Pulmonary oedema and cardiac injury are well known complications of subarachnoid haemorrhage (SAH). Massive release of catecholamines, probably due to hypothalamic ischaemic stress, results in specific myocardial lesions and hydrostatic pressure injury to the pulmonary capillaries causing neurogenic pulmonary oedema (NPO). Catastrophic NPO and cardiac failure may present simultaneously or in isolation. They represent the severe end of a clinical spectrum of respiratory and cardiac impairment, which results in hypoxia and hypotension – major detrimental factors influencing outcome in acute brain injury.

 

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