused in conjunction with these medications; 5,6• use multiple shifting agents in addition toremoval strategies above.For severe elevation (≥6.5 mmol l −1 ) with toxicECG changes, protect the heart first with:• calcium chloride, i.e., 10 ml 10% calcium chlorideIV over 2—5 min to antagonise the toxic effects ofhyperkalaemia at the myocardial cell membrane.This protects the heart by reducing the risk ofVF, but does not lower serum potassium (onset in1—3 min). Use in addition to potassium removaland shifting strategies stated above.Patient in cardiac arrest. If the patient is incardiac arrest, there are no modifications to BLSin the presence of electrolyte abnormalities. ForALS, follow the universal algorithm. The generalapproach to treatment depends on the degree ofhyperkalaemia, rate of rise of serum potassium andthe patient’s clinical condition.In cardiopulmonary arrest, protect the heartfirst, then apply shifting and removal strategiesusing:• calcium chloride: 10 ml of 10% calcium chlorideIV by rapid bolus injection to antagonise the toxiceffects of hyperkalaemia at the myocardial cellmembrane;• sodium bicarbonate: 50 mmol IV by rapid injection(if severe acidosis or renal failure);• dextrose/insulin: 10 units short-acting insulin and50 g glucose IV by rapid injection;• haemodialysis: consider this for cardiac arrestinduced by hyperkalaemia, which is resistant tomedical treatment.Indications for dialysis. Haemodialysis is themost effective method of removal of potassiumfrom the body. The principal mechanism of actionis the diffusion of potassium ions across thetransmembrane potassium ion gradient. The typicaldecline in serum potassium is 1 mmol l −1 inthe first 60 min, followed by 1 mmol l −1 over thenext 2 h. Consider haemodialysis early for hyperkalaemiaassociated with established renal failure,oliguric acute renal failure (

S138arrhythmias when cardiac arrest is imminent. ContinuousECG monitoring is essential during IV infusion,and the dose should be titrated after repeatedsampling of serum potassium levels.Many patients who are potassium deficient arealso deficient in magnesium. Magnesium is importantfor potassium uptake and for the maintenanceof intracellular potassium levels, particularlyin the myocardium. Repletion of magnesiumstores will facilitate more rapid correction ofhypokalaemia and is recommended in severe casesof hypokalaemia. 8Calcium and magnesium disordersThe recognition and management of calcium andmagnesium disorders is summarised in Table 7.1.SummaryElectrolyte abnormalities are among the most commoncauses of cardiac arrhythmias. Of all theelectrolyte abnormalities, hyperkalaemia is mostrapidly fatal. A high degree of clinical suspicion andimmediate treatment of the underlying electrolyteabnormalities can prevent many patients from progressingto cardiac arrest.7b. PoisoningGeneral considerationsPoisoning is an infrequent cause of cardiac arrest,but remains a leading cause in victims younger than40 years. 9—12 Most research on this topic consistsprimarily of small case series, animal studies andcase reports.Self-poisoning with therapeutic or recreationaldrugs is the main reason for hospital admission.Drug toxicity can also be caused by inappropriatedosing and drug interactions. Accidental poisoningis commonest in children. Homicidal poisoning isuncommon. Industrial accidents, warfare or terrorismmay cause extensive chemical or radiationexposure. Decontamination and safe managementfor mass casualty incidents is not part of theseguidelines.ResuscitationTreatment of the self-poisoning (‘overdose’)patient is based on an ABCDE approach to preventcardiorespiratory arrest whilst awaiting drugelimination. 13 Airway obstruction and respiratoryJ. Soar et al.arrest secondary to a decreased conscious level isa common cause of death. Alcohol excess is oftenassociated with self-poisoning.• After opening and clearing the airway, check forbreathing and a pulse. Avoid mouth-to-mouthresuscitation in the presence of toxins, suchas cyanide, hydrogen sulphide, corrosives andorganophosphates. Ventilate the patient’s lungsusing a pocket- or bag-mask and the highestpossible concentration of oxygen. Be careful inparaquat poisoning as pulmonary injury may beexacerbated by high concentrations of oxygen. 14• There is a high incidence of pulmonary aspirationof gastric contents after poisoning. Intubateunconscious patients who cannot protect theirairway early, using a rapid-sequence inductionwith cricoid pressure to decrease the risk of aspiration(see section 4d). This must be undertakenby persons trained in the technique.• In the event of cardiac arrest, provide standardbasic and advanced life support.• With the exception of torsades de pointes(see below), cardioversion is indicated for lifethreateningtachyarrhythmias (see section 4f).• Drug-induced hypotension is common after selfpoisoning.This usually responds to fluid therapy,but occasionally inotropic support is required.• Once resuscitation is under way, try to identifythe poison(s). Relatives, friends and ambulancecrews can usually provide useful information.Examination of the patient may reveal diagnosticclues, such as odours, needle puncture marks,pinpoint pupils, tablet residues, signs of corrosionin the mouth or blisters associated with prolongedcoma.• Measure the patient’s temperature; hypo- orhyperthermia may occur after drug overdose (seesections 7d and 7e).• Consult regional or national poisons centresfor information on treatment of the poisonedpatient. 15,16 The World Health Organizationlists poison centres on its website:http://www.who.int/ipcs/poisons/centre/en/.Specific therapeutic measuresThere are few specific therapeutic measures forpoisons that are useful immediately. The emphasisis on intensive supportive therapy, with correctionof hypoxia, hypotension and acid/base and electrolytedisorders.Therapeutic measures include limiting absorptionof ingested poisons, enhancing elimination,or the use of specific antidotes. For up-to-dateguidance in severe or uncommon poisonings, seek

Table 7.1Calcium (Ca 2+ ) and magnesium (Mg 2+ ) disorders with associated clinical presentation, ECG manifestations and recommended treatmentDisorder Causes Presentation ECG TreatmentHypercalcaemia (Ca 2+ Primary or tertiary Confusion Short QT interval Fluid replacement IV>2.6 mmol l −1 hyperparathyroidism Weakness Prolonged QRS interval Furosemide, 1 mg kg −1 IVMalignancy Abdominal pain Flat T waves Hydrocortisone, 200—300 mg IVSarcoidosis Hypotension AV-block Pamidronate, 60—90 mg IVDrugs Arrhythmias Cardiac arrest Calcitonin, 4—8 units kg −1 8h −1 IMCardiac arrestReview medicationHaemodialysisHypocalcaemia (Ca 2+ Chronic renal failure Paraesthesia Prolonged QT interval Calcium chloride 10%, 10—40 ml 1.1 mmol l −1 )Hypomagnesaemia(Mg 2+

S140advice from a poisons centre.• Activated charcoal is known to adsorb certaindrugs. Its value decreases over time after ingestion.There is no evidence that ingestion of charcoalimproves clinical outcome. According to evidencefrom volunteer studies, consider giving asingle dose of activated charcoal to patients whohave ingested a potentially toxic amount of poison(known to be adsorbed by activated charcoal)up to 1 h previously. 17 Give it only to patientswith an intact or protected airway. Multiple dosesof activated charcoal can be beneficial in lifethreateningpoisoning with carbemazepine, dapsone,phenobarbital, quinine and theophylline.• Gastric lavage followed by activated charcoaltherapy is useful only within 1 h of ingesting thepoison. 17 Generally this should be carried outafter tracheal intubation. Delayed gastric lavagehas very little effect on drug absorption and maypropel drugs further along the gastrointestinaltract. 18 Do not give ipecacuanha syrup to inducevomiting; there is little evidence of benefit. 19• There is little evidence for the use of laxatives,e.g., lactulose or magnesium citrate, to enhancedrug elimination from the gut. 20• Whole-bowel irrigation by enteral administrationof a polyethylene glycol solution can reducedrug absorption by cleansing the gastrointestinaltract. It can be useful in cases of potentiallytoxic ingestion of sustained release or entericcoateddrugs, oral iron poisoning and the removalof ingested packets of illicit drugs. 21• Urine alkalinisation (pH 7.5) by giving IV sodiumbicarbonate can be useful in moderate-to-severesalicylate poisoning in patients who do not needhaemodialysis. 22 Urine alkalinisation can also beuseful in tricyclic overdose (see below).• Haemodialysis or haemoperfusion can be usefulfor elimination of specific life-threateningtoxins. Haemodialysis removes drugs or metabolitesthat are water soluble, have a low volumeof distribution and low plasma proteinbinding. 23 It may be considered for poisoningwith methanol, ethylene glycol, salicylatesand lithium. Haemoperfusion involves passingblood through an absorptive-containing cartridge(usually charcoal). This technique removes substancesthat have a high degree of plasma proteinbinding. Charcoal haemoperfusion may beindicated for intoxications with carbamazepine,phenobarbital, phenytoin and theophylline.• Specific antidotes (see below) which may beeffective include: N-acetylcysteine for paracetamol;high-dose atropine for organophosphateinsecticides; sodium nitrite, sodium thiosulphateJ. Soar et al.or dicobalt edetate for cyanides; digoxin-specificFab antibodies for digoxin; flumazenil for benzodiazepines;and naloxone for opioids. Reversalof benzodiazepine intoxication with flumazenilis associated with significant toxicity in patientswith benzodiazepine dependence or co-ingestionof proconvulsant medications, such as tricyclicantidepressants. 24 The routine use of flumazenilin the comatose patient with an overdose is notrecommended.Specific antidotesThese guidelines will address only some causes ofcardiorespiratory arrest due to poisoning.Opioid poisoningOpioid poisoning commonly causes respiratorydepression followed by respiratory insufficiency orrespiratory arrest. The respiratory effects of opioidsare reversed rapidly by the opiate antagonistnaloxone. In severe respiratory depression, theevidence shows fewer adverse events when airwayopening, oxygen administration and ventilationare carried out before giving naloxone in casesof opioid-induced respiratory depression; 25—30 however,the use of naloxone can prevent the need forintubation. The preferred route for giving naloxonedepends on the skills of the rescuer: IV, intramuscular(IM), subcutaneous (SC), endotracheal (ET)and intranasal (IN) routes can be used. The non-IV routes can be quicker because time is saved innot having to establish IV access, which can beextremely difficult in an IV drug abuser. The initialdoses of naloxone are 400 mcg IV, 27 800 mcgIM, 800 mcg SC, 27 2mg IN 31 or 1—2 mg ET. Largeopioid overdoses may require titration to a totalnaloxone dose of 6—10 mg. The duration of actionof naloxone is approximately 45—70 min, but respiratorydepression can persist for 4—5 h after opioidoverdose. Thus, the clinical effects of naloxone maynot last as long as those of a significant opioid overdose.Titrate the dose until the victim is breathingadequately and has protective airway reflexes.Acute withdrawal from opioids produces a stateof sympathetic excess and may cause complications,such as pulmonary oedema, ventriculararrhythmia and severe agitation. Use naloxonereversal of opiate intoxication with caution inpatients suspected of opioid dependence.There is no good evidence that naloxoneimproves outcome once cardiac arrest associatedwith opioid toxicity has occurred. Cardiac arrest isusually secondary to a respiratory arrest and associatedwith severe brain hypoxia. Prognosis is poor. 26

European Resuscitation Council Guidelines for Resuscitation 2005S141Giving naloxone is unlikely to be harmful. Once cardiacarrest has occurred, follow the standard resuscitationprotocols.Tricyclic antidepressantsSelf-poisoning with tricyclic antidepressants is commonand can cause hypotension, seizures andarrhythmias. Anticholinergic effects include mydriasis,fever, dry skin, delirium, tachycardia, ileusand urinary retention. Most life-threatening problemsoccur within the first 6 h after ingestion. Awidening QRS complex indicates a greater risk ofarrhythmias. There is evidence to support the use ofsodium bicarbonate to treat arrhythmias induced bytricyclic antidepressants and/or hypotension. 32—47The exact threshold for starting treatment basedon QRS duration has not been established. No studyhas investigated the optimal target arterial or urinarypH with bicarbonate therapy, but an arterialpH of 7.45—7.55 has been commonly accepted andseems reasonable. Hypertonic saline may also beeffective in treating cardiac toxicity. 48Cocaine toxicitySympathetic overstimulation associated withcocaine toxicity may cause agitation, symptomatictachycardia, hypertensive crisis, hyperthermia andmyocardial ischaemia with angina. Glyceryl trinitrateand phentolamine reverse cocaine-inducedcoronary vasoconstriction, labetalol has no significanteffect, and propranolol makes it worse. 49—52Small doses of IV benzodiazepines (midazolam,diazepam, lorazepam) are effective first-linedrugs. Use nitrates only as second-line therapy formyocardial ischaemia. Labetalol (alpha- and betablocker)is useful for the treatment of tachycardiaand hypertensive emergencies due to cocainetoxicity.Drug-induced severe bradycardiaSevere bradycardia from poisoning or drug overdosemay be refractory to standard ALS protocolsbecause of prolonged receptor binding or directcellular toxicity. Atropine may be life saving inorganophosphate, carbamate or nerve agent poisoning.Give atropine for bradycardia caused byacetylcholinesterase-inhibiting substances. Large(2—4 mg) and repeated doses may be required toachieve a clinical effect. Isoprenaline may be usefulat high doses in refractory bradycardia induced bybeta-antagonist receptor blockade. Heart block andventricular arrhythmias associated with digoxin ordigitalis glycoside poisoning may be treated effectivelywith digoxin-specific antibody fragments. 53Antibody-specific therapy may also be effective inpoisoning from plants as well as Chinese herbalmedications containing digitalis glycosides. 53—55Vasopressors, inotropes, calcium, glucagon,phosphodiesterase inhibitors and insulin-glucosemay all be useful in beta-blocker and calcium channelblocker overdose. 56—58 Transcutaneous pacingmay be effective for severe bradycardia caused bypoisoning and overdose (see section 3).Further treatment and prognosisA long period of coma in a single position can causepressure sores and rhabdomyolysis. Measure electrolytes(particularly potassium), blood glucose andarterial blood gases. Monitor temperature becausethermoregulation is impaired. Both hypothermiaand hyperthermia (hyperpyrexia) can occur afterthe overdose of some drugs. Retain samples of bloodand urine for analysis.Be prepared to continue resuscitation for a prolongedperiod, particularly in young patients asthe poison may be metabolised or excreted duringextended life support measures.Alternative approaches which may be effectivein severely poisoned patients include:• higher doses of medication than in standard protocols;• non-standard drug therapies;• prolonged CPR.7c. DrowningOverviewDrowning is a common cause of accidental death inEurope. The most important and detrimental consequenceof drowning is hypoxia. The duration ofhypoxia is the critical factor in determining thevictim’s outcome. Therefore, oxygenation, ventilationand perfusion should be restored as rapidlyas possible. Immediate resuscitation at the sceneis essential for survival and neurological recoveryafter drowning. This will require bystander provisionof CPR plus immediate activation of the EMSsystem. Victims who have spontaneous circulationand breathing when they reach hospital usuallyrecover with good outcomes.EpidemiologyThe World Health Organization (WHO) estimatesthat, worldwide, drowning accounts for

S142approximately 450,000 deaths each year. A further1.3 million disability-adjusted life-years are losteach year as a result of premature death or disabilityfrom drowning; 59 97% of deaths from drowningoccur in low- and middle-income countries. 59 In2002, there were 427 deaths from drowning in theUnited Kingdom (Royal Society for the Preventionof Accidents 2002) and 4073 in the United States(National Center for Injury Prevention 2002),yielding an annual incidence of drowning of 0.8and 1.45 per 100,000 population, respectively.Death from drowning is more common in youngmales and is the leading cause of accidental deathin Europe in this group. 59 Alcohol consumption is acontributory factor in up to 70% of drownings. 60The guidelines in this chapter focus on the treatmentof the individual drowning victim rather thanthe management of mass casualty aquatic incidents.Definitions, classifications and reportingOver 30 different terms have been used to describethe process and outcome from submersion- andimmersion-related incidents. 61 To improve clarityand to help comparability of future scientific andepidemiological reports, the International LiaisonCommittee on Resuscitation (ILCOR) has proposednew definitions related to drowning. 62 Drowningitself is defined as a process resulting in primary respiratoryimpairment from submersion/immersion ina liquid medium. Implicit in this definition is thata liquid/air interface is present at the entranceof the victim’s airway, preventing the victim frombreathing air. The victim may live or die after thisprocess, but whatever the outcome, he or she hasbeen involved in a drowning incident. Immersionmeans to be covered in water or other fluid. Fordrowning to occur, usually at least the face andairway must be immersed. Submersion implies thatthe entire body, including the airway, is under thewater or other fluid.ILCOR recommends that the following terms,previously used, should no longer be used: dry andwet drowning, active and passive drowning, silentdrowning, secondary drowning and drowned versusnear-drowned. 62Basic life supportAquatic rescue and recovery from the waterJ. Soar et al.Always be aware of personal safety and minimisethe danger to yourself and the victim at all times.Whenever possible, attempt to save the drowningvictim without entry into water. Talking to the victim,reaching with a rescue aid (e.g., stick or clothing),or throwing a rope or buoyant rescue aid maybe effective if the victim is close to dry land. Alternatively,use a boat or other water vehicle to assistwith the rescue. Avoid entry into the water wheneverpossible. If entry into the water is essential,take a buoyant rescue aid or flotation device.Remove all the drowning victims from the waterby the fastest and safest means available and resuscitateas quickly as possible. The incidence ofcervical spine injury in drowning victims is low(approximately 0.5%). 63 Spinal immobilisation canbe difficult to perform in the water and can delayremoval from the water and adequate resuscitationof the victim. Poorly applied cervical collarscan also cause airway obstruction in unconsciouspatients. 64 Despite potential spinal injury, victimswho are pulseless and apnoeic should be removedfrom water as quickly as possible (even if a backsupport device is not available), while attemptingto limit neck flexion and extension. Cervicalspine immobilisation is not indicated unless signs ofsevere injury are apparent or the history is consistentwith the possibility of severe injury. 65 Thesecircumstances include a history of diving, waterslideuse, signs of trauma or signs of alcohol intoxication.Whenever possible, remove the victim fromthe water in a horizontal position to minimise therisks of post-immersion hypotension and cardiovascularcollapse. 66Rescue breathingThe first and most important treatment for thedrowning victim is alleviation of hypoxaemia.Prompt initiation of rescue breathing or positivepressure ventilation increases the survival. 67,68 Inthe apnoeic victim, start rescue breathing as soonas the victim’s airway is opened and the rescuer’ssafety ensured. This can sometimes be achievedwhen the victim is still in shallow water. It is likelyto be difficult to pinch the victim’s nose, so mouthto-noseventilation may be used as an alternative tomouth-to-mouth ventilation. If the victim is in deepwater, start in-water rescue breathing if trained todo so, ideally with the support of a buoyant rescueaid, 69 although in-water, unsupported resuscitationmay also be possible. 70 Untrained rescuers shouldnot attempt to perform any form of resuscitationwith a victim in deep water.If there is no spontaneous breathing after openingthe airway, give rescue breaths for approximately1 min. 69 If the victim does not start breathingspontaneously, further management depends onthe distance from land. If the victim can be broughtto land in

European Resuscitation Council Guidelines for Resuscitation 2005S143breaths while towing. If more than an estimated5 min from land, give further rescue breaths over1 min, then bring the victim to land as quickly aspossible without further attempts at ventilation. 69There is no need to clear the airway of aspiratedwater. The majority of drowning victims aspirateonly a modest amount of water, and this isabsorbed rapidly into the central circulation. Anattempt to remove water from the air passagesby any means other than suction is unnecessaryand dangerous. Abdominal thrusts cause regurgitationof gastric contents and subsequent aspiration.They have been associated with other lifethreateninginjuries and should not be performedunless there are clear signs of foreign-body airwayobstruction. 71Chest compressionAs soon as the victim is removed from water,check for breathing. A healthcare professional whois trained in pulse checking may also check forpulse, but this may be even more difficult to findin a drowning victim, particularly if cold. If thevictim is not breathing, start chest compressionsimmediately. Chest compression is ineffective inwater. 72,73DefibrillationIf the victim is unresponsive and not breathing andan AED is available, attach it to the victim andturn it on. Before attaching the AED pads, drythe victim’s chest to enable adherence. Delivershocks according to the AED prompts. If the victimis hypothermic with a core body temperature≤30 ◦ C (86 ◦ F), limit defibrillation to a total of threeattempts until the core body temperature risesabove 30 ◦ C (86 ◦ F). 74Regurgitation during resuscitationRegurgitation of stomach contents is common followingresuscitation from drowning and will complicateefforts to maintain a patent airway. In onestudy, regurgitation occurred in two-thirds of victimswho received rescue breathing and 86% of victimswho required compression and ventilation. 75If regurgitation occurs, turn the victim’s mouth tothe side and remove the regurgitated material usingdirected suction if possible. If spinal cord injury issuspected, log-roll the victim, keeping the head,neck and torso aligned, before aspirating the regurgitatedmaterial. Log-rolling will require severalrescuers.Advanced life supportAirway and breathingGive high-flow oxygen during the initial assessmentof the spontaneously breathing drowningvictim. Consider non-invasive ventilation or continuouspositive airway pressure if the victim fails torespond to treatment with high-flow oxygen. 76 Usepulse oximetry and arterial blood gas analysis totitrate the concentration of inspired oxygen andto provide an indicator of the adequacy of ventilation.Consider early intubation and controlledventilation for victims who fail to respond to theseinitial measures or who have a reduced level ofconsciousness. Take care to ensure optimal preoxygenationbefore intubation. Use a rapid-sequenceinduction with cricoid pressure to reduce the highrisk of aspiration. 77 Protect the airway of the victimin cardiopulmonary arrest early in the resuscitationattempt, ideally with a tracheal tube. Reducedpulmonary compliance requiring high inflation pressuresmay limit the use of adjuncts, such as thelaryngeal mask airway. Initiate ventilation with ahigh-inspired oxygen concentration as soon as possible,to treat the severe hypoxaemia that is likelyto be present.Circulation and defibrillationFollow standard advanced life support protocols. Ifsevere hypothermia is present (core body temperature≤30 ◦ Cor86 ◦ F), limit defibrillation attemptsto three, and withhold IV drugs until the corebody temperature increases above these levels. Ifmoderate hypothermia is present, give IV drugs atlonger than standard intervals (see section 7d).During prolonged immersion, victims maybecome hypovolaemic from the hydrostatic pressureof water on the body. Give IV fluid to correctthe hypovolaemia but avoid excessive volumes,which may cause pulmonary oedema. After returnof spontaneous circulation, use haemodynamicmonitoring to guide fluid resuscitation.Discontinuing resuscitation effortsMaking a decision to discontinue resuscitationefforts on a victim of drowning is notoriously difficult.No single factor can accurately predict goodor poor survival with 100% certainty. Decisions madein the field frequently prove later to have beenincorrect. 78 Continue resuscitation unless thereis clear evidence that resuscitation attempts arefutile (e.g., massive traumatic injuries, rigor mortis,putrefaction etc.), or timely evacuation to

S144a medical facility is not possible. Neurologicallyintact survival has been reported in several victimssubmerged for greater than 60 min. 79,80Post-resuscitation careSalt versus fresh waterMuch attention has been focused in the past on differencesbetween salt- and fresh-water drowning.Extensive data from animal studies and human caseseries have shown that, irrespective of the tonicityof the inhaled fluid, the predominant pathophysiologicalprocess is hypoxaemia, driven by surfactantwash-out and dysfunction, alveolar collapse,atelectasis and intrapulmonary shunting. Small differencesin electrolyte disturbance are rarely of anyclinical relevance and do not usually require treatment.Lung injuryVictims of drowning are at high risk of developingacute respiratory distress syndrome (ARDS) forupto 72 h after submersion. Protective ventilationstrategies improve survival in patients with ARDS. 81The propensity towards alveolar collapse mayrequire the use of PEEP or other alveolar recruitmentmanoeuvres to reverse severe hypoxaemia. 82Extracorporeal membrane oxygenation and nitricoxide administration have been used in some centresfor refractory hypoxaemia in drowning victimsbut the efficacy of these treatments is unproven. 65Pneumonia is common after drowning. Prophylacticantibiotics have not been shown to be ofbenefit, although they may be considered aftersubmersion in grossly contaminated water such assewage. Give broad-spectrum antibiotics if signs ofinfection develop subsequently. 65HypothermiaVictims of submersion may develop primary orsecondary hypothermia. If the submersion occursin icy water (37 ◦ C) during thesubsequent period of intensive care (InternationalLife Saving Federation, 2003).Other supportive careAttempts have been made to improve neurologicaloutcome following drowning with the use ofbarbiturates, intracranial pressure (ICP) monitoringand steroids. None of these interventions has beenshown to alter the outcome. In fact, signs of highICP serve as a symptom of significant neurologicalhypoxic injury, and no evidence that attempts toalter the ICP will affect the outcome. 657d. HypothermiaDefinitionHypothermia exists when the body core temperatureis below 35 ◦ C and is classified arbitrarily asmild (35—32 ◦ C), moderate (32—30 ◦ C) or severe(less than 30 ◦ C). Hypothermia can occur in peoplewith normal thermoregulation who are exposedto cold environments, particularly wet or windyconditions, or following immersion in cold water.When thermoregulation is impaired, for example,in the elderly and very young, hypothermia mayfollow a mild cold insult. The risk of hypothermiais also increased by drug or alcohol ingestion,illness, injury or neglect. Hypothermia may be suspectedfrom the clinical history or a brief externalexamination of a collapsed patient. A low-readingthermometer is needed to measure the core temperatureand confirm diagnosis.In some cases, hypothermia may exert a protectiveeffect on the brain after cardiac arrest. 84,85Intact neurological recovery may be possible afterhypothermic cardiac arrest, although those withnon-asphyxial arrest have a better prognosis thanthose with asphyxial hypothermic arrest. 86—88 Lifesavingprocedures should not be withheld on thebasis of clinical presentation alone. 87Decision to resuscitateBeware of pronouncing death in a hypothermicpatient, as cold alone may produce a very slow,

