Blood Pressure Management for Acute Ischemic and Hemorrhagic Stroke: The Evidence

Abstract

Hypertension is the most common modifiable risk factor for stroke (both ischemic and hemorrhagic types). In the hyperacute phase, a majority of patients shows an elevated blood pressure (BP) at the time of presentation because of sympathetic hyperactivity or a physiological response to tissue ischemia. Therefore, BP may decrease spontaneously in a few hours and may drop further when complete recanalization is achieved. In stroke guidelines, an elevated BP is usually left untreated up to a systolic BP (SBP) of 220 mm Hg and a diastolic BP of 120 mm Hg. This recommendation is based on the BP level that corresponds to the upper limit of the pressure autoregulation zone above which cerebral blood flow is directly dependent on BP. However, in patients in whom administration of recombinant tissue-type plasminogen activator is indicated, BP should be controlled to a level < 185/110 mm Hg before infusion and should be maintained at levels < 180/105 mm Hg to limit the risk of intracerebral hemorrhage (ICH). In cases where endovascular thrombectomy is considered, the optimal intra- and postprocedural BP target have not yet been clearly identified. Expert opinion recommends that intraprocedural BP reduction could be associated with a risk of poor outcomes, and therefore, SBP may be reduced only to 120 to 140 mm Hg after successful reperfusion therapy. However, this recommendation is primarily based on observational studies and requires validation in prospective trials. It has been observed that in patients presenting with an ICH, there is no perihematomal penumbra noted and rapid BP reduction is generally well tolerated without a risk of neurological worsening. Multiple trials describing acute reduction of BP recommend SBP reduction only to 140 mm Hg because while there is no benefit of better functional outcomes below that level, there exists a definite risk of increased renal complications.

Brain–heart interaction after acute ischemic stroke

“…Cerebral autoregulation: between blood pressure and hemodynamics Cerebral autoregulation plays an essential role in maintaining cerebral blood flow and cerebral perfusion pressure within constant ranges to ensure adequate irrigation of the brain [61]. However, AIS can dysregulate this vulnerable system, leading to secondary brain damage [61]. Blood pressure control plays a pivotal role in the prevention of both AIS and post-AIS secondary brain damage [46,61].…”

“…However, AIS can dysregulate this vulnerable system, leading to secondary brain damage [61]. Blood pressure control plays a pivotal role in the prevention of both AIS and post-AIS secondary brain damage [46,61]. The main mechanisms involved in hypertension after AIS are still unclear, although the same mechanisms responsible for other cardiac complications have been proposed and may account for the increase in systolic blood pressure (> 140 mmHg) [61].…”

“…Blood pressure control plays a pivotal role in the prevention of both AIS and post-AIS secondary brain damage [46,61]. The main mechanisms involved in hypertension after AIS are still unclear, although the same mechanisms responsible for other cardiac complications have been proposed and may account for the increase in systolic blood pressure (> 140 mmHg) [61]. Among AIS subtypes, the lacunar infarct is the most closely associated with hypertension, suggesting an important role of the small lacunar vessels [62].…”

Gut Microbiota in Acute Ischemic Stroke: From Pathophysiology to Therapeutic Implications

“…Diabetes and hypertension have been identified as systemic activators of immune response and are two of the most important risk factors for AIS (65). Intensive management of hypertension in AIS patients is recommended to reduce the risk of chronic myocardial dysfunction and cardiac remodeling (66)(67)(68). Hypertensive and pre-hypertensive patients have a different gut microbiota composition as compared to non-hypertensive patients.…”

Anesthetic Management for Endovascular Treatment of Stroke in Patients With Coronavirus Disease 2019: A Case Series

“… 2 Neurogenic hypertension occurs shortly after an ischemic insult to maintain cerebral perfusion pressure. 3 It is mediated by an increased excitatory drive of the rostral ventrolateral medulla sympathoexcitatory neurons. 4 It is possible that ventrolateral medulla neuronal dysfunction through viral infection could result in blunting of the sympathetic nervous response to cerebral ischemia.…”