Advance Life Support Manual

Mercy Health Learning
Advanced Life Support
2 nd Edition
1

2

© Published by Mercy Health
Authors 1 st
Edition:
Kelly-Ann Humphry’s, Emergency Nurse Educator (2010)
Patty Dillon , Emergency Nurse Educator (2015)
Patty Dillon (2014 &2015) Lynn O’Neill( 2014)
Julie O’Connell (2011)
Reviewed: Kamaree Berry & Rachel Mol (2014) John Caluza
Authors
2 nd Edition:
Karen Wynne Critical Care Program Lead
(2016)
Caroline Cooper-Blair Medical Surgical
Program Lead (2016)
Version: 2016 Review Date: March 2017
This document is bound by copyright and has been produced for the intended use of Mercy Health
employees only. No part of this document may be reproduced, stored, broadcasted or transmitted in any
form or by any electronic, recording, mechanical, copying or any other means, without prior notice or
permission, except as permitted by the Copyright Act.
A high standard of accuracy is maintained when completing and producing this document. However, the
contents of this document may be altered and / or revised without prior notice; no responsibility is taken
for any consequential issues that may result from using this document.
Acknowledgments to the ACCCN 2014 Advanced Life Support Manual which has been acknowledged
throughout this package as a resource for theory.
For more information, please contact:
Karen Wynne
Critical Care Program Lead
MPHI
Ph: 87543483
KWynne@mercy.com.au
Clinical Nurse Educator (Emergency)
Patty Dillon
Ph: 8754 3524
PDillon@mercy.com.au
3

Table of Contents
Learning Objectives
Basic Life Support
Principles and Practices
Advanced Life Support
Principles and Practices
4 H’s and 4 T’s of Resuscitation
ALS Algorithm
5-8
9-13
Tachycardia and Bradycardia Algorithm 14-15
Non-technical skills in ALS 16
Advanced Airway
Management
Intubation
Complications
Laryngeal
Mask Airway
(LMA)
17-24
Defibrillation Technique and Considerations 25-31
Cardiac Conduction and Arrhythmia Recognition 32-37
Arrhythmia Revision 38-47
Pharmacology 48-52
Roles in an arrest 53--54
Post Resuscitation Care
Bibliography
55-56
Assessment Tool 57-58
Paediatric Considerations 60-63
4

Introduction
Overview
The purpose of this package is to ensure consistency and continuity of Advanced Life Support (ALS) techniques
for Mercy Health and to ensure a high standard of Advanced Life Support (ALS) knowledge and proficiency
amongst suitably qualified nurses through an annual assessment process.
This package must be reviewed and activities completed as required for every Grade 2 Registered Nurse (RN) and
above undertaking this skill set and practical assessment competency.
Learning Outcomes
At this end of this package and following practical training the RN will be able to:
• Define / describe the difference between basic and advanced life support
• Define the roles of team members in an arrest
• Discuss the importance of advanced airway management – adult
• Recognise and discuss the relevant arrhythmias and treatment for each
• Discuss medications used in emergency situations including indications, action, dosage and complications
• Demonstrate the ability to provide Leadership in an arrest scenario
Resources
In addition to the content provided in this package, the list of resources is located in the bibliography at the end
of this package to assist staff to successfully complete the necessary requirements.
5

Basic Life Support
Overview
Basic Life Support (BLS) is considered the preservation of life by the initial establishment of, and / or
maintenance of airway, breathing and circulation and related emergency care, including the use of an
automated external defibrillator. Basic life support is only a temporary measure to maintain ventilation
and circulation. Even with effective cardiac compressions, only 20-30% of the pre-arrest cardiac output is
maintained.
Review of Key BLS Information
• BLS can commence when the:
a) patient is not moving and is unresponsive
b) patient is not breathing, breathing abnormally
• DRSABCD forms the key steps in BLS:
Danger – Response – Send for help – Airway open – Breathing normally– Circulation start CPR – Defibrillator attach
AED (see Figure 1: ARC BLS Algorithm)
• Mouth-to-mouth resuscitation is not performed in hospitals – a bag and mask are used (eg. Air Viva with oxygen flow at
15 L / minute)
• The use of the head tilt and chin lift manoeuver are used to open the airway
• Hand position – middle of lower half of sternum for all age groups
• Depth of compression should be 1/3 chest
• Infants: Two finger method and Adults: Heal of hand
• BLS ratio is 30 compressions: 2 breaths for one (1) or two (2) rescuers – if unwilling / unable to perform rescue breaths
continue with chest compressions
• BLS ratio for children with 2 rescuers is: 15 compressions : 2 breaths.
• If only chest compressions are given, they should be continuous at a rate of approximately 100 - 120 compressions / minute
• AED pads should be firmly applied to a bare chest with a smooth rolling action to eliminate any air bubbles
• AED adult pads can be used for children over the age of 9
• AED child pads are used on infants / children between the ages of 1 and 8
• BLS can cease when the:
a) patient has regained spontaneous respirations
b) patient has resumed a rhythm with an effective cardiac output
c) medical officer has declared the patient deceased
6

Figure 1: ARC Basic Life Support Flowchart
Australian Resuscitation Council. (2010). Basic life support. Retrieved 07 February, 2014 from http://www.resus.org.au/flowcharts.html
7

The previous flow chart is for Basic life support in the community or outside a hospital setting as per
Resuscitation Council of Australia.
The policy is to initiate medical assistance as soon as possible and obtain medical intervention. If the
patient becomes unconscious/ unresponsive then the emergency code blue will be initiated and CPR
commenced on the patient. Advance life support steps will need to be initiated to ensure the safety of
the patient.
Please review the below flow chart for management of the patient with a foreign airway obstruction.
Figure 5: Airway Obstruction Flowchart
8

9
Advanced Life Support
Overview
Advanced Life Support (ALS) is considered the prevention or restoration of life by the establishment and / or
maintenance of airway, breathing and circulation using invasive techniques such as defibrillation, advanced
airway management, intravenous access and drug therapy.
Principles and Practices
Excellent cardiopulmonary resuscitation (CPR) and early defibrillation for
treatable arrhythmias remain the cornerstones of basic and advanced
life support.
In the past, clinicians frequently interrupted CPR to check for pulses, perform tracheal intubation and obtain
venous access. The Australian guidelines strongly recommend that every effort be made NOT to interrupt
CPR. Interventions such as intubation, medication administration and invasive monitoring are performed
during the briefest interruption to CPR.
It is important that good CPR and early defibrillation is undertaken in the attempt to achieve successful
outcomes within a hospital environment. Ventricular Fibrillation (VF) is in many situations the primary
rhythm in sudden cardiac arrest. The vast majority of survivors of a cardiac arrest come from this group.
Key Principles
CPR to commence with chest compressions rather than ventilation
Use combination of unresponsiveness & absence of breathing or abnormal breathing to identify cardiac
arrest
Fallibility of pulse check even in the hands of clinicians
Increased emphasis on high quality chest compressions with minimal interruptions
Simultaneous breaths & compressions are to be avoided
When using a defibrillator in manual mode, it is safe to charge the defibrillator while chest
compressions continue in preparation for rhythm analysis & possible defibrillation
Only single shocks are recommended
After each defibrillation continue a further 2 minutes of CPR, unless responsiveness or normal
breathing becomes apparent.
Administer 100% oxygen when available
Obtain intravenous or intra- osseous access
Consider airway adjuncts, but attempts to secure the airway should not interrupt CPR for
more than 20 seconds
Adrenaline should be administered every second cycle and other drugs/anti arrhythmic should be
considered to reverse causes of the arrest (see sections of medications)
Indications
Airway obstruction, respiratory and circulatory arrest are the conditions requiring BLS and ALS. Common
underlying problems include:
Ischaemic heart disease
Acute severe asthma
Drug overdose/toxicity

Near drowning
Trauma
Electrolyte abnormalities
Post surgical complications
It is most important to be aware of and understand the 4 H’s and the T’s……..
The H’s and T’s of advanced life support is a mnemonic that is used to help recall the major contributing factors
to cardiac arrest. The H’s and T’s will most commonly be associated with pulseless electrical activity (PEA) but
they will help to identify underlying causes to any of arrhythmias associated with ALS. Please see below for
further detail.
THE H’s
Hypovolemia
Hypoxia
Hyper-/hypokalaemia
Hypo/Hyperthermia.
THE T’s
Toxins
Tamponade (cardiac)
Tension pneumothorax
Thrombosis (coronary and pulmonary)
Hypovolemia
Hypovolemia or the loss of fluid volume is most commonly due to haemorrhage from trauma or post surgery.
After CPR has commenced the most import intervention is obtaining intravenous access/IO access. Treatment is
based on delivering circulatory volume to the patient. Administration of 20ml/kg Normal Saline immediately if
hypovolaemia is the suspected cause of cardiac arrest.
Hypoxia
Low circulating oxygen levels will cause energy failure at the cellular level and if uncorrected will eventually
result in arrest. Ensure that the patient’s airway is open, and that the patient has chest rise and fall and bilateral
breath sounds with ventilation. Also ensure that your oxygen source is connected properly.
10