European Resuscitation Council Guidelines for Resuscitation 2005S145small-volume, irregular pulse and an unrecordableblood pressure. Hypothermia protects the brain andvital organs, and associated arrhythmias are potentiallyreversible either before or during rewarming.At 18 ◦ C the brain can tolerate periods of circulatoryarrest for 10 times longer than at 37 ◦ C. Dilatedpupils can be caused by a variety of insults and mustnot be taken as a sign of death.On discovering a hypothermic cardiac arrestvictim in cold environment, it is not always easyto distinguish between primary and secondaryhypothermia. Cardiac arrest could be caused primarilyby hypothermia, or hypothermia could followa normothermic cardiac arrest (e.g., cardiacarrest caused by myocardial ischaemia in a personin cold environment).Do not confirm death until the patient has beenrewarmed or until attempts to raise the core temperaturehave failed; prolonged resuscitation maybe necessary. In the prehospital setting, resuscitationshould be withheld only if the patient hasobvious lethal injuries or if the body is completelyfrozen making resuscitation attempts impossible. 89In the hospital setting, use clinical judgment todetermine when to stop resuscitating a hypothermicarrest victim.ResuscitationAll the principles of prevention, basic and advancedlife support apply to the hypothermic patient. Donot delay the urgent procedures, such as intubationand insertion of vascular catheters. Intubationcan provoke VF in a patient with severehypothermia. 87,90• Clear the airway and, if there is no spontaneousrespiratory effort, ventilate the patient’s lungswith high concentrations of oxygen. If possible,use warmed (40—46 ◦ C) and humidified oxygen.Consider careful tracheal intubation when indicatedaccording to the ALS algorithm.• Palpate a major artery and, if available, look atthe ECG for up to 1 min and look for signs of lifebefore concluding that there is no cardiac output.If a Doppler ultrasound probe is available,use it to establish whether there is peripheralblood flow. If the victim is pulseless, start chestcompressions immediately. If there is any doubtabout whether a pulse is present, start CPR.• Once resuscitation is under way, confirmhypothermia with a low-reading thermometer.The method of temperature measurementshould be the same throughout resuscitation andrewarming. Use oesophageal, bladder, rectal ortympanic temperature measurements. 91,92Use the same ventilation and chest compressionrates as for a normothermic patient. Hypothermiacan cause stiffness of the chest wall, making ventilationand chest compression difficult.The hypothermic heart may be unresponsiveto cardioactive drugs, attempted electrical pacingand attempted defibrillation. Drug metabolismis slowed, leading to potentially toxic plasmaconcentrations of any drug given repeatedly. 90The evidence for the efficacy of drugs in severehypothermia is limited and based mainly on animalstudies. Adrenaline may be effective in increasingcoronary perfusion pressure, but not survival,in severe hypothermic cardiac arrest. 93,94 The efficacyof amiodarone is also reduced. 95 For thesereasons, withhold adrenaline and other drugs untilthe patient has been warmed to a temperaturegreater than 30 ◦ C. Once 30 ◦ C has been reached,the intervals between doses should be doubled. Asthe patient’s temperature returns towards normal,the standard drug protocols should be used.Remember to rule out other primary causes ofcardiorespiratory arrest using the four Hs and fourTs approach (e.g., drug overdose, hypothyroidism,trauma).ArrhythmiasAs the body core temperature decreases, sinusbradycardia tends to give way to atrial fibrillation(AF) followed by ventricular fibrillation (VF) andfinally asystole. 96 Follow the standard treatmentprotocols.Severely hypothermic victims (core temperature

S146heat loss and rapid transfer to the hospital. Removecold or wet clothing as soon as possible. Cover thedry casualties with blankets and keep them out ofthe wind.Rewarming may be passive external, activeexternal, or active internal. Passive warming isachieved with blankets and a warm room, and issuitable for conscious victims with mild hypothermia.In severe hypothermia or cardiac arrest,active warming is required, but this must notdelay transport to a hospital where more advancedrewarming techniques are available. Several techniqueshave been described, although there are noclinical trials of outcome to determine the bestrewarming method. Studies show that forced airrewarming and warm IV fluids are effective inpatients with severe hypothermia and a perfusingrhythm. 99,100 Other warming techniques includethe use of warm humidified gases, gastric, peritoneal,pleural or bladder lavage with warm fluids(at 40 ◦ C), and extracorporeal blood warming withpartial bypass. 87,90,101—103In the patient with cardiac arrest and hypothermia,cardiopulmonary bypass is the preferredmethod of active internal rewarming because italso provides circulation, oxygenation and ventilation,while the core body temperature is increasedgradually. 104,105 Survivors in one case series had anaverage of 65 min of conventional CPR before cardiopulmonarybypass. 105 Unfortunately, facilitiesfor cardiopulmonary bypass are not always availableand a combination of methods may have to beused.During rewarming, patients will require largevolumes of fluids as their vascular space expandswith vasodilation. Warm all the IV fluids. Use continuoushaemodynamic monitoring and, if possible,treat the patient in a critical care unit. Avoidhyperthermia during and after the warming period.Although there are no formal studies, once ROSChas been achieved use standard strategies for postresuscitationcare, including mild hypothermia ifappropriate (section 4g). There is no evidencefor the routine use of steroids, barbiturates orantibiotics. 106,1077e. HyperthermiaDefinitionJ. Soar et al.Hyperthermia occurs when the body’s abilityto thermoregulate fails, and core temperatureexceeds the one that is normally maintainedby homeostatic mechanisms. Hyperthermia maybe exogenous, caused by environmental conditions,or secondary to endogenous heat production.Environment-related hyperthermia occurs whereheat, usually in the form of radiant energy, isabsorbed by the body at a rate faster than that canbe lost by thermoregulatory mechanisms. Hyperthermiaoccurs along a continuum of heat-relatedconditions, starting with heat stress, progressingto heat exhaustion, to heat stroke (HS) and finallymultiorgan dysfunction and cardiac arrest in someinstances. 108Malignant hyperthermia (MH) is a rare disorder ofskeletal muscle calcium homeostasis characterisedby muscle contracture and life-threatening hypermetaboliccrisis following exposure of geneticallypredisposed individuals to halogenated anaestheticsand depolarising muscle relaxants. 109,110The key features and treatment of heat stressand heat exhaustion are included in Table 7.2.Heat stroke (HS)HS is a systemic inflammatory response with acore temperature above 40.6 ◦ C, accompanied bymental state change and varying levels of organdysfunction. There are two forms of HS: classicnon-exertion heat stroke (CHS) occuring duringhigh environmental temperatures and ofteneffecting the elderly during heat waves; 111 exertionheat stroke (EHS) occuring during strenuousphysical exercise in high environmental temperaturesand/or high humidity usually effectinghealthy young adults. 112 Mortality from HS rangesbetween 10 and 50%. 113Predisposing factorsThe elderly are at an increased risk for heat-relatedillness because of underlying illness, medicationuse, declining thermoregulatory mechanisms andlimited social support. There are several risk factors:lack of acclimatisation, dehydration, obesity,alcohol, cardiovascular disease, skin conditions(psoriasis, eczema, scleroderma, burn, cysticfibrosis), hyperthyroidism, phaeochromocytomaand drugs (anticholinergics, diamorphine, cocaine,amphetamine, phenothiazines, sympathomimetics,calcium channel blockers, beta-blockers).Clinical presentationHeat stroke can resemble septic shock and may becaused by similar mechanisms. 114 Features include:• core temperature 40.6 ◦ C or more;• hot, dry skin (sweating is present in about 50% ofcases of exertional heat stroke);

European Resuscitation Council Guidelines for Resuscitation 2005S147Table 7.2 Heat stress and heat exhaustionCondition Features TreatmentHeat stress Normal or mild temperature elevation RestHeat oedema: swelling of feet and anklesElevation of oedematous limbsHeat syncope: vasodilation causing hypotension CoolingHeat cramps: sodium depletion causing cramps Oral rehydrationSalt replacementHeat exhaustion Systemic reaction to prolonged heat exposure As above(hours to days)Temperature >37 ◦ C and

S148Malignant hyperthermia (MH)MH is a life-threatening genetic sensitivity of skeletalmuscles to volatile anaesthetics and depolarisingneuromuscular blocking drugs, occurring duringor after anaesthesia. Stop triggering agents immediately;give oxygen, correct acidosis and electrolyteabnormalities. Start active cooling and givedantrolene. 135Modifications to cardiopulmonaryresuscitation and post-resuscitation careThere are no specific studies on cardiac arrest inhyperthermia. If cardiac arrest occurs, follow standardprocedures for basic and advanced life supportand cool the patient. There are no data onthe effects of hyperthermia on defibrillation threshold;therefore, attempt defibrillation according tocurrent guidelines, while continuing to cool thepatient. Animal studies suggest that the prognosisis poor compared with normothermic cardiacarrest. 136,137 The risk of unfavourable neurologicaloutcome increases for each degree of body temperature>37 ◦ C. 138 Provide post-resuscitation careaccording to the normal guidelines.7f. AsthmaIntroductionApproximately 300 million people of all agesand ethnic backgrounds suffer from asthmaworldwide. 139 Asthma still causes many deaths inyoung adults, mostly among those with chronicsevere asthma, adverse psychosocial circumstancesand poor medical management. National and internationalguidance for the management of asthmaalready exists. 139,140 The following guidelines focuson the treatment of patients with near-fatal asthmaand cardiac arrest.Causes of cardiac arrestCardiac arrest in the asthmatic person is often aterminal event after a period of hypoxaemia; occasionally,it may be sudden. Cardiac arrest in asthmaticshas been linked to:• severe bronchospasm and mucous plugging leadingto asphyxia (this condition causes the vastmajority of asthma-related deaths);• cardiac arrhythmias caused by hypoxia, which isthe common cause of asthma-related arrhythmia.Arrhythmias can be caused by stimulant drugsJ. Soar et al.(e.g., beta-adrenergic agonists, aminophylline)or electrolyte abnormalities;• dynamic hyperinflation, i.e., autopositive endexpiratorypressure (auto-PEEP), can occur inmechanically ventilated asthmatics. Auto-PEEPis caused by air trapping and ‘breath stacking’(breathed air entering and being unable toescape). Gradual build-up of pressure occurs andreduces blood flow and blood pressure;• tension pneumothorax (often bilateral).The four Hs and four Ts approach to reversiblecauses helps identify these causes in cardiac arrest.DiagnosisWheezing is a common physical finding, but severitydoes not correlate with the degree of airwayobstruction. The absence of wheezing may indicatecritical airway obstruction, whereas increasedwheezing may indicate a positive response to bronchodilatortherapy. SaO 2 may not reflect progressivealveolar hypoventilation, particularly if oxygenis being given. The SaO 2 may initially decrease duringthe therapy because beta-agonists cause bothbronchodilation and vasodilation and may increaseintrapulmonary shunting initially.Other causes of wheezing include: pulmonaryoedema, chronic obstructive pulmonary disease(COPD), pneumonia, anaphylaxis, 141 pneumonia,foreign bodies, pulmonary embolism, bronchiectasisand subglottic mass. 142The severity of an asthma attack is defined inTable 7.3.Key interventions to prevent arrestThe patient with severe asthma requires aggressivemedical management to prevent deterioration.Base assessment and treatment on an ABCDEapproach. Experienced clinicians should treat thesehigh-risk patients in a critical care area. The specificdrugs and the treatment sequence will varyaccording to local practice.OxygenUse a concentration of inspired oxygen that willachieve an SaO 2 ≥92%. High-flow oxygen by maskis sometimes necessary. Consider rapid-sequenceinduction and tracheal intubation if, despite effortsto optimise drug therapy, the patient has:• decreased conscious level, coma;• profuse sweating;• reduced muscle tone (clinical signs of hypercarbia);

European Resuscitation Council Guidelines for Resuscitation 2005S149Table 7.3 The severity of asthma 140AsthmaNear-fatalLife-threateningAcute severeModerate exacerbationBrittlePEF, peak expiratory flow.FeaturesRaised PaCO 2 and/or requiring mechanical ventilation with raised inflation pressuresAny one of:PEF 50—75% best or predictedNo features of acute severe asthmaType 1: wide PEF variability (>40% diurnal variation for >50% of the time over a period>150 days) despite intense therapyType 2: sudden severe attacks on a background of apparently well controlled asthma• findings of severe agitation, confusion and fightingagainst the oxygen mask (clinical signs ofhypoxemia).Elevation of the PaCO 2 alone does not indicatethe need for tracheal intubation. Treat the patient,not the numbers.Nebulised beta 2 -agonistsSalbutamol, 5 mg nebulised, is the cornerstone oftherapy for acute asthma in most of the world.Repeated doses every 15—20 min are often needed.Severe asthma may necessitate continuous nebulisedsalbutamol. Nebuliser units that can bedriven by high-flow oxygen should be available.The hypoventilation associated with severe or nearfatalasthma may prevent effective delivery of nebuliseddrugs.Intravenous corticosteroidsOxygen and beta-agonists are the most importanttherapies initially, but give corticosteroids (hydrocortisone,200 mg IV,) early. Although there is nodifference in clinical effects between oral and IVformulations of corticosteroids, 143 the IV route ispreferable because patients with near-fatal asthmamay vomit or be unable to swallow.Nebulised anticholinergicsNebulised anticholinergics (ipratropium, 0.5 mg4—6 h) may produce additional bronchodilation insevere asthma or in those who do not respond tobeta-agonists. 144,145Intravenous salbutamolSeveral studies have shown intravenous salbutamol(250 mcg IV slowly) to provide additional benefitin severe asthmatics who are already receivingnebulised salbutamol. 146 Give an infusion of3—20 mcg min −1 .Intravenous magnesium sulphateMagnesium sulphate (2 g, IV slowly) may be useful asa bronchodilator in severe or near-fatal asthma. ACochrane meta-analysis of seven studies concludedthat magnesium is beneficial, particularly for thosewith the most severe exacerbations. 147 Magnesiumcauses bronchial smooth muscle relaxation independentof the serum magnesium level and has onlyminor side effects (flushing, light-headedness).Intravenous theophyllineTheophylline is given IV as aminophylline, amixture of theophylline with ethylenediamine,

S150which is 20 times more soluble than theophyllinealone. Aminophylline should only be consideredin severe or near-fatal asthma. A loading doseof 5mgkg −1 is given over 20—30 min (unless onmaintenance therapy), followed by an infusion of500—700 mcg kg −1 h −1 . Addition of this drug to highdoses of beta-agonists increases side effects morethan it increases bronchodilation. Check levels toavoid toxicity.Subcutaneous or intramuscular adrenaline andterbutalineAdrenaline and terbutaline are adrenergic agentsthat may be given subcutaneously to patientswith acute severe asthma. The dose of subcutaneousadrenaline is 300 mcg up to a total of threedoses at 20-min intervals. Adrenaline may cause anincrease in heart rate, myocardial irritability andincreased oxygen demand; however, its use (evenin patients over 35 years old) is well tolerated. 148Terbutaline is given in a dose of 250 mcg subcutaneously,which can be repeated in 30—60 min.These drugs are more commonly given to childrenwith acute asthma and, although most studies haveshown them to be equally effective, 149 one studyconcluded that terbutaline was superior. 150 Thesealternative routes may need to be considered whenIV access is impossible.Intravenous fluidsSevere or near-fatal asthma is associated withdehydration and hypovolaemia, and this will furthercompromise the circulation in patients withdynamic hyperinflation of the lungs. If there is evidenceof hypovolaemia or dehydration, give IV fluids.HelioxHeliox is a mixture of helium and oxygen (usually80:20 or 70:30). A recent meta-analysis of fourclinical trials did not support the use of helioxin the initial treatment of patients with acuteasthma. 151KetamineKetamine is a parenteral dissociative anaestheticwith bronchodilatory properties. One case seriessuggested substantial effectiveness, 152 but the singlerandomised trial published to date showedno benefit to ketamine compared with standardcare. 153Non-invasive ventilationJ. Soar et al.Non-invasive ventilation decreases the intubationrate and mortality in COPD; 154 however, its rolein patients with severe acute asthma is uncertain.Although promising, a recent Cochrane review suggeststhat more studies are needed. 155Management of cardiac arrestBasic life supportGive basic life support according to the standardguidelines. Ventilation will be difficult because ofincreased airway resistance; try to prevent gastricinflation.Advanced life supportModifications to standard ALS guidelines. Considerthe need for intubation early. The peakairway pressures recorded during the ventilationof patients with severe asthma (mean67.8 ± 11.1 cmH 2 0 in 12 patients) are significantlyhigher than the normal lower oesophageal sphincterpressure (approximately 20 cmH 2 0). 156 There isa significant risk of gastric inflation and hypoventilationof the lungs when attempting to ventilatea severe asthmatic without a tracheal tube. Duringcardiac arrest this risk is even higher becausethe lower oesophageal sphincter pressure is substantiallyless than normal. 157The new recommended respiratory rate(10 breaths min −1 ) and tidal volume requiredfor a normal chest rise during CPR should notcause dynamic hyperinflation of the lungs (gastrapping). Tidal volume depends on the inspiratorytime and inspiratory flow, while lung emptyingdepends on the expiratory time and expiratoryflow. In mechanically ventilated severe asthmatics,increasing the expiratory time (achievedby reducing the respiratory rate) provides onlymoderate gains in terms of reduced gas trappingwhen a minute volume of less than 10 l min −1 isused. 156There is limited evidence from the casereports of unexpected ROSC in patients withsuspected gas trapping when the tracheal tube isdisconnected. 158—161 If dynamic hyperinflation ofthe lungs is suspected during CPR, compression ofthe chest wall and/or a period of apnoea (disconnectionof tracheal tube) may relieve gas trappingif dynamic hyperinflation occurs. Although thisprocedure is supported by limited evidence, it isunlikely to be harmful in an otherwise desperatesituation.

European Resuscitation Council Guidelines for Resuscitation 2005S151Dynamic hyperinflation increases transthoracicimpedance. 162 Consider the higher shock energiesfor defibrillation if initial defibrillation attemptsfail.There is no good evidence for the use of openchestcardiac compressions in patients with asthmaassociatedcardiac arrest. Working through the fourHs and four Ts will identify potentially reversiblecourses of asthma related cardiac arrest. Tensionpneumothorax can be difficult to diagnose in cardiacarrest; it may be indicated by unilateral expansionof the chest wall, shifting of the trachea andsubcutaneous emphysema. Release air from thepleural space with needle decompression. Insert alarge-gauge cannula in the second intercostal spacein the mid clavicular line, being careful to avoiddirect puncture of the lung. If air is emitted, inserta chest tube. Always consider bilateral pneumothoracesin asthma-related cardiac arrest.Post-resuscitation careThe following should be added to usual managementafter ROSC:• Optimise the medical management of bronchospasm.• Use permissive hypercapnia; it may not be possibleto achieve normal oxygenation and ventilationin a patient with severe bronchospasm.Efforts to achieve normal arterial blood gas valuesmay worsen lung injury. Mild hypoventilationreduces the risk of barotraumas, and hypercapnoeais typically well-tolerated. 163 Target lowerarterial blood oxygen saturations (e.g., 90%).• Provide sedation (neuromuscular paralysis ifneeded) and controlled ventilation. Despite theabsence of formal studies, ketamine and inhalationalanaesthetics have bronchodilator propertiesthat may be useful in the asthmatic patientwho is difficult to ventilate.• Involve a senior critical care doctor early.7g. AnaphylaxisIntroductionAnaphylaxis is a rare, but potentially reversible,cause of cardiac arrest. Although the managementof cardiac arrest secondary to anaphylaxis followsthe general principles described elsewhere in theseguidelines, the pathophysiological processes occurringduring anaphylaxis may require additional specifictherapy.Anaphylaxis is a severe life-threatening, generalisedor systemic hypersensitivity reaction.Investigations will show whether the reactionis allergic (immunoglobulin E (IgE) or non IgEmediated) or non-allergic anaphylaxis. The termanaphylactoid reaction is no longer used. An anaphylacticreaction is generally defined as a severe,systemic allergic reaction characterized by multisysteminvolvement, including the airway, vascularsystem, gastrointestinal tract and skin. Severecases may cause complete airway obstructionsecondary to laryngeal oedema, bronchospasm,hypotension, cardiovascular collapse and death.Other symptoms include rhinitis, conjunctivitis,abdominal pain, vomiting, diarrhoea and a senseof impending doom. There is also usually a colourchange; the patient may appear either flushed orpale. Anaphylactic reactions vary in severity, andprogress may be rapid, slow or (unusually) biphasic.Rarely, manifestations may be delayed (this mayoccur with latex allergy), or persist for more than24 h.PathophysiologyInitial exposure to an allergen may trigger animmune response that sensitises the body to subsequentexposure. This sensitisation results inantigen-specific IgE bound to the cell membrane ofbasophils and mast cells. On repeat exposure, theantigen is bound by the IgE, triggering release ofa series of inflammatory mediators including histamines,leukotrienes, prostaglandins, thromboxanesand bradykinins. These mediators act systemicallyto cause increased mucous membrane secretion,increased capillary permeability and markedlyreduced vascular smooth muscle tone. This causesthe clinical symptoms of angioedema and airwayswelling, bronchospasm, hypotension and cardiovascularcollapse.Anaphylaxis is caused by a hypersensitivity reactionin which histamine, serotonin and othervasoactive substances are released from basophilsand mast cells in response to an IgE-mediated reaction.Antigen-specific immunoglobulins are producedafter initial exposure to an allergen. Subsequentre-exposure to this allergen provokes ananaphylactic reaction, although many anaphylacticreactions occur without known previous exposure.AetiologyAlthough anaphylaxis is relatively common, progressionto a severe life-threatening reaction israre. Any antigen capable of activating IgE can theoreticallybe a trigger for anaphylaxis. The com-

S152monest causes of life-threatening reactions aredrugs, stinging insects and food. In as many as 5%of the cases, the antigen triggering the anaphylaxiscannot be identified.DrugsNeuromuscular blocking drugs (particularly suxamethonium)and antibiotics are the most commontriggers for drug-induced anaphylaxis. 164 Aspirin,non-steroidal anti-inflammatory drugs and IV contrastagents are also common causes of lifethreateninganaphylaxis.LatexLatex, or natural rubber, is a significant trigger ofanaphylaxis among hospitalised patients because offrequent instrumentation and operations in whichlatex products are used. Avoidance is the onlyeffective therapy, and the availability of latex-freeclinic and hospital environments, including patientand operating rooms, is now a priority. 165 Lifethreateninganaphylactic reactions to latex are veryrare 166,167 with a decade-long registry of anaphylacticdeaths in England not registering any latexassociateddeaths. 168,169Stinging insectsThe prevalence of IgE-mediated systemic reactionsto insect stings is 2.8% in temperateclimates, although higher in countries, such asAustralia where exposure to insect stings is morecommon. 170 The stinging insects belong to theHymenoptera order and include hornets, wasps,honeybees and fire ants. Most stings cause localreactions with pain and swelling at the site butprogress to anaphylaxis in susceptible persons.Fatal anaphylaxis occurs in people who are re-stungafter a previous sting has induced IgE antibodies.Fatal reactions occur within 10—15 min, with cardiovascularcollapse being the commonest cause ofdeath. 168,169,171FoodsLife-threatening allergic reactions to food areincreasing. Peanuts, seafood (in particular prawnsand shellfish) and wheat are the foods associatedmost frequently with life-threateninganaphylaxis. 172 Bronchospasm, angioedema, airwayobstruction and asphyxia comprise the mostcommon fatal mechanism. 168,169,171Signs and symptomsJ. Soar et al.Anaphylaxis should be considered when two ormore body systems are affected (cutaneous, respiratory,cardiovascular, neurological or gastrointestinal),with or without cardiovascular or airwayinvolvement. Symptoms may be particularlysevere in patients with asthma, those taking betaadrenoceptorblockers and during neuraxial anaesthesia:states associated with reduced endogenouscatecholamine response. The speed of the onset ofsigns and symptoms is related to the likely severityof the ensuing anaphylaxis.Early signs and symptoms include urticaria, rhinitis,conjunctivitis, abdominal pain, vomiting anddiarrhoea. Flushing is common but pallor may alsooccur. Marked upper airway (laryngeal) oedemaand bronchospasm may develop, causing stridorand wheezing (or high airway pressures in ventilatedpatients). In asthmatics, this may be particularlysevere and difficult to treat. Cardiovascularcollapse is the most common peri-arrestmanifestation. Vasodilation causes relative hypovolaemia,exacerbated by true volume loss asincreased capillary permeability results in extravasationof intravascular fluid. Additional cardiac dysfunctionmay follow from underlying disease orfrom the development of myocardial ischaemiafrom adrenaline administration. 168,169,171Differential diagnosisThe lack of any consistent clinical manifestationand a wide range of possible presentations maycause diagnostic difficulty. In each case, take asfull a history and examination as possible. The historyof previous allergic reactions, as well as thatof the recent incident is important. Pay particularattention to the condition of the skin, the pulserate, the blood pressure and the upper airways,and auscultate the chest. Measure and record thepeak flow where possible. Consider the diagnosisof other conditions only after anaphylaxis has beenexcluded; failure to identify and treat anaphylaxiscan be fatal: 173,174• ACE inhibitors may cause angioedema withmarked swelling of the upper airway. This reactionmay occur at any time and is not related to aninitial exposure to the drug. The best treatmentfor this form of angioedema is unclear, but earlyrecognition and appropriate airway managementare critical. 175• Hereditary angioedema is familial and indistinguishablefrom the early angioedema of anaphylaxisor drug-related angioedema. An important

European Resuscitation Council Guidelines for Resuscitation 2005S153distinguishing feature is the absence of urticariawith hereditary angioedema. This is treated withC1 esterase inhibitor, either as a specific concentrateor contained within fresh frozen plasma.• Severe asthma may present with bronchospasmand stridor, which are also common features ofsevere anaphylaxis. However, asthma attacks donot usually present with urticaria or angioedema.• Rarely, panic attacks may be associated withfunctional stridor as a result of forced adductionof the vocal cords. As with asthma, there is nourticaria, angioedema, hypoxia or hypotension.• Vasovagal reactions cause sudden collapse andextreme bradycardia that may be mistaken forabsence of a pulse. Recovery is usually relativelyrapid, and is not associated with urticaria,angioedema or bronchospasm.Considerations in relation to treatmentWide variations in aetiology, severity and organinvolvement preclude standardised treatment recommendations.The lack of clinical trials necessitatesguidelines based on consensus opinion.Adrenaline is generally agreed to be the mostimportant drug for any severe anaphylactic reaction.As an alpha-agonist, it reverses peripheralvasodilation and reduces oedema. Its beta-agonistproperties dilate the airways, increase the force ofmyocardial contraction and suppress histamine andleukotriene release.Adrenaline is most effective when given earlyafter the onset of the reaction, but it is not withoutrisk, particularly when given IV. When given intramuscularly,adrenaline is very safe. Adverse effectsare extremely rare, and the only patient reportedto have had a myocardial infarction after intramuscularinjection had numerous risk factors forcoronary disease. Sometimes there has been uncertaintyas to whether complications (e.g., myocardialischaemia) have been due to the effects of theallergen itself or to adrenaline given as treatmentfor it. 168,176Rarely, adrenaline may fail to reverse the clinicalmanifestations of anaphylaxis, particularly in latereactions or in patients treated with beta-blockers.Other measures then assume greater importance,particularly volume replacement.General resuscitation measuresAll victims should recline in a position of comfort.Remove the likely allergen (i.e., stop drug infusionor blood transfusion). Lying flat, with or without legelevation, may be helpful for hypotension but nothelpful for breathing difficulties. Airway obstructioncan develop rapidly due to soft tissue swelling.Consider early tracheal intubation; delay may makeintubation extremely difficult.OxygenGive high-flow oxygen (10—15 l min −1 ).AdrenalineGive adrenaline intramuscularly to all patients withclinical signs of shock, airway swelling or definitebreathing difficulty; adrenaline will be absorbedrapidly. Inspiratory stridor, wheeze, cyanosis, pronouncedtachycardia and decreased capillary fillingindicate a severe reaction. For adults, givean IM dose of adrenaline, 0.5 ml of 1:1000 solution(500 mcg). If the patient’s condition fails toimprove, repeat the dose after about 5 min. In somecases several doses may be needed, particularly ifimprovement is transient. The IM route is preferableto SC administration because absorption ismore rapid in shock. 177,178IV adrenaline (in a dilution of at least 1:10,000;never 1:1000) is hazardous and must be reservedfor patients with profound shock that is immediatelylife threatening and for special indications,for example during anaesthesia. A further 10-folddilution to 1:100,000 adrenaline enables finer titrationof the dose and increases its safety by reducingthe risk of unwanted adverse effects. This shouldbe carried out with a minimum of electrocardiographicmonitoring. Doctors experienced in the useof IV adrenaline may prefer to use the IV route inany patient with signs of severe anaphylaxis.AntihistamineGive an H 1 -antihistamine (e.g., chlorphenamine10—20 mg) by slow IV injection. Consider also anH 2 -blocker, e.g., ranitidine, 50 mg IV. 179HydrocortisoneGive hydrocortisone by slow IV injection aftersevere attacks to help avert late sequelae. This isparticularly important for asthmatics (who are at anincreased risk of severe or fatal anaphylaxis) if theyhave been treated with corticosteroids previously.Corticosteroids are considered as slow-acting drugsand may take up to 4—6 h to have an effect, even ifgiven IV. However, they may help in the emergencytreatment of an acute attack, and they also havea role in preventing or shortening the protractedreactions.

