Drugs

Adrenaline remains as the only drug that is effective in restoring circulation in cardiac arrest. The consensus initial dose is 0.01mg/kg intravascularly or 0.1mg/kg by the endotracheal route. The subsequent doses should be 0.1mg/kg at 3 to 5 minute interval to allow the peak effect of intravascular adrenaline to take place. Its mechanism of action is believed to be its a-adrenergic activity that increases the aortic diastolic pressure and hence, myocardial perfusion. Adrenaline also selectively diverts blood flow to the vital organs such as the brain and heart from the skin, muscle and splanchnic circulation. However, adrenaline increases myocardial oxygen demand and afterload.

Strangely, though, studies using pure a-agonist such as methoxamine and phenylephrine have not demonstrated any clear benefit over adrenaline. This is possibly the beneficial b 1 effect on cerebral vasodilatation. Noradrenaline, which has both a and b 1 effects without b 2 effects, theoretically may be advantageous since it lacks the b 2 smooth muscle vasodilatation which reduces the aortic diastolic pressure. However, it has not been proven to be superior to adrenaline. Recently, vasopressin has been shown to have greater improvement in myocardial and coronary blood flow compared to adrenaline in ventricular fibrillation models. More work needs to be done in this area.

The use of high dose adrenaline in cardiac arrest in adults has not produced optimistic results. Large multicentre trials have demonstrated increased ROSC rates but no improvement in long term survival and neurological outcome. The poor outcome is attributed to the limited improvement in myocardial perfusion in adult patients with coronary heart disease and a fixed cardiac narrowing, from high dose adrenaline is offset by the increased in myocardial demand. There is suggestion that children with normal coronaries would benefit from high dose adrenaline. However, the benefits of high dose adrenaline in the paediatric population remains unproven due to the small sample size of the studies.

There are concerns over the use of high dose adrenaline. The combination of severe a vasoconstriction with increase in myocardial oxygen consumption may lead to systemic hypertension, intracranial haemorrhage, ventricular dysrhythmias, myocardial ischema and necrosis as it has been shown in some animal studies. There is also the potential that high dose adrenaline may produce more survivors but in a vegetative state.

Poor ventilation and perfusion leads to a mixed respiratory and metabolic acidosis during cardiac arrest. It is believed that acidosis reduces the effectiveness of adrenaline, myocardial contractility, increases pulmonary vascular resistance but decreases the systemic vascular resistance and reduces the synthesis of adenosine triphosphate. However, cellular acidosis is poorly reflected by the arterial blood gas. The key treatment for the acidosis is restoration of tissue perfusion. Administration of sodium bicarbonate would theoretically then overcome this problem by buffering the accumulated metabolic acids. However, unless ventilation and perfusion is adequate to eliminate the formed CO2, the Handerson-Hasselbach equation would not proceed to the right. In fact, the increased CO2 formed may worsen the intracellular acidosis. Furthermore, overzealous bicarbonate administration may produce metabolic alkalosis with a left shift of the oxyhaemoglobin dissociation curve and poor tissue oxygen delivery, depressed myocardial function, hypokalemia, hypernatremia and hyperosmolality. Results from animal studies have been encouraging but again the empiric administration of sodium bicarbonate during prolonged cardiac arrest has not been proven to improve outcome in humans. Bicarbonate should not be used routinely in paediatric resuscitation but it may be used to transiently increase the pH so that adrenaline is affective in restoring the circulation.

Hypocalcemia in infants may present with poor contractility because contractility is more dependant on extracellular calcium as the intracellular calcium release from sarcoplasmic reticulum is deficient. However, recent data suggest that calcium antagonises the action of adrenaline and its major action on blood pressure is due to vasoconstriction rather than positive inotropic action. Furthermore, there is concern that calcium administration may worsen reperfusion injury. Hence, calcium is only indicated to correct documented ionized hypocalcemia and to antagonise the actions of hyperkalemia, hypermagnesemia and calcium channel blocker toxicity.

Magnesium is useful in treatment of tachy-arrhythmias especially those resistant to lignocaine, torsades de pointes and preventing arrhythmias post myocardial infarct. However it's role, dosage and administration in CPR is uncertain.

Lignocaine has been recommended for treatment of ventricular tachycardia and ventricular fibrillation based on its extensive use in adults. It is a membrane-stabilising drug which will cause myocardial depression and may stabilise existing arrhythmias.

Bradycardia in children is often due to hypoxia and should be treated with adequate oxygenation. Atropine can be used to antagonise excessive vagal stimulation with 0.02mg/kg. A minimum of 0.1mg should be used based on a study that demonstrated paradoxical bradycardia with lesser doses in infants.

Adenosine has become the drug of choice for supraventricular tachycardia and is safe and effective in children. Verapamil is however not recommended because it has been reported to produce bradycardia, hypotension and asystole in infants because of their immature autonomic system and importance of heart rate in maintaining cardiac output.

Cerebral resuscitation

There have been efforts to improve neurological outcome post cardiac arrest patients. Attempts to increase post-ischaemic cerebral blood flow with calcium channel blockers have not shown improvement in neurological outcome. However, cerebral cooling in animal studies has consistently improved neurological outcome. The use of a simple portable external head cooling device requires further investigation.

Automatic External Defibrillator

The benefit of automatic external defibrillator (AED) in adults has been demonstrated. Sedgwick et al showed that 43% patients defibrillated within 4 minutes survived and 87% of the survivors were neurologically intact. Successful defibrillation is inversely related to the time of the first shock.

Its use in the paediatric population is limited as the conventional wisdom is that ventricular fibrillation is rare cause of cardiac arrest in the paediatric population.

However, recent studies have shown that ventricular fibrillation account for 20% of paediatric cardiac arrests. The overall survival rate in patients with ventricular fibrillation was better than patients with pulseless electrical activity or asystole.

The limitation in the use of AED in children are the energy dose, the paddle size and the reliability of these devices in detecting ventricular tachycardia and ventricular fibrillation. The preset voltage in the AED would exceed the recommended voltage in a child. The initial voltage recommended is 2J/kg increasing to a maximum of 4J/kg in a series of 3 shocks. Whether this would be damaging to the myocardium remains unclear. The chest wall of children older than 8 years old or more than 10kg is probably large enough to accommodate the adult size paddle. The impedance of the adult paddle is approximately half of the children paddle.