Pathways Leading To Cardiorespiratory Arrest

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Cardiac arrest in infancy and childhood is rarely due to primary cardiac disease. This is different from the adult situation where the primary arrest is often cardiac, and cardiorespiratory function may remain near normal until the moment of arrest. In childhood most cardiac arrests are secondary to hypoxia, underlying causes including birth asphyxia, inhalation of foreign body, bronchiolitis, asthma, and pneumothorax. Respiratory arrest also occurs secondary to neurological dysfunction such as that caused by some poisons or during convulsions. Raised intracranial pressure (ICP) due to head injury or acute encephalopathy eventually leads to respiratory arrest, but severe neuronal damage has already been sustained before the arrest occurs.

Whatever the cause, by the time of cardiac arrest the child has had a period of respiratory insufficiency which will have caused hypoxia and respiratory acidosis. The combination of hypoxia and acidosis causes cell damage and death (particularly in more sensitive organs such as the brain, liver, and kidney), before myocardial damage is severe enough to cause cardiac arrest.

Most other cardiac arrests are secondary to circulatory failure (shock). This will have resulted often from fluid or blood loss, or from fluid maldistribution within the circulatory system. The former may be due to gastroenteritis, burns, or trauma whilst the latter is often caused by sepsis or anaphylaxis. As all organs are deprived of essential nutrients and oxygen as shock progresses to cardiac arrest, circulatory failure, like respiratory failure, causes tissue hypoxia and acidosis. In fact, both pathways may occur in the same condition. The pathways leading to cardiac arrest in children are summarised in Figure 1.2.





Blood loss

Septic shock

Foreign body



Cardiac disease


Raised ICP









Figure 1.2. Pathways leading to cardiac arrest in childhood (with examples of underlying causes)

The worst outcome is in children who have had an out-of-hospital arrest and who arrive apnoeic and pulseless. These children have a poor chance of intact neurological survival. There has often been a prolonged period of hypoxia and ischaemia before the start of adequate cardiopulmonary resuscitation. Earlier recognition of seriously ill children and paediatric cardiopulmonary resuscitation training for the public could improve the outcome for these children.


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