Hyper-/hypokalemia
Hypokalaemia is defined as a serum potassium level less than 3.5mmoll/L with severe hypokalaemia defined as
a serum potassium less than 2.5mmol/L. Causes include gastrointestinal loss, drugs, renal losses, metabolic
alkalosis, magnesium depletion and poor dietary intake. Treatment includes 5mmol bolus of Potassium Chloride
K+. The major signs of hypokalaemia or low serum potassium are flattened T-waves, prominent U-waves, and
possibly a widened QRS complex. Hyperkalaemia is defined as a serum potassium level of more than 5.5mmol/L
and severe as greater than 6.5mmol/L. Causes include renal failure, drugs, rhabdomyolysis, metabolic acidosis
and endocrine disorders. Symptoms include flattened or absent P waves, peaked T wave, widened QRS complex
and bradycardia. Treatment includes administration of 10mls of Calcium Chloride, Glucose/Insulin infusion to
move potassium back into the cells and dialysis to move potassium from the body.
Hypo-Hyperthermia
Hypothermia is defined as a core body temperature less than 35 degrees Celsius. Low core temperature results
in less oxygen being delivered to the tissues. Hyperthermia occurs when the body’s core temperature exceeds
what is normally maintained by homeostatic mechanisms. Treatment is based on supportive therapies like
managing a patient’s ABC and attempting to return the core body temperature to normal. Malignant
hyperthermia is a rare disorder that is characterised by muscle contracture and life threatening hypermetabolic
crisis following exposure to halogenated anaesthetics and muscle relaxants.
The T’s include:
Toxins
Accidental overdose of a number of different kinds of medications can cause pulseless arrest. Some of the most
common include: tricyclics, digoxin, beta-blockers, and calcium channel blockers and illegal substances and
envenomation from venomous creatures such as snakes, jellyfish.
Tamponade
Cardiac tamponade is an emergency condition in which fluid accumulates in the pericardium (sac in which the
heart is enclosed). The build-up of fluid results in ineffective pumping of the blood which can lead to pulseless
arrest. ECG symptoms include narrow QRS complex and rapid heart rate. Physical signs include jugular vein
distention (JVD), no pulse or difficulty palpating a pulse, and muffled heart sounds due to fluid inside the
pericardium. The recommended treatment for cardiac tamponade is pericardiocentesis.
Tension Pneumothorax
Tension pneumothorax occurs when air is allowed to enter the plural space and is prevented from escaping
naturally. Physical signs include JVD, tracheal deviation, unequal breath sounds, difficulty with ventilation, and
no pulse felt with CPR. Treatment of tension pneumothorax is needle decompression or drain insertion.
Thrombosis (pulmonary/cardiac)
Cardiac thrombosis is the impedance of blood flow within a coronary artery caused by blood that has clotted
within the vessel. The clotted blood causes an acute myocardial infarction which destroys heart muscle and can
lead to sudden death depending on the location of the blockage. Treatments for coronary thrombosis before
cardiac arrest include use of fibrinolytic therapy, or PCI (percutaneous coronary intervention). The most
common PCI procedure is coronary angioplasty with or without stent placement.
Thrombosis (pulmonary embolism)
11

Pulmonary thrombus or pulmonary embolism (PE) is a blockage of the main artery of the lung which can rapidly
lead to respiratory collapse and sudden death. Treatment includes pulmonary thrombectomy and fibrinolytic
therapy.
Factors that determine whether an individual will survive after cardio respiratory arrest include:
Time interval to initiation of BLS
Efficient and effective CPR
Time interval to defibrillation
Cardiac rhythm
Patient characteristics and co-morbidities e.g age, previous health, underlying disease
Body Temperature
The chain of survival
The best chance of survival after cardiac arrest is if:
The victim is witnessed to collapse
CPR is commenced immediately
The cardiac rhythm is ventricular fibrillation or pulseless ventricular tachycardia
Defibrillation is performed as soon as possible
When spontaneous return of circulation (ROC) is established, post resuscitation care is initiated.
12

During CPR
Airway adjuncts (LMA/ETT)
Oxygen
Waveform capnography
IV/IO Access
Plan actions before interrupting CPR
Drugs
Shockable
Adrenaline 1mg after 2 nd shock
(Then every 2 nd loop)
Amiodarone 300mg after 3 rd shock
Non Shockable
Adrenaline 1mg immediately
(Then every 2 nd loop)
Consider and Correct
Hypoxia
Hypovolaemia
Hyper/hypokalaemia/Metabolic disorders
Hypothermia/Hyperthermia
Tension pneumothorax
Tamponade
Toxins
Thrombosis
Post Resuscitation Care
Re-evaluate ABCDE
12 lead ECG
Treat precipitating causes
Re-evaluate oxygenation and ventilation
Temperature control (Cool)
Recognising the Deteriorating Patient
According to the Australian Resuscitation Council, the signs of clinical deterioration are similar despite the
underlying cause. They will in general reflect failing respiratory, cardiovascular and neurological systems. The
following algorithms relate to guidelines for managing the patient presenting with tachycardia or bradycardia.
(Algorithm care of ACCN 2014)
13

Algorithm care of ACCCN 2014)
14

(Algorithm care of ACCCN 2014)
15

Non-Technical Skills in the Emergency Situation
Skills like compression, airway management, intravenous cannulation and rhythm recognition are essential
technical skills in managing cardiac arrest. However, non-technical skill like situational awareness, decision
making, team work and leadership, are often overlooked in regards to their importance, but can have a huge
impact in the success of cardiac arrest management. These are the skills that can affect our performance as
health care professionals.
Situational awareness
Situational awareness is described as how aware we are of the current environment/situation, its gravity and
how our decisions make impact on current happenings. In a cardiac arrest situation, situational awareness
includes:
Being aware of the location of the arrest
Gaining information about the cardiac arrest i.e. events leading up to the event from staff who have
been with the patient.
Considering the causes and making a diagnosis
Establishing team members roles in the arrest, especially determining who is team leader
Establishing actions/interventions already initiated by the initial responders i.e. have chest
compressions been commenced, is the monitor attached, what rhythm is the patient in, has
defibrillation been given, have any drugs been administered?
Determining immediate needs and implementing interventions which take priority
Establishing adequate communication within the team
Decision Making
In a high intensity situation like cardiac arrest, decision making will usually fall onto the shoulders of the team
leader. Although decisions will fall to the team leader, all team members should feel comfortable to have some
input. Once any decision is made communication of the decision and possible interventions/s is the key!
Team Work and Team Leadership
Team work and team leadership is essential in the successful management of a cardiac arrest. The team needs
to work towards a common goal and should be managed by a competent tea leader. An effective team is made
up of members who are competent, committed, communicate well, supportive, accountable, and identifies the
need for help and participates actively in non-judgmental feedback and debriefing. A team leader is someone
who provides guidance, direction and instruction and should be a person who is willing to delegate tasks, a
good communicator and shows tolerance, has good situational awareness, is assertive when needed but can
stay calm and keep the team focused.
During the resuscitation the Team Leader needs to be identified early, their role includes allocating roles to the
other team members, making decisions as per the current resuscitation guidelines initiate debriefing after the
resuscitation attempt and support both staff and family who have been involved.
16

