ABSTRACT
The brain and cerebral circulation are highly vulnerable to the effects of blood pressure (BP) instability. Untreated hypertension is an important risk factor for cerebral infarction, intracerebral hemorrhage (ICH), and, to a lesser extent, subarachnoid hemorrhage (SAH) ( 1-4 ). The deleterious effects of acutely elevated BP in the presence of these and other cerebral insults, however, must be balanced against the physiologic regulation of cerebral perfusion pressure (CPP) and risks of reduced cerebral blood fl ow (CBF). After a surge in intracranial pressure (ICP), such as following subarachnoid or other intracranial hemorrhage, ICP may temporarily surpass mean arterial BP (MABP), such that CPP falls to zero, with resultant loss of consciousness. The elevated systemic BP after such events is presumably an autoregulatory phenomenon and may represent a component of the Cushing response, along with bradycardia and irregular respiratory effort, if ICP continues to be elevated. Rapid treatment of such hypertension is thought to be detrimental because decreased CPP may worsen brain injury by aggravating ischemia ( 5-7 ). Systemic hypertension has been shown to be protective in several brain injury paradigms, including mass lesions, infarction, and traumatic brain injury ( 7-10 ). The rationale for lowering BP in these same conditions is to decrease the risk for new or ongoing hemorrhage, depending on the mechanism of injury. The optimal BP might depend on several factors, including presence of chronic hypertension, suspected intracranial hypertension, age, etiology of injury, and time since onset ( 5 ). Guidelines for acute BP control are often controversial, vague, or nonexistent. It is therefore important to review the relevant pathophysiology in order to make rational decisions under a variety of clinical conditions.