S154J. Soar et al.Inhaled bronchodilatorsAn inhaled beta 2 agonist, such as salbutamol(5 mg, repeated if necessary), may help reversethe refractory bronchospasm. Inhaled ipratropium(500 mcg, repeated as necessary) may be particularlyuseful for the treatment of bronchospasmin patients on beta-blockers. Some cases of nearfatalasthma may really be anaphylaxis, resultingin mistaken overtreatment with conventional bronchodilatorsrather than more specific treatmentwith adrenaline. 141Intravenous fluidsIf severe hypotension does not respond rapidly todrug treatment, give fluid; a rapid infusion of 1—2 lmay be required. Further fluid is likely to be necessary.Potential therapiesVasopressin. There are case reports thatvasopressin may benefit severely hypotensivepatients. 180,181Atropine. Case reports also suggest that, whenrelative or severe bradycardia is present, there maybe a role for atropine. 174Glucagon. For patients unresponsive toadrenaline, especially those receiving betablockers,glucagon may be effective. This agentis short-acting (1—2 mg every 5 min IM, or IV).Nausea, vomiting and hyperglycaemia are commonside effects.EnvenomationRarely, insect envenomation by bees, but notwasps, leaves a venom sac. Immediately scrapeaway any insect parts at the site of the sting. 182Squeezing may increase envenomation.Cardiac arrestIn addition to the ALS drugs, consider the followingtherapies.Rapid fluid resuscitationNear-fatal anaphylaxis produces profound vasodilationand a relative hypovolaemia. Massive volumereplacement is essential. Use at least two largeborecannulae with pressure bags to give large volumes(as much as 4—8 l IV fluid may be necessary inthe immediate resuscitation period).AntihistaminesGive an antihistamine IV if antihistamine has notalready been given before the arrest. 179SteroidsSteroids given during a cardiac arrest will have littleimmediate effect but, if ROSC is restored, they maybe effective in the post-resuscitation period.Prolonged CPRPatients with anaphylaxis are often young, withhealthy hearts and cardiovascular systems. EffectiveCPR may maintain sufficient oxygen deliveryuntil the catastrophic effects of the anaphylacticreaction resolve.Airway obstructionAirway obstruction may occur rapidly in severe anaphylaxis,particularly in patients with angioedema.Warning signs are lingual and labial swelling,hoarseness and oropharyngeal swelling. Considerearly, elective intubation. As airway obstructionprogresses, both LMAs and Combitubes are likelyto be difficult to insert. Tracheal intubation andcricothyroidotomy will also become increasinglydifficult. Attempts at tracheal intubation may exacerbatelaryngeal oedema. Early involvement of asenior anaesthetist is mandatory when managingthese patients.ObservationWarn patients with even moderate attacks of thepossibility of an early recurrence of symptoms and,in some circumstances, keep them under observationfor 8—24 h. This caution is particularly applicableto:• severe reactions with slow onset due to idiopathicanaphylaxis;• reactions in severe asthmatics or with a severeasthmatic component;• reactions with the possibility of continuingabsorption of allergen;• patients with a previous history of biphasicreactions. 179,183—187A patient who remains symptom-free for 4 h aftertreatment may be discharged. 188

European Resuscitation Council Guidelines for Resuscitation 2005S155Investigations and further managementMeasurement of mast cell tryptase may help withretrospective diagnosis of anaphylaxis. 189,190 Takethree 10-ml clotted blood samples:• immediately after the reaction has been treated;• about 1 h after reaction;• about 6 h and up to 24 h after reaction.It is important to identify the allergen after successfulresuscitation from anaphylaxis, to preventrecurrence. Refer the patient to a specialist clinic.Patients at very high risk of anaphylaxis may carrytheir own adrenaline syringe for self-administrationand wear a ‘MedicAlert’ type bracelet. Report reactionsto drugs to the appropriate monitoring agency.7h. Cardiac arrest following cardiacsurgeryCardiac arrest following major cardiac surgery(both on and off bypass) is relatively common in theimmediate postoperative phase, with a reportedincidence of 0.7% in the first 24 h 191 and 1.4%within the first 8 days. 192 Cardiac arrest is usuallycaused by specific pathology that is reversibleif treated promptly and appropriately, and therefore,has a relatively high survival rate. Cardiacarrest is usually preceded by physiologicaldeterioration, 193 although it may occur suddenlyin stable patients. 191 Continuous monitoring on theintensive care unit (ICU) enables immediate interventionat the time of arrest. Survival to hospitaldischarge of patients suffering from cardiacarrest during the first 24 h after adult cardiacsurgery is reported as 54% 192 —79% 191,194 and 41%in children. 193AetiologyPerioperative myocardial infarction is the commonestcause of sudden cardiac arrest and is often secondaryto graft occlusion. 191,192The main causes of cardiac arrest in the initialpostoperative period include:• myocardial ischaemia;• tension pneumothorax;• haemorrhage causing hypovolaemic shock;• cardiac tamponade;• disconnection of pacing system in pacingdependentpatient;• electrolyte disturbances (particularly hypo/hyperkalaemia).DiagnosisAn immediate decision on the likely cause of cardiacarrest must be made to enable rapid interventionand successful resuscitation. Auscultation ofthe chest, examination of the ECG and chest radiograph,transoesophageal/transthoracic echocardiographyand measurement of blood loss from chestdrains will aid in identifying the cause of the arrest.Actively seek and exclude reversible causes of cardiacarrest: the four Hs and four Ts. Myocardialischaemia often causes myocardial irritability andprogressive hypotension before an arrest. A tensionpneumothorax and cardiac tamponade will causeprogressive hypotension and an increasing centralvenous pressure. Increasing airway pressures andpoor air entry in the affected lung will differentiatebetween the two conditions. Lack of drainage ofblood from the chest drains does not exclude haemorrhageor tamponade, because drains may blockwith clot.TreatmentTreatment of cardiac arrest following cardiacsurgery follows the same principles of BLS andALS that have already been described in theseguidelines. Seek assistance from experienced clinicianswithout delay. Exclude immediately correctablecauses, such as pacing-lead disconnectionand tension pneumothorax. Extreme bradycardia orasystole may respond to pacing via internal pacingwires(if present) connected to an external pacemaker.Ensure correction of hypo/hyperkalaemiaand hypomagnesaemia. Rapid restoration of an adequateblood volume is important, ensuring thathaemoglobin levels are maintained no lower than8.0gdl −1 . Be careful when giving IV adrenaline, asthe resulting hypertension may cause catastrophicfailure of anastomoses.External chest compressionsExternal chest compressions may be necessary butmay cause sternal subluxation, fractured ribs anddamage to grafts. Continuous observation of theinvasive blood pressure will enable the force ofcompression to be optimised. Effective externalchest compressions should take precedence overthe concerns of damage to grafts.Internal cardiac massageMechanical factors (e.g., haemorrhage, tamponade,graft occlusion) account for a substantialproportion of causes of sudden cardiac arrest

S156occurring in haemodynamically stable patients duringthe immediate postoperative period. 191 Correctionof this pathology may require chest reopeningand therefore internal cardiac massage. Upto 10% of patients may need chest reopening followingcardiac surgery. 195 Overall survival to dischargethe following internal cardiac massage is17% 196 —25%. 195 Cardiac arrest on the ICU, arrestwithin 24 h of surgery, and reopening within 10 minof arrest are independent predictors of survival. 195The high incidence of potentially correctablemechanical causes of arrest, in conjunction withthe high survival rate achieved by open CPR, supportsan early approach to open-chest CPR in thesepatients. 191,197 Reopen the patient’s chest immediatelyif there is no output with external chestcompressions or if there is a shockable rhythmrefractory to cardioversion. Management of asystoleusually requires prompt chest opening. Openingof the chest is relatively straightforward and,if indicated, should be undertaken within 10 min ofcardiac arrest. Consider training the non-surgicalmedical staff to open the wound and remove sternalwires, while a surgeon is summoned. Make surethat a chest opening kit is immediately available onthe ICU. The invasive blood pressure will guide theeffectiveness of internal cardiac massage Removethe blood clot carefully, either manually or by suctioning,to avoid damaging the grafts. Early identificationand treatment of underlying pathology ischallenging under these circumstances and requiresan experienced surgeon.Reinstitution of emergency cardiopulmonarybypassThe need for emergency cardiopulmonary bypass(CPB) may occur in approximately 0.8% patients,occurring at a mean of 7 h postoperatively, 198 andis usually indicated to correct surgical bleeding orgraft occlusion and rest an exhausted myocardium.Emergency institution of CPB should be availableon all units undertaking cardiac surgery. Survival todischarge the rates of 32%, 195 42% 198 and 56.3% 199have been reported when CPB is reinstituted on theICU. Survival rates decline rapidly when this procedureis undertaken more than 24 h after surgeryand when performed on the ward rather than theICU. Emergency CPB should probably be restrictedto patients who arrest within 72 h of surgery, assurgically remediable problems are unlikely afterthis time. 195 Ensuring adequate re-anticoagulationbefore commencing CPB, or the use of a heparinbondedCPB circuit, is important. The need for afurther period of aortic cross-clamping does notpreclude a favourable outcome. 198Internal defibrillationJ. Soar et al.Internal defibrillation using paddles applied directlyacross the ventricles requires considerably lessenergy than that used for external defibrillation.Biphasic shocks are substantially more effectivethan the monophasic shocks for direct defibrillation.For biphasic shocks, starting at 5 J createsthe optimum conditions for lowest threshold andcumulative energy, whereas 10 or 20 J offers optimumconditions for more rapid defibrillation andfewer shocks. 200 Monophasic shocks require approximatelydouble these energy levels. 2007i. Traumatic cardiorespiratory arrestIntroductionCardiac arrest secondary to traumatic injury hasa very high mortality, with an overall survival ofjust 2.2% (range, 0—3.7%) (Table 7.4). 201—207 Inthose who survive, neurological disability is common,being absent in only 0.8% of those sufferingfrom traumatic cardiorespiratory arrest (TCRA).Diagnosis of traumatic cardiorespiratoryarrestThe diagnosis of TCRA is made clinically: the traumapatient is unresponsive, apnoeic and pulseless. Bothasystole and organised cardiac activity without cardiacoutput are regarded as TCRA.Commotio cordisCommotio cordis is actual or near cardiac arrestcaused by a blunt impact to the chest wall overthe heart. 208—211 A blow on the chest during thevulnerable phase of the cardiac cycle may causemalignant arrhythmias (usually VF). Syncope afterchest wall impact may be caused by non-sustainedarrhythmic events. Commotio cordis occurs mostlyduring sports (most commonly baseball) and recreationalactivities, and victims are usually youngmales (mean age 14 years). The Commotio CordisRegistry in Minneapolis is accruing 5—15 cases ofcommotio cordis each year. The overall survival ratefrom commotio cordis is 15%, but reaches 25% ifresuscitation is started within 3 min. 211Trauma secondary to medical eventsA cardiorespiratory arrest caused by a medicalpathology (e.g., cardiac arrhythmia, hypoglycaemia,seizure) may precipitate a secondary

European Resuscitation Council Guidelines for Resuscitation 2005S157traumatic event (e.g., fall, road traffic accident,etc.). Traumatic injuries may not be the primarycause of a cardiorespiratory arrest.Mechanism of injuryBlunt traumaOf 1242 patients with cardiac arrest after blunttrauma, 19 (1.5%) survived, but only 2 (0.16%) hada good neurological outcome (Table 7.4).Penetrating traumaOf 839 patients with cardiac arrest after penetratinginjury, there were 16 (1.9%) survivors, ofwhom 12 (1.4%) had a good neurological outcome(Table 7.4).Signs of life and initial ECG activityThere are no reliable predictors of survival forTCRA. One study reported that the presence ofreactive pupils and sinus rhythm correlated significantlywith survival. 217 In a study of penetratingtrauma, pupil reactivity, respiratory activity andsinus rhythm were correlated with survival but wereunreliable. 207 Three studies reported no survivorsamong patients presenting with asystole or agonalrhythms. 202,207,218 Another reported no survivors inPEA after blunt trauma. 219 Based on these studies,the American College of Surgeons and the NationalAssociation of EMS Physicians produced prehospitalguidelines on withholding resuscitation. 220 Theyrecommend withholding resuscitation in:• blunt trauma victims presenting apnoeic andpulseless, and without organised ECG activity;• penetrating trauma victims found apnoeic andpulseless after rapid assessment for signs of life,such as pupillary reflexes, spontaneous movementor organised ECG activity.A recent retrospective study questions theserecommendations: in a series of 184 TCRA victims,several survivors met the criteria for nonresuscitation.221TreatmentSurvival from TCRA is correlated with duration ofCPR and prehospital time. 205,222—226 Prolonged CPRis associated with a poor outcome; the maximumCPR time associated with a favourable outcome is16 min. 205,222—224 The level of prehospital interventionwill depend on the skills of local EMS providers,but treatment on scene should focus on good qualityBLS and ALS and exclusion of reversible causes.Look for and treat any medical condition that mayhave precipitated the trauma event. Undertakeonly the essential lifesaving interventions on sceneand, if the patient has signs of life, transfer rapidlyto the nearest appropriate hospital. Consider onscenethoracostomy for appropriate patients. 227,228Do not delay for unproven interventions, such asspinal immobilisation. 229Resuscitative thoracotomyPrehospital. Resuscitative thoracotomy has beenreported as futile if out-of-hospital time hasexceeded 30 min; 225 others consider thoracotomyto be futile in patients with blunt trauma requiringmore than 5 min of prehospital CPR and in patientswith penetrating trauma requiring more than 15 minof CPR. 226 With these time limits in mind, one UKservice recommends that, if surgical interventioncannot be accomplished within 10 min after lossof pulse in patients with penetrating chest injury,on-scene thoracotomy should be considered. 227Following this approach, of 39 patients whounderwent thoracotomy at scene, 4 patients survivedand 3 of these made a good neurologicalrecovery.Hospital. A relatively simple technique forresuscitative thoracotomy has been describedrecently. 228,230 The American College of Surgeonshas published practice guidelines for emergencydepartment thoracotomy (EDT) based on a metaanalysisof 42 outcome studies including 7035EDTs. 231 The overall survival rate was 7.8%, andof 226 survivors (5%), only 34 (15%) exhibited aneurological deficit. The investigators concludedthe following:• After blunt trauma, EDT should be limited tothose with vital signs on arrival and a witnessedcardiac arrest (estimated survival rate 1.6%).• Emergency department thoracotomy is bestapplied to patients with penetrating cardiacinjuries, who arrive at the trauma centre aftershort on-scene and transport times, with witnessedsigns of life or ECG activity (estimatedsurvival rate 31%).• Emergency department thoracotomy should beundertaken in penetrating non-cardiac thoracicinjuries even though survival rates are low.• Emergency department thoracotomy should beundertaken in patients with exsanguinatingabdominal vascular injury even though survivalrates are low. This procedure should be used as

S158J. Soar et al.Table 7.4Survival after traumatic cardiac arrestSource Entry criteria Number of survivorsneurologically intactBouillon 212Pulseless, requiringCPR at scene22443Number of survivors ofpenetrating traumaneurologically intactNumber of survivorsof blunt traumaneurologically intactBattistella 202Pasquale 206Fisher 213Hazinski 214Pulseless, requiringCPR at scene, en routeor in EDCPR before or onhospital admissionChildren requiring CPRbefore or on admissionafter blunt traumaChildren requiring CPRor being severelyhypotensive onadmission after blunttraumaShimazu 203 TCRA on admission 26774Calkins 215Children requiring CPRafter blunt trauma604 300 30416 12 49 9 0106 21 853 1 265 381 10 038 651 10 025 252 22 2Yanagawa 216 OHCA in blunt trauma 332 3326 60 0Rosemurgy 201 CPR before admission 138 42 960 0 00 0 0Stratton 207Unconscious, pulselessat sceneCera 217 CPR on admission 16115?879 497 3829 4 53 3 0For each study, the first number indicates the number of patients in cardiac arrest, the second indicates the numbers of survivorsand the third indicates the number of survivors with a good neurological outcome. CPR = cardiopulmonary resuscitation;ED = emergency department; TCRA = traumatic cardiorespiratory arrest; OHCA = out-of-hospital cardiac arrest.an adjunct to definitive repair of abdominal vascularinjury.Airway managementEffective airway management is essential to maintainoxygenation of the severely compromisedtrauma victim. In one study, tracheal intubation onsceneof patients with TCRA doubled the toleratedperiod of CPR, i.e., the mean time of CPR for survivorswho were intubated in the field was 9.1 minversus 4.2 min for those who were not intubated. 224Tracheal intubation of trauma victims is a difficultprocedure with a high failure rate if carriedout by less experienced care providers. 232—235Use the basic airway management manoeuvres andalternative airways to maintain oxygenation if trachealintubation cannot be accomplished immediately.If these measures fail, a surgical airway isindicated.

European Resuscitation Council Guidelines for Resuscitation 2005S159VentilationIn low cardiac output states positive pressure ventilationcauses further circulatory depression, oreven cardiac arrest, by impeding venous return tothe heart. 236 Monitor ventilation with capnometryand adjust to achieve normocapnia. This mayenable slow respiratory rates and low tidal volumes,and the corresponding decrease in transpulmonarypressure may increase venous return and cardiacoutput.Chest decompressionEffective decompression of a tension pneumothoraxcan be achieved quickly by lateral thoracostomy,which is likely to be more effective than needlethoracostomy and quicker than inserting a chesttube. 237Effectiveness of chest compressions in TCRAIn hypovolaemic cardiac arrest or cardiac tamponade,chest compressions are unlikely to be aseffective as in cardiac arrest from other causes; 238nonetheless, return of spontaneous circulation withALS in patients with TCRA is well described. Chestcompressions are still the standard of care inpatients with cardiac arrest, irrespective of aetiology.Haemorrhage controlEarly haemorrhage control is vital. Handle thepatient gently at all times, to prevent clot disruption.Apply external compression and pelvic andlimb splints when appropriate. Delays in surgicalhaemostasis are disastrous for patients with exsanguinatingtrauma.PericardiocentesisIn patients with suspected trauma-related cardiactamponade, needle pericardiocentesis is probablynot a useful procedure. 239 There is no evidenceof benefit in the literature. It may increase scenetime, cause myocardial injury and delay effectivetherapeutic measures, such as emergency thoracotomy.Fluids and blood transfusion on sceneFluid resuscitation of trauma victims before haemorrhageis controlled is controversial, and there isno clear consensus on when it should be startedand what fluids should be given. 240 Limited evidenceand general consensus support a more conservativeapproach to IV fluid infusion, with permissivehypotension until surgical haemostasis isachieved. 241,242 In the UK, the National Institute forClinical Excellence (NICE) has published guidelineson prehospital fluid replacement in trauma. 243 Therecommendations include giving 250 ml boluses ofcrystalloid solution until a radial pulse is achieved,and not delaying rapid transport of trauma victimsfor fluid infusion in the field. Prehospital fluid therapymay have a role in prolonged entrapments, butthere is no reliable evidence for this. 244,245UltrasoundUltrasound is a valuable tool in the evaluation of thecompromised trauma victim. Haemoperitoneum,haemo- or pneumothorax and cardiac tamponadecan be diagnosed reliably in minutes even in theprehospital phase. 246 Diagnostic peritoneal lavageand needle pericardiocentesis have virtually disappearedfrom clinical practice since the introductionof sonography in trauma care. Prehospital ultrasoundis now available, although its benefits are yetto be proven.VasopressorsThe possible role of vasopressors (e.g., vasopressin)in trauma resuscitation is unclear and is basedmainly on case reports. 2477j. Cardiac arrest associated withpregnancyOverviewMortality related to pregnancy in developed countriesis rare, occurring in an estimated 1:30,000deliveries. 248 The fetus must always be consideredwhen an adverse cardiovascular event occurs in apregnant woman. Resuscitation guidelines for pregnancyare based largely on case series and scientificrationale. Most reports address the causes in developedcountries, whereas the majority of pregnancyrelateddeaths occur in the developing world.Significant physiological changes occur duringpregnancy, e.g., cardiac output, blood volume,minute ventilation and oxygen consumption allincrease. Furthermore, the gravid uterus may causesignificant compression of iliac and abdominal vesselswhen the mother is in the supine position,resulting in reduced cardiac output and hypotension.