17

ADVANCED AIRWAY MANAGEMENT
AND
VENTILATION DURING CPR
18

Advanced Airway Management
Airway management is the first step in the resuscitation of a patient. Initial measures to manage the airway
of a collapsed person include the removal of any foreign matter to clear the airway, backward head tilt, jaw
thrust and chin lift. Advanced measures may include the insertion of an endotracheal tube (ETT) to secure
the airway and provide ventilation either via a bag-valve circuit or mechanical ventilation with oxygen.
Intubation attempts should not delay
CPR for any longer than 20 seconds. LMA may be considered if professional trained in its use as an
alternative to bag- mask ventilation during CPR
ETT
Intubation
Rapid
Sequence
Induction
• Accomplished by passing a tube, either nasally or orally through the larynx and into the trachea
• Indication include:
a) To secure or maintain an airway in the unconscious or obtund patient
b) To protect the airway from regurgitation or aspiration in patients with a depressed level of
consciousness or ineffective upper airway reflexes
c) To provide high concentrations of oxygen, mechanical ventilation, or general anaesthesia
d) For management of secretions in patients who are unable to effectively clear secretions and
whose respiratory state is compromised as a result
• Unless the patient is in cardiac arrest the patient will require medications to ensure that the tube
can be passed safely and correctly
• This technique minimises the risk of hypoxaemia and aspiration of vomitus
• Steps as follows:
• Explanation to the patient (if conscious) or to family / next of kin
• IV access
• Monitoring equipment
• Medications required for intubation:
• Thiopentone
• Suxamethonium
• Propofol
• Morphine
• Midazolam
• Vecuronium
• Diazepam
Rapid
Sequence
Induction
cont.
Preparation
• Medication preparation will depend on the type of sedation/anaesthetic the
RMO chooses. This will be patient depended. The list above are some of the
medications used for intubation.
• Intubation Equipment as follows:
a) Bag-valve-mask circuit
b) Suction with Yankaeur sucker attached and selection of Y-suction
catheters
c) Magill’s forceps, laryngoscope blade and handle
d) Introducer, intubating bougie tube and lubricant
e) Appropriate size endotracheal tube (ETT), with one size smaller and
larger available. In the emergency department we typically use sizes
between 6.5 and 8.0
f) 10mL syringe for inflating the cuff
g) Tape for securing the ETT and endotracheal mount
h) Waveform capnography and stethoscope
19

Rapid
Sequence
Induction
cont.
Pre-oxygenation
Pre-treatment
Pressure
• Pre-oxygenation with 100% oxygen via a tight fitting mask with the patient in
a supine ‘sniffing’ position
• Attach waveform capnography to AirViva
• Goal is to prevent potential adverse effects of laryngoscopy and
neuromuscular blocking agents (generally Suxamethonium)
• Adjunctive medications may be given such as atropine to reduce bradycardia
• After pre-treatment has been addressed, the sedative may be given
• Exact sedative agents that are used depend on operator preference and
patient condition (eg. head injury, raised intracranial pressure)
• Once the sedative is given and consciousness lost, cricoid pressure (Sellick’s
manoeuvre) is applied
• Performed to prevent the inhalation of regurgitated gastric contents, helps
the passage of the tube, and visualise the vocal cords
• One person needs to be solely responsible for this task
Procedure
• Identify the cricoid cartilage (directly below the Adam’s apple)
• When advised, place the thumb and middle finger on either side of the
cricoid cartilage
• Place the index finger above, in the space between the cricoid and thyroid
cartilage.
• Maintain firm, even pressure directly backwards and release only when
advised by the person responsible for the intubation
Cricoid Location:
Paralysis
• Immediately follows the induction agent
• The muscle relaxant of choice is generally Suxamethonium (1.5mg/kg); a
depolarising agent
• Acts at the motor neuron junction causing fasciculation and paralysis for 3-5
minutes
20

Passing ETT
Post-management
• On cessation of muscle fasciculation, muscle tone is lost and laryngoscopy
can be performed
• The ETT is passed through the vocal cords and into the trachea
• The cuff is inflated and the ETT secured with tape
• Cricoid pressure is only released when the ETT position is checked (via
waveform capnography) and secured
• Proof of placement includes clinical assessment (eg. auscultation of breath
sounds, chest wall movement)
• Capnography remains the standard for confirming intubation of the trachea
• Chest x-ray is performed to ensure that the ETT is 2cm above the carina
• Lip level is also documented
• Once the ETT is secured and correct position confirmed, the patient should
be monitored closely
• Position of the ETT should be checked at least once a shift and more
frequently if patient condition changes
Intubation Complications
Immediate
Long Term
• Oesophageal intubation
• Intubation of the right main bronchus
• Trauma to the nose and / or mouth
• Aspiration of gastric contents
• Cardiac arrhythmias
• Hypoxia
• Bronchospasm or laryngospasm
• Tracheal stenosis
• Infection
• Laryngeal damage
• Tracheo-oesophageal fistula
• Tube obstruction from biting or secretions
• Loss of voice
• Displacement of the tube
Adapted from:
Australian Resuscitation Guidelines (2010)
Laryngeal Mask Airway (LMA)
The LMA is commonly used in patients undergoing short surgical procedures. The LMA was
developed in the 1980’s to address the gap between facemasks and endotracheal tubes in
anaesthesia. It is now considered appropriate for LMA’s to be used in the setting of cardiac arrest
as an alternative to endotracheal tubes for airway management. The design aims to:
• Provide a direct connection with the airway
• Avoid some of the hazards of intubation
• Provide greater security and convenience than the bag-valve mask
The LMA sits in the hypo-pharynx with the tip resting against the upper oesophageal sphincter. It
provides ventilation and oxygenation when used correctly, however it does not protect against
passive regurgitation and aspiration of gastric contents as the endotracheal tube does. Therefore
intubation remains standard for airway maintenance in a cardiac arrest.
The LMA is available in many sizes ranging from small masks used for neonates/infants to large masks
21

used for adults.
Table 1.1: LMA Size and Cuff Volume
LMA Size Weight Cuff Volume
1 <5kg Up to 4mL
2 Up to 20kg Up to 10 mL
2.5 20 – 30kg Up to 14 mL
3 30 – 50kg Up to 20 mL
4 50 – 70kg Up to 30 mL
5 70 – 100kg Up to 40 mL
6 Over 100kg
Prior to use, the cuff should be inflated to ensure there is no herniation of the cuff. Herniation of the
cuff may lead to airway obstruction. The equipment required to insert a LMA are:
• Appropriate sized LMA and water based lubricant
• 50mL syringe to inflate the cuff and tape to secure the LMA
• Suction and ventilating device
Insertion Procedure
• If possible, ventilate the patient with 100% oxygen using a bag-valve-mask device before
inserting the LMA
• At the same time, check the integrity of the cuff
• Deflate the cuff and lubricate the back and sides of the mask
• Tilt the patient’s head (if appropriate), open the mouth fully and insert the tip of the mask
along the hard palate with the open side facing, but not touching the tongue
• Insert the mask further, along the posterior pharyngeal wall, with index finger initially
providing support for the tube
• Resistance will be felt as the tip of the LMA lies at the upper end of the oesophagus
• Fully inflate the cuff
• Note the slight rise of the LMA
• Secure the LMA with tape and check its position during ventilation
• Note that a completely tight fit is not usually obtain - there may be a slight leak of gas
• If insertion is not accomplished within 20 seconds, re-establish ventilation using a bag-valvemask
Complications
• Inability to ventilate patient – withdraw the mask and re-insert
• Coughing or laryngeal spasm is usually due to attempting to insert the LMA in patient
whose laryngeal reflexes are still present.
• Inadvertent displacement – more common with smaller LMA’s due to rotation when the
bag-valve circuit is attached
22

• Aspiration of gastric contents is possible
Figure 1.2 LMA Steps for Insertion
1
3 4.
www.ijciis.org
23

24

DEFIBRILLATION TECHNIQUE
AND
CONSIDERATIONS
25

Defibrillation
Introduction
Early defibrillation is the key link in the chain of survival following VT or VT cardiac arrest. Defibrillation
has been shown to improve outcomes from these lethal arrhythmias. It is vital to know that although
defibrillation is essential to the successful management of VT/VF cardiac arrests, the importance of
effective, uninterrupted chest compressions cannot be emphasized enough.
Indications
Influencing
Factors
Types of
Defibrillators
Energy
• Ventricular fibrillation
• Pulseless ventricular tachycardia
• Fine ventricular fibrillation masquerading as asystole
• Time elapsed since onset of rhythm
• Biphasic versus Monophasic waveform – biphasic achieve higher first-shock success rates
• Size of the electrode – 12cm electrodes may have greater defibrillation success than 8cm pads
• Transthoracic impedance
• Electrode position – apex-anterior position recommended by ARC; however alternate positions
such as anterior-posterior and apex-posterior may also be used
Monophasic
• The energy is delivered in one direction only
• The current flows from one paddle to the other
• Higher energy levels are required – 200 to 360J
• Does not compensate for differences in thoracic impedance
Biphasic
• The energy is delivered in two directions
• Initially the current flows in a positive direction, then reverses and flows in the opposite
direction
• Lower energy levels are used – 150 to 200J
• Has the ability to compensate for variations in thoracic impedance
• For monophasic defibrillators, energy levels are set at 360J for the initial shock and remain set
at 360J for all subsequent shocks
• For biphasic defibrillators, energy levels are set at 150J for the initial shock and remain set at
150J for all subsequent shocks
Figure 3.1 Types Defibrillators
Adapted from: www.philips.com
Manual Mode
• Requires the operator to analyse the rhythm and decide if defibrillation is indicated
• Only staff members trained and deemed competent in ALS should operate the defibrillator in
manual mode
• All other staff members should operate the defibrillator in Automatic mode
26

