Chapter 8 - Collateral Flow Enhancement: Blood Pressure Lowering and Alteration of Blood Viscosity

Summary

In acute ischaemic stroke, cerebral blood flow autoregulatory mechanisms may be disrupted so that cerebral perfusion becomes reliant on systemic blood pressure. Too low blood pressure may lead to progression of the infarction and too high blood pressure may cause cerebral oedema or haemorrhagic transformation of the infarct. In patients with BP = 220/120 mm Hg who do not receive intravenous thrombolysis, it is reasonable to lower BP by 15% during the first 24 hours after stroke onset. Patients who have elevated blood pressure and are otherwise eligible for treatment with intravenous rt-PA should have their blood pressure lowered so that systolic blood pressure is < 185 mm Hg and their diastolic blood pressure is < 110 mm Hg before thrombolytic treatment is administered. Acute stroke patients should be assessed for dehydration and a fluid balance chart should be kept. Underlying causes of hypotension should be treated rapidly. There is no beneficial effect of hemodilution treatment for acute ischaemic stroke. Fibrinogen-depleting agents that reduce viscosity may marginally reduce risk of recurrent ischaemic stroke, but more greatly increases symptomatic intracranial haemorrhage. Methylxanthine derivatives such as pentoxyphylline and propenofylline that reduce viscosity and produce vasodilation have insufficient evidence to support their use.