S160CausesThere are many causes of cardiac arrest in pregnantwomen. A review of nearly 2 million pregnancies inthe UK 248 showed that maternal death was associatedwith:• pre-existing cardiac disease;• thromboembolism;• suicide;• hypertensive disorders of pregnancy;• sepsis;• ectopic pregnancy;• haemorrhage;• amniotic fluid embolism;Pregnant women can also suffer the same causesof cardiac arrest as women of the same agegroup.Key interventions to prevent cardiac arrestIn an emergency, use an ABCDE approach. Manycardiovascular problems associated with pregnancyare caused by caval compression. Treat a distressedor compromised pregnant patient as follows:• Place the patient in the left lateral position ormanually and gently displace the uterus to theleft.• Give 100% oxygen.• Give a fluid bolus.• Immediately re-evaluate the need for any drugsbeing given.• Seek expert help early.Modifications to BLS guidelines for cardiacarrestAfter 20 weeks’ gestation, the pregnant woman’suterus can press down against the inferior vena cavaand the aorta, impeding venous return and cardiacoutput. Uterine obstruction of venous return cancause pre-arrest hypotension or shock and, in thecritically ill patient, may precipitate arrest. 249,250After cardiac arrest, the compromise in venousreturn and cardiac output by the gravid uteruslimit the effectiveness of chest compressions. Noncardiacarrest data show that the gravid uterus canbe shifted away from the cava in most cases byplacing the patient in 15 degrees of left lateraldecubitus position. 251 Tilt may be accomplished bymanual or mechanical means. There is no evidenceto guide the hand position for optimum chest compressionsin the pregnant patient. A hand positionhigher than the normal position for chest compressionmay be needed to adjust for the elevationJ. Soar et al.of the diaphragm and abdominal contents causedby the gravid uterus. Attempt defibrillation usingstandard energy doses. 252 There is no evidencethat shocks from a direct current defibrillator haveadverse effects on the fetal heart. Left lateral tiltand large breasts will make it difficult to place anapical defibrillator paddle. Adhesive defibrillatorpads are preferable to paddles in pregnancy.Modifications to advanced life supportThere is a greater potential for gastro-oesophagealsphincter insufficiency and risk of pulmonary aspirationof gastric contents. Early tracheal intubationwith correctly applied cricoid pressure decreasesthis risk. Tracheal intubation will make ventilationof the lungs easier in the presence of increasedintra-abdominal pressure.A tracheal tube 0.5—1 mm internal diameter (ID)smaller than that used for a non-pregnant womanof similar size may be necessary because of maternalairway narrowing from oedema and swelling. 253Tracheal intubation may be more difficult in thepregnant patient. 254 Expert help, a failed intubationdrill and the use of alternative airway devicesmay be needed (see section 4d). 255Reversible causesRescuers should attempt to identify common andreversible causes of cardiac arrest in pregnancyduring resuscitation attempts. The 4 Hs and 4 Tsapproach helps to identify all the common causes ofcardiac arrest in pregnancy. Pregnant patients areat risk of all the other causes of cardiac arrest fortheir age group (e.g., anaphylaxis, drug overdose,trauma). Consider the use of abdominal ultrasoundby a skilled operator to detect pregnancy and possiblecauses during cardiac arrest in pregnancy; however,do not delay other treatments. Specific causesof cardiac arrest in pregnancy include the following:HaemorrhageLife-threatening haemorrhage can occur bothantenatally and postnatally. Associations includeectopic pregnancy, placental abruption, placentapraevia and uterine rupture. 248 A massive haemorrhageprotocol must be available in all units andshould be updated and rehearsed regularly in conjunctionwith the blood bank. Women at high risk ofbleeding should be delivered in centres with facilitiesfor blood transfusion, intensive care and otherinterventions, and plans should be made in advancefor their management. Treatment is based on an

European Resuscitation Council Guidelines for Resuscitation 2005S161ABCDE approach. The key step is to stop the bleeding.Consider the following:• fluid resuscitation including use of rapid transfusionsystem and cell salvage; 256• correction of coagulopathy. There may be a rolefor recombinant Factor VIIa; 257• oxytocin and prostaglandins to correct uterineatony; 258• uterine compression sutures; 259• radiological embolisation; 260• hysterectomy;• aortic cross-clamping in catastrophic haemorrhage.261DrugsIatrogenic overdose is possible in eclamptic womenreceiving magnesium sulphate, particularly if thewoman becomes oliguric. Give calcium to treatmagnesium toxicity (see life-threatening electrolyteabnormalities).Central neural blockade for analgesia or anaesthesiamay cause problems due to sympatheticblockade (hypotension, bradycardia) or local anaesthetictoxicity. 262Cardiovascular diseasePulmonary hypertension causes most deaths fromcongenital heart disease. Peripartum cardiomyopathy,myocardial infarction and aneurysm or dissectionof the aorta or its branches cause most deathsfrom acquired cardiac disease. 263,264 Patients withknown cardiac disease need to be managed in a specialistunit. Pregnant women with coronary arterydisease may suffer an acute coronary syndrome.Percutaneous coronary intervention is the reperfusionstrategy of choice for ST-elevation myocardialinfarction in pregnancy because fibrinolytics arerelatively contraindicated. 265Pre-eclampsia and eclampsiaEclampsia is defined as the development of convulsionsand/or unexplained coma during pregnancy orpostpartum in patients with signs and symptoms ofpre-eclampsia. 266,267 Magnesium sulphate is effectivein preventing approximately half of the casesof eclampsia developing in labour or immediatelypostpartum in women with pre-eclampsia.Life-threatening pulmonary embolismSuccessful use of fibrinolytics for massive, lifethreateningpulmonary embolism in pregnantwomen has been reported. 268—271Amniotic fluid embolismAmniotic fluid embolism may present with breathlessness,cyanosis, arrhythmias, hypotension andhaemorrhage associated with disseminated intravascularcoagulopathy. 272 Presentation is variableand may be similar to anaphylaxis. Treatment issupportive, as there is no specific therapy. Successfuluse of cardiopulmonary bypass for womensuffering life-threatening amniotic fluid embolismduring labour and delivery is reported. 273If immediate resuscitation attempts failConsider the need for an emergency hysterotomyor Caesarean section as soon as a pregnant womangoes into cardiac arrest. In some circumstancesimmediate resuscitation attempts will restore aperfusing rhythm; in early pregnancy this mayenable the pregnancy to proceed to term. Wheninitial resuscitation attempts fail, delivery ofthe fetus may improve the chances of successfulresuscitation of the mother and fetus. 274—276 Thebest survival rate for infants over 24—25 weeks’gestation occurs when delivery of the infant isachieved within 5 min after the mother’s cardiacarrest. 274,277—279 This requires that the providercommence the hysterotomy at about 4 min aftercardiac arrest. Delivery will relieve caval compressionand improve chances of maternal resuscitation.The Caesarean delivery also enables accessto the infant so that newborn resuscitation canbegin.Decision-making for emergency hysterotomyConsider gestational age. The gravid uterusreaches a size that will begin to compromise aortocavalblood flow at approximately 20 weeks’ gestation;however, fetal viability begins at approximately24—25 weeks. Portable ultrasounds areavailable in some emergency departments and mayaid in determination of gestational age (in experiencedhands) and positioning, provided their usedoes not delay the decision to perform emergencyhysterotomy. 280• At gestational age

S162of the delivered infant, which is unlikely at thisgestational age.• At gestational age approximately ≥24—25 weeks,initiate emergency hysterotomy to save the lifeof both the mother and the infant.Planning for emergencies. Advanced life supportin pregnancy requires coordination of maternalresuscitation, Caesarean delivery of the fetus andnewborn resuscitation within 5 min. To achieve this,units likely to deal with cardiac arrest in pregnancyshould:• have plans and equipment for resuscitation ofboth the pregnant woman and newborn in place;• ensure early involvement of obstetric and neonatalteams;• ensure regular training in obstetric emergencies.7k. ElectrocutionIntroductionElectrical injury is a relatively infrequent butpotentially devastating multisystem injury withhigh morbidity and mortality, causing 0.54 deathsper 100,000 people each year. Most electricalinjuries in adults occur in the workplace and areassociated generally with high voltage, whereaschildren are at risk primarily at home, where thevoltage is lower (220 V in Europe, Australia and Asia;110 V in the USA and Canada). 281 Electrocution fromlightning strikes is rare, but worldwide it causes1000 deaths each year. 282Electric shock injuries are caused by the directeffects of current on cell membranes and vascularsmooth muscle. The thermal energy associated withhigh-voltage electrocution will also cause burns.Factors influencing the severity of electrical injuryinclude whether the current is alternating (AC) ordirect (DC), voltage, magnitude of energy delivered,resistance to current flow, pathway of currentthrough the patient, and the area and duration ofcontact. Skin resistance is decreased by moisture,which increases the likelihood of injury. Electriccurrent follows the path of least resistance; conductiveneurovascular bundles within limbs are particularlyprone to damage.Contact with AC may cause tetanic contractionof skeletal muscle, which may prevent release fromthe source of electricity. Myocardial or respiratoryfailure may cause immediate death.• Respiratory arrest may be caused by paralysis ofthe central respiratory control system or the respiratorymuscles.J. Soar et al.• Current may precipitate ventricular fibrillation(VF) if it traverses the myocardium duringthe vulnerable period (analogous to an R-on-T phenomenon). 283 Electrical current may alsocause myocardial ischaemia because of coronaryartery spasm. Asystole may be primary, or secondaryto asphyxia following respiratory arrest.Current that traverses the myocardium is morelikely to be fatal. A transthoracic (hand-to-hand)pathway is more likely to be fatal than a vertical(hand-to-foot) or straddle (foot-to-foot) pathway.There may be extensive tissue destruction along thecurrent pathway.Lightning strikeLightning strikes deliver as much as 300 kilovoltsover a few ms. Most of the current froma lightning strike passes over the surface of thebody in a process called ‘external flashover’. Bothindustrial shocks and lightning strikes cause deepburns at the point of contact. For industry thepoints of contact are usually on the upper limbs,hands and wrists, whereas for lightning they aremostly on the head, neck and shoulders. Injurymay also occur indirectly through ground currentor current ‘splashing’ from a tree or other objectthat is hit by lightning. 284 Explosive force maycause blunt trauma. 285 The pattern and severityof injury from a lightning strike varies considerably,even among affected individuals from a singlegroup. 286—288 As with industrial and domesticelectric shock, death is caused by cardiac 287—291 orrespiratory arrest. 284,292 In those who survive theinitial shock, extensive catecholamine release orautonomic stimulation may occur, causing hypertension,tachycardia, non-specific ECG changes(including prolongation of the QT interval and transientT-wave inversion), and myocardial necrosis.Creatine kinase may be released from myocardialand skeletal muscle. Lightning can also cause centraland peripheral nerve damage; brain haemorrhageand oedema, and peripheral nerve injury arecommon. Mortality from lightning injuries is as highas 30%, with up to 70% of survivors sustaining significantmorbidity. 293—295DiagnosisThe circumstances surrounding the incident are notalways known. Unconscious patients with linear orpunctuate burns or feathering should be treated asa victims of lightning strike. 284

European Resuscitation Council Guidelines for Resuscitation 2005S163RescueEnsure that any power source is switched off anddo not approach the casualty until it is safe.High voltage (above domestic mains) electricitycan arc and conduct through the ground for upto a few metres around the casualty. It is safeto approach and handle casualties after lightningstrike, although it would be wise to move to a saferenvironment, particularly if lightning has been seenwithin 30 min. 284ResuscitationStart standard basic and advanced life support withoutdelay.• Airway management may be difficult if there areelectrical burns around the face and neck. Earlytracheal intubation is needed in these cases, asextensive soft-tissue oedema may develop causingairway obstruction. Head and spine traumacan occur after electrocution. Immobilise thespine until evaluation can be performed.• Muscular paralysis, especially after high voltage,may persist for several hours; 294 ventilatory supportis required during this period.• VF is the commonest initial arrhythmia after highvoltageAC shock; treat with prompt attempteddefibrillation. Asystole is more common after DCshock; use standard protocols for this and otherarrhythmias.• Remove smouldering clothing and shoes to preventfurther thermal injury.• Vigorous fluid therapy is required if there issignificant tissue destruction. Maintain a goodurine output to enhance the excretion of myoglobin,potassium and other products of tissuedamage. 291• Consider early surgical intervention in patientswith severe thermal injuries.• Maintain spinal immobilisation if there is a likelihoodof head or neck trauma. 296,297• Conduct a thorough secondary survey to excludetraumatic injuries caused by tetanic muscularcontraction or by the person being thrown. 297,298• Electrocution can cause severe, deep soft-tissueinjury with relatively minor skin wounds, becausecurrent tends to follow neurovascular bundles;look carefully for features of compartment syndrome,which will necessitate fasciotomy.Patients struck by lightning are most likely todie if they suffer immediate cardiac or respiratoryarrest and are not treated rapidly. When multiplevictims are struck simultaneously by lightning,rescuers should give highest priority to patientsin respiratory or cardiac arrest. Victims with respiratoryarrest may require only ventilation toavoid secondary hypoxic cardiac arrest. Resuscitativeattempts may have higher success ratesin lightning victims than in patients with cardiacarrest from other causes, and efforts maybe effective even when the interval before theresuscitative attempt is prolonged. 292 Dilated ornon-reactive pupils should never be used as a prognosticsign, particularly in patients suffering a lightningstrike. 284There are conflicting reports on the vulnerabilityof the fetus to electric shock. The clinical spectrumof electrical injury ranges from a transientunpleasant sensation for the mother with no effecton her fetus, to fetal death either immediately ora few days later. Several factors, such as the magnitudeof the current and the duration of contact,are thought to affect outcome. 299Further treatment and prognosisImmediate resuscitation in young victims of cardiacarrest due to electrocution can result in survival.Successful resuscitation has been reported afterprolonged life support. All those who survive electricalinjury should be monitored in hospital if theyhave a history of cardiorespiratory problems or havesuffered:• loss of consciousness;• cardiac arrest;• electrocardiographic abnormalities;• soft-tissue damage and burns.Severe burns (thermal or electrical), myocardialnecrosis, the extent of central nervous systeminjury, and secondary multisystem organ failuredetermine the morbidity and long-term prognosis.There is no specific therapy for electrical injury,and the management is symptomatic. Preventionremains the best way to minimise the prevalenceand severity of electrical injury.References1. Guidelines 2000 for Cardiopulmonary Resuscitation andEmergency Cardiovascular Care: International Consensuson Science. Part 8: Advanced challenges in resuscitation.Section 1. Life-threatening electrolyte abnormalities. Circulation2000;102:I-122—217.2. Niemann JT, Cairns CB. Hyperkalemia and ionized hypocalcemiaduring cardiac arrest and resuscitation: possible culpritsfor postcountershock arrhythmias? Ann Emerg Med1999;34:1—7.3. Ahmed J, Weisberg LS. Hyperkalemia in dialysis patients.Semin Dial 2001;14:348—56.

S1644. Mahoney B, Smith W, Lo D, Tsoi K, Tonelli M, Clase C. Emergencyinterventions for hyperkalaemia. Cochrane DatabaseSyst Rev 2005. CD003235.5. Ngugi NN, McLigeyo SO, Kayima JK. Treatment ofhyperkalaemia by altering the transcellular gradient inpatients with renal failure: effect of various therapeuticapproaches. East Afr Med J 1997;74:503—9.6. Allon M, Shanklin N. Effect of bicarbonate administrationon plasma potassium in dialysis patients: interactions withinsulin and albuterol. Am J Kidney Dis 1996;28:508—14.7. Rastegar A, Soleimani M. Hypokalaemia and hyperkalaemia.Postgrad Med J 2001;77:759—64.8. Cohn JN, Kowey PR, Whelton PK, Prisant LM. New guidelinesfor potassium replacement in clinical practice: a contemporaryreview by the National Council on Potassium inClinical Practice. Arch Intern Med 2000;160:2429—36.9. Litovitz TL, Felberg L, White S, Klein-Schwartz W. 1995annual report of the American Association of Poison ControlCenters Toxic Exposure Surveillance System. Am J EmergMed 1996;14:487—537.10. McCaig LF, Burt CW. Poisoning-related visits to emergencydepartments in the United States, 1993—1996. J ToxicolClin Toxicol 1999;37:817—26.11. Fingerhut LA, Cox CS. Poisoning mortality, 1985—1995. PublicHealth Rep 1998;113:218—33.12. Watson WA, Litovitz TL, Klein-Schwartz W, et al. 2003annual report of the American Association of Poison ControlCenters Toxic Exposure Surveillance System. Am J EmergMed 2004;22:335—404.13. Zimmerman JL. Poisonings and overdoses in the intensivecare unit: general and specific management issues. CritCare Med 2003;31:2794—801.14. Suntres ZE. Role of antioxidants in paraquat toxicity. Toxicology2002;180:65—77.15. Facility assessment guidelines for regional toxicology treatmentcenters. American Academy of Clinical Toxicology. JToxicol Clin Toxicol 1993;31:211—7.16. Poison information and treatment systems. American Collegeof Emergency Physicians. Ann Emerg Med 1996;28:384.17. Chyka PA, Seger D, Krenzelok EP, Vale JA. Positionpaper: single-dose activated charcoal. Clin Toxicol (Phila)2005;43:61—87.18. Vale JA, Kulig K. Position paper: gastric lavage. J ToxicolClin Toxicol 2004;42:933—43.19. Krenzelok EP. Ipecac syrup-induced emesis.. no evidenceof benefit. Clin Toxicol (Phila) 2005;43:11—2.20. Position paper: cathartics. J Toxicol Clin Toxicol2004;42:243—53.21. Position paper: whole bowel irrigation. J Toxicol Clin Toxicol2004;42:843—54.22. Proudfoot AT, Krenzelok EP, Vale JA. Position Paper on urinealkalinization. J Toxicol Clin Toxicol 2004;42:1—26.23. Golper TA, Bennett WM. Drug removal by continuousarteriovenous haemofiltration. A review of the evidencein poisoned patients. Med Toxicol Adverse Drug Exp1988;3:341—9.24. Pitetti RD, Singh S, Pierce MC. Safe and efficacious use ofprocedural sedation and analgesia by nonanesthesiologistsin a pediatric emergency department. Arch Pediatr AdolescMed 2003;157:1090—6.25. Osterwalder JJ. Naloxone — for intoxications with intravenousheroin and heroin mixtures — harmless or hazardous?A prospective clinical study. J Toxicol Clin Toxicol1996;34:409—16.26. Sporer KA, Firestone J, Isaacs SM. Out-of-hospital treatmentof opioid overdoses in an urban setting. Acad EmergMed 1996;3:660—7.J. Soar et al.27. Wanger K, Brough L, Macmillan I, Goulding J, MacPhail I,Christenson JM. Intravenous vs. subcutaneous naloxone forout-of-hospital management of presumed opioid overdose.Acad Emerg Med 1998;5:293—9.28. Hasan RA, Benko AS, Nolan BM, Campe J, Duff J, ZureikatGY. Cardiorespiratory effects of naloxone in children. AnnPharmacother 2003;37:1587—92.29. Sporer KA. Acute heroin overdose. Ann Intern Med1999;130:584—90.30. Schneir AB, Vadeboncoeur TF, Offerman SR, et al. Massiveoxycontin ingestion refractory to naloxone therapy. AnnEmerg Med 2002;40:425—8.31. Kelly AM, Kerr D, Dietze P, Patrick I, Walker T, KoutsogiannisZ. Randomised trial of intranasal versus intramuscularnaloxone in prehospital treatment for suspected opioidoverdose. Med J Aust 2005;182:24—7.32. Brown TC. Sodium bicarbonate treatment for tricyclicantidepressant arrhythmias in children. Med J Aust1976;2:380—2.33. Hoffman JR, Votey SR, Bayer M, Silver L. Effect of hypertonicsodium bicarbonate in the treatment of moderateto-severecyclic antidepressant overdose. Am J Emerg Med1993;11:336—41.34. Knudsen K, Abrahamsson J. Epinephrine and sodium bicarbonateindependently and additively increase survivalin experimental amitriptyline poisoning. Crit Care Med1997;25:669—74.35. Nattel S, Mittleman M. Treatment of ventricular tachyarrhythmiasresulting from amitriptyline toxicity in dogs.J Pharmacol Exp Ther 1984;231:430—5.36. Nattel S, Keable H, Sasyniuk BI. Experimental amitriptylineintoxication: electrophysiologic manifestations and management.J Cardiovasc Pharmacol 1984;6:83—9.37. Pentel P, Benowitz N. Efficacy and mechanism of action ofsodium bicarbonate in the treatment of desipramine toxicityin rats. J Pharmacol Exp Ther 1984;230:12—9.38. Brown TC, Barker GA, Dunlop ME, Loughnan PM. Theuse of sodium bicarbonate in the treatment of tricyclicantidepressant-induced arrhythmias. Anaesth IntensiveCare 1973;1:203—10.39. Brown TC. Tricyclic antidepressant overdosage: experimentalstudies on the management of circulatory complications.Clin Toxicol 1976;9:255—72.40. Hedges JR, Baker PB, Tasset JJ, Otten EJ, Dalsey WC,Syverud SA. Bicarbonate therapy for the cardiovascular toxicityof amitriptyline in an animal model. J Emerg Med1985;3:253—60.41. Sasyniuk BI, Jhamandas V, Valois M. Experimentalamitriptyline intoxication: treatment of cardiac toxicitywith sodium bicarbonate. Ann Emerg Med 1986;15:1052—9.42. Stone CK, Kraemer CM, Carroll R, Low R. Does a sodiumfreebuffer affect QRS width in experimental amitriptylineoverdose? Ann Emerg Med 1995;26:58—64.43. McCabe JL, Cobaugh DJ, Menegazzi JJ, Fata J. Experimentaltricyclic antidepressant toxicity: a randomized,controlled comparison of hypertonic saline solution,sodium bicarbonate, and hyperventilation. Ann Emerg Med1998;32:329—33.44. Sasyniuk BI, Jhamandas V. Mechanism of reversal oftoxic effects of amitriptyline on cardiac Purkinjefibers by sodium bicarbonate. J Pharmacol Exp Ther1984;231:387—94.45. Sasyniuk BI, Jhamandas V. Frequency-dependent effects ofamitriptyline on V max in canine Purkinje fibers and its alterationby alkalosis. Proc West Pharmacol Soc 1986;29:73—5.46. Bou-Abboud E, Nattel S. Molecular mechanisms of thereversal of imipramine-induced sodium channel blockade

European Resuscitation Council Guidelines for Resuscitation 2005S165by alkalinization in human cardiac myocytes. CardiovascRes 1998;38:395—404.47. Levitt MA, Sullivan Jr JB, Owens SM, Burnham L, FinleyPR. Amitriptyline plasma protein binding: effect of plasmapH and relevance to clinical overdose. Am J Emerg Med1986;4:121—5.48. McKinney PE, Rasmussen R. Reversal of severe tricyclicantidepressant-induced cardiotoxicity with intravenoushypertonic saline solution. Ann Emerg Med 2003;42:20—4.49. Brogan WCI, Lange RA, Kim AS, Moliterno DJ, Hillis LD.Alleviation of cocaine-induced coronary vasoconstrictionby nitroglycerin. J Am Coll Cardiol 1991;18:581—6.50. Lange RA, Cigarroa RG, Yancy Jr CW, et al. Cocaineinducedcoronary-artery vasoconstriction. N Engl J Med1989;321:1557—62.51. Lange RA, Cigarroa RG, Flores ED, et al. Potentiationof cocaine-induced coronary vasoconstriction by betaadrenergicblockade. Ann Intern Med 1990;112:897—903.52. Boehrer JD, Moliterno DJ, Willard JE, Hillis LD, Lange RA.Influence of labetalol on cocaine-induced coronary vasoconstrictionin humans. Am J Med 1993;94:608—10.53. Bosse GM, Pope TM. Recurrent digoxin overdose and treatmentwith digoxin-specific Fab antibody fragments. JEmerg Med 1994;12:179—85.54. Eddleston M, Rajapakse S, Rajakanthan, et al. Anti-digoxinFab fragments in cardiotoxicity induced by ingestion ofyellow oleander: a randomised controlled trial. Lancet2000;355:967—72.55. Dasgupta A, Szelei-Stevens KA. Neutralization of freedigoxin-like immunoreactive components of orientalmedicines Dan Shen and Lu-Shen-Wan by the Fab fragmentof antidigoxin antibody (Digibind). Am J Clin Pathol2004;121:276—81.56. Bailey B. Glucagon in beta-blocker and calcium channelblocker overdoses: a systematic review. J Toxicol Clin Toxicol2003;41:595—602.57. Dewitt CR, Waksman JC. Pharmacology, pathophysiologyand management of calcium channel blocker and betablockertoxicity. Toxicol Rev 2004;23:223—38.58. Wax PM, Erdman AR, Chyka PA, et al. beta-blocker ingestion:an evidence-based consensus guideline for out-ofhospitalmanagement. Clin Toxicol (Phila) 2005;43:131—46.59. Peden MM, McGee K. The epidemiology of drowning worldwide.Inj Control Saf Promot 2003;10:195—9.60. Driscoll TR, Harrison JA, Steenkamp M. Review of the roleof alcohol in drowning associated with recreational aquaticactivity. Inj Prev 2004;10:107—13.61. Papa L, Hoelle R, Idris A. Systematic review of definitionsfor drowning incidents. Resuscitation 2005;65:255—64.62. Idris AH, Berg RA, Bierens J, et al. Recommended guidelinesfor uniform reporting of data from drowning: The ‘‘Utsteinstyle’’. Resuscitation 2003;59:45—57.63. Watson RS, Cummings P, Quan L, Bratton S, Weiss NS. Cervicalspine injuries among submersion victims. J Trauma2001;51:658—62.64. Dodd FM, Simon E, McKeown D, Patrick MR. The effect of acervical collar on the tidal volume of anaesthetised adultpatients. Anaesthesia 1995;50:961—3.65. International Liaison Committee on Resuscitation 2005.International Consensus on Cardiopulmonary Resuscitationand Emergency Cardiovascular Care Science with TreatmentRecommendations. Resuscitation 2005;67:157—341.66. Golden FS, Hervey GR, Tipton MJ. Circum-rescue collapse:collapse, sometimes fatal, associated with rescueof immersion victims. J R Nav Med Serv 1991;77:139—49.67. Goh SH, Low BY. Drowning and near-drowning—–somelessons learnt. Ann Acad Med Singapore 1999;28:183—8.68. Quan L, Wentz KR, Gore EJ, Copass MK. Outcome andpredictors of outcome in pediatric submersion victimsreceiving prehospital care in King County. Wash Pediatr1990;86:586—93.69. Szpilman D, Soares M. In-water resuscitation—–is it worthwhile?Resuscitation 2004;63:25—31.70. Perkins GD. In-water resuscitation: a pilot evaluation.Resuscitation 2005;65:321—4.71. Rosen P, Stoto M, Harley J. The use of the Heimlich maneuverin near-drowning: Institute of Medicine report. J EmergMed 1995;13:397—405.72. March NF, Matthews RC. New techniques in external cardiaccompressions. Aquatic cardiopulmonary resuscitation.JAMA 1980;244:1229—32.73. March NF, Matthews RC. Feasibility study of CPR in thewater. Undersea Biomed Res 1980;7:141—8.74. Thomas R, Cahill CJ. Successful defibrillation in profoundhypothermia (core body temperature 25.6 degrees C).Resuscitation 2000;47:317—20.75. Manolios N, Mackie I. Drowning and near-drowning on Australianbeaches patrolled by life-savers: a 10-year study,1973—1983. Med J Aust 1988;148:165—7, 70—71.76. Modell JH, Calderwood HW, Ruiz BC, Downs JB, ChapmanJr R. Effects of ventilatory patterns on arterial oxygenationafter near-drowning in sea water. Anesthesiology1974;40:376—84.77. Golden FS, Tipton MJ, Scott RC. Immersion, near-drowningand drowning. Br J Anaesth 1997;79:214—25.78. Wyatt JP, Tomlinson GS, Busuttil A. Resuscitation ofdrowning victims in south-east Scotland. Resuscitation1999;41:101—4.79. Schmidt U, Fritz KW, Kasperczyk W, Tscherne H. Successfulresuscitation of a child with severe hypothermia after cardiacarrest of 88 min. Prehosp Disaster Med 1995;10:60—2.80. Bolte RG, Black PG, Bowers RS, Thorne JK, Corneli HM. Theuse of extracorporeal rewarming in a child submerged for66 min. JAMA 1988;260:377—9.81. The acute respiratory distress syndrome network. Ventilationwith lower tidal volumes as compared with traditionaltidal volumes for acute lung injury and the acute respiratorydistress syndrome. N Engl J Med 2000;342:1301—8.82. Moran I, Zavala E, Fernandez R, Blanch L, Mancebo J.Recruitment manoeuvres in acute lung injury/acuterespiratory distress syndrome. Eur Respir J Suppl2003;42:37s—42s.83. Nolan JP, Morley PT, Vanden Hoek TL, Hickey RW. Therapeutichypothermia after cardiac arrest. An advisory statementby the Advancement Life support Task Force of the InternationalLiaison committee on Resuscitation. Resuscitation2003;57:231—5.84. Holzer M, Behringer W, Schorkhuber W, et al. Mildhypothermia and outcome after CPR. Hypothermia for CardiacArrest (HACA) Study Group. Acta Anaesthesiol ScandSuppl 1997;111:55—8.85. Sterz F, Safar P, Tisherman S, Radovsky A, Kuboyama K,Oku K. Mild hypothermic cardiopulmonary resuscitationimproves outcome after prolonged cardiac arrest in dogs.Crit Care Med 1991;19:379—89.86. Farstad M, Andersen KS, Koller ME, Grong K, Segadal L,Husby P. Rewarming from accidental hypothermia by extracorporealcirculation. A retrospective study. Eur J CardiothoracSurg 2001;20:58—64.87. Schneider SM. Hypothermia: from recognition to rewarming.Emerg Med Rep 1992;13:1—20.