Steps
• Continue CPR with minimal interruption
• Apply self-adhesive pads ensuring that skin is clean and dry
• Remove GTN patches / paste, electrodes and clip hair if the chest is excessively hairy
• To place adhesive multi-function pads in the apex-anterior position roll the pads against the
patent’s skin starting at the opposite end of the wire ensuring no air is caught under the pads.
• Continue with CPR.
Procedure
Steps cont.
Single Shock
Protocol
• Connect the pads to the adaptor cable
• To lock the adapter by sliding the pads adapter into the defibrillator cable. It can only go one
way!
• If the pads are not connected correctly to the adaptor cable, the energy may not be delivered
to the patient
• If the ‘Pads Off’ message is displayed, check all patient connections
• Select the energy level required – 150J (biphasic).
• Continue chest compressions whilst applying pads and press ‘Charge’
• Re-check the rhythm to ensure the rhythm is unchanged – should be VF or VT
• Once the defibrillator has charged, there will be an audible ‘Stand Clear’ statement made by the
defibrillator
• The operator must also call out ‘Stand Clear’ to ensure all staff have heard
• Whilst calling ‘Stand Clear’, the operator must visually inspect the area to ensure that no-one is
in contact with the patient or the bed / trolley
• Confirm that the shock is still indicated and if so, press ‘Shock’
• When delivered, the shock will produce a sudden contraction of the patient’s muscles
• As soon as the shock has been delivered, recommence CPR
• DO NOT wait to assess rhythm until two (2) minutes CPR completed
• After defibrillation, recommence CPR for two (2) minutes
• Reassess the rhythm and pulse and need for defibrillation every two (2) minutes
• Continue until return of signs of life or decision is made to discontinue resuscitation
Figure 3.1: Pad Placement
Adapted from: www.philips.com
Hazards and
Complications
Safety
Considerations
• Burns
• Electrocution
• Worsening of the arrhythmia
• Explosions from GTN or oxygen
• Changes in cardiac enzymes – less with biphasic defibrillators
• In patients who have implanted defibrillators or pacemakers the pads / paddles should be
positioned at least 10cm away from the device
• After defibrillation the device should be checked as damage to these devices may occur
• Be aware of electrical hazards in the presence of water and flammable substances
• Do not operate the defibrillator with wet hands or whilst standing in water
• If a shock / tingle experienced when touched do not use and send the device for repair
• If using paddles, never have them charged anywhere except for on the patient
27

Troubleshooting
• If the defibrillation is unsuccessful, take the following steps
a) Recommence CPR
b) Check skin contact, leads and pad / paddle position
c) Ensure that the defibrillator is not on ‘Synch’ mode
d) Consider alternative pad placement
28

Defibrillation versus Cardioversion
Defibrillation is an unsynchronised direct current shock to terminate VF / pulseless VT. Cardioversion is
an elective procedure to revert an arrhythmia by delivering a synchronised direct current shock.
The electrical discharge is timed to occur at a designated point in the cardiac cycle; the R wave
This minimises the chance of worsening the arrhythmia by ensuring that the energy is
not delivered during the vulnerable period just prior to the T wave
Not appropriate in an emergency situation
Synchronised
Cardioversion
Arrhythmias
Haemodynamically stable VT (with pulse)
Supraventricular tachycardia
Atrial flutter
Atrial fibrillation
Procedure
As per defibrillation with the additional steps:
Activate the ‘Synchronise’ button
There should be a marker on the R wave visible and ‘Sync’ should be displayed on the
screen
Energy levels are generally lower than for defibrillation; energy levels may be as low as 25
to 50J
The discharge button(s) must be pressed and held until the charge is delivered
Discharge may not occur immediately as the defibrillator will wait to synchronise with the
R wave
After cardioversion, the patient should be monitored for further arrhythmias
Adapted from:
Philip’s Heartstart XL+ (2011)
Philips Heartstream XL (2001)
Transcutaneous Pacing
External, transcutaneous pacing is when an electrical pacing impulse is delivered to the patient via external
pacing pads. This is used in emergency situations, or until other forms of pacing can be initiated (eg.
insertion of transvenous wires).
Indications
Advantages
Limitations
Pad Placement
• Drug resistant symptomatic bradycardia and cardiac arrest.
• Prophylactic use in high-risk patients (pacemaker ready but not turned on) for scheduled
cardioversion, PA catheter insertion and cardiac catheterisation
• Can be established quickly
• Is easy to perform and requires minimal training
• Avoids the risk of central venous cannulation
• Can be performed by doctors, nurses and paramedics
• Has a limited role when used to treat asystole or refractory symptomatic bradyarrhythmia in
cardiac arrest victims
• It is associated with considerable pain and discomfort and the patient must be sedated & have
adequate analgesia
• Offer many functions and combine monitoring, pacing and defibrillation
• Recommended pad placement is anterior-posterior position (defibrillation can also be
performed in this position)
• Anterior-apex positioning may be used
29

Modes of Pacing
Demand Mode
Fixed Mode
• Preferred mode, seen to be safer
• The pacemaker will deliver impulses to the patient if the patient’s rate falls below the heart
rate that the pacemaker has been set at
• If using a Philips medical defibrillator, it will only work in the demand mode when three or five
lead ECG electrodes are attached to the patient
• When using the demand mode, adjust the lead selection and / or amplitude to provide the
tallest R wave
• Not selecting a lead, the unit will automatically default to lead 1
• Also referred to as asynchronous pacing
• Used when there is excessive artefact such as motion interfering with the pacing unit’s ability to
detect an R wave
• The pacing unit will deliver impulses to the patient at the set rate; irrespective of the patient’s
inherent rate (eg. the unit does not sense the patient’s own HR)
• This may be a problem if the pacing unit fires during the relative refractory period potentially
causing ventricular arrhythmias
• ECG electrodes are not required for pacing in this mode but there will be no ECG trace on the
display
Procedure
Prepare the
patient
Pad Placement
Switch Pacer
On
Select Mode
Set Rate
Capture HR
Evaluate
• Psychologically –Explain the procedure to the patient and provide reassurance.
• Sedation - Type of sedation used are usually RMO dependent and relevant to the patients
condition. Typically Midazolam or Morphine may be used for pacing. Other medication such as
low dose Propofol or Fentanyl may be considered. Pain relieve and sedation is required for pain
relieve and sedation required for pacing.
• Skin Preparation Skin preparation involves removing any GTN patches, ensuring the skin is dry,
removing chest hair by means of clipping. Ensure the skin is dry prior to applying the pads. If
the patient has a pacemaker, do not place pads over the pacemaker. Ensure at least 5cm
distance is maintained and consider placing the pads in the anterior/posterior position. ?
• Apply the pads (anterior – posterior)
• Avoid placing them over electrodes, lines, patches
• Press the button labelled “Pacer” until a green light appears next to the button and a dialogue
box appears in the display – see figure X
• In the display you will see “Pacer Stopped”. This means that the pacer is turned on but no
impulses are being sent to the patient. The pacer turns on in the mode which was last used
• The emergency department uses two different types of pacing unit. The Phillips Heartstart XL
and the Phillips heartstart XL+ Please refer to the manufacturers guidelines for pacing using the
different units.
• Press the button labelled ‘Mode’ on the Philips XL model.
• The newer Philips Heartstart XL+ defibrillator will default to the demand mode.
• Select the demand mode; unless otherwise instructed
• Only select fixed mode if there is excessive movement of the patient
• To change the mode when the pacer is in use, the pacer must be stopped by pressing the ‘Start
/ Stop’ button
• Set according to patient condition and medical orders
• Set by pressing the button labelled ‘Rate’ and adjust up or down in accordance with the arrows
on the ‘Rate’ button
• Start the pacemaker and increase the output (mA) by pressing the button labelled ‘Output’ and
adjust up or down in accordance with the arrows on the output button until a pacing spike is
noted
• Continue to increase the output until a pacing spike is noted, followed by a wide QRS complex
• Every time a pacing spike is seen, a QRS complex should follow (referred to as ‘Capture’)
• Cardiac output should improve and therefore close monitoring of the patient is needed
• ‘Capture’ must be maintained whilst the patient is being paced
30

