Blood Pressure in Acute Stroke

One of the oldest questions in acute stroke management, and perhaps the most challenging since it has yet to be solved after more than half a century of published research, is how to manage high blood pressure (BP). The problem might be summed up as follows:> To treat , or not to treat : that is the question:> > Whether ’tis nobler in the mind to suffer> > The slings and arrows of outrageous pressure ,> > Or to take drugs against a sea of blood ,> > And by opposing end them? To live : to walk ;> > —With apologies to Shakespeare , Hamlet Act III, Scene I To treat, or not to treat, high BP was debated >30 years ago in 1985,1–3 and yet there is no definitive answer here in 2018. Part of the debate is driven by opposing arguments based on epidemiology and pathophysiology and part by the failure of every large trial to provide a definitive answer. There is considerable evidence that high BP is associated independently with a poor outcome after ischemic stroke (IS) whether defined by early recurrence or death, or late death and dependency.4,5 Similarly, high BP is related to hematoma expansion6 and functional outcome after intracerebral hemorrhage (ICH).7 A straightforward conclusion of this epidemiological evidence is that high BP should be lowered. In contrast, pathophysiological concerns are based on the presence of dysfunctional cerebral autoregulation during acute stroke, and so lowering BP will reduce tissue perfusion, increase lesion size, and thereby worsen outcome.8There are many causes of high BP in acute stroke, including prior hypertension, acute neuroendocrine stimulation (via the renin-angiotensin-aldosterone system [RAAS], sympathetic autonomic nervous, and corticotrophin-cortisol systems), the Cushing reflex (due to raised intracranial pressure), and stress associated with admission to hospital and …