S16688. Gilbert M, Busund R, Skagseth A, Nilsen PÅ, Solbø JP. Resuscitationfrom accidental hypothermia of 13.7 ◦ C with circulatoryarrest. Lancet 2000;355:375—6.89. Danzl DF, Pozos RS, Auerbach PS, et al. Multicenterhypothermia survey. Ann Emerg Med 1987;16:1042—55.90. Reuler JB. Hypothermia: pathophysiology, clinical settings,and management. Ann Intern Med 1978;89:519—27.91. Lefrant JY, Muller L, de La Coussaye JE, et al. Temperaturemeasurement in intensive care patients: comparison of urinarybladder, oesophageal, rectal, axillary, and inguinalmethods versus pulmonary artery core method. IntensiveCare Med 2003;29:414—8.92. Robinson J, Charlton J, Seal R, Spady D, Joffres MR.Oesophageal, rectal, axillary, tympanic and pulmonaryartery temperatures during cardiac surgery. Can J Anaesth1998;45:317—23.93. Krismer AC, Lindner KH, Kornberger R, et al. Cardiopulmonaryresuscitation during severe hypothermia in pigs:does epinephrine or vasopressin increase coronary perfusionpressure? Anesth Analg 2000;90:69—73.94. Kornberger E, Lindner KH, Mayr VD, et al. Effects ofepinephrine in a pig model of hypothermic cardiac arrestand closed-chest cardiopulmonary resuscitation combinedwith active rewarming. Resuscitation 2001;50:301—8.95. Stoner J, Martin G, O’Mara K, Ehlers J, Tomlanovich M.Amiodarone and bretylium in the treatment of hypothermicventricular fibrillation in a canine model. Acad EmergMed 2003;10:187—91.96. Mattu A, Brady WJ, Perron AD. Electrocardiographicmanifestations of hypothermia. Am J Emerg Med2002;20:314—26.97. Southwick FS, DalglishS P.H. Jr. Recovery after prolongedasystolic cardiac arrest in profound hypothermia: a casereport and literature review. JAMA 1980;243:1250—3.98. Ujhelyi MR, Sims JJ, Dubin SA, Vender J, Miller AW.Defibrillation energy requirements and electrical heterogeneityduring total body hypothermia. Crit Care Med2001;29:1006—11.99. Kornberger E, Schwarz B, Lindner KH, Mair P. Forcedair surface rewarming in patients with severe accidentalhypothermia. Resuscitation 1999;41:105—11.100. Roggla M, Frossard M, Wagner A, Holzer M, Bur A,Roggla G. Severe accidental hypothermia with or withouthemodynamic instability: rewarming without theuse of extracorporeal circulation. Wien Klin Wochenschr2002;114:315—20.101. Weinberg AD, Hamlet MP, Paturas JL, White RD, McAninchGW. Cold weather emergencies: principles of patient management.Branford, CN: American Medical Publishing Co.;1990.102. Zell SC, Kurtz KJ. Severe exposure hypothermia: a resuscitationprotocol. Ann Emerg Med 1985;14:339—45.103. Althaus U, Aeberhard P, Schupbach P, Nachbur BH, MuhlemannW. Management of profound accidental hypothermiawith cardiorespiratory arrest. Ann Surg 1982;195:492—5.104. Walpoth BH, Walpoth-Aslan BN, Mattle HP, et al. Outcomeof survivors of accidental deep hypothermia and circulatoryarrest treated with extracorporeal blood warming. N EnglJ Med 1997;337:1500—5.105. Silfvast T, Pettila V. Outcome from severe accidentalhypothermia in Southern Finland—–a 10-year review. Resuscitation2003;59:285—90.106. Moss J. Accidental severe hypothermia. Surg GynecolObstet 1986;162:501—13.J. Soar et al.107. Safar P. Cerebral resuscitation after cardiac arrest:research initiatives and future directions [published correctionappears in Ann Emerg Med. 1993;22:759]. AnnEmerg Med 1993;22(pt 2):324—49.108. Bouchama A, Knochel JP. Heat stroke. N Engl J Med2002;346:1978—88.109. Wappler F. Malignant hyperthermia. Eur J Anaesthesiol2001;18:632—52.110. Ali SZ, Taguchi A, Rosenberg H. Malignant hyperthermia.Best Pract Res Clin Anaesthesiol 2003;17:519—33.111. Bouchama A. The 2003 European heat wave. Intensive CareMed 2004;30:1—3.112. Coris EE, Ramirez AM, Van Durme DJ. Heat illness in athletes:the dangerous combination of heat, humidity andexercise. Sports Med 2004;34:9—16.113. Grogan H, Hopkins PM. Heat stroke: implications for criticalcare and anaesthesia. Br J Anaesth 2002;88:700—7.114. Bouchama A, De Vol EB. Acid-base alterations in heatstroke.Intensive Care Med 2001;27:680—5.115. Akhtar MJ, al-Nozha M, al-Harthi S, Nouh MS. Electrocardiographicabnormalities in patients with heat stroke. Chest1993;104:411—4.116. el-Kassimi FA, Al-Mashhadani S, Abdullah AK, Akhtar J.Adult respiratory distress syndrome and disseminatedintravascular coagulation complicating heat stroke. Chest1986;90:571—4.117. Waruiru C, Appleton R. Febrile seizures: an update. ArchDis Child 2004;89:751—6.118. Berger J, Hart J, Millis M, Baker AL. Fulminant hepatic failurefrom heat stroke requiring liver transplantation. J ClinGastroenterol 2000;30:429—31.119. Huerta-Alardin AL, Varon J, Marik PE. Bench-to-bedsidereview: Rhabdomyolysis—–an overview for clinicians. CritCare 2005;9:158—69.120. Wolff ED, Driessen OMJ. Theophylline intoxication in achild. Ned Tijdschr Geneeskd 1977;121:896—901.121. Sidor K, Mikolajczyk W, Horwath-Stolarczyk A. Acute poisoningin children hospitalized at the Medical UniversityHospital No 3 in Warsaw, between 1996 and 2000. PediatrPolska 2002;77:509—16.122. Boyer EW, Shannon M. The serotonin syndrome. N Engl JMed 2005;352:1112—20.123. Bhanushali MJ, Tuite PJ. The evaluation and managementof patients with neuroleptic malignant syndrome. NeurolClin 2004;22:389—411.124. Abraham E, Matthay MA, Dinarello CA, et al. Consensusconference definitions for sepsis, septic shock, acute lunginjury, and acute respiratory distress syndrome: time for are-evaluation. Crit Care Med 2000;28:232—5.125. Savage MW, Mah PM, Weetman AP, Newell-Price J.Endocrine emergencies. Postgrad Med J 2004;80:506—15.126. Hadad E, Weinbroum AA, Ben-Abraham R. Drug-inducedhyperthermia and muscle rigidity: a practical approach.Eur J Emerg Med 2003;10:149—54.127. Halloran LL, Bernard DW. Management of drug-inducedhyperthermia. Curr Opin Pediatr 2004;16:211—5.128. Armstrong LE, Crago AE, Adams R, Roberts WO, Maresh CM.Whole-body cooling of hyperthermic runners: comparisonof two field therapies. Am J Emerg Med 1996;14:355—8.129. Horowitz BZ. The golden hour in heat stroke: use of icedperitoneal lavage. Am J Emerg Med 1989;7:616—9.130. Bernard S, Buist M, Monteiro O, Smith K. Induced hypothermiausing large volume, ice-cold intravenous fluid incomatose survivors of out-of-hospital cardiac arrest: a preliminaryreport. Resuscitation 2003;56:9—13.

European Resuscitation Council Guidelines for Resuscitation 2005S167131. Schmutzhard E, Engelhardt K, Beer R, et al. Safetyand efficacy of a novel intravascular cooling device tocontrol body temperature in neurologic intensive carepatients: a prospective pilot study. Crit Care Med 2002;30:2481—8.132. Al-Senani FM, Graffagnino C, Grotta JC, et al. A prospective,multicenter pilot study to evaluate the feasibilityand safety of using the CoolGard system and icy catheterfollowing cardiac arrest. Resuscitation 2004;62:143—50.133. Behringer W, Safar P, Wu X, et al. Veno-venous extracorporealblood shunt cooling to induce mild hypothermia in dogexperiments and review of cooling methods. Resuscitation2002;54:89—98.134. Hadad E, Cohen-Sivan Y, Heled Y, Epstein Y. Clinical review:treatment of heat stroke—–should dantrolene be considered?Crit Care 2005;9:86—91.135. Krause T, Gerbershagen MU, Fiege M, Weisshorn R, WapplerF. Dantrolene—–a review of its pharmacology, therapeuticuse and new developments. Anaesthesia 2004;59:364—73.136. Eshel G, Safar P, Sassano J, Stezoski W. Hyperthermiainducedcardiac arrest in dogs and monkeys. Resuscitation1990;20:129—43.137. Eshel G, Safar P, Radovsky A, Stezoski SW. Hyperthermiainducedcardiac arrest in monkeys: limited efficacy of standardCPR. Aviat Space Environ Med 1997;68:415—20.138. Zeiner A, Holzer M, Sterz F, et al. Hyperthermia after cardiacarrest is associated with an unfavorable neurologicoutcome. Arch Intern Med 2001;161:2007—12.139. Masoli M, Fabian D, Holt S, Beasley R. The global burdenof asthma: executive summary of the GINA DisseminationCommittee report. Allergy 2004;59:469—78.140. BTS/SIGN. British Thoracic Society, Scottish IntercollegiateGuidelines Network (SIGN). British guideline on the managementof asthma. Thorax 2003;58(Suppl. I):i1—94.141. Rainbow J, Browne GJ. Fatal asthma or anaphylaxis? EmergMed J 2002;19:415—7.142. Kokturk N, Demir N, Kervan F, Dinc E, Koybasioglu A, TurktasH. A subglottic mass mimicking near-fatal asthma: achallenge of diagnosis. J Emerg Med 2004;26:57—60.143. Ratto D, Alfaro C, Sipsey J, Glovsky MM, Sharma OP. Areintravenous corticosteroids required in status asthmaticus?JAMA 1988;260:527—9.144. Aaron SD. The use of ipratropium bromide for the managementof acute asthma exacerbation in adults and children:a systematic review. J Asthma 2001;38:521—30.145. Rodrigo G, Rodrigo C, Burschtin O. A meta-analysis ofthe effects of ipratropium bromide in adults with acuteasthma. Am J Med 1999;107:363—70.146. Munro A, Jacobs M. Best evidence topic reports. Is intravenousaminophylline better than intravenous salbutamolin the treatment of moderate to severe asthma? Emerg MedJ 2004;21:78—80.147. Rowe BH, Bretzlaff JA, Bourdon C, Bota GW, Camargo JrCA. Magnesium sulfate for treating exacerbations of acuteasthma in the emergency department. Cochrane DatabaseSyst Rev 2000:CD001490.148. Cydulka R, Davison R, Grammer L, Parker M, Mathews IVJ. The use of epinephrine in the treatment of older adultasthmatics. Ann Emerg Med 1988;17:322—6.149. Victoria MS, Battista CJ, Nangia BS. Comparison of subcutaneousterbutaline with epinephrine in the treatmentof asthma in children. J Allergy Clin Immunol1977;59:128—35.150. Victoria MS, Battista CJ, Nangia BS. Comparison betweenepinephrine and terbutaline injections in the acute managementof asthma. J Asthma 1989;26:287—90.151. Rodrigo GJ, Rodrigo C, Pollack CV, Rowe B. Use of heliumoxygenmixtures in the treatment of acute asthma: a systematicreview. Chest 2003;123:891—6.152. Petrillo TM, Fortenberry JD, Linzer JF, Simon HK. Emergencydepartment use of ketamine in pediatric status asthmaticus.J Asthma 2001;38:657—64.153. Howton JC, Rose J, Duffy S, Zoltanski T, Levitt MA. Randomized,double-blind, placebo-controlled trial of intravenousketamine in acute asthma. Ann Emerg Med 1996;27:170—5.154. Antonelli M, Pennisi MA, Montini L. Clinical review: noninvasiveventilation in the clinical setting—–experience fromthe past 10 years. Crit Care 2005;9:98—103.155. Ram FS, Wellington S, Rowe BH, Wedzicha JA. Non-invasivepositive pressure ventilation for treatment of respiratoryfailure due to severe acute exacerbations of asthma.Cochrane Database Syst Rev 2005:CD004360.156. Leatherman JW, McArthur C, Shapiro RS. Effect of prolongationof expiratory time on dynamic hyperinflation inmechanically ventilated patients with severe asthma. CritCare Med 2004;32:1542—5.157. Bowman FP, Menegazzi JJ, Check BD, Duckett TM. Loweresophageal sphincter pressure during prolonged cardiacarrest and resuscitation. Ann Emerg Med 1995;26:216—9.158. Lapinsky SE, Leung RS. Auto-PEEP and electromechanicaldissociation. N Engl J Med 1996;335:674.159. Rogers PL, Schlichtig R, Miro A, Pinsky M. Auto-PEEP duringCPR. An ‘‘occult’’ cause of electromechanical dissociation?Chest 1991;99:492—3.160. Rosengarten PL, Tuxen DV, Dziukas L, Scheinkestel C, MerrettK, Bowes G. Circulatory arrest induced by intermittentpositive pressure ventilation in a patient withsevere asthma. Anaesth Intensive Care 1991;19:118—21.161. Sprung J, Hunter K, Barnas GM, Bourke DL. Abdominaldistention is not always a sign of esophageal intubation:cardiac arrest due to ‘‘auto-PEEP’’. Anesth Analg1994;78:801—4.162. Deakin CD, McLaren RM, Petley GW, Clewlow F, Dalrymple-Hay MJ. Effects of positive end-expiratory pressure ontransthoracic impedance—–implications for defibrillation.Resuscitation 1998;37:9—12.163. Mazzeo AT, Spada A, Pratico C, Lucanto T, Santamaria LB.Hypercapnia: what is the limit in paediatric patients? Acase of near-fatal asthma successfully treated by multipharmacologicalapproach. Paediatr Anaesth 2004;14:596—603.164. Mertes PM, Laxenaire MC, Alla F. Anaphylactic and anaphylactoidreactions occurring during anesthesia in France in1999—2000. Anesthesiology 2003;99:536—45.165. Yunginger JW. Latex allergy in the workplace: anoverview of where we are. Ann Allergy Asthma Immunol1999;83:630—3.166. Dreyfus DH, Fraser B, Randolph CC. Anaphylaxis to latexin patients without identified risk factors for latex allergy.Conn Med 2004;68:217—22.167. Ownby DR. A history of latex allergy. J Allergy Clin Immunol2002;110:S27—32.168. Pumphrey RS. Lessons for management of anaphylaxisfrom a study of fatal reactions. Clin Exp Allergy2000;30:1144—50.169. Pumphrey RS. Fatal anaphylaxis in the UK, 1992—2001.Novartis Found Symp 2004;257:116—28, discussion 28—32,57—60, 276—285.170. Incorvaia C, Senna G, Mauro M, et al. Prevalence of allergicreactions to Hymenoptera stings in northern Italy. AllergImmunol (Paris) 2004;36:372—4.

S168171. Pumphrey RS, Roberts IS. Postmortem findings after fatalanaphylactic reactions. J Clin Pathol 2000;53:273—6.172. Mullins RJ. Anaphylaxis: risk factors for recurrence. ClinExp Allergy 2003;33:1033—40.173. Brown AF. Anaphylaxis: quintessence, quarrels, and quandaries.Emerg Med J 2001;18:328.174. Brown AF. Anaphylaxis gets the adrenaline going. EmergMed J 2004;21:128—9.175. Ishoo E, Shah UK, Grillone GA, Stram JR, FuleihanNS. Predicting airway risk in angioedema: staging systembased on presentation. Otolaryngol Head Neck Surg1999;121:263—8.176. Pumphrey R. Anaphylaxis: can we tell who is at riskof a fatal reaction? Curr Opin Allergy Clin Immunol2004;4:285—90.177. Simons FE, Gu X, Simons KJ. Epinephrine absorption inadults: intramuscular versus subcutaneous injection. JAllergy Clin Immunol 2001;108:871—3.178. Simons FER, Chan ES, Gu X, Simons KJ. Epinephrine forthe out-of-hospital (first-aid) treatment of anaphylaxis ininfants: is the ampule/syringe/needle method practical? JAllergy Clin Immunol 2001;108:1040—4.179. Winbery SL, Lieberman PL. Histamine and antihistaminesin anaphylaxis. Clin Allergy Immunol 2002;17:287—317.180. Kill C, Wranze E, Wulf H. Successful treatment of severeanaphylactic shock with vasopressin. Two case reports. IntArch Allergy Immunol 2004;134:260—1.181. Williams SR, Denault AY, Pellerin M, Martineau R. Vasopressinfor treatment of shock following aprotinin administration.Can J Anaesth 2004;51:169—72.182. Visscher PK, Vetter RS, Camazine S. Removing bee stings.Lancet 1996;348:301—2.183. Yocum MW, Butterfield JH, Klein JS, Volcheck GW,Schroeder DR, Silverstein MD. Epidemiology of anaphylaxisin Olmsted County: a population-based study. J Allergy ClinImmunol 1999;104(pt 1):452—6.184. Ellis AK, Day JH. Diagnosis and management of anaphylaxis.CMAJ 2003;169:307—11.185. Smith PL, Kagey-Sobotka A, Bleecker ER, et al. Physiologicmanifestations of human anaphylaxis. J Clin Invest1980;66:1072—80.186. Stark BJ, Sullivan TJ. Biphasic and protracted anaphylaxis.J Allergy Clin Immunol 1986;78:76—83.187. Brazil E, MacNamara AF. Not so immediate’’ hypersensitivity:the danger of biphasic anaphylactic reactions. J AccidEmerg Med 1998;15:252—3.188. Brady Jr WJ, Luber S, Carter CT, Guertler A, LindbeckG. Multiphasic anaphylaxis: an uncommon eventin the emergency department. Acad Emerg Med 1997;4:193—7.189. Joint Working Party of the Association of Anaesthetists ofGreat Britain and Ireland and the British Society for Allergyand Clinical Immunology. Suspected anaphylactic reactionsassociated with anaesthesia. 3rd ed. London: The Associationof Anaesthetists of Great Britain and Ireland and BritishSociety for Allergy and Clinical Immunology; 2003.190. Payne V, Kam PC. Mast cell tryptase: a review ofits physiology and clinical significance. Anaesthesia2004;59:695—703.191. Anthi A, Tzelepis GE, Alivizatos P, Michalis A, PalatianosGM, Geroulanos S. Unexpected cardiac arrest after cardiacsurgery: incidence, predisposing causes, and outcomeof open chest cardiopulmonary resuscitation. Chest1998;113:15—9.192. Wahba A, Gotz W, Birnbaum DE. Outcome of cardiopulmonaryresuscitation following open heart surgery. ScandCardiovasc J 1997;31:147—9.J. Soar et al.193. Rhodes JF, Blaufox AD, Seiden HS, et al. Cardiac arrestin infants after congenital heart surgery. Circulation1999;100:II194—9.194. Dimopoulou I, Anthi A, Michalis A, Tzelepis GE. Functionalstatus and quality of life in long-term survivorsof cardiac arrest after cardiac surgery. Crit Care Med2001;29:1408—11.195. Mackay JH, Powell SJ, Osgathorp J, Rozario CJ. Six-yearprospective audit of chest reopening after cardiac arrest.Eur J Cardiothorac Surg 2002;22:421—5.196. Pottle A, Bullock I, Thomas J, Scott L. Survival to dischargefollowing open chest cardiac compression (OCCC). A 4-yearretrospective audit in a cardiothoracic specialist centre—–Royal Brompton and Harefield NHS Trust, United Kingdom.Resuscitation 2002;52:269—72.197. Raman J, Saldanha RF, Branch JM, et al. Open cardiac compressionin the postoperative cardiac intensive care unit.Anaesth Intensive Care 1989;17:129—35.198. Birdi I, Chaudhuri N, Lenthall K, Reddy S, Nashef SA. Emergencyreinstitution of cardiopulmonary bypass followingcardiac surgery: outcome justifies the cost. Eur J CardiothoracSurg 2000;17:743—6.199. Rousou JA, Engelman RM, Flack III JE, Deaton DW, Owen SG.Emergency cardiopulmonary bypass in the cardiac surgicalunit can be a lifesaving measure in postoperative cardiacarrest. Circulation 1994;90:II280—4.200. Schwarz B, Bowdle TA, Jett GK, et al. Biphasic shocks comparedwith monophasic damped sine wave shocks for directventricular defibrillation during open heart surgery. Anesthesiology2003;98:1063—9.201. Rosemurgy AS, Norris PA, Olson SM, Hurst JM, Albrink MH.Prehospital traumatic cardiac arrest: the cost of futility. JTrauma 1993;35:468—73.202. Battistella FD, Nugent W, Owings JT, Anderson JT.Field triage of the pulseless trauma patient. Arch Surg1999;134:742—5.203. Shimazu S, Shatney CH. Outcomes of trauma patientswith no vital signs on hospital admission. J Trauma1983;23:213—6.204. Stockinger ZT, McSwain Jr NE. Additional evidence in supportof withholding or terminating cardiopulmonary resuscitationfor trauma patients in the field. J Am Coll Surg2004;198:227—31.205. Fulton RL, Voigt WJ, Hilakos AS. Confusion surroundingthe treatment of traumatic cardiac arrest. J Am Coll Surg1995;181:209—14.206. Pasquale MD, Rhodes M, Cipolle MD, Hanley T, Wasser T.Defining ‘‘dead on arrival’’: impact on a level I trauma center.J Trauma 1996;41:726—30.207. Stratton SJ, Brickett K, Crammer T. Prehospital pulseless,unconscious penetrating trauma victims: field assessmentsassociated with survival. J Trauma 1998;45:96—100.208. Maron BJ, Gohman TE, Kyle SB, Estes III NA, Link MS.Clinical profile and spectrum of commotio cordis. JAMA2002;287:1142—6.209. Maron BJ, Estes III NA, Link MS. Task Force 11: commotiocordis. J Am Coll Cardiol 2005;45:1371—3.210. Nesbitt AD, Cooper PJ, Kohl P. Rediscovering commotiocordis. Lancet 2001;357:1195—7.211. Link MS, Estes M, Maron BJ. Sudden death caused bychest wall trauma (commotio cordis). In: Kohl P, Sachs F,Franz MR, editors. Cardiac mechano-electric feedback andarrhythmias: from pipette to patient. Philadelphia: ElsevierSaunders; 2005. p. 270—6.212. Bouillon B, Walther T, Kramer M, Neugebauer E. Trauma andcirculatory arrest: 224 preclinical resuscitations in Colognein 1990 [in German]. Anaesthesist 1994;43:786—90.