Figure 3.2: Pacer Pad Placement
Adapted from: www.phillips.com
Troubleshooting
Failure to
‘Capture’
Failure to Sense
• Occurs when:
a) the output (mA) have not been set high enough
b) in both fixed and demand modes
c) pads are not in place and / or in contact with the patient
• Only occurs in demand mode
• Seen when the pacemaker discharges inappropriately (eg. after the patient’s own QRS
complex and may occur in the relative refractory period)
• Pads are not sensing the patient’s heart beat
• Pads are not in place and / or in contact with the patient
• If the monitoring ECG electrode falls off during pacing in demand mode, the pacer will stop
delivering impulses and the message ‘Pacer Stop and Leads Off’ will appear
• If a pad comes off in either mode, the pacer will stop delivering impulses and the messages
Other
‘Pacer Stop and Pads Off’ will appear
• Resume by pressing ‘Pacer Start / Stop’ button
• The three leads on the pacer need to be placed on the patient for the pacing unit to work
Additional Requirements
• Evaluate pads for correct positioning and patient comfort
a) Check the pads every 30 minutes to ensure the patient is not getting burnt
b) Consider repositioning the pads every few hours to avoid skin irritation
c) Pads should be changed after eight (8) hours of continuous pacing
Care of Patient
and Pacer
• Ensure patient is adequately sedated as pacing involves initiating a shock. Administering a
sedative or dissociative agent with or without analgesia will induce a state, which will allow the
patient to tolerate the unpleasant procedure.
• Ensure ‘Capture’ is maintained by:
a) each pacing spike should be followed with a QRS complex
b) checking for a pulse with each QRS complex to ensure PEA / EMD does not exist
• Ongoing evaluation / review of patient condition
31

• If the patient does not improve check all connections including the leads
CPR and
Defibrillation
• Identify length of time pacer is to be used as transcutaneous pacing is only a temporary
measure and used for a few hours
• Turn off pacing unit during CPR to prevent inappropriate stimulation of the patient
• When the defibrillator is charged by pressing the ‘Charge’ button on the front of the
defibrillator unit, the pacer stops pacing
• Prior to discharge, ‘Stand Clear’ must be called out and a visual check carried out to ensure that
no-one is touching the patient or bed
• To deliver the shock press and hold the ‘Shock’ button on the front of the defibrillator
• The shock is delivered through the multi-function pads
• After the shock has been delivered, the pacer remains off - recommence pacing, by pressing the
‘Pacer Start / Stop’ button this is the same of both models of pacing unit in the emergency
department.
• Pacing will resume at the settings prior to defibrillation
Adapted from:
Philips Heartstream XL Resource Guide
(2001) Philips Heartstart XL+ resource
manual (2011)
32

33

Cardiac Conduction
&
Arrhythmia Recognition
34

Cardiovascular Considerations
Overview
The section below will examine the conduction of the heart as well as common cardiac arrhythmias.
Understanding and interpreting arrhythmias is an important element of Advance life support.
The cardiovascular system consists of the heart, lungs and blood vessels. The cardiovascular system is
responsible for transportation of vital nutrients, gases and hormones throughout the body. The section
below look at some of the cardiovascular considerations.
THE ECG COMPLEX
The P wave represents atrial depolarization, which also means atrial contraction. A normal P wave is rounded
and symmetrical in shape/morphology. They should not be notched or peaked. If the P waves that are present
are of normal morphology then the rhythm was initiated in the SA node.
35

The QRS complex represents ventricular depolarization, which also means ventricular contraction. The Q is the
first negative deflection below the baseline after the P wave, the R is a deflection upwards (not always after a
Q) and the S is an deflection below the baseline after the R wave. The QRS complex should be 0.06-0.10
seconds long.
The T wave represents the repolarization ( the resting phase) of the ventricles. In many leads the T wave is
barely noticeable and may only be slightly rounded. The T wave is usually rounded and asymmetrical an d in
the same direction as the QRS complex (if the QRS is positive then the T wave is usually positive). Atrial
repolarization is not usually seen as it is occurring at the same time as the QRS is shown. The QRS complex is
much bigger and therefore it hides atrial depolarization.
The P-R interval represents the time that it takes for the impulse to travel to the ventricles during atrial
depolarization. A normal P-R interval is 0.12 – 0.20 seconds (3-5 small squares on the ECG paper). It is
measured from the beginning of the P wave to the beginning of the QRS complex.
ST segment- this represents the time between the end of ventricular depolarization and the beginning of
ventricular repolarization (rest). This is a short space of time where nothing is happening electrically, so the ST
segment is isoelectric (flat). An elevated of depressed ST segment can indicate an abnormality.
-
Conduction Pathways
All cardiac cells have the potential for
• Automaticity – the ability to initiate an impulse
• Excitability – the ability to respond to an impulse
• Conductivity – the ability to transmit an impulse
The specialised conduction system facilitates the spread of impulses from the atria to the ventricles and
enables rhythmic and optimal contraction of the myocardium with optimal cardiac output. The conduction
system consists of:-
Sinoatrial Node (SA node)
Atrioventricular Node (AV node
Bundle of His
Right and Left Bundle Branches
Purkinje Fibres
The sinoatrial (SA) node
The SA node is usually called the pacemaker of the heart. This is because it is the part of the heart that
36

isresponsible for initiating each beat in a normally functioning heart. The cells of the SA node naturally
discharge approximately 60-100 times/minute. As this rate is higher than any of the other conducting cells
within the heart, the SA node is referred to as the primary pacemaker. In a healthy heart the impulses then
travel via the internodal tracts to the AV node. The AV node then delays the impulses by 0.04 second to
prevent the ventricles from contracting too early, and thereby allowing them to complete their filling phase.
If the SA node fails, the AV node may initiate an impulse.
The Atrioventricular (AV) node
The AV node usually conducts an impulse that has been initiated in the SA node however if the SA node
fails the AV node can initiate an impulse. If the AV node does become the secondary pacemaker of the
heart it will usually initiate the impulse at 40 – 60 times/minute.
From the AV node, the impulse travels to the Bundle of His which then divides into the right bundle branch
and the left bundle branch. The impulse then continues down through the Purkinje fibres which extend
deep into the myocardial tissue. The Purkinje fibres may also act as a pacemaker (tertiary) if the SA node
and AV node fail. The rate generated by these fibres is usually somewhere between 20-40
impulses/minute.
Figure 2.1
Source www.studyblue.com
37

Coronary Circulation
The role of the coronary artery system is to maintain blood flow and supply to the myocardium through the
right and left coronary arteries. Both originate as a single branch from the ascending aorta from which the
left coronary artery further divides into the left anterior descending (LAD) and left circumflex artery (LCx).
The LAD artery supplies the surface of the left ventricle towards the apex of the heart. It also supplies blood
to the anterior wall of the left ventricle, intraventricular septum, the right bundle branch and left anterior
fascicle of the left bundle branch. The LAD artery further branches into the septal perforators and diagonal
arteries which help to supply blood to the walls of both ventricles.
The right coronary artery supplies blood to the right atrium, right ventricle and part of the inferior and
posterior surfaces of the left ventricle. It also supplies blood to the SA node in 50% of the population. The
Bundle of His and AV node also receive blood from the right coronary artery.
The coronary arteries can only fill when the left ventricle is in diastole (relaxed) which is significant for two
reasons:
1. During tachycardia the diastolic period is shortened which reduces the coronary capillary perfusion
time. This can lead to reduced myocardial oxygen supply when demand is actually increased.
2. During CPR, the coronary arteries also fill during diastole – the time during the release of cardiac
compressions. To maintain adequate coronary capillary perfusion pressure during CPR, a high aortic
pressure needs to be maintained. To achieve high aortic pressure, interruptions to cardiac
compressions need to be minimised.
38

