Pediatric Cardiopulmonary Emergency Drugs

In a cardiorespiratory arrest, drugs are usually given intravenously. However, prior to obtaining vascular or intraosseous access, many drugs can be administered via the tracheal route, namely epinephrine (adrenaline), lignocaine, naloxone and atropine. At least two to three times the intravenous dose, and, in the case of epinephrine (adrenaline), 10 times, the dose should be mixed with 2–3 ml of 0.9% saline. The dose is usually administered via a tracheal suction catheter, which is advanced past the trachea in order to maximise delivery of the drug. This route is a lastresort drug delivery and absorption from this route is very unpredictable.

Atropine

Persistent myocardial hypoxia results in bradycardia, which, left untreated, will lead to a cardiopulmonary arrest Atropine in a dose of 20 µg kg−1 is useful to antagonise the vagally induced bradycardia during tracheal intubation. The pupils should be examined prior to the administration of atropine as it causes bilateral pupillary dilatation and hence interferes with neurological assessment in head injuries.

Epinephrine (adrenaline)

Despite experience with cardiopulmonary resuscitation over the last 30 years,epinephrine (adrenaline) still remains the sole drug effective in restoring circulation in patients following cardiac arrest. Its alpha-receptor activity is thought to be responsible for increasing the aortic diastolic pressure and subsequently coronary artery perfusion. Peripheral arterial vasoconstriction increases the afterload and myocardial perfusion but also has a tendency to increase myocardial oxygen demand. Enhancement of the contractile state of the heart and stimulation of spontaneous cardiac contractions is responsible for the successful return of circulatory activity. It has been postulated that a drug with pure alpha-receptor agonist properties may in fact be more effective, but studies comparing epinephrine (adrenaline) with norepinephrine (noradrenaline) have shown no clear benefit. 

Sodium bicarbonate

Metabolic acidosis rapidly develops during cardiopulmonary resuscitation as a result of anaerobic metabolism owing to the absence of oxygen. Myocardial contractility is inevitably depressed by this state of acidosis. The use of alkalising agents, namely sodium bicarbonate, is not routinely recommended in the initial stages of resuscitation as it can produce a transient increase in intracellular acidosis. The generation of carbon dioxide, whose elimination is already impaired will result in a left shift in the oxygen dissociation curve and further limit the supply of oxygen. Sodium bicarbonate can reliably be used in the treatment of hyperkalemia and, as worsening acidosis renders epinephrine (adrenaline) ineffective, its use may be advocated if return of spontaneous circulation has not occurred after the second dose of epinephrine (adrenaline).

Fluid administration

In the pre-arrest state, the tissues are often poorly perfused and administration of 20 ml kg−1 of crystalloids (0.9% saline) or colloid (4.5% human albumin solution) as a fluid bolus will result in rapid expansion of the circulatory volume. The controversy regarding crystalloid versus colloid administration in resuscitation will continue until published

evidence is available.

Glucose

Once vascular access has been obtained, blood should be taken to check the blood glucose as hypoglycemia (<3 mmol l−1) can develop following cardiac arrest. Prompt correction with 5 ml kg−1 bolus of 10% dextrose is essential as the hypoglycemic state may worsen neurological outcome.