Pathophysiology of subarachnoid haemorrhage. Experimental and clinical data

Abstract

When a saccular aneurysm suddenly ruptures the intracranial pressure (ICP) abruptly rises to reach a level at about the diastolic blood pressure in 1 to 2 minutes. Unless a haematoma is formed ICP will soon fall and reach a steady level in about 10 minutes. In the days following the initial SAH several pathophysiological events take place. Regional CBF and the cerebral metabolic rate of oxygen (CMRO2) are reduced resulting in so-called luxury perfusion due to an uncoupling between flow and metabolism. The arteriovenous difference of oxygen is always reduced. CMRO2 falls parallel to increasing severity of vasospasm. CBF below 20 ml/100 g/min in cases of severe diffuse spasm inevitably result in brain tissue infarction. The development of vasospasm, which reaches a maximum between the 5th and 9th day after SAH, is accompanied by CSF lactacidosis and intracranial hypertension. The reactivity of the cerebral arteries after SAH is often impaired. Cerebral autoregulation to arterial hypotension is disturbed even in mild cases, and globally fails in severe vasospasm. On the other hand the reactivity of the cerebral vasculature to changes in arterial PCO2 is always preserved although reduced. Only in the presence of severe tissue acidosis will both modes of reactivity be damaged--so-called total vasoparalysis.