Arrhythmias
Most cases of adult cardiac arrest occur outside the hospital setting. The three primary mechanisms for out
of hospital arrest are Ventricular Fibrillation (VF), Ventricular Tachycardia (VT) and bradyarrhythmias
(including asystole). There is always a concern that patients who develop an arrhythmia may suffer from
one that causes their death, may be potentially lethal, and may cause cardiac failure. It is important to
identify the arrhythmia, have an understanding of the clinical significance and modes of treatment related
to that arrhythmia.
Ventricular Tachycardia (VT)
Figure 1 Ventricular Tachycardia:
• Develops when three or more consecutive premature ventricular contractions (PVC) occur in a row
• The rate is greater than 100 beats / minute
• Originates due to an ectopic pacemaker somewhere in the bundle branch, Purkinje network or ventricular
myocardium
• The patient may or may not be conscious with this arrhythmia
Rate
P Wave
Rhythm
QRS
Treatment
• Rapid > 100 beats/minute, usually between 140-200 beats/minute
• Usually absent, however may be obscured by the QRS complex
• Ventricular rhythm is essentially regular; may be some beat-to-beat variation
• Wide and bizarre, > 0.12 seconds in duration and usually identical
• Treatment of VT is governed by the haemodynamic and conscious state of the patient
• If the patient is uncompromised (eg. pulse is present and the patient is conscious), then treatment
relies on the use of antiarrhythmics such as amiodarone, lignocaine and magnesium
• Elective cardioversion may also be needed if reversion of VT is unsuccessful with medications or
the patient’s condition is deteriorating
39

Ventricular Fibrillation (VF)
Figure 2: Ventricular Fibrillation
• There is totally disorganised depolarization and contraction of small areas of the ventricular myocardium
• There is no effective ventricular pumping activity
• Ventricular fibrillation (VF) is never accompanied by a pulse or BP
• Patients who are awake and responsive, the ECG pattern of VF is caused by a loose lead artifact or electrical
interference
Rate
P Wave
Rhythm
QRS
Treatment
• No coordinated ventricular beats are present - rate cannot be determined
• Cannot be determined
• Totally irregular
• Cannot be identified
• The only definitive treatment for VF is defibrillation – the earlier the better
• VF is treated according to the Australian Resuscitation Council (ARC) Adult Cardiorespiratory Arrest
Flowchart
Torsades de Pointes
Figure 3: Torsades de Pointes
French term meaning ‘twisting of the points’
Torsades is a form of VT which rotates around the isoelectric line of the ECG, thereby continually changing its axis
This arrhythmia may be paroxysmal, starting and stopping abruptly, or may deteriorate into VF
Rate
P Wave
Rhythm
QRS
Treatment
• 150 to 250 beats/minute
• Absent
• Irregular
• Widened with undulating height
• The underlying cause must be determined and treated accordingly
• Torsades de pointes is very sensitive to magnesium
• The magnesium is usually enough to cause reversion
• If the patient is haemodynamically unstable, then defibrillation is indicated; however, it should be
noted that Torsades can be resistant to defibrillation
• Overdrive pacing and isoprenaline may also be considered
40

Asystole
Figure 4: Asystole
• The complete absence of any cardiac electrical activity
• The patient is unresponsive with no cardiac output and it is usually the result of prolonged cardiac arrest without
effective resuscitation
• The ECG recording shows an almost flat baseline
• If the patient has a pacemaker which continues to function, a pacing spike may be seen but a QRS complex does
not occur in response to the pacemaker
• If asystole is seen on the monitor, assess the patient, ensure all leads are connected, electrodes have good contact
and increase the gain on the monitor before initiating treatment
Rate
P Wave
Rhythm
QRS
Treatment
• None
• May or may not be identifiable
• None
• Absent
• Asystole is treated according to the Australian Resuscitation Council (ARC) Adult Cardiorespiratory
Arrest Flowchart - Defibrillation is not indicated in the treatment of asystole
• The mainstays of treatment for asystole are effective and prompt CPR and the administration of
Adrenaline 1mg IV every 3 minutes
• Atropine no longer recommended for routine use for cardiac arrests due to asystole or PEA
• During resuscitation, consideration and treatment of reversible causes should be sought and
treated accordingly
41

Figure 5:
PEA
Source: www.study.com
• Pulseless electrical activity (PEA) is the presence of electrical complexes without accompanying contraction of the
heart; resulting in complete circulatory collapse
• On the ECG / monitor there will be evidence of organised electrical activity, but there will be no palpable pulse or
measurable blood pressure
• The observed rhythm degenerates into VF or asystole and the prognosis for PEA is very poor
• PEA may also be referred to as electromechanical dissociation (EMD)
Rate
P Wave
Rhythm
QRS
Treatment
• Generally < 60 beats/minute which may persist regardless of treatment
• Organised atrial activity can be present or absent
• Can be normal
• Wide complexes (such as idioventricular and escape rhythms) or organised electrical activity with
narrow QRS complexes
• PEA is treated according to the Australian Resuscitation Council (ARC) Adult Cardiorespiratory
Arrest Flowchart
• The mainstays of treatment for PEA are effective and prompt CPR and the administration of
Adrenaline 1mg IV every 3 minutes
• Atropine no longer recommended for routine use for cardiac arrests due to asystole or PEA
• Reversible causes must be sought and treated appropriately if the patient is to survive
• Defibrillation is not indicated in the treatment of PEA
42

Sinus Bradycardia
Figure 6: Sinus Bradycardia
• An impulse originating from the SA node at a rate of less than 60 beats/minute
• Sinus bradycardia may occur normally during sleep or in a person with a well-conditioned heart (eg. athletes)
• Unless the patient is symptomatic, then no treatment is necessary
Rate
P Wave
Rhythm
QRS
Treatment
• Less than 60 beats/minute
• Present, identical and upright, precedes each QRS complex
• Regular
• Normal duration and configuration unless there is an underlying block
• Unless the patient is symptomatic (eg. dizziness, syncope, hypotensive) treatment is not required
• In the symptomatic patient treatment includes:
a) Identifying the underlying cause and treat accordingly
b) 1 st line medication: Atropine 500– 600mcg to 1mg given IV in increments every 3 to 5
minutes (maximum total dose 3mg)
c) 2 nd line medication: Low dose adrenaline (as a bolus or as an infusion)
d) 2–10mcgs/ minute to maintain satisfactory HR with a mean arterial pressure of 70mmHg
e) Isoprenaline 20mcg bolus IV +/- infusion titrated to effect
f) Consider IV glucogon or insulin/glucose/potassium therapy if a beta blocker or calcium
channel blocker is the cause of the bradyarrythmia
g) Do not give atropine to heart transplant patients as the heart is denervated
h) If pharmacological treatment is not successful, prepare the patient for transcutaneous pacing
Adapted from: Australian Resuscitation Council (2010)
ECG Interpretation made incredibly easy (2012)
43

Atrioventricular Blocks
An atrioventricular (AV) block is characterised by delayed conduction or non-conduction of atrial impulses
through the conduction system (AV node, bundle of His or the bundle branches) during a time when the
tissue is not physiologically refractory. AV blocks are divided into the following groups:
• 1st degree AV block
• 2nd degree AV block (type I and II)
• 3rd AV block
The clinical effect of the block depends on how many of the impulses are completely blocked, how
slow the ventricular rate is, and how the block affects the heart.
First Degree AV Block
Figure 6: First Degree AV Block
• First degree AV block occurs when atrial activity is conducted to the ventricles but there is a constant delay in
conduction resulting in a prolonged PR interval (> 0.20 second)
Rate
P Wave
Rhythm
QRS
PR Interval
Treatment
• Usually normal
• Present, identical and upright, precedes each QRS complex
• Regular
• Normal duration and configuration
• Consistently prolonged i.e. > 0.20s – This is the distinguishing feature of this block
• Identify underlying causes and treat as needed
• If the block is new and related to underlying cause, continue to monitor the patient
• There are no indications for treatment in isolated first degree block
44

Second Degree AV Block – Type 1
Figure 7: Second Degree AV Block Type 1
• Second Degree AV Block (Type 1) may also be referred to as Mobitz Type I block or Wenckebach
• The AV conduction time progressively lengthens until a P wave is not conducted
• On the ECG this is shown as a progressive prolongation of the PR interval before an atrial impulse fails to
stimulate the ventricle, resulting in a “missed” or “dropped” QRS complex
• It is believed to be caused by a prolongation of the refractory period of the AV node
Rate
P Wave
Rhythm
QRS
PR Interval
Treatment
• Usually normal, atrial rate is greater than the ventricular rate
• Normal size and configuration
• Irregular due to dropped QRS complexes
• Normal duration and configuration, complexes lost periodically
• Progressively lengthens until a P wave is not followed by a QRS complex
• The stable patient requires no treatment and management is aimed at excluding ischaemia
• If the patient is symptomatic (eg. bradycardic, hypotensive etc) then IV atropine may be given
(incremental doses of 0.5mg to 1.0mg)
• Cardiac pacing may be indicated especially if the ventricular response rate is slow and the patient
does not respond to atropine
Second Degree AV Block – Type 2
Figure 8: Second Degree AV Block Type 2
Second Degree AV Block (Type 2) may also be referred to as Mobitz Type II block
This block is generally less common than Type 1 however it is much more serious
It occurs when occasional impulses from the SA node fail to conduct the ventricles
On the ECG, this is represented as a constant PR interval with the regular, intermittent failure of a P wave to
conduct the ventricles (“dropped” QRS complex)
45

