Only 53%-58% of patients with a subarachnoid haemorrhage (SAB) following the 
rupture of a cerebral aneurysm survive without neurological damage. Morbidity 
and mortality are closely related to the delayed ischaemic neurological deficit 
due to cerebral vasospasm. The following review gives an account of 
pathophysiological mechanisms; the importance of treatment with calcium 
antagonists, hypervolaemic haemodilution, and induced arterial hypertension is 
discussed in light of the current literature. PATHOPHYSIOLOGY. In addition to 
other vasoactive substances in the blood, haemoglobin, which is released from 
lysed erythrocytes on the 2nd to 4th day after the haemorrhage, plays an 
important role in inducing vasospasm. An inflammatory angiopathy ensues, with 
complete resolution after 6-12 weeks. The cerebral blood flow (CBF) is reduced 
depending on the extent of vasospasm. Irreversible infarction may follow the 
decrease of CBF below a critical value. Severe vasospasm causes autoregulatory 
disturbances and reduced responsiveness of cerebral vessels to CO2. CALCIUM 
ANTAGONISTS. The calcium blocker nimodipine causes dilatation of small pial 
vessels with increased CBF. However, systemic vasodilation with the subsequent 
fall in blood pressure may limit the increase in CBF. Furthermore, it is known 
that nimodipine decreases intracellular calcium concentrations resulting in some 
protection against ischaemic cellular injury. Seven placebo-controlled clinical 
studies have shown that nimodipine improves the outcome of patients with severe 
neurological damage due to cerebral vasospasm. HYPERVOLAEMIC HAEMODILUTION. 
Volume expansion and haemodilution to a hematocrit of 30%-33% is suggested to 
improve cerebral perfusion during vasospasm. The central venous and pulmonary 
capillary wedge pressures should be 10-12 mm Hg and 15-18 mm Hg, respectively. 
But there is no evidence of improved outcome with this measure, and pulmonary 
edema is a frequent side effect. However, impairment of cerebral perfusion and 
increased neurological damage can be demonstrated with hypovolaemia and 
haemoconcentration. INDUCED ARTERIAL HYPERTENSION. In the presence of cerebral 
vasospasm and resulting autoregulatory disturbances, cerebral perfusion can be 
increased by raising systemic arterial pressure. This measure, too, fails to 
improve neurological outcome. CONCLUSION. Treatment of cerebral vasospasm 
following a SAB aims to avoid any impairment of cerebral perfusion. Hypovolaemia 
and haemoconcentration have to be corrected. Normoventilation should be 
established to avoid hypocapnic vasoconstriction. Nimodipine should be 
administered continuously after a SAB. In view of the autoregulatory 
disturbances, systemic hypotension with its danger of decreased CBF must be 
prevented. The importance of hypervolaemic haemodilution and/or induced arterial 
hypertension is not clear. Despite therapeutic efforts, the number of patients 
who have survived a SAB without a substantial neurological deficit has not 
increased.