Monday, June 25, 2018

Blood Pressure in Acute Stroke To Treat or Not to Treat: That Is Still the Question

Are we EVER going to get a blood pressure protocol? Or will we wait until stroke survivors are in charge? This question has been out there forever. Is your doctor and stroke hospital still sitting on their asses WAITING FOR SOMEONE ELSE TO SOLVE THE PROBLEM? 

 Blood Pressure in Acute Stroke To Treat or Not to Treat: That Is Still the Question

Philip M. Bath, Jason P. Appleton, Kailash Krishnan, Nikola Sprigg
https://doi.org/10.1161/STROKEAHA.118.021254


This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.


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 1985,13 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.8
There 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 …
View Full Text

No comments:

Post a Comment