Rate
P Wave
Rhythm
QRS
PR Interval
• Atrial rate usually normal, the ventricular rate is slow
• Present, identical and upright
• Atrial rhythm is regular, ventricular rhythm is irregular due to “dropped” QRS complexes
• Typically > 0.12 sec due to an underlying bundle branch block
• Constant; may be normal or prolonged
Treatment
Treatment is directed at increasing the ventricular rate when the patient is symptomatic
Atropine may be used; however it may not always be effective due to the location of the block
Isoprenaline may be ordered instead to increase the ventricular rate as a temporary measure prior
to pacing
In patients who remain symptomatic despite medications, cardiac pacing is indicated
It can be hard to distinguish between Type I and Type II AV – the following may assist:
If the QRS is normal and PR interval is lengthened = Type I
If the QRS is wide and PR interval normal = Type II
Second Degree AV Block – Type 2
Figure 9: Third Degree AV Block
• Third Degree AV Block may also be referred to as Complete Heart Block
• Atrial impulses cannot conduct through the AV node to depolarise the ventricles
• Therefore the atria and ventricles work independently of each other (atrial and ventricular dissociation)
• Depending on the site of the block, either the junctional or ventricular fibres will provide a slow escape beat
Rate
P Wave
Rhythm
QRS
PR Interval
• Atrial rate is normal; the ventricular rate is generally slow < 40 beats/min
• Normal shape and size, completely dissociated from the QRS
• Atrial and ventricular rates are essentially regular
• Depends on where the ventricular beat originates; > 0.12 sec if the beat originates in the ventricles
or there is an underlying bundle branch block
• Not applicable as the atria and the ventricles work independently of each other
46

Treatment
• Treatment is aimed at improving the ventricular rate and thereby improving cardiac output
• The patient will generally be haemodynamically compromised and therefore treatment should be
initiated promptly
• Atropine and / or Isoprenaline may be used as a temporary measure until the patient can be paced
• Isoprenaline may worsen the patient’s condition as a result of vasodilatation and coronary
hypoperfusion and therefore should be used cautiously
• In the ED, transcutaneous pacing may be used temporarily whilst the patient awaits transfer to a
specialist unit
Supraventricular Tachycardia (SVT)
Figure 10: SVT
• Collective term for all arrhythmias occurring above the Bundle of His, but do not fit the criteria for atrial fibrillation,
atrial flutter, sinus tachycardia
Rate
P Wave
Rhythm
QRS
PR Interval
Treatment
• 160 to 240 beats/minute
• Difficult to see due to the rapid rate – may be buried in the QRS complex or T waves
• Regular
• Usually normal < 0.10 sec, unless there is an underlying bundle branch block causing a widened
QRS
• Not visible
• Confirm diagnosis on 12-lead ECG – narrow complex tachycardia
• If haemodynamically unstable synchronised DC reversion is indicated. Can give IV adenosine but
do not delay synchronised cardioversion
• If stable (eg. Systolic BP > 100mmHg) vagal manoeuvres such as carotid sinus massage may be of
benefit
• IV Adenosine administered in increments of 6mg, 12mg and 12mg can be given as first-line
management
• If unsuccessful and BP remains >100mmHg, Verapamil 2.5mg-5mg IV or diltiazem 15-20mg as
second-line management depending on medical orders
• If SVT fails to respond to medications, then consider atrial flutter and treat accordingly. If no
atrial activity observed then synchronised DC reversion is indicated
Adapted from:
ECG Interpretations made incredibly easy (2011)
The only ECG book you’ll ever need ((2012)
Australian Resuscitation Council (2010)
47

Pharmacology
&
Routes of Administration
48

49

Pharmacology
Despite the historical use of medication in a cardiac arrest, research has shown that no one drug has been
found to improve survival to hospital discharge. Some medications would appear to improve the return of
spontaneous circulation (ROSC) and therefore should be given.
The role of medications in resuscitation are:
Improve organ and tissue perfusion
Facilitation of defibrillation
Preventing the recurrence of arrhythmias
Normalising metabolic abnormalities
Administration routes
(ACCCN; 2014)
Obtaining vascular allows for medications and fluids to be given as well as the taking of blood sample and is a
critical aspect of advanced life support. The preferred site for vascular access the largest and most accessible
vein that can be cannulated without interrupting resuscitation attempts. If this cannot be achieved in a timely
manner then it reasonable to consider the intraosseous (IO) route.
Intravenous access
Peripheral access preferred to central venous access (CVC) unless CVC access already established.
Large bore cannula (14-16 gauge) into a proximal vein
Flushed by 20-30 mL of NaCl (normal saline)
Butterflies should not be used
Intraosseous
Traditionally used in children, intraosseous is considered to be a safe alternative to intravenous access for
adults too.
Used if IV access is not accessible
Common sites include is the anterior aspect of the tibia, 2-3cm below the tibial tuberosity
Alternative sites include the distal femur and medial malleolus
Fluid / drugs will not flow under gravity and will need to be ‘pushed’
http://2.bp.blogspot.com/-
PtxK4T2BeM4/Tumywf91yiI/AAAAAAAACSI/zJZRKZjUKCc/s1600/Proximal%2BTibia%2BIO%2Bsite%2Bfrom%2BVidacare.jpg
Endotracheal
The endotracheal route whilst still a viable option in paediatric life support is no longer recommended for adult
50

life support.
51

ALS Algorithm Pharmacology: Quick Reference Guide (ACCCN; 2014)
Rhythm
Shockable
VT/VF
Non- Shockable
EMD/PEA or
Asystole
Adrenaline 1mg
After 2 nd Shock
Adrenaline 1mg
Immediately
Amiodarone
300mg
After 3 rd Shock
Adrenaline 1mg
Every 2 nd Loop
Adrenaline 1mg
Every 2 nd Loop
Consider medications for reversible causes:
Hypovolaemia – N/Saline or Hartmanns 20mls/Kg
Hyperkalaemia/Hypocalcaemia/Calcium Channel Overdose – Calcium Chloride 5-10ml 10%
Hypokalaemia/Hypomagnesia – Potassium Chloride 5 mmol
Torsade de Pointes/Hypomagnesia/Hypokalaemia – Magnesium Sulphate 10 mmol
Hypoglycaemia – Glucose 25g (50 mls 50% solution)
Hyperkalaemia/Tricyclic Antidrepressant Overdose – Sodium Bicarbonate 50 mmol
Narcotic Overdose – Naloxone 200-400mcg
Symptomatic Bradycardia (pulse with low hypotension) – Atropine 500mcg up to 3mg
51

Medications used in Resuscitation
Medications used in Resuscitation
Group Name Dose Notes
Vasoactive
Agents
Adrenaline Shockable (VF/VT) Arrest
1mg IV every 3-5 minutes
First dose after 2nd defibrillation; repeat
every 2 nd loop
Non-Shockable (EMD/PEA/Asystole) Arrest
1mg IV every 3-5 minutes
Give immediately then every 2 nd loop
A naturally occurring catecholamine
Adrenaline stimulates alpha receptors to produce vasoconstriction and beta receptors to produce
increased myocardial contractility, heart rate and bronchodilation
Vasopressin 1 dose 40 units IV given instead of 1mg
Adrenaline – given once only.
Anti-Arrhythmics Amiodarone 300mg IV after 3 rd defibrillation
150mg may be repeated for refractory VF/VT
followed by IV infusion: 900mg /24hrs
Pharmacology
for reversible
causes
Lignocaine
Magnesium
Crystalloid Fluids:
Normal Saline or
Hartmanns
Calcium Chloride
(CaCl)
Calcium
Gluconate
Potassium
Chloride (K+)
1mg/kg IV after 3 rd defibrillation IF
Amiodarone not available
0.5mg/kg IV can be repeated for refractory
VT/VF
5mmol IV
2 nd dose 5mmol IV may be given after 10-15
minutes
20mls/kg IV
5-10mls of 10% (6.8mmol Ca) IV
10mls of 10% IV may be given if calcium
chloride not available
5mmol bolus IV
May continue with adrenaline 1mg every second loop
Increases the action potential and refractory period in the atria, AV node and ventricles
Give in 5% Dextrose only
To be given if Amiodarone not available. Do not give if Amiodarone already administered
Indicated for Torsades de Pointes; Digoxin toxicity or documented hypomagnesaemia or
hypokalaemia
Indicated for hypovolaemia
Indicated for hyperkalaemia; hypocalcaemia; calcium channel overdose; hypermagnesaemia
Calcium may increase myocardium and cerebral injury.
Extravasation can cause tissue necrosis
Indicated for documented hypokalaemia; persistent VF secondary to hypokalaemia.
Rapid or excessive use may cause hyperkalaemia; bradycardia; hypotension; asystole
Extravasation can cause tissue necrosis
Glucose 25g of 50% solution IV (50mls of 50% solution) Hypoglycaemia is often present in critical illness and may cause cardiac arrest
Naloxone 200 – 400mcg IV Rapid acting opioid antagonist
Repeat doses or infusion may be required as naloxone has shorter half-life than opioids
Sodium 50 mmol IV Indicated for Trycyclic antidepressant overdose; hyperkalaemia; pre-existing metabolic acidosis
52