European Resuscitation Council Guidelines for Resuscitation 2005S169213. Fisher B, Worthen M. Cardiac arrest induced by blunttrauma in children. Pediatr Emerg Care 1999;15:274—6.214. Hazinski MF, Chahine AA, Holcomb III GW, Morris Jr JA. Outcomeof cardiovascular collapse in pediatric blunt trauma.Ann Emerg Med 1994;23:1229—35.215. Calkins CM, Bensard DD, Partrick DA, Karrer FM. A criticalanalysis of outcome for children sustaining cardiac arrestafter blunt trauma. J Pediatr Surg 2002;37:180—4.216. Yanagawa Y, Saitoh D, Takasu A, Kaneko N, Sakamoto T,Okada Y. Experience of treatment for blunt traumaticout-of-hospital cardiopulmonary arrest patients over 24years: head injury vs. non-head injury. No Shinkei Geka2004;32:231—5.217. Cera SM, Mostafa G, Sing RF, Sarafin JL, Matthews BD, HenifordBT. Physiologic predictors of survival in post-traumaticarrest. Am Surg 2003;69:140—4.218. Esposito TJ, Jurkovich GJ, Rice CL, Maier RV, Copass MK,Ashbaugh DG. Reappraisal of emergency room thoracotomyin a changing environment. J Trauma 1991;31:881—5, discussion5—7.219. Martin SK, Shatney CH, Sherck JP, et al. Blunt traumapatients with prehospital pulseless electrical activity(PEA): poor ending assured. J Trauma 2002;53:876—80, discussion80—81.220. Domeier RM, McSwain Jr NE, Hopson LR, et al. Guidelinesfor withholding or termination of resuscitation in prehospitaltraumatic cardiopulmonary arrest. J Am Coll Surg2003;196:475—81.221. Pickens JJ, Copass MK, Bulger EM. Trauma patientsreceiving CPR: predictors of survival. J Trauma 2005;58:951—8.222. Gervin AS, Fischer RP. The importance of prompt transportof salvage of patients with penetrating heart wounds. JTrauma 1982;22:443—8.223. Branney SW, Moore EE, Feldhaus KM, Wolfe RE. Criticalanalysis of two decades of experience with postinjuryemergency department thoracotomy in a regional traumacenter. J Trauma 1998;45:87—94, discussion -5.224. Durham III LA, Richardson RJ, Wall Jr MJ, Pepe PE, MattoxKL. Emergency center thoracotomy: impact of prehospitalresuscitation. J Trauma 1992;32:775—9.225. Frezza EE, Mezghebe H. Is 30 min the golden period to performemergency room thoratomy (ERT) in penetrating chestinjuries? J Cardiovasc Surg 1999;40:147—51.226. Powell DW, Moore EE, Cothren CC, et al. Is emergencydepartment resuscitative thoracotomy futile care for thecritically injured patient requiring prehospital cardiopulmonaryresuscitation? J Am Coll Surg 2004;199:211—5.227. Coats TJ, Keogh S, Clark H, Neal M. Prehospital resuscitativethoracotomy for cardiac arrest after penetratingtrauma: rationale and case series. J Trauma2001;50:670—3.228. Wise D, Davies G, Coats T, Lockey D, Hyde J, Good A.Emergency thoracotomy: ‘‘how to do it’’. Emerg Med J2005;22:22—4.229. Kwan I, Bunn F, Roberts I. Spinal immobilisation for traumapatients. Cochrane Database Syst Rev 2001. CD002803.230. Voiglio EJ, Coats TJ, Baudoin YP, Davies GD, WilsonAW. Resuscitative transverse thoracotomy. Ann Chir2003;128:728—33.231. Practice management guidelines for emergency departmentthoracotomy. Working Group, Ad Hoc Subcommitteeon Outcomes, American College of Surgeons-Committee onTrauma. J Am Coll Surg 2001;193:303—9.232. Jones JH, Murphy MP, Dickson RL, Somerville GG, BrizendineEJ. Emergency physician-verified out-of-hospital intubation:miss rates by paramedics. Acad Emerg Med2004;11:707—9.233. Jemmett ME, Kendal KM, Fourre MW, Burton JH. Unrecognizedmisplacement of endotracheal tubes in a mixedurban to rural emergency medical services setting. AcadEmerg Med 2003;10:961—5.234. Katz SH, Falk JL. Misplaced endotracheal tubes byparamedics in an urban emergency medical services system.Ann Emerg Med 2001;37:32—7.235. Deakin CD, Peters R, Tomlinson P, Cassidy M. Securing theprehospital airway: a comparison of laryngeal mask insertionand endotracheal intubation by UK paramedics. EmergMed J 2005;22:64—7.236. Pepe PE, Roppolo LP, Fowler RL. The detrimental effectsof ventilation during low-blood-flow states. Curr Opin CritCare 2005;11:212—8.237. Deakin CD, Davies G, Wilson A. Simple thoracostomy avoidschest drain insertion in prehospital trauma. J Trauma1995;39:373—4.238. Luna GK, Pavlin EG, Kirkman T, Copass MK, Rice CL. Hemodynamiceffects of external cardiac massage in traumashock. J Trauma 1989;29:1430—3.239. Gao JM, Gao YH, Wei GB, et al. Penetrating cardiacwounds: principles for surgical management. World J Surg2004;28:1025—9.240. Kwan I, Bunn F, Roberts I. Timing and volume of fluid administrationfor patients with bleeding. Cochrane DatabaseSyst Rev 2003. CD002245.241. Pepe PE, Mosesso VN, Falk JL. Prehospital fluid resuscitationof the patient with major trauma. Prehosp Emerg Care2002;6:81—91.242. Bickell WH, Wall Jr MJ, Pepe PE, et al. Immediate versusdelayed fluid resuscitation for hypotensive patients withpenetrating torso injuries. N Engl J Med 1994;331:1105—9.243. National Institute for Clinical Excellence. Prehospital initiationof fluid replacement therapy for trauma. London:National Institute for Clinical Excellence; 2004.244. Sumida MP, Quinn K, Lewis PL, et al. Prehospital bloodtransfusion versus crystalloid alone in the air medical transportof trauma patients. Air Med J 2000;19:140—3.245. Barkana Y, Stein M, Maor R, Lynn M, Eldad A. Prehospitalblood transfusion in prolonged evacuation. J Trauma1999;46:176—80.246. Walcher F, Kortum S, Kirschning T, Weihgold N, Marzi I. Optimizedmanagement of polytraumatized patients by prehospitalultrasound. Unfallchirurg 2002;105:986—94.247. Krismer AC, Wenzel V, Voelckel WG, et al. Employing vasopressinas an adjunct vasopressor in uncontrolled traumatichemorrhagic shock. Three cases and a brief analysis of theliterature. Anaesthesist 2005;54:220—4.248. Department of Health, Welsh Office, Scottish OfficeDepartment of Health, Department of Health and SocialServices, Northern Ireland. Why mothers die. Report onconfidential enquiries into maternal deaths in the UnitedKingdom, 2000—2002. London: The Stationery Office;2004.249. Page-Rodriguez A, Gonzalez-Sanchez JA. Perimortemcesarean section of twin pregnancy: case report and reviewof the literature. Acad Emerg Med 1999;6:1072—4.250. Cardosi RJ, Porter KB. Cesarean delivery of twins duringmaternal cardiopulmonary arrest. Obstet Gynecol1998;92:695—7.251. Kinsella SM. Lateral tilt for pregnant women: why 15degrees? Anaesthesia 2003;58:835—6.252. Nanson J, Elcock D, Williams M, Deakin CD. Do physiologicalchanges in pregnancy change defibrillation energy requirements?Br J Anaesth 2001;87:237—9.

S170253. Johnson MD, Luppi CJ, Over DC. Cardiopulmonary resuscitation.In: Gambling DR, Douglas MJ, editors. Obstetricanesthesia and uncommon disorders. Philadelphia: W.B.Saunders; 1998. p. 51—74.254. Rahman K, Jenkins JG. Failed tracheal intubation in obstetrics:no more frequent but still managed badly. Anaesthesia2005;60:168—71.255. Henderson JJ, Popat MT, Latto IP, Pearce AC. Difficultairway society guidelines for management of the unanticipateddifficult intubation. Anaesthesia 2004;59:675—94.256. Catling S, Joels L. Cell salvage in obstetrics: the time hascome. Br J Obstet Gynaecol 2005;112:131—2.257. Ahonen J, Jokela R. Recombinant factor VIIa for lifethreateningpost-partum haemorrhage. Br J Anaesth2005;94:592—5.258. Bouwmeester FW, Bolte AC, van Geijn HP. Pharmacologicaland surgical therapy for primary postpartum hemorrhage.Curr Pharm Des 2005;11:759—73.259. El-Hamamy E, CBL. A worldwide review of the uses of theuterine compression suture techniques as alternative tohysterectomy in the management of severe post-partumhaemorrhage. J Obstet Gynaecol 2005;25:143—9.260. Hong TM, Tseng HS, Lee RC, Wang JH, Chang CY. Uterineartery embolization: an effective treatment for intractableobstetric haemorrhage. Clin Radiol 2004;59:96—101.261. Yu S, Pennisi JA, Moukhtar M, Friedman EA. Placentalabruption in association with advanced abdominal pregnancy.A case report. J Reprod Med 1995;40:731—5.262. Wlody D. Complications of regional anesthesia in obstetrics.Clin Obstet Gynecol 2003;46:667—78.263. Ray P, Murphy GJ, Shutt LE. Recognition and managementof maternal cardiac disease in pregnancy. Br J Anaesth2004;93:428—39.264. Abbas AE, Lester SJ, Connolly H. Pregnancy and the cardiovascularsystem. Int J Cardiol 2005;98:179—89.265. Doan-Wiggins L. Resuscitation of the pregnant patient sufferingsudden death. In: Paradis NA, Halperin HR, NowakRM, editors. Cardiac arrest: the science and practiceof resuscitation medicine. Baltimore: Williams & Wilkins;1997. p. 812—9.266. Sibai B, Dekker G, Kupferminc M. Pre-eclampsia. Lancet2005;365:785—99.267. Sibai BM. Diagnosis, prevention, and management ofeclampsia. Obstet Gynecol 2005;105:402—10.268. Dapprich M, Boessenecker W. Fibrinolysis with alteplasein a pregnant woman with stroke. Cerebrovasc Dis2002;13:290.269. Turrentine MA, Braems G, Ramirez MM. Use of thrombolyticsfor the treatment of thromboembolic disease duringpregnancy. Obstet Gynecol Surv 1995;50:534—41.270. Thabut G, Thabut D, Myers RP, et al. Thrombolytic therapyof pulmonary embolism: a meta-analysis. J Am Coll Cardiol2002;40:1660—7.271. Patel RK, Fasan O, Arya R. Thrombolysis in pregnancy.Thromb Haemost 2003;90:1216—7.272. Tuffnell DJ. Amniotic fluid embolism. Curr Opin ObstetGynecol 2003;15:119—22.273. Stanten RD, Iverson LI, Daugharty TM, Lovett SM, TerryC, Blumenstock E. Amniotic fluid embolism causing catastrophicpulmonary vasoconstriction: diagnosis by transesophagealechocardiogram and treatment by cardiopulmonarybypass. Obstet Gynecol 2003;102:496—8.274. Katz VL, Dotters DJ, Droegemueller W. Perimortemcesarean delivery. Obstet Gynecol 1986;68:571—6.J. Soar et al.275. Guidelines 2000 for Cardiopulmonary Resuscitation andEmergency Cardiovascular Care: International Consensuson Science. Part 8: advanced challenges in resuscitation.Section 3. Special challenges in ECC. 3F: cardiac arrestassociated with pregnancy. Resuscitation 2000;46:293—5.276. Cummins RO, Hazinski MF, Zelop CM. Chapter 4, Part 6:cardiac arrest associated with pregnancy. In: Cummins R,Hazinski M, Field J, editors. ACLS—–the reference textbook.Dallas: American Heart Association; 2003, p. 143—158.277. Oates S, Williams GL, Rees GA. Cardiopulmonary resuscitationin late pregnancy. BMJ 1988;297:404—5.278. Strong THJ, Lowe RA. Perimortem cesarean section. Am JEmerg Med 1989;7:489—94.279. Boyd R, Teece S. Towards evidence based emergencymedicine: best BETs from the Manchester Royal Infirmary.Perimortem caesarean section. Emerg Med J2002;19:324—5.280. Moore C, Promes SB. Ultrasound in pregnancy. Emerg MedClin N Am 2004;22:697—722.281. Budnick LD. Bathtub-related electrocutions in the UnitedStates, 1979 to 1982. JAMA 1984;252:918—20.282. Lightning-associated deaths—–United States, 1980—1995.MMWR Morb Mortal Wkly Rep 1998;47:391—4.283. Geddes LA, Bourland JD, Ford G. The mechanism underlyingsudden death from electric shock. Med Instrum1986;20:303—15.284. Zafren K, Durrer B, Herry JP, Brugger H. Lightning injuries:prevention and on-site treatment in mountains and remoteareas. Official guidelines of the International Commissionfor Mountain Emergency Medicine and the Medical Commissionof the International Mountaineering and ClimbingFederation (ICAR and UIAA MEDCOM). Resuscitation2005;65:369—72.285. Cherington M. Lightning injuries. Ann Emerg Med1995;25:517—9.286. Fahmy FS, Brinsden MD, Smith J, Frame JD. Lightning: themultisystem group injuries. J Trauma 1999;46:937—40.287. Patten BM. Lightning and electrical injuries. Neurol Clin1992;10:1047—58.288. Browne BJ, Gaasch WR. Electrical injuries and lightning.Emerg Med Clin North Am 1992;10:211—29.289. Kleiner JP, Wilkin JH. Cardiac effects of lightning stroke.JAMA 1978;240:2757—9.290. Lichtenberg R, Dries D, Ward K, Marshall W, Scanlon P. Cardiovasculareffects of lightning strikes. J Am Coll Cardiol1993;21:531—6.291. Cooper MA. Emergent care of lightning and electricalinjuries. Semin Neurol 1995;15:268—78.292. Milzman DP, Moskowitz L, Hardel M. Lightning strikes at amass gathering. S Med J 1999;92:708—10.293. Cooper MA. Lightning injuries: prognostic signs for death.Ann Emerg Med 1980;9:134—8.294. Kleinschmidt-DeMasters BK. Neuropathology of lightningstrike injuries. Semin Neurol 1995;15:323—8.295. Stewart CE. When lightning strikes. Emerg Med Serv2000;29:57—67, quiz 103.296. Duclos PJ, Sanderson LM. An epidemiological descriptionof lightning-related deaths in the United States. Int J Epidemiol1990;19:673—9.297. Epperly TD, Stewart JR. The physical effects of lightninginjury. J Fam Pract 1989;29:267—72.298. Whitcomb D, Martinez JA, Daberkow D. Lightning injuries.S Med J 2002;95:1331—4.299. Goldman RD, Einarson A, Koren G. Electric shock duringpregnancy. Can Fam Physician 2003;49:297—8.

Resuscitation (2005) 67S1, S171—S180European Resuscitation Council Guidelines forResuscitation 2005Section 8. The ethics of resuscitation andend-of-life decisionsPeter J.F. Baskett, Petter A. Steen, Leo BossaertIntroductionSuccessful resuscitation attempts have broughtextended, useful and precious life to many, andhappiness and relief to their relatives and lovedones. And yet, there are occasions when resuscitationattempts have merely prolonged suffering andthe process of dying. In few cases resuscitation hasresulted in the ultimate tragedy—–the patient in apersistent vegetative state. Resuscitation attemptsare unsuccessful in 70—95% of cases and death ultimatelyis inevitable. All would wish to die withdignity.Several ethical decisions are required to ensurethat the decisions to attempt or withhold cardiopulmonaryresuscitation (CPR) are appropriate, andthat patients and their loved ones are treated withdignity. These decisions may be influenced by individual,international and local cultural, legal, traditional,religious, social and economic factors. 1—10Sometimes the decisions can be made in advance,but often they have to be made in a matter of secondsat the time of the emergency. Therefore, itis important that healthcare providers understandthe principles involved before they are put in asituation where a resuscitation decision must bemade.This section of the guidelines deals with ethicalaspects and decisions, including• advance directives, sometimes known as livingwills;• when not to start resuscitation attempts;• when to stop resuscitation attempts;• decision making by non-physicians;• when to withdraw treatment from those in a persistentvegetative state following resuscitation;• decisions about family members or loved oneswho wish to be present during resuscitation;• decisions about research and training on therecently dead;• the breaking of bad news to relatives and lovedones;• staff support.PrinciplesThe four key principles are beneficence, nonmaleficence,justice and autonomy. 11Beneficence implies that healthcare providersmust provide benefit while balancing benefit andrisks. Commonly this will involve attempting resuscitation,but on occasion it will mean withholding0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.doi:10.1016/j.resuscitation.2005.10.005

S172cardiopulmonary resuscitation (CPR). Beneficencemay also include responding to the overall needs ofthe community, e.g. establishing a programme ofpublic access to defibrillation.Non maleficence means doing no harm. Resuscitationshould not be attempted in futile cases, norwhen it is against the patient’s wishes (expressedwhen the individual is in a mentally competentstate).Justice implies a duty to spread benefits and risksequally within a society. If resuscitation is provided,it should be made available to all who will benefitfrom it within the available resources.Autonomy relates to patients being able to makeinformed decisions on their own behalf, rather thanbeing subjected to paternalistic decisions beingmade for them by the medical or nursing professions.This principle has been introduced particularlyduring the past 30 years, arising fromlegislature such as the Helsinki Declaration ofHuman Rights and its subsequent modificationsand amendments. 12 Autonomy requires that thepatient is adequately informed, competent, freefrom undue pressure and that there is consistencyin the patient’s preferences.Advance directivesAdvance directives have been introduced in manycountries, emphasising the importance of patientautonomy. Advance directives are a method of communicatingthe patient’s wishes concerning futurecare, particularly towards the end of life, andmust be expressed while the patient is mentallycompetent and not under duress. Advance directivesare likely to specify limitations concerningterminal care, including the withholding ofCPR.The term advance directive applies to anyexpression of patient preferences, including meredialogue between patient and/or close relativesand loved ones and/or medical or nursing attendants.This may help healthcare attendants inassessing the patient’s wishes should the patientbecome mentally incompetent. However, problemscan arise. The relative may misinterpret the wishesof the patient, or may have a vested interest inthe death (or continued existence) of the patient.Healthcare providers tend to underestimate sickpatients’ desire to live.Written directions by the patient, legally administeredliving wills or powers of attorney may eliminatesome of these problems but are not withoutlimitations. The patient should describe as preciselyas possible the situation envisaged when lifeP.J.F. Baskett et al.support should be withheld or discontinued. Thismay be aided by a medical adviser. For instance,many would prefer not to undergo the indignityof futile CPR in the presence of end-stage multiorganfailure with no reversible cause, but wouldwelcome the attempt at resuscitation should ventricularfibrillation (VF) occur in association with aremediable primary cardiac cause. Patients oftenchange their minds with change in circumstances,and therefore the advanced directive should be asrecent as possible and take into account any changeof circumstances.In sudden out-of-hospital cardiac arrest, theattendants usually do not know the patient’s situationand wishes, and an advance directive isoften not readily available. In these circumstances,resuscitation is begun immediately and questionsaddressed later. There is no ethical difference instopping the resuscitation attempt that has startedif the healthcare providers are later presented withan advance directive limiting care. The family doctorcan provide an invaluable link in these situations.There is considerable international variationin the medical attitude to written advancedirectives. 1 In some countries, the writtenadvanced directive is considered to be legallybinding and disobedience is considered an assault;in others, the advance directive is flagrantlyignored if the doctor does not agree with thecontents. However, in recent years, there hasbeen a growing tendency towards compliance withpatient autonomy and a reduction in patronisingattitudes by the medical profession. 1When to withhold a resuscitationattemptWhereas patients have a right to refuse treatment,they do not have an automatic right to demandtreatment; they cannot insist that resuscitationmust be attempted in any circumstance. A doctoris required only to provide treatment that islikely to benefit the patient, and is not requiredto provide treatment that would be futile. However,it would be wise to seek a second opinionin making this momentous decision, for fear thatthe doctor’s own personal values, or the questionof available resources, might influence his or heropinion. 13The decision to withhold a resuscitation attemptraises several ethical and moral questions. Whatconstitutes futility? What exactly is being withheld?Who should decide? Who should be consulted? Whoshould be informed? Is informed consent required?

European Resuscitation Council Guidelines for Resuscitation 2005S173When should the decision be reviewed? What religiousand cultural factors should be taken into consideration?What constitutes futility?Futility exists if resuscitation will be of no benefitin terms of prolonging life of acceptable quality. Itis problematic that, although predictors for nonsurvivalafter attempted resuscitation have beenpublished, 14—17 none has been tested on an independentpatient sample with sufficient predictivevalue, apart from end-stage multi-organ failurewith no reversible cause. Furthermore, studies onresuscitation are particularly dependent on systemfactors such as time to CPR, time to defibrillation,etc. These may be prolonged in any study but notapplicable to an individual case.Inevitably, judgements will have to be made,and there will be grey areas where subjective opinionsare required in patients with heart failure andsevere respiratory compromise, asphyxia, majortrauma, head injury and neurological disease. Theage of the patient may feature in the decision butis only a relatively weak independent predictor ofoutcome 18,19 ; however, age is frequently associatedwith a prevalence of comorbidity, which does havean influence on prognosis. At the other end of thescale, most doctors will err on the side of interventionin children for emotional reasons, even thoughthe overall prognosis is often worse in children thanin adults. It is therefore important that cliniciansunderstand the factors which influence resuscitationsuccess.What exactly should be withheld?Do not attempt resuscitation (DNAR) means that,in the event of cardiac or respiratory arrest, CPRshould not be performed; DNAR means nothingmore than that. Other treatment should be continued,particularly pain relief and sedation, asrequired. Ventilation and oxygen therapy, nutrition,antibiotics, fluid and vasopressors, etc., are continuedas indicated, if they are considered to becontributing to the quality of life. If not, orders notto continue or initiate any such treatments shouldbe specified independently of DNAR orders.DNAR orders for many years in many countrieswere written by single doctors, often without consultingthe patient, relatives or other health personnel,but there are now clear procedural requirementsin many countries such as the USA, UK andNorway.Who should decide not to attemptresuscitation?This very grave decision is usually made by thesenior doctor in charge of the patient after appropriateconsultations. Decisions by committee areimpractical and have not been shown to work,and hospital management personnel lack the trainingand experience on which to base a judgement.Decisions by legal authorities are fraughtwith delays and uncertainties, particularly if thereis an adversarial legal system, and should be soughtonly if there are irreconcilable differences betweenthe parties involved. In especially difficult cases,the senior doctor may wish to consult his or herown medical defence society for a legal opinion.Medical emergency teams (METs), acting inresponse to concern about a patient’s conditionfrom ward staff, can assist in initiating thedecision-making process concerning DNAR (see Section4a). 20,21Who should be consulted?Although the ultimate decision for DNAR shouldbe made by the senior doctor in charge of thepatient, it is wise for this individual to consult othersbefore making the decision. Following the principleof patient autonomy it is prudent, if possible,to ascertain the patient’s wishes about a resuscitationattempt. This must be done in advance,when the patient is able to make an informedchoice. Opinions vary as to whether such discussionsshould occur routinely for every hospital admission(which might cause undue alarm in the majorityof cases) or only if the diagnosis of a potentiallylife-threatening condition is made (when there isa danger that the patient may be too ill to make abalanced judgement). In presenting the facts to thepatient, the doctor must be as certain as possible ofthe diagnosis and the prognosis and may seek a secondor third medical opinion in this matter. It is vitalthat the doctor should not allow personal life valuesto distort the discussion—–in matters of acceptabilityof a certain quality of life, the patient’s opinionshould prevail.It is considered essential for the doctor to havediscussions with close relatives and loved ones if atall possible. Whereas they may influence the doctor’sdecision, it should be made clear to them thatthe ultimate decision will be that of the doctor. Itis unfair and unreasonable to place the burden ofdecision on the relative.The doctor would also be wise to discuss thematter with the nursing and junior medical personnel,who are often closer to the patient and

S174more likely to be given personal information. Thepatient’s family doctor may have very close andlong-term insight into the patient’s wishes and thefamily relationships, based on years of knowledgeof the particular situation.Who should be informed?Once the decision has been made it must be communicatedclearly to all who may be involved,including patient and relatives. The decision andthe reasons for it, and a record of who has beeninvolved in the discussions should be written down,ideally on a special DNAR form that should beplaced in a place of prominence in the patient’snotes, and should be recorded in the nursingrecords. Sadly, there is evidence of a reluctanceto commit such decisions to writing by doctors insome centres in some countries. 22When to abandon the resuscitationattemptThe vast majority of resuscitation attempts do notsucceed and have to be abandoned. Several factorswill influence the decision to stop the resuscitativeeffort. These will include the medical history andanticipated prognosis, the period between cardiacarrest and start of CPR, the interval to defibrillationand the period of advanced life support (ALS) withcontinuing asystole and no reversible cause.In many cases, particularly in out-of-hospital cardiacarrest, the underlying cause of arrest may beunknown or merely surmised, and the decision ismade to start resuscitation while further informationis gathered. If it becomes clear that the underlyingcause renders the situation to be futile, thenresuscitation should be abandoned if the patientremains in asystole with all ALS measures in place.Additional information (such as an advance directive)may become available and may render discontinuationof the resuscitation attempt ethicallycorrect.In general, resuscitation should be continuedas long as VF persists. It is generally acceptedthat ongoing asystole for more than 20 min in theabsence of a reversible cause, and with all ALS measuresin place, constitutes grounds for abandoningthe resuscitation attempt. 23 There are, of course,reports of exceptional cases that prove the generalrule, and each case must be assessed individually.In out-of-hospital cardiac arrest of cardiac origin,if recovery is going to occur, a return of spontaneouscirculation usually takes place on site.P.J.F. Baskett et al.Patients with primary cardiac arrest, who requireongoing CPR without any return of a pulse duringtransport to hospital, rarely survive neurologicallyintact. 24Many will persist with the resuscitation attemptfor longer if the patient is a child. This decisionis not generally justified on scientific grounds, forthe prognosis after cardiac arrest in children is certainlyno better, and probably worse, than in adults.Nevertheless, the decision to persist in the distressingcircumstances of the death of a child isquite understandable, and the potential enhancedrecruitment of cerebral cells in children after anischaemic insult is an as yet unknown factor to bereckoned with.The decision to abandon the resuscitationattempt is made by the team leader, but afterconsultation with the other team members, whomay have valid points to contribute. Ultimately, thedecision is based on the clinical judgement that thepatient’s arrest is unresponsive to ALS. The finalconclusion should be reached by the team leadertaking all facts and views into consideration anddealing sympathetically, but firmly, with any dissenter.When considering abandoning the resuscitationattempt, a factor that may need to be taken intoaccount is the possibility of prolonging CPR andother resuscitative measures to enable organ donationto take place. Mechanical chest compressionsmay be valuable in these circumstances, 25 but thishas not been studied. The issue of initiating lifeprolongingtreatment with the sole purpose of harvestingorgans is debated by ethicists, and there isvariation between the different countries of Europeas to the ethics of this process; at present no consensusexists.Decision-making by non-physiciansMany cases of out-of-hospital cardiac arrest areattended by emergency medical technicians orparamedics, who face similar dilemmas of whento determine if resuscitation is futile and whenit should be abandoned. In general, resuscitationis started in out-of-hospital cardiac arrest unlessthere is a valid advanced directive to the contraryor it is clear that resuscitation would be futilein cases of a mortal injury, such as decapitation,hemicorporectomy, known prolonged submersion,incineration, rigor mortis, dependent lividity andfetal maceration. In such cases, the non-physicianis making a diagnosis of death but is not certifyingdeath (which can be done only by a physician inmost countries).

