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European Resuscitation Council Guidelines for Resuscitation 2010 ...

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C.D. Deakin et al. / <strong>Resuscitation</strong> 81 (<strong>2010</strong>) 1305–1352 1323<br />

prone to failure because of kinking of the cannula, and is unsuitable<br />

<strong>for</strong> patient transfer.<br />

4f Assisting the circulation<br />

Drugs and fluids <strong>for</strong> cardiac arrest<br />

This topic is divided into: drugs used during the management<br />

of a cardiac arrest; anti-arrhythmic drugs used in the peri-arrest<br />

period; other drugs used in the peri-arrest period; fluids; and routes<br />

<strong>for</strong> drug delivery. Every ef<strong>for</strong>t has been made to provide accurate<br />

in<strong>for</strong>mation on the drugs in these guidelines, but literature from<br />

the relevant pharmaceutical companies will provide the most upto-date<br />

data.<br />

Drugs used during the treatment of cardiac arrest<br />

Only a few drugs are indicated during the immediate management<br />

of a cardiac arrest, and there is limited scientific evidence<br />

supporting their use. Drugs should be considered only after initial<br />

shocks have been delivered (if indicated) and chest compressions<br />

and ventilation have been started. The evidence <strong>for</strong> the optimal<br />

timing and order of drug delivery, and the optimal dose, is limited.<br />

There are three groups of drugs relevant to the management of<br />

cardiac arrest that were reviewed during the <strong>2010</strong> Consensus Conference:<br />

vasopressors, anti-arrhythmics and other drugs. Routes of<br />

drug delivery other than the optimal intravenous route were also<br />

reviewed and are discussed.<br />

Vasopressors<br />

Despite the continued widespread use of adrenaline and<br />

increased use of vasopressin during resuscitation in some countries,<br />

there is no placebo-controlled study that shows that the<br />

routine use of any vasopressor during human cardiac arrest<br />

increases survival to hospital discharge, although improved shortterm<br />

survival has been documented. 245,246 The primary goal of<br />

cardiopulmonary resuscitation is to re-establish blood flow to vital<br />

organs until the restoration of spontaneous circulation. Despite the<br />

lack of data from cardiac arrest in humans, vasopressors continue<br />

to be recommended as a means of increasing cerebral and coronary<br />

perfusion during CPR.<br />

Adrenaline (epinephrine) versus vasopressin<br />

Adrenaline has been the primary sympathomimetic agent<br />

<strong>for</strong> the management of cardiac arrest <strong>for</strong> 40 years. 438 Its<br />

alpha-adrenergic, vasoconstrictive effects cause systemic vasoconstriction,<br />

which increases coronary and cerebral perfusion<br />

pressures. The beta-adrenergic actions of adrenaline (inotropic,<br />

chronotropic) may increase coronary and cerebral blood flow, but<br />

concomitant increases in myocardial oxygen consumption, ectopic<br />

ventricular arrhythmias (particularly when the myocardium is<br />

acidotic), transient hypoxaemia due to pulmonary arteriovenous<br />

shunting, impaired microcirculation, 281 and worse post-cardiac<br />

arrest myocardial dysfunction 283,284 may offset these benefits.<br />

The potentially deleterious beta-effects of adrenaline have led<br />

to exploration of alternative vasopressors. Vasopressin is a naturally<br />

occurring antidiuretic hormone. In very high doses it is a<br />

powerful vasoconstrictor that acts by stimulation of smooth muscle<br />

V1 receptors. Three randomised controlled trials 439–441 and a<br />

meta-analysis 442 demonstrated no difference in outcomes (ROSC,<br />

survival to discharge, or neurological outcome) with vasopressin<br />

versus adrenaline as a first line vasopressor in cardiac arrest. Two<br />

more recent studies comparing adrenaline alone or in combination<br />

with vasopressin also demonstrated no difference in ROSC, survival<br />

to discharge or neurological outcome. 443,444 There are no alternative<br />

vasopressors that provide survival benefit during cardiac arrest<br />

resuscitation when compared with adrenaline.<br />

Participants at the <strong>2010</strong> Consensus Conference debated in depth<br />

the treatment recommendations that should follow from this evidence.<br />

Despite the absence of data demonstrating an increase in<br />

long-term survival, adrenaline has been the standard vasopressor<br />

in cardiac arrest. It was agreed that there is currently insufficient<br />

evidence to support or refute the use of any other vasopressor as<br />

an alternative to, or in combination with, adrenaline in any cardiac<br />

arrest rhythm to improve survival or neurological outcome. Current<br />

practice still supports adrenaline as the primary vasopressor <strong>for</strong> the<br />

treatment of cardiac arrest of all rhythms. Although the evidence<br />

of benefit from the use of adrenaline is limited, it was felt that the<br />

improved short-term survival documented in some studies 245,246<br />

warranted its continued use, although in the absence of clinical<br />

evidence, the dose and timing have not been changed in the <strong>2010</strong><br />

guidelines.<br />

Adrenaline<br />

Indications.<br />

• Adrenaline is the first drug used in cardiac arrest of any cause:<br />

it is included in the ALS algorithm <strong>for</strong> use every 3–5 min of CPR<br />

(alternate cycles).<br />

• Adrenaline is preferred in the treatment of anaphylaxis (Section<br />

8g). 294<br />

• Adrenaline is a second-line treatment <strong>for</strong> cardiogenic shock.<br />

Dose. During cardiac arrest, the initial IV/IO dose of adrenaline<br />

is 1 mg. There are no studies showing survival benefit <strong>for</strong> higher<br />

doses of adrenaline <strong>for</strong> patients in refractory cardiac arrest. In some<br />

cases, an adrenaline infusion is required in the post-resuscitation<br />

period.<br />

Following return of spontaneous circulation, even small doses<br />

of adrenaline (50–100 g) may induce tachycardia, myocardial<br />

ischaemia, VT and VF. Once a perfusing rhythm is established, if<br />

further adrenaline is deemed necessary, titrate the dose carefully to<br />

achieve an appropriate blood pressure. Intravenous doses of 50 g<br />

are usually sufficient <strong>for</strong> most hypotensive patients. Use adrenaline<br />

cautiously in patients with cardiac arrest associated with cocaine<br />

or other sympathomimetic drugs.<br />

Use.<br />

Adrenaline is available most commonly in two dilutions:<br />

• 1 in 10,000 (10 ml of this solution contains 1 mg of adrenaline).<br />

• 1 in 1000 (1 ml of this solution contains 1 mg of adrenaline).<br />

Both these dilutions are used routinely in Europe.<br />

Anti-arrhythmics<br />

As with vasopressors, the evidence that anti-arrhythmic drugs<br />

are of benefit in cardiac arrest is limited. No anti-arrhythmic drug<br />

given during human cardiac arrest has been shown to increase survival<br />

to hospital discharge, although amiodarone has been shown<br />

to increase survival to hospital admission. 285,286 Despite the lack<br />

of human long-term outcome data, the balance of evidence is in<br />

favour of the use anti-arrhythmic drugs <strong>for</strong> the management of<br />

arrhythmias in cardiac arrest.<br />

Amiodarone<br />

Amiodarone is a membrane-stabilising anti-arrhythmic drug<br />

that increases the duration of the action potential and refractory<br />

period in atrial and ventricular myocardium. Atrioventricular

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