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Drug Therapy

Adrenaline (epinephrine)is the main drug used during resuscitation from cardiac arrest. A 1mg dose should be given at least every
three minutes during the arrest. Intravenous adrenaline enhances cerebral and myocardial blood flow by increasing peripheral vascular
resistance and raising aortic diastolic pressure. These peripheral vascular actions are primarily alpha1 (α 1), and alpha2 (α 2),
receptor-mediated. Beta1(β 1) and Beta2 (β 2) receptor actions also occur though a beta effect has not been shown to be beneficial in
restoring spontaneous circulation in VF, asystole or EMD. Indeed, β 1 effects may increase myocardial oxygen demand and increase
the risk of arrhythmias in a beating heart. Recently, high dose adrenaline (5mg) has been tried during resuscitation in an attempt to
improve the survival of cardiac arrest but there was no improvement in outcome.

The ALS algorithm suggests the use of antiarrhythmics, buffers, atropine and pacing. Antiarrhythmic drugs are considered in figure 7.

Atropine as a single dose of 3mg is sufficient to block vagal tone completely and should be used once in cases of asystole. It is also
indicated for symptomatic bradycardia in a dose of 0.5mg - 1mg.

Sodium bicarbonate In prolonged arrests, the effects of acidosis become significant. The use of sodium bicarbonate as a buffer has
been controversial; it is associated with hyperosmolarity and carbon dioxide production, and may worsen intra-cellular acidosis.
Carbon dioxide-consuming buffers, such as Carbicarb and THAM have been developed, but no buffer has been shown to improve
outcome. Nevertheless, sodium bicarbonate continues to be recommended (50mls of 8.4% solution) after 15 minutes of cardiac arrest
or when the arterial pH is less than 7.1, or the base deficit is more negative than -10. It should be used early in arrests caused by
acidosis, hyperkalaemia or tricyclic overdosage, but must not be given by the tracheal route or mixed with calcium or adrenaline

Drug Delivery

Drugs for ACLS

Despite widespread and long-standing use, no drug has definitively been shown to increase survival to hospital discharge

in patients with cardiac arrest. Some drugs do appear to improve the return of spontaneous circulation and thus may

reasonably be given (for dosing, including pediatric, see Table 3: Respiratory and Cardiac Arrest: Drugs for

Resuscitation* ).

Table 3

Drugs for Resuscitation*

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In a patient with a peripheral IV line, drug administration is followed by a fluid bolus (“wide open” IV in adults; 3 to 5 mL in

young children) to flush the agent into the central circulation. In a patient without IV or intraosseous access, atropine


, when indicated, may be given via the endotracheal tube at 2 to 2.5 times the IV dose.
First-line drugs: Epinephrine

is the main drug used in cardiac arrest although its benefit is increasingly challenged. It is given q 3 to 5 min. Epinephrine

has combined α- and β-adrenergic effects. The α-adrenergic effects may augment coronary diastolic pressure, thereby

increasing subendocardial perfusion during chest compressions. Epinephrine

also increases the likelihood of successful defibrillation. However, β-adrenergic effects may be detrimental because they

increase O2 requirements (especially of the heart) and cause vasodilation. Intracardiac injection of epinephrine

is not recommended because pneumothorax, coronary artery laceration, and cardiac tamponade may occur.

A single dose of vasopressin

40 units is an alternative to epinephrine

(adults only); it is not proven superior to epinephrine

sulfate is a parasympatholytic drug that increases heart rate and conduction through the atrioventricular node. It is given

for asystole (except in children), bradyarrhythmias, and high-degree atrioventricular nodal block, although no survival

benefit has been demonstrated.


can be given once if defibrillation is unsuccessful following epinephrine


. It is also of potential value if VT or VF recurs following successful defibrillation; a lower dose is given over 10 min

followed by a continuous infusion.

Other drugs: Ca chloride is recommended for patients with hyperkalemia, hypermagnesemia, hypocalcemia, or Ca

channel blocker toxicity. In others, because intracellular Ca is already higher than normal, additional Ca is likely to be

detrimental. Because cardiac arrest in patients on renal dialysis is often a result of or accompanied by hyperkalemia,

these patients may benefit from a trial of Ca if bedside K determination is unavailable. Caution is necessary because Ca

exacerbates digitalis toxicity and can of itself cause cardiac arrest.

Mg sulfate has not been shown to improve outcome in randomized clinical studies. However, it may be helpful in patients

with torsades de pointes or known or suspected Mg deficiency (ie, alcoholics, protracted diarrhea).


is a 2nd-line drug for treatment of refractory VF or VT. However,procainamide

s not recommended in pulseless arrest in pediatric patients.


may rarely be used to treat VF or VT, but only when it is due to digitalis toxicity and is refractory to other drugs. Dose is 50

mg/min given until rhythm improves or total dose reaches 18 mg/kg.

NaHCO3 is no longer recommended unless cardiac arrest is caused by hyperkalemia, hypermagnesemia, or tricyclic

antidepressant overdose with complex ventricular arrhythmias. In pediatric patients, NaHCO3 should be considered when

cardiac arrest is prolonged (> 10 min); it is administered only if there is good ventilation. When NaHCO3 is used, arterial

pH should be monitored before infusion and after each 50-mEq dose (1 to 2 mEq/kg in children).

and bretylium are no longer used during CPR.

Drugs used during cardiac arrest

Only a small number of drugs are indicated during cardiac arrest and there is little in the way of scientific evidence for their

use. However many drugs have also been disgarded because of lack of evidence for efficiency. One must always

remember that although drugs can be very useful during a cardiac arrest, good chest compressions and adequate

ventilation are paramount.

The drugs are listed in alphabetical order.



 Cardiac arrest from any cause


 1mg IV / IO every 3-5 mins

 3mg (diluted to 10-20mls with sterile water endotracheally every 3-5 mins if IV / IO access is unavailable)


Adrenaline is a naturally occurring sympathomimetic that possesses both alpha (α) and beta

(β) adrenergic agonist activity. α1 and α2stimulation leads to marked peripheral vasoconstriction and a subsequent

increase in systemic vascular resistance. This, in turn, leads to an increase in both cerebral and coronary perfusion. In the

beating heart, stimulation of β1 receptors leads to increased force and rate of contraction of the heart which can have a

negative impact on the situation by increasing myocardial oxygen demand, thus increasing the risk of

myocardial ischaemia. However, β-adrenergic stimulation may enhance cerebral blood flow.

Adrenaline is arrhythmogenic. After successful resuscitation, adrenaline can induce ventricular fibrillation (VF).



 Refractory ventricular fibrillation (VF) / pulseless ventricular tachycardia (VT)


 300mg IV


The major, acute, side effects of amiodarone are bradycardia and hypotension. Use of amiodarone should be considered

if VF / VT persists after 3 shocks.


Amiodarone is a Vaughan-Williams class III anti-arrhythmic agent that has many actions, many of which are not fully

understood. It acts as a membrane stabilising drug and it increases the duration of both the action potential and the

refractory period in both atrial and ventricular myocardium. Amiodarone is also mildly inotropic and and causes peripheral

vasodilatation, largely due to the solvent it is dissolved in (Polysorbate 80).





Beta-blocker overdose



Polymorphic VT (ie Torsades de Points)


2g IV over 10 minutes


Hypomagnesaemia can lead to polymorphic VT which is shock-refractory.