European Resuscitation Council Guidelines for Resuscitation 2005S175But what of the decision to abandon a resuscitationattempt? Should paramedics trained in ALSbe able to declare death after 20 min of asystole inthe absence of reversible causes, bearing in mindthe very negative results achieved with ongoingCPR during transport? Opinions vary from countryto country. 26 In some countries it is routine, andit is surely unreasonable to expect paramedics tocontinue with resuscitation in the precise circumstanceswhere it would be abandoned by a doctor.In making this recommendation, it is essentialthat times are recorded very accurately and writtenguidelines provided. 27 The answer would appearto lie in superior training and thereafter confidencein those who have been trained to make thedecision.Similar decisions and a diagnosis of death mayhave to be made by nurses in nursing homesfor the aged and terminally ill without a residentdoctor. It is to be hoped that a decision onthe merits of a resuscitation attempt will havebeen made previously, and the matter of DNARshould always be addressed for all patients in theseestablishments.Mitigating circumstancesCertain circumstances, for example hypothermiaat the time of cardiac arrest, will enhance thechances of recovery without neurological damage,and the normal prognostic criteria (such as asystolepersisting for more than 20 min) are not applicable.Furthermore, sedative and analgesic drugs mayobscure the assessment of the level of consciousnessin the patient who has a return of spontaneouscirculation.Withdrawal of treatment after aresuscitation attemptPrediction of the final neurological outcome inpatients remaining comatose after regaining aspontaneous circulation is difficult during the first3 days (see Section 4g). There are no specific clinicalsigns that can predict outcome in the first fewhours after the return of a spontaneous circulation.Use of therapeutic hypothermia after cardiac arrestmakes attempts at predicting neurological outcomeeven more difficult.In a very small number of distressing cases,patients regain spontaneous circulation but remainin persistent vegetative state (PVS). Continuedexistence in this state may not be in the patient’sbest interest compared with the alternative ofdying. If remaining alive but in PVS is considerednot to be in the patient’s best interests, considerationmust be given to the potential withdrawal offood and fluids to terminate life. These are profoundlydifficult decisions, but generally there isagreement between relatives and the doctors andnurses on the correct course of action. In thesecases, decisions can often be made without theneed for legal intervention. Difficulties arise ifthere is a disagreement between the doctors andnurses and the relatives, or between the relatives.In Europe, although there also may be extremeviews, it seems that the majority are content toleave the decision to the family and physicians inprivate.Family presence during resuscitationThe concept of a family member being present duringthe resuscitation process was introduced in the1980s 28 and has become accepted practice in manyEuropean countries. 29—38 Many relatives would liketo be present during resuscitation attempts and, ofthose who have had this experience, over 90% wouldwish to do it again. 33 Most parents would wish to bewith their child at this time. 39Relatives have considered several benefits frombeing permitted to be present during a resuscitationattempt, including• help in coming to terms with the reality of deathand easing the bereavement process;• being able to communicate with, and touch, theirloved one in their final moments while they werestill warm. Many feel that their loved one appreciatedtheir presence at that moment, and thismay be quite possible if consciousness returnsduring effective CPR (as has been recorded particularlywith mechanical CPR on occasions);• feeling that they had been present during thefinal moments and that they had been a supportto their loved one when needed;• feeling that they had been there to see thateverything that could be done, was done.Several measures are required to ensure that theexperience of the relative is the best under the circumstances.• The resuscitation should be seen to be conductedcompetently, under good team leadership, withan open and welcoming attitude to relatives.• Brief the relatives, in terms that they can understand,before entering; and ensure that continualsupport is provided by a member of staff(usually a nurse) trained in this subject. Ensure

S176that relatives understand that the choice to bepresent is entirely theirs, and do not provokefeelings of guilt, whatever their decision.• Make the relatives aware of the proceduresthey are likely to see (e.g., tracheal intubation,insertion of central venous catheters) andthe patient’s response (e.g., convulsive movementsafter defibrillation). Emphasise the importanceof not interfering with any procedures andexplain clearly the dangers of doing so.• In the majority, of cases it will be necessary toexplain that the patient has not responded to theresuscitation attempt and that the attempt hasto be abandoned. This decision should be madeby the team leader, involving the members of theteam. Explain to the relatives that there may bea brief interval while equipment is removed, andthat then they will be able to return to be withtheir loved one at their leisure, alone or supported,as they wish. Certain tubes and cannulaemay have to be left in place for medicolegal reasons.• Finally, there should be an opportunity for therelative to reflect, ask questions about the causeand the process, and be given advice about theprocedure for registering the death and the supportservices available.In the event of an out-of-hospital arrest, therelatives may already be present, and possibly performingbasic life support (BLS). Offer them theoption to stay; they may appreciate the opportunityto help and travel in the ambulance to hospital. Ifdeath is pronounced at the scene, offer the relativesthe help and support of their family doctor orcommunity nurse and bereavement councillor.For resuscitation staff, both in and out hospital,it is worth offering training in the matter of relativesbeing present. 40With increasing experience of family presenceduring resuscitation attempts, it is clear that problemsrarely, if ever, arise. In the majority ofinstances, relatives come in and stay for just afew minutes and then leave, satisfied that theyhave taken the opportunity to be there to supporttheir loved one and say goodbye as theywould have wished. Ten years ago most staffwould not have countenanced the presence ofrelatives during resuscitation, but a recent surveyhas shown an increasingly open attitude andappreciation of the autonomy of both patient andrelatives. 1 Perhaps this is related to a generallymore permissive and less autocratic attitude. Internationalcultural and social variations still exist,and must be understood and appreciated withsensitivity.P.J.F. Baskett et al.Training and research on the recentlydeadAnother matter that has raised considerable debateis the ethics, and in some cases the legality,of undertaking training and/or research on therecently dead.TrainingThe management of resuscitation can be taughtusing scenarios with manikins and modern simulators,but training in certain skills required duringresuscitation is notoriously difficult. External chestcompressions and, to an extent, expired air ventilationand insertion of oropharyngeal and nasopharyngealairways can be taught using manikins; butdespite technological advances in manikins and simulators,many other skills that are needed on aregular basis during resuscitation can be acquiredsatisfactorily only through practice on humans,dead or alive. These other skills include, for example,central and peripheral venous access, arterialpuncture and cannulation, venous cut-down, bagmaskventilation, tracheal intubation, cricothyroidotomy,needle thoracostomy, chest drainageand open-chest cardiac massage. Some of theseskills may be practised during routine clinical work,mostly involving anaesthesia, and to a lesser degreesurgery; but others such as cricothyroidotomy, needlethoracostomy and open chest cardiac massagecannot, and are needed only in a life-threateningemergency when it is difficult to justify a teachingexercise. In modern day practice, with practitionersbeing called increasingly to account and patientautonomy prevailing, it is becoming more and moredifficult to obtain permission for student practice ofskills in the living. Gone are the days when admissionto a ‘teaching hospital’ implied automatic consentfor students to practise procedures on patientsunder supervision as they wished. And yet the publicexpect, and are entitled to, competent practitionersfor generation after generation.So the question arises as to whether it is ethicallyand morally appropriate to undertake trainingand practice on the living or the dead. There is awide diversity of opinion on this matter. 41 Many,particularly those in the Islamic nations, find theconcept of any skills training and practice on therecently dead completely abhorrent because of aninnate respect for the dead body. Others will acceptthe practice of non-invasive procedures that do notleave a mark, such as tracheal intubation; and someare open and frank enough to accept that any proceduremay be learned on the dead body with the

European Resuscitation Council Guidelines for Resuscitation 2005S177justification that the learning of skills is paramountfor the well-being of future patients.One option is to request informed consent forthe procedure from the relative of the deceased.However, only some will obtain permission, 1,40 andmany find this very difficult to do in the harrowingcircumstances of breaking bad news simultaneouslyto the recently bereaved. As a result, frequentlyonly non-invasive procedures are practised, on thebasis that what is not seen will not cause distress.The days of undertaking any procedure without consentare rapidly coming to an end, and perhaps itis now becoming increasingly necessary to mount apublicity campaign to exhort the living to give permissionfor training on their dead body through anadvance directive, in much the same way as permissionfor transplant of organs may be given. Itmay be that an ‘opt-out’ rather than an ‘opt-in’arrangement may be adopted, but this will requirechanges in the law in most countries. It is advisedthat healthcare professionals learn local and hospitalpolicies regarding this issue and follow theestablished policy.ResearchThere are important ethical issues relating toundertaking randomized clinical trials for patientsin cardiac arrest who cannot give informed consentto participate in research studies. Progress inimproving the dismal rates of successful resuscitationwill only come through the advancement ofscience through clinical studies. The utilitarian conceptin ethics looks to the greatest good for thegreatest number of people. This must be balancedwith respect for patient autonomy, according towhich patients should not be enrolled in researchstudies without their informed consent. Over thepast decade, legal directives have been introducedinto the USA and the European Union 42,43 that placesignificant barriers to research on patients duringresuscitation without informed consent fromthe patient or immediate relative. 44 There aredata showing that such regulations deter researchprogress in resuscitation. 45 It is indeed possible thatthese directives may in themselves conflict withthe basic human right to good medical treatmentas set down in the Helsinki Agreement. 12 Researchin resuscitation emanating from the USA has fallendramatically in the last decade, 46 and it appearsvery likely that the European Union will followsuit as the rules bite there. 47 The US authoritieshave, to a very limited extent, sought to introducemethods of exemption, 42 but these are still associatedwith problems and almost insurmountabledifficulties. 45Research on the recently dead is likely toencounter similar restrictions unless previous permissionis granted as part of an advance directiveby the patient, or permission can be given immediatelyby the relative who is next of kin. Legalownership of the recently dead is established onlyin a few countries, but in many countries it is atleast tacitly agreed that the body ‘belongs’ to therelatives (unless there are suspicious circumstancesor the cause of death is unknown), and permissionfor any research must be granted by the next of kinunless there is an advance directive giving consent.Obtaining consent from relatives in the stressfulcircumstances of immediate bereavement is unenviableand potentially damaging to the relationshipbetween doctor and relative.Research can still be carried out during postmortemexamination, for instance to study thetraumatic damage resulting from the use of specificmethods of chest compression, but all bodyparts must be returned to the patient unless specificpermission is obtained from relatives to dootherwise.Breaking bad news and bereavementcounsellingBreaking news of the death of a patient to a relativeis an unenviable task. It is a moment thatthe relative will remember for ever, so it is veryimportant to do it as correctly and sensitively aspossible. It also places a considerable stress on thehealthcare provider who has this difficult duty. Bothmay need support in the ensuing hours and days. Itis salutatory that the breaking of bad news is seldomtaught in medical school or at postgraduatelevel. 1Contacting the family in the case of deathwithout the relatives being presentIf the relatives are not present when the patientdies, they must be contacted as soon as possible.The caller may not be known to the relative andmust take great care to ensure that his or heridentity is made quite clear to the relative and,in turn, the caller must make sure of the relationshipof the call recipient to the deceased. Inmany cases it is not stated on the telephone thatthe patient has actually died, unless the distanceand travel time are prolonged (e.g., the relativeis in another country). Many find that it is betterto say that the patient is seriously and criticallyill or injured and that the relatives should cometo hospital immediately, so that a full explanation

S178can be given face to face. It is wise to request thatrelatives to ask a friend to drive them to hospital,and to state that nothing will be gained by drivingat speed. When the relatives arrive they should begreeted right away by a competent and knowledgeablemember of staff, and the situation explainedimmediately. Delays in being told the facts areagonising.Who should break the bad news to therelative?Gone are the days when it was acceptable for thepatronising senior doctor to delegate the breakingof bad news to a junior assistant. Nowadays, it isgenerally agreed that it is the duty of the seniordoctor or the team leader to talk to the relatives.Nevertheless, it is wise to be accompanied by anexperienced nurse who may be a great comfort forthe patient (and indeed the doctor).Where and how should bad news be given?The environment where bad news is given is vitallyimportant. There should be a room set aside forrelatives of the seriously ill that is tastefully andcomfortably furnished, with free access to a telephone,television and fresh flowers daily (whichmay be provided by the florist who runs the flowershop that is in most hospitals in Europe).There are some basic principles to be followedwhen breaking bad news, that should be adhered toif grave errors are to be avoided and the relative isnot to be discomforted. It is essential to know thefacts of the case and to make quite sure to whomwho you are talking. Body language is vital; alwayssit at the same level as the patient and relative;do not stand up when they are sitting down. Makesure you are cleanly dressed; wearing blood-stainedclothing is not good. Do not give the impressionthat you are busy and in a hurry. Give the newsthey are anxious to hear immediately, using thewords ‘‘dead’’ or ‘‘has died’’, ‘‘I am very sorry tohave to tell you that your father/husband/son hasdied’’. Do not leave any room for doubt by usingsuch phrases as ‘‘passed on’’ or left us’’ or ‘‘goneup above’’.Discussing the medical details comprehensivelyat this stage is not helpful; wait until they are askedfor. Touching may be appropriate, such as holdinghands or placing an arm on the shoulder, but peopleand customs vary and the doctor needs to be awareof these. Do not be ashamed if you shed a tear yourself.Allow time for the news to be assimilated bythe relative. Reactions may vary, includingP.J.F. Baskett et al.• relief (‘‘I am so glad his suffering is over,’’ or‘‘He went suddenly—–that is what he would havewished’’);• anger with the patient (‘‘I told him to stop smoking,’’or ‘‘He was too fat to play squash,’’ or‘‘Look at the mess he has left me in’’);• self-guilt (‘‘If only I had not argued with him thismorning before he left for work,’’ or ‘‘Why did Inot tell the doctor he got chest pain?’’);• anger with the medical system (‘‘Why did theambulance take so long?’’ or ‘‘The doctor wasfar too young and did not know what he/she wasdoing’’);• uncontrollable wailing and crying and anguish;• complete expressionless catatonia.It may be useful to reassure the family that theydid everything correctly, such as calling for help andgetting to the hospital but, in the vast majority ofcases, healthcare providers are unable to restartthe heart.Some time may elapse before conversation canresume and, at this stage, ask relatives if they haveany questions about the medical condition and thetreatment given. It is wise to be completely openand honest about this, but always say ‘‘He did notsuffer’’.In the majority of cases the relative will wishto see the body. It is important that the body andbedclothes are clean and all tubes and cannulaeare removed, unless these are needed for postmortemexamination. The image of the body willleave an impression on the relative that will last forever. A post-mortem examination may be required,and this should requested with tact and sensitivity,explaining that the procedure will be carriedout by a professional pathologist and will help todetermine the precise cause of death.ChildrenBreaking bad news to children may be perceived topresent a special problem, but experience seemsto indicate that it is better to be quite open andhonest with them, so helping to dispel the nightmarishfantasies that children may concoct aboutdeath. It is helpful to contact the school, so thatthe teachers and fellow pupils can be prepared toreceive the child back into the school environmentwith support and sensitivity.ClosureIn many cases this will be the relative’s firstexperience of death, and help should be offeredwith the bewildering administration of the official

European Resuscitation Council Guidelines for Resuscitation 2005S179registration of death, funeral arrangements andsocioeconomic support by the hospital or communitysocial worker. Depending on religious beliefs,the hospital padre or priest may have a vital role toplay. Whenever possible, family physicians shouldbe informed immediately by telephone or e-mailwith the essential details of the case, so that theycan give full support to the relatives. A followuptelephone call to the relative a day or twolater from a member of the hospital staff whowas involved, offering to be of help and to answerany questions that the relative may have forgottenabout at the time, is always appreciated.Staff debriefAlthough many members of staff seem, and oftenare, little affected by death in the course of theirwork, this should not be assumed. Their senseof accomplishment and job satisfaction may beaffected adversely, and there may be feelings ofguilt, inadequacy and failure. This may be particularlyapparent in, but not restricted to, very juniormembers of staff. A team debrief of the eventusing positive and constructive critique techniquesshould be conducted and personal bereavementcounselling offered to those with a particular need.How this is done will vary with the individual andwill range from an informal chat in the pub or cafe(which seems to deal effectively with many cases)to professional counselling. It should be explainedthat distress after a death at work may be a normalreaction to an abnormal situation.ConclusionsResuscitation has given many a new lease of life,to the delight of themselves and their relatives,but has the potential to bring misery to a few. Thischapter addresses how that misery can be reducedby not attempting resuscitation in inappropriatecircumstances or in cases with a valid advanceddirective, and when to discontinue the resuscitationattempt in cases of futility or PVS.Ethical issues such as training and research onthe recently dead, and the presence of family membersduring the resuscitation attempt, place furtherburdens on the medical profession but must bedealt with sympathetically, and with an appreciationof growing patient autonomy and human rightsthroughout the world.Finally, the breaking of bad news is one of themost difficult tasks to be faced by the medical andnursing professions. It requires time, training, compassionand understanding.References1. Baskett PJ, Lim A. The varying ethical attitudes towardsresuscitation in Europe. Resuscitation 2004;62:267—73.2. Sprung CL, Cohen SL, Sjokvist P, et al. End-of-life practicesin European intensive care units: the Ethicus Study. JAMA2003;290:790—7.3. Richter J, Eisemann MR, Bauer B, Kreibeck H, Astrom S.Decision-making in the treatment of elderly people: a crossculturalcomparison between Swedish and German physiciansand nurses. Scand J Caring Sci 2002;16:149—56.4. da Costa DE, Ghazal H, Al Khusaiby S. Do not resuscitateorders and ethical decisions in a neonatal intensive careunit in a Muslim community. Arch Dis Child Fetal NeonatalEd 2002;86:F115—9.5. Ho NK. Decision-making: initiation and withdrawing life supportin the asphyxiated infants in developing countries. SingaporeMed J 2001;42:402—5.6. Richter J, Eisemann M, Zgonnikova E. Doctors’ authoritarianismin end-of-life treatment decisions. A comparisonbetween Russia, Sweden and Germany. J Med Ethics2001;27:186—91.7. Cuttini M, Nadai M, Kaminski M, et al. End-of-life decisions inneonatal intensive care: physicians’ self-reported practicesin seven European countries. EURONIC Study Group. Lancet2000;355:2112—8.8. Konishi E. Nurses’ attitudes towards developing a do notresuscitate policy in Japan. Nurs Ethics 1998;5:218—27.9. Muller JH, Desmond B. Ethical dilemmas in a cross-culturalcontext. A Chinese example. West J Med 1992;157:323—7.10. Edgren E. The ethics of resuscitation; differences betweenEurope and the USA-Europe should not adopt Americanguidelines without debate. Resuscitation 1992;23:85—9.11. Beauchamp TL, Childress J, editors. Principles of biomedicalethics. 3rd ed. Oxford: Oxford University Press; 1994.12. Declaration of Helsinki. Ethical principles for medicalresearch involving human subjects adopted by the 18th WMAGeneral Assembly, Helsinki, Finland, June 1964 and amendedat the 29th, 35th, 41st, 48th, and 52nd WMA Assemblies.Geneva, 1964.13. Aasland OG, Forde R, Steen PA. Medical end-of-life decisionsin Norway. Resuscitation 2003;57:312—3.14. Danciu SC, Klein L, Hosseini MM, Ibrahim L, Coyle BW, KehoeRF. A predictive model for survival after in-hospital cardiopulmonaryarrest. Resuscitation 2004;62:35—42.15. Dautzenberg PL, Broekman TC, Hooyer C, Schonwetter RS,Duursma SA. Review: patient-related predictors of cardiopulmonaryresuscitation of hospitalized patients. AgeAgeing 1993;22:464—75.16. Haukoos JS, Lewis RJ, Niemann JT. Prediction rules for estimatingneurologic outcome following out-of-hospital cardiacarrest. Resuscitation 2004;63:145—55.17. Herlitz J, Engdahl J, Svensson L, Young M, Angquist KA, HolmbergS. Can we define patients with no chance of survivalafter out-of-hospital cardiac arrest? Heart 2004;90:1114—8.18. Herlitz J, Engdahl J, Svensson L, Angquist KA, Young M,Holmberg S. Factors associated with an increased chanceof survival among patients suffering from an out-of-hospitalcardiac arrest in a national perspective in Sweden. Am HeartJ 2005;149:61—6.19. Ebell MH. Prearrest predictors of survival following inhospitalcardiopulmonary resuscitation: a meta-analysis. JFam Pract 1992;34:551—8.20. Hillman K, Parr M, Flabouris A, Bishop G, Stewart A. Redefiningin-hospital resuscitation: the concept of the medicalemergency team. Resuscitation 2001;48:105—10.

S18021. The MERIT study investigators. Introduction of the medicalemergency team (MET) system: a cluster-randomised controlledtrial. Lancet 2005;365:2091—7.22. Sovik O, Naess AC. Incidence and content of written guidelinesfor ‘‘do not resuscitate’’ orders. Survey at six differentsomatic hospitals in Oslo. Tidsskr Nor Laegeforen1997;117:4206—9.23. Bonnin MJ, Pepe PE, Kimball KT, Clark Jr PS. Distinct criteriafor termination of resuscitation in the out-of-hospitalsetting. JAMA 1993;270:1457—62.24. Kellermann AL, Hackman BB, Somes G. Predicting the outcomeof unsuccessful prehospital advanced cardiac life support.JAMA 1993;270:1433—6.25. Steen S, Liao Q, Pierre L, Paskevicius A, Sjoberg T. Evaluationof LUCAS, a new device for automatic mechanical compressionand active decompression resuscitation. Resuscitation2002;55:285—99.26. Naess A, Steen E, Steen P. Ethics in treatment decisionsduring out-of-hospital resuscitation. Resuscitation1997;35:245—56.27. Joint Royal Colleges Ambulance Liaison Committee. Newsletter1996 and 2001. Royal College of Physicians: London.28. Doyle CJ, Post H, Burney RE, Maino J, Keefe M, Rhee KJ. Familyparticipation during resuscitation: an option. Ann EmergMed 1987;16:673—5.29. Adams S, Whitlock M, Higgs R, Bloomfield P, Baskett PJ.Should relatives be allowed to watch resuscitation? BMJ1994;308:1687—92.30. Hanson C, Strawser D. Family presence during cardiopulmonaryresuscitation: Foote Hospital emergency department’snine-year perspective. J Emerg Nurs 1992;18:104—6.31. Cooke MW. I desperately needed to see my son. BMJ1991;302:1023.32. Gregory CM. I should have been with Lisa as she died. AccidEmerg Nurs 1995;3:136—8.33. Boie ET, Moore GP, Brummett C, Nelson DR. Do parents wantto be present during invasive procedures performed on theirchildren in the emergency department? A survey of 400 parents.Ann Emerg Med 1999;34:70—4.34. Boudreaux ED, Francis JL, Loyacano T. Family presence duringinvasive procedures and resuscitations in the emergencydepartment: a critical review and suggestions for futureresearch. Ann Emerg Med 2002;40:193—205.35. Martin J. Rethinking traditional thoughts. J Emerg Nurs1991;17:67—8.P.J.F. Baskett et al.36. Robinson SM, Mackenzie-Ross S, Campbell Hewson GL, EglestonCV, Prevost AT. Psychological effect of witnessedresuscitation on bereaved relatives. Lancet 1998;352:614—7[comment].37. Baskett PJF. The ethics of resuscitation. In: Colquhoun MC,Handley AJ, Evans TR, editors. The ABC of resuscitation. 5thed. London: BMJ Publishing Group; 2004.38. Azoulay E, Sprung CL. Family-physician interactions in theintensive care unit. Crit Care Med 2004;32:2323—8.39. Bouchner H, Vinci R, Waring C. Pediatric procedures: do parentswant to watch? Pediatrics 1989;84:907—9.40. Resuscitation Council (UK) Project Team. Should relativeswitness resuscitation? London, UK: Resuscitation Council;1996.41. Morag RM, DeSouza S, Steen PA, et al. Performing procedureson the newly deceased for teaching purposes: what if wewere to ask? Arch Intern Med 2005;165:92—6.42. US Department of Health and Human Services. Protection ofhuman subjects: informed consent and waiver of informedconsent requirements in certain emergency circumstances.In: 61 Federal Register 51528 (1996) codified at CFR #50.24and #46.408; 1996.43. Fontaine N, Rosengren B. Directive/20/EC of the EuropeanParliament and Council of 4th April 2001 on the approximationof the laws, regulations and administrative provisionsof the Member States relating to the implementation ofgood clinical practice in the conduct of trials on medicalproducts for human use. Off J Eur Commun 2001;121:34—44.44. Lemaire F, Bion J, Blanco J, et al. The European UnionDirective on Clinical Research: present status of implementationin EU member states’ legislations with regardto the incompetent patient. Intensive Care Med 2005;31:476—9.45. Nichol G, Huszti E, Rokosh J, Dumbrell A, McGowan J, BeckerL. Impact of informed consent requirements on cardiacarrest research in the United States: exception from consentor from research? Resuscitation 2004;62:3—23.46. Mosesso Jr VN, Brown LH, Greene HL, et al. Conductingresearch using the emergency exception from informed consent:the public access defibrillation (PAD) trial experience.Resuscitation 2004;61:29—36.47. Sterz F, Singer EA, Bottiger B, et al. A serious threat toevidence based resuscitation within the European Union.Resuscitation 2002;53:237—8.