Pharmacology
for reversible
causes
(continued)
Bicarbonate
Do not administer routinely for prolonged arrest or cardiac arrest induced acidosis
Do not administer simultaneously by the same route as other drugs
Atropine 500mcg - 3mg max IV Indicated for symptomatic bradycardia – doses < 500mcg may result in further bradycardia
No longer recommended for asystole or bradycardia without a pulse (PEA/EMD)
Isoprenaline
Adenosine
20mcg IV stat
0.5mcg – 20mcg/min titrated to HR (Infusion
concentration 20mcg/ml = 1mg/50ml)
6mg initially; 12mg after 1-2 minutes if no
change in rhythm.
Further 12mg may be given if still no change
Indicated for symptomatic bradycardia and AV unresponsive to atropine; pharmacological pacing in
Torsades de Pointes
Indicated for tachycardia with narrow and regular QRS complexes
Ref: ACCCN 2014
53

Team Roles for Resuscitation Team Members:
It is an expectation that all members of an ALS team can work within all roles of the ALS team and each
team member is responsible for being fully competent in the use of all equipment that is at hand during a
resuscitation. A team approach is essential to ensure coordinated activities and clear communication.
Communication is crucial and clearly defined roles can assist with organising a situation that can be difficult to
manage. The following provides guidance on the roles team members can be assigned during a resuscitation.
Basic Life Support & Documentation
Co-ordination of basic life support team members
Ensure interchange of compression person every two minutes/or when fatigued
Documents ALS treatment, vital signs, rhythm interpretation
Communication to group of two minute loops and end of loop sequence
Observes and reports on timing interruptions to compressions notifies group if > 5 seconds.
Defibrillation and Cardiac Monitoring
Attaches defibrillator and monitor to patient and places into manual mode.
Performs rhythm analysis during rhythm checks and performs defibrillation
Connects ETCO2 monitoring if available
Vital sign checks post arrest
Airway Management
Prepares airway management devices e.g LMA, Intubation equipment
Assists with LMA insertion or Intubation
Assists with manual ventilation where necessary
Prepares for an ABG
54

IV Cannulation & Drugs
Gathers cannulation equipment and cannulates the patient
Prepare intraosseous equipment when necessary
Prepares, checks and administers medications
Prepares, checks and administers IV fluids
Team Leader
Gives direction to ALS and BLS team members
Assesses and provides feedback on CPR technique
Follows ALS algorithm and co-ordinates events to minimize interruptions to CPR
Obtains history of patient and performs patient assessment to identify possible cause of arrest
Debriefs ALS and BLS team
Manage transfer of patient to relevant department post resuscitation
55

Post Resuscitation Care
Overview
Hypoxic brain injury, myocardial injury or organ failure are the predominant causes of morbidity and
mortality after cardiac arrests. Interventions in the post resuscitation period are likely to significantly
influence the final outcome. The aims of therapy after initial resuscitation are to:
• Continue respiratory support
• Maintain cerebral perfusion
• Treat and prevent cardiac arrhythmias
• Determine and treat the cause of the arrest
Treatment Recommendations
Intubation and ventilation
Blood pressure
Oxygenation
Control of Arterial Carbon
Dioxide
Blood Glucose Control
Temperature Control
Resuscitation Related
Injuries
Adapted from: Australina Resucitation Council (2012)
• Must be continued in the immediate post arrest period guided by appropriate
monitoring
• Aim for a BP equal to the patient’s usual BP or at least a systolic pressure greater
than 100mmHg
• If need titrate small IV incremental doses of adrenalin, or consider the need for
intravascular volume expansion
• Once return of spontaneous circulation (ROSC) has been established and the oxygen
saturation of arterial blood (SaO 2) can be monitored reliably (by pulse oximetry and /
or ABG analysis) the inspired oxygen can be titrated to achieve a SaO 2 of 94-98%
• Ventilate to normocarbia (PaCO2 35 – 40mmHg)
• Monitored frequently according to the patient’s condition
• Hyperglycaemia (>mmols) should be treated with insulin but avoid hypoglycaemia
• Monitor unconscious patients as they are at risk of unrecognised hypoglycaemia
• Induced hypothermia has been shown to be beneficial in some patients still
comatose after ROSC
• Rib fractures & other injuries are common but acceptable consequences of CPR
• All patients should be reassessed & re evaluated for post resuscitation related
injuries
• Other complications are incorrect placement of tubes; replacement of IV lines may
need to be attended to
56

Bibliography
ACCCN National Adult Advanced Life Support Program Manual 2014 Edition
Australian Commission on Safety and Quality in Health Care. (2012). National Safety and Quality Health
Service Standards. Sydney: Commonwealth of Australia. Australian Commission on Safety and
Quality in Health Care. (2012). NSQHS Standards: Hospital accreditation workbook. Sydney:
Commonwealth of Australia.
Australian Commission on Safety and Quality in Health Care. (2012). Standard 1: Governance for safety and
quality in health service organisations – Safety and quality improvement guide. Sydney: Commonwealth of
Australia.
Australian Commission on Safety and Quality in Health Care. (2012). Standard 9: Recognising and responding
to clinical deterioration in acute health care – Safety and quality improvement guide. Sydney:
Commonwealth of Australia.
Australian and New Zealand Resuscitation Council. (2010) Available from:
https//www.resus.org.au/policy/guidelines/index.asp
57

ALS PERFORMANCE CRITERIA
Staff Name & ID Number………………………………………………………
Department………………………………………………………………………….
CRITERIA PERFORMANCE DEMONSTRATED NEEDED
PROMPTING
1. Demonstrated effective
basic life support
Follows ARC algorithm DRSABCD
Confirms safe environment
Assess Response
Activate emergency response
Clears and opens airway uses correct head
tilt
chin lift draw thrust technique
Assess for normal breathing
Commences compressions at rate of 100-
120/minute
Demonstrates correct depth
Confirms rise and fall of chest during
ventilations
Apply and follow prompts of SAED/AED
2. Demonstrate advanced
airway management skills
Correct bag mask ventilation technique
Bag connected to oxygen
Size and fit an oropharyngeal airway
Size and fit a laryngeal mask airway
Demonstrates set up of intubation
equipment
58

Demonstrates knowledge of assisting with
intubation-cricoid pressure/confirms
correct positioning of ET tube
3.Demonstrate safe
defibrillation technique
4.Follows ALS algorithm and
manages ALS simulation
Connects patient to monitor
Demonstrates safety when charging pads
during compressions
Communicates correct rhythm analysis
Identifies if shockable or non-shockable
Visually confirms “ALL CLEAR” prior to
shocking
Demonstrates synchronized cardioversion
Confirms Leadership Role
Communicates with BLS team throughout
the simulation
Demonstrates situational awareness and
prioritises throughout simulation
Minimise interruptions to compressions
throughout simulation
Correctly identify rhythm and select
appropriate side of the ALS algorithm
Initiate appropriate treatment (e.g
defibrillation, IV/IO, advanced airway
management)
Orders correct drug, doses, administration
intervals
Assess reversible causes
Treat reversible causes
Manage post resuscitation cares relevant to
the patient scenario
FURTHER COMMENTS:
SATISFACTORY/FURTHER TRAINING RECOMMENDED
Assessor signature:
59
Date: