What are the mechanisms of hypertension following an ischemic (lack of blood flow) stroke?

From the Guidelines

Hypertension following an ischemic stroke is primarily caused by the brain's autoregulatory response to ischemia, which triggers an immediate blood pressure elevation to increase perfusion to the damaged area, accompanied by activation of the sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS) 1. The mechanisms of hypertension following an ischemic stroke are complex and multifactorial.

• The brain's autoregulatory response to ischemia triggers an immediate blood pressure elevation as the body attempts to increase perfusion to the damaged area.
• Activation of the sympathetic nervous system releases catecholamines like norepinephrine and epinephrine, causing vasoconstriction and increased cardiac output.
• The RAAS is simultaneously activated, leading to fluid retention and vasoconstriction through angiotensin II production 1.
• Baroreceptor dysfunction in the carotid sinus and aortic arch impairs normal blood pressure regulation.
• Inflammation at the stroke site releases cytokines that damage endothelial cells, reducing nitric oxide production and causing further vasoconstriction.
• Stress-related cortisol elevation contributes to sodium retention and vascular sensitivity to catecholamines.
• Pre-existing hypertension is often exacerbated by these mechanisms, creating a dangerous cycle.
• Damage to specific brain regions that regulate blood pressure, particularly in the brainstem or insular cortex, can disrupt central blood pressure control. According to the most recent guidelines, management typically involves careful blood pressure monitoring with gradual reduction, avoiding rapid decreases that could compromise cerebral perfusion in the vulnerable penumbra surrounding the infarct 1. In patients not receiving i.v. thrombolysis or mechanical thrombectomy, there is no evidence for actively lowering BP unless it is extremely high (e.g. >220/120 mmHg) 1. If BP is extremely high, an initial moderate relative reduction of 10%–15% over a period of hours may be considered 1. For stable patients who remain hypertensive (≥140/90 mmHg) ≥3 days after an acute ischemic stroke, initiation or reintroduction of BP-lowering medication is recommended 1.

From the Research

Mechanisms of Hypertension Following an Ischemic Stroke

The mechanisms of hypertension following an ischemic stroke are complex and not fully