Resuscitation (2005) 67S1, S181—S189European Resuscitation Council Guidelines forResuscitation 2005Section 9. Principles of training in resuscitationPeter J. F. Baskett, Jerry P. Nolan, Anthony Handley, Jasmeet Soar,Dominique Biarent, Sam RichmondIntroductionThere are a variety of methods used for trainingin resuscitation. None are perfect and, in theabsence of frequent practice, retention of knowledgeand skills is suboptimal. The optimal intervalfor retraining has not been established, butrepeated refresher training at intervals of less than6 months seems to be needed for most individualswho are not undertaking resuscitation on a regularbasis. 1—12ObjectivesThe objective of training is to equip the learnerwith the ability to be able to undertake resuscitationin a real clinical situation at the level at whichthey would be expected to perform, be they be laybystander, first responder in the community or hospital,a healthcare professional working in an acutearea, or a member of the medical emergency orcardiac arrest response team.MethodsTraining should follow the principles of adult educationand learning. Generally this will mean anestablished European Resuscitation Council (ERC)course with small-group (four to eight members)participation using interactive discussion andhands-on practice for skills and clinical scenariosfor problem-solving and team leadership. 13The ratio of instructors to candidates shouldrange from 1:3 to 1:6, depending on the type ofcourse.Core knowledge should be acquired by candidatesbefore the course by study of the coursemanual or an interactive CD designed for the purpose.The course should aim to produce an improvementin competence in the learner, and thereshould be a test of core knowledge and an ongoingassessment of practical skills and scenario management.Sophisticated manikins, simulators and virtualreality techniques may be incorporated intothe scenario-based training. 14For basic life support (BLS) by lay people or firstresponders, home-based learning using a video orinteractive CD with a simple manikin may offera valuable alternative to traditional instructorbasedcourses. 15—19 This method minimises candidatedisruption and instructor time and finances.However, the role of the instructor should not beunderestimated and, in addition to explaining situationsthat were unforeseen on the original videoor CD, the instructor can act as a role modeland provide invaluable enthusiasm and motivation.0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.doi:10.1016/j.resuscitation.2005.10.006

S182Group participation has also been demonstrated toenhance the overall learning process.EthosThe course should be taught by trained instructorswho have undertaken the relevant specific ERCcourse in teaching and assessment. Teaching shouldbe conducted by encouragement with constructivefeedback on performance rather than humiliation.First names are encouraged among bothfaculty and candidates to reduce apprehension,and the mentor/mentee system is used to enhancefeedback and support for the candidate. Stress isinevitable, 20 particularly during assessment, butthe aim of the instructors is to enable the candidatesto do their best.LanguageInitially, the ERC courses were taught in English byan international faculty. 13 As local instructors havebeen trained, and manuals and course materialshave been translated into different languages, thecourses, particularly the provider courses, are nowtaught increasingly in the candidates’ native language.InstructorsA tried and tested method has evolved for identifyingand training instructors.Identification of instructor potentialsInstructors will be individuals who, in the opinion ofthe faculty, have demonstrated good competencein the subjects at a provider course and, importantly,have shown qualities of leadership and clinicalcredibility and skills that involve being articulate,supportive and motivated. These individualswill be invited to take part in an instructor coursecalled the Generic Instructor Course (GIC) in thecase of Advanced Life Support (ALS) and EuropeanPaediatric Life Support (EPLS) courses, or BasicLife Support (BLS)/Automated External Defibrillation(AED) Instructor Course in the BLS and AEDcourses. An instructor course for Immediate LifeSupport (ILS) is under development.The instructor coursesThese are conducted for instructor potentials (IPs)by experienced instructors and, in the case of theP.J.F. Baskett et al.GIC, include an educator who has undertaken specifictraining in medical educational practice andthe principles of adult learning. Details of theseinstructor courses are given below. There are noformal tests for candidates during the course, butassessment is done by the faculty and feedback isgiven as appropriate.Instructor candidate stageFollowing successful completion of an instructorcourse, the individual is designated as an instructorcandidate (IC), normally taught on two separatecourses under supervision, and is given constructivefeedback on performance. After experience of twocourses, the IC normally progresses to full instructorstatus, but occasionally the faculty decides thata further course is required or, rarely, that the candidateis not suitable to progress to be an instructor.An appeal can be lodged with the relevant InternationalCourse Committee, which makes the finaldecision.Course director statusSelected individuals may progress to the status ofthe course director. They will be selected by theirpeers and approved by the relevant committee ofthe National Resuscitation Council or the relevantInternational Course Committee. Course directorsmust be relatively senior individuals with considerableclinical credibility, good judgement and impeccablepowers of assessment and fairness. They willhave embraced the educational principles inherentin the instructor course. Normally, individualswill have had experience of teaching on at least sixcourses and will have been appointed course codirectoron at least one occasion.Interchange of instructorsInterchange between instructors of different disciplinesis possible. For instance, an ALS instructormay proceed directly to be an IC on an EPLScourse, provided that he or she has passed the EPLScourse and has been identified as an IP and viceversa. There is no need to repeat the GIC. Similarly,current instructors in the Advanced TraumaLife Support (ATLS) Course of the American Collegeof Surgeons, having been identified as an IP inthe relevant provider course, may proceed directlyto being an IC in ALS or EPLS. Current AmericanHeart Association Advanced Cardiac Life Support(ACLS) or Paediatric Advanced Life Support (PALS)instructors may proceed directly to IC status in therelevant course.

European Resuscitation Council Guidelines for Resuscitation 2005S183Code of conductAll instructors must adhere to the code of conductfor the instructors, which is set out in Appendix A.The Basic Life Support (BLS) andAutomated External Defibrillator (AED)coursesBLS and AED courses are appropriate for a widerange of providers. These may include clinical andnon-clinical healthcare professionals (particularlythose who are less likely to be faced with havingto manage a cardiac arrest), general practitioners,dentists, medical students, first-aid workers, lifeguards,those with a duty of care for others (suchas school teachers and care workers), and membersof first-responder schemes, as well as members ofthe general public.Provider course formatThe aim of these provider courses is to enable eachcandidate to gain competency in BLS or the useof AED. Details of appropriate competencies havebeen published by the ERC BLS Working Group andmay be found on http://www.erc.edu. BLS and AEDcourses are developed and managed by the ERCInternational BLS Course Committee (ICC).Each BLS or AED provider course lasts approximatelyhalf a day and consists of skill demonstrationsand hands-on practice, with a minimumnumber of lectures. The recommended ratio ofinstructors to candidates is 1:6, with at least onemanikin and one AED for each group of six candidates.Formal assessment is not usually undertaken,but each candidate receives individual feedback onperformance. Those who need a certificate of competencyfor professional or personal use may beassessed continuously during the course or definitivelyat the end.BLS provider and AED provider manuals, togetherwith certificates, may be purchased from the ERC.Approved alternative manuals, translated if necessaryinto the local language, may also be used.Instructor courseMany of the candidates attending a BLS or AEDprovider course are lay people, and some subsequentlywant to become instructors themselves. Forthis reason, the ERC has developed a 1-day BLS/AEDinstructor course. Candidates for this course mustbe healthcare professionals, or lay people who holdthe ERC BLS or AED provider certificate and are designatedas IP. The aim is to be as inclusive as possibleregarding the course attendance, the over-ridingcriterion being that all candidates should have thepotential and knowledge to teach the subject.The BLS/AED instructor course follows the principlesof the GIC, with an emphasis on teachinglay people. Following successful completion of thecourse, each candidate becomes an IC and teachestwo BLS or AED courses before becoming a fullinstructor.Introducing courses into a countryMany ERC BLS and AED provider courses are run by,or under the control of, the National ResuscitationCouncil. The normal procedure for introducing ERCBLS/AED courses into a country is that ERC internationalinstructors visit that country to run a 2-daycombined BLS provider, AED provider and BLS/AEDinstructor course. If there are local instructors(e.g., those who have passed an ERC course successfully,or who are ERC ALS instructors), theyteach on the course in a 1:1 ratio of international tolocal instructor, with the course director (an internationalinstructor) as an additional person who cansupport local instructors. After a successful coursethe local instructors become full ERC instructors,and the outstanding local instructors are selectedto become instructor trainers. Subsequent coursesare normally held in the language of the countryconcerned, and training materials are translatedinto that language. The candidates who are on thecombined course qualify, hopefully, as ERC BLS/AEDICs. They then need to teach on one or two providercourses, under the supervision of full instructors,before becoming full instructors themselves.The Immediate Life Support (ILS) courseThe ILS course is for the majority of healthcareprofessionals who attend cardiac arrests rarelybut have the potential to be first respondersor cardiac-arrest team members. 21 The courseteaches the healthcare professionals the skills thatare most likely to result in successful resuscitationwhile awaiting the arrival of the resuscitationteam. 22 Importantly, the ILS course alsoincludes a section on preventing cardiac arrest,and complements other short courses that focus onmanaging sick patients in the first 24 h of critical illnesswhen critical care expertise is not immediatelyavailable. 23—25 There is a large group of potentialcandidates including nurses, nursing students, doctors,medical students, dentists, physiotherapists,radiographers and cardiac technicians.

S184Current ALS instructors and ICs can teach andassess on ILS courses. There is also a pilot projectunderway to develop specific ILS instructors. Theremust be at least 1 instructor for every 6 candidates,with a maximum of 30 candidates on acourse.Course formatThe ILS course is delivered over 1 day and compriseslectures, hands-on skills teaching and cardiacarrestscenario teaching (CASTeach) using manikins.The programme includes a number of options thatallow instructors to tailor the course to their candidategroup.Course contentThe course covers those skills that are most likelyto result in successful resuscitation: causes and preventionof cardiac arrest, starting CPR, basic airwayskills and defibrillation (AED or manual). There areoptions to include the teaching of the laryngealmask airway and drug treatments during cardiacarrest. Once all the skills have been covered, thereis a cardiac arrest demonstration by the instructorsthat outlines the first-responder role to thecandidates. This is followed by the CASTeach stationwhere candidates practise. ILS candidates arenot usually expected to undertake the role of theteam leader. Candidates should be able to starta resuscitation attempt and continue until moreexperienced help arrives. When appropriate, theinstructor takes over as a resuscitation team leader.This is not always necessary, as in some scenariosresuscitation may be successful before more experiencedhelp arrives. Set scenarios are used thatare adapted to the workplace and the clinical roleof the candidate.AssessmentP.J.F. Baskett et al.Candidate’s performances are assessed continuouslyand they must show their competencethroughout the ILS course. There are no formaltesting stations, removing the threat associatedwith spot testing at the end of the course. Candidatesare sent the assessment forms with the precoursematerials. The forms indicate clearly howtheir performance will be measured against a predeterminedcriteria. Assessment on the ILS courseenables the candidate to see what is expected andframe learning around achievement of these outcomes.The following practical skills are assessed onthe ILS course: airway management, BLS and defibrillation.With a supportive approach, the majorityof candidates achieve the course learning outcomes.EquipmentThe ILS course is designed to be straightforwardto run. Most courses are conducted in hospitalswith small groups of candidates (average 12 candidates).The course requires lecture facilities anda skills teaching area for each group of six candidates.There needs to be at least one ALS manikinfor every six candidates. The course should be suitablefor local needs. Course centres should tryas far as possible to train candidates to use theequipment (e.g., defibrillator type) that is availablelocally.Course report and results sheetA course report and the results sheet are compiledby the course director and filed with the NationalResuscitation Council and the ERC.The Advanced Life Support (ALS) courseThe target candidates for this course are doctorsand senior nurses working in emergency areas ofthe hospital and those who may be members ofthe medical emergency or cardiac arrest teams. 26The course is also suitable for senior paramedicsand certain hospital technicians. The ILS course ismore suitable for first-responder nurses, doctorswho rarely encounter cardiac arrest in their practice,and emergency medical technicians. Up to 32candidates can be accommodated on the course,with a ratio of at least 1 instructor for every 3 candidates.Up to a maximum of 50% of the instructorsmay be ICs. Groups for teaching should not exceedeight candidates and should be six ideally. Eachinstructor acts as a mentor for a small group of candidates.The course normally lasts for two to twoand a half days.Course formatThe course format has very few formal lectures(four), and teaching concentrates on hands-onskills, clinically based scenarios in small groups withemphasis on the team leader approach and interactivegroup discussions. Mentor/mentee sessions areincluded, to allow candidates to give and receivefeedback. Faculty meetings are held at the beginningof the course and at the end of each day of the

European Resuscitation Council Guidelines for Resuscitation 2005S185course. Social occasions, such as course and facultydinners, add greatly to the course interaction andenjoyment.Course contentThe course content is based on the currentERC guidelines for resuscitation. Candidates areexpected to have studied the ALS course manualcarefully before the course.The course aims to train candidates to highlightthe causes of cardiac arrest, identify sick patients indanger of deterioration and manage cardiac arrestand the immediate periarrest problems encounteredin and around the first hour or so of the event.It is not a course in advanced intensive care or cardiology.Competence in BLS is expected before thecandidate enrols for the course.Emphasis is placed on the techniques of safedefibrillation and ECG interpretation, the managementof the airway and ventilation, the managementof periarrest rhythms, simple acid/base balanceand special circumstances relating to cardiacarrest. Post-resuscitation care, ethical aspectsrelated to resuscitation and care of the bereavedare included in the course.Assessment and testingEach candidate is assessed individually andreviewed at the end of each day by the facultyat their meeting. Feedback is given as required.There is a testing scenario towards the end ofthe course, and an on going assessment of themanagement of the sick patient and the needto be able to defibrillate effectively and safely.There is a multiple-choice question paper takenat the end of the course to test core knowledge.Candidates are required to achieve 75% to pass thistest.Course venue and equipmentThe course requires four practical rooms, a lectureroom, a faculty room and facilities for lunches andrefreshments. At least two digital projectors andcomputers and up to four flip charts are needed.The practical rooms each should have an adult ALSmanikin with ECG simulator and a defibrillator. Fouradult airway manikins are required, together withthe equipment for simple airway care and ventilation,tracheal intubation and placing a supraglotticairway, such as the laryngeal mask. Intravenouscannulae, syringes, infusion fluids and simulateddrugs make up the list.Course report and results sheetA course report and the results sheet are compiledby the course director and filed with the nationalresuscitation council and the ERC.The European Paediatric Life Support(EPLS) courseThe EPLS course is designed for healthcare workerswho are involved in the resuscitation of a newborn,an infant or a child whether in or out of hospitalThe course aims at providing caregivers with theknowledge and skills for the management of thecritically ill child during the first hour of illnessand to prevent progression of diseases to cardiacarrest.Competence in basic paediatric life support is aprerequisite, although a 90-min refresher course onBLS and relief of foreign-body airway obstructionis included. The EPLS course is suitable for doctors,nurses, emergency medical technicians andparamedics, etc., who have a duty to respondto sick newborns, infants and children in theirpractice. 27,28 EPLS is not a course in neonatal orpaediatric intensive care aimed at the advancedproviders.The course can accommodate 24 candidates witha ratio of at least 1 instructor for every 4 candidates.In exceptional circumstances, 28 candidatesmay be accepted with extra instructors. Experiencein paediatrics is necessary to keep scenariosrealistic and to answer candidates’ questions, soa minimum of 50% of the faculty must have regularexperience in neonatal or paediatric practice.Up to a maximum of 50% of the instructors may beICs. Groups for teaching should not exceed eightcandidates and ideally should be five or six; twoinstructors act as mentors for a group of five toseven candidates. The course normally lasts for twoto two and a half days.Course formatThe new course format has fewer formal lectures(three). Teaching of knowledge and skills is givenin small groups using clinically based scenarios.The emphasis is on assessment and treatment ofthe sick child, team working and leadership. Formalmentor/mentee sessions are included, to allowcandidates to give and receive feedback. Facultymeetings are held at the beginning of the courseand at the end of each day of the course. Feedbackis also given to ICs after each series of workshopsand after their lectures.

S186Course contentThe course content follows the current ERC guidelinesfor neonatal and paediatric resuscitation. Thecourse candidates are expected to have studied themanual before attending the course. In the futurethey also may receive a CD or a DVD for hometraining in BLS. 15 A precourse MCQ is sent with themanual to candidates 4—6 weeks before the course.It is collected at the beginning and feedback is givenduring the course.The EPLS is aimed at training the candidatesto understand the causes and mechanisms of cardiorespiratoryarrest in neonates and children, torecognise and treat the critically ill neonate, infantor child and to manage cardiac arrest if it occurs.Skills taught include airway management, bag-maskventilation, log roll and cervical collar placement,oxygen delivery, an introduction to intubation andvascular access, safe defibrillation, cardioversionand AED use.Each candidate is assessed individually andreviewed by the faculty. Feedback is given asrequired. A BLS assessment follows the BLSrefresher course, and a second scenario-based testat the end of the course emphasises the assessmentof the sick child and the core skills. There is amultiple-choice question paper taken at the end ofthe course to test the core knowledge. Candidatesare required to achieve 75% to pass this test.Course venue and equipmentThe course requires four practical rooms, a lectureroom, a faculty room and facilities for lunches andrefreshments. At least one digital projector andcomputer and up to four flip charts are needed.Paediatric manikins (infant and child for basic andadvanced techniques) and adjuncts must be availablein each classroom. One defibrillator, one AEDand one rhythms simulator device must also beavailable.Course report and results sheetA course report and the results sheet are compiledby the course director and filed with the nationalresuscitation council and the ERC.The Newborn Life Support (NLS) courseThis course is designed for health workers likely tobe present at the birth of a baby in the course oftheir job. It aims to give those who may be calledP.J.F. Baskett et al.upon to start resuscitation at birth the backgroundknowledge and skills to approach the managementof the newborn infant during the first 10—20 minin a competent manner. The course is suitable formidwives, nurses and doctors and, like most suchcourses, works best with candidates from a mixtureof specialties.The course is usually conducted over 1 day andruns best with 24 candidates, though up to 32 maybe permitted. There should be one instructor forevery three candidates in addition to the coursedirector.Course formatThe NLS manual is sent to each of the candidates 4weeks before the course. Each candidate receivesa multiple-choice questionnaire, with the manualand is asked to complete this and bring it to thecourse. There are two 30-min and two 15-min lectures.The candidates are then divided into fourgroups and pass through three workstations beforelunch. The afternoon is taken up by a demonstrationscenario, followed by 2 h of scenario teachingin small groups and finally a theoretical andpractical assessment by an MCQ and an individualpractical airway test. The course concentrates onairway management but also covers chest compression,umbilical venous access and drugs.Course venue and equipmentThe venue requires a lecture room, four goodsizedpractical rooms, a faculty room and facilitiesfor lunch and refreshments. A digital projector isrequired in the lecture theatre and a flip chart ora black/white board in each practical room. Ideally,one of the practical rooms should have handwashingfacilities. At least four infant BLS and fourinfant ALS manikins (ideally six of each) should beavailable, as well as other airway adjuncts. FourResuscitaires, ideally complete with gas cylinders,should also be available.Course report and results sheetA course report and results sheet are compiled bythe course director and lodged with the nationalresuscitation council and the ERC.The Generic Instructor Course (GIC)This course is for candidates who have been recommendedas IP, emanating from the ALS or EPLS

European Resuscitation Council Guidelines for Resuscitation 2005S187provider courses. In some, the MIMMS course isundertaken under the auspices of the ALSG, andIPs from that course may take the GIC to qualifyas ICs for teaching that course. There should be amaximum of 24 candidates, with a ratio of at least1 instructor to 3 candidates. Instructors must allbe fully experienced ERC instructors, not ICs. A keyperson is the educator. Groups should not exceed sixcandidates. The emphasis of the course is on developinginstruction skills. Core knowledge of the originalprovider course is assumed. The course lasts fortwo to two and a half days.Course formatThe course format is largely interactive. The educatorplays a key role and leads many of the discussionsand feedback. There is one formal lecture oneffective teaching and adult learning, conductedby the educator. This lecture is interspersed withgroup activities. The remainder of the course isconducted in small group discussions and skill- andscenario-based hands-on sessions.Mentor/mentee sessions are included, and thereis a faculty meeting at the beginning of the courseand at the end of each day.Course contentThe course concentrates on teaching techniquesand skills. Candidates are expected to have studiedthe GIC manual carefully before the course(reference manual). The theoretical background ofadult learning and effective teaching is coveredby the educator at the beginning of the course.The features of PowerPoint and the flip chart aredemonstrated, and candidates have an opportunityto present a 5-min lecture and are given personalfeedback on their performance. The principle ofequipment familiarisation, followed by a demonstrationby the faculty with subsequent candidatepractice, is followed in all aspects of the course.The teaching of skills is based on the four-stageapproach. Scenario-based sessions use scenariosfrom the candidate’s original provider course.Emphasis is placed on the role of the instructorthroughout this teaching day, and each candidatehas the opportunity to adopt the instructor role.Constructive feedback is a key element of theinstructor role.During the second day, the emphasis movesto assessment and, after demonstrations by thefaculty, all candidates are offered the opportunityto act in the instructor assessor role for theassessment of skills and scenario leadership. Furthersessions include the conduct of open andclosed discussions and the role and qualities of theinstructor.AssessmentEach candidate has ongoing assessment by the facultythroughout the course. Candidates’ performancesand attitudes are discussed at the dailyfaculty meetings and feedback is given as required.Successful candidates may proceed to the status ofIC.Course venue and equipmentThis is as for the original provider course. If thecandidates come from mixed backgrounds, then avariety of equipment is required.Course report and results sheetA course report is compiled by the course directorand the educator. This and the results sheet arefiled with the national resuscitation council and theERC.The Educator Master Class (EMC)This course, normally held annually, is designed forthose aspiring to become medical educators for theGIC. Suitable candidates are selected by the faculty,and generally must have a background andqualification in medical education or must havedemonstrated a special commitment to educationalpractice over a number of years. They should haveexperience of a provider course and a GIC, andshould have studied the background reading for thecourse.The instructors for the course are experiencededucators. A maximum of 18 candidates can beaccommodated with 6 instructors. The groupsshould comprise a maximum of six candidates. Thecourse lasts just under 2 days.Course formatThe course consists mainly of closed discussiongroups for the whole course, led by one or twoof the instructors, together with break-out smallgroup discussions and problem solving.Course contentThe course covers the theoretical framework formedical educators, assessment and quality control,

S188teaching methodologies, critical appraisal, the roleof the mentor, multiprofessional education strategiesand continued development of the medicaleducator.AssessmentEach candidate has ongoing assessment by the facultythroughout the course. Individual progress isdiscussed at a faculty meeting at the end of eachday, and candidates are given the feedback asappropriate. Successful candidates may proceed tothe status of educator candidate (EC), where theywill be supervised and assessed by an experiencededucator and course director until it is decidedwhether or not they will be suitable educators towork on their own.Course venue and equipmentThe course venue requires a lecture room and threebreak-out rooms. A digital projector and three flipcharts are needed; no manikins are required.Course report and resultsThe course director compiles a course report afterconsultation with the faculty. This, and the resultssheet, are conveyed to the educator’s nationalresuscitation council and the ERC.Appendix A. European ResuscitationCouncil Code of ConductThe Code of Conduct applies to all who instruct, orotherwise assist, at courses held under the auspicesof the ERC.It is essential that these individuals• fully understand that accreditation, and continuingaccreditation, of the individual instructor orassistant is dependent on observing this code aswell as completing the necessary requirementsfor re-certification• ensure that courses approved by the ERC are runin accordance with the ethos and regulations currentlyin force using the manuals, slides and othermaterials to ensure that consistent standards ofattitude, knowledge and skills are achieved• behave at all times while participating in coursesor social events related to the courses, which arerun under the auspices of the ERC, in a responsiblemanner and observe and other applicableprofessional codes of conductP.J.F. Baskett et al.• cooperate with other instructors, educators andadministrators (the faculty) and recognise andrespect their individual contributions• avoid any abuse of their position and maintainconfidentiality about candidates’ results and performance.References1. Makker R, Gray-Siracusa K, Evers M. Evaluation of advancedcardiac life support in a community teaching hospital by useof actual cardiac arrests. Heart Lung 1995;24:116—20.2. Anthonypillai F. Retention of advanced cardiopulmonaryresuscitation knowledge by intensive care trained nurses.Intensive Crit Care Nurs 1992;8:180—4.3. Azcona LA, Gutierrez GE, Fernandez CJ, Natera OM, Ruiz-Speare O, Ali J. Attrition of advanced trauma life support(ATLS) skills among ATLS instructors and providers in Mexico.J Am Coll Surg 2002;195:372—7.4. Birnbaum ML, Robinson NE, Kuska BM, Stone HL, FrybackDG, Rose JH. Effect of advanced cardiac life-support trainingin rural, community hospitals. Crit Care Med 1994;22:741—9.5. Hammond F, Saba M, Simes T, Cross R. Advanced life support:retention of registered nurses’ knowledge 18 months afterinitial training. Aust Crit Care 2000;13:99—104.6. Kaye W, Mancini ME, Rallis SF. Advanced cardiac life supportrefresher course using standardized objective-based megacode testing. Crit Care Med 1987;15:55—60.7. Kaye W, Wynne G, Marteau T, et al. An advanced resuscitationtraining course for preregistration house officers. J RColl Physicians Lond 1990;24:51—4.8. O’Steen DS, Kee CC, Minick MP. The retention of advancedcardiac life support knowledge among registered nurses. JNurs Staff Dev 1996;12:66—72.9. Schwid HA, O’Donnell D. Anesthesiologists’ managementof simulated critical incidents. Anesthesiology1992;76:495—501.10. Young R, King L. An evaluation of knowledge and skill retentionfollowing an in-house advanced life support course. NursCrit Care 2000;5:7—14.11. Stross JK. Maintaining competency in advanced cardiac lifesupport skills. JAMA 1983;249:3339—41.12. Su E, Schmidt TA, Mann NC, Zechnich AD. A randomized controlledtrial to assess decay in acquired knowledge amongparamedics completing a pediatric resuscitation course.Acad Emerg Med 2000;7:779—86.13. Baskett P. Progress of the advanced life support courses inEurope and beyond. Resuscitation 2004;62:311—3.14. Chamberlain DA, Hazinski MF. Education in resuscitation.Resuscitation 2003;59:11—43.15. Braslow A, Brennan RT, Newman MM, Bircher NG, BatchellerAM, Kaye W. CPR training without an instructor: developmentand evaluation of a video self-instructional systemfor effective performance of cardiopulmonary resuscitation.Resuscitation 1997;34:207—20.16. Todd KH, Braslow A, Brennan RT, et al. Randomized, controlledtrial of video self-instruction versus traditional CPRtraining. Ann Emerg Med 1998;31:364—9.17. Todd KH, Heron SL, Thompson M, Dennis R, O’Connor J,Kellermann AL. Simple CPR: a randomized, controlled trial ofvideo self-instructional cardiopulmonary resuscitation trainingin an African American church congregation. Ann EmergMed 1999;34:730—7.

European Resuscitation Council Guidelines for Resuscitation 2005S18918. Batcheller AM, Brennan RT, Braslow A, Urrutia A, Kaye W.Cardiopulmonary resuscitation performance of subjects overforty is better following half-hour video self-instruction comparedto traditional four-hour classroom training. Resuscitation2000;43:101—10.19. Lynch B, Einspruch E, Nichol G, Becker L, Aufderheide T, IdrisA. Effectiveness of a 30-minute CPR self-instruction programfor lay responders: a controlled randomized study. Resuscitation2005;67:31—43.20. Sandroni C, Fenici P, Cavallaro F, Bocci MG, ScapigliatiA, Antonelli M. Haemodynamic effects of mentalstress during cardiac arrest simulation testing onadvanced life support courses. Resuscitation 2005;66:39—44.21. Soar J, Perkins GD, Harris S, Nolan JP. The immediate lifesupport course. Resuscitation 2003;57:21—6.22. Soar J, McKay U. A revised role for the hospital cardiac arrestteam. Resuscitation 1998;38:145—9.23. Smith GB, Osgood VM, Crane S. ALERT—–a multiprofessionaltraining course in the care of the acutely ill adult patient.Resuscitation 2002;52:281—6.24. Smith GB, Poplett N. Impact of attending a 1-day multiprofessionalcourse (ALERT) on the knowledge of acute carein trainee doctors. Resuscitation 2004;61:117—22.25. Featherstone P, Smith GB, Linnell M, Easton S, Osgood VM.Impact of a one-day inter-professional course (ALERT TM )on attitudes and confidence in managing critically ill adultpatients. Resuscitation 2005;65:329—36.26. Nolan J. Advanced life support training. Resuscitation2001;50:9—11.27. Buss PW, McCabe M, Evans RJ, Davies A, Jenkins H. A surveyof basic resuscitation knowledge among resident paediatricians.Arch Dis Child 1993;68:75—8.28. Carapiet D, Fraser J, Wade A, Buss PW, Bingham R. Changesin paediatric resuscitation knowledge among doctors. ArchDis Child 2001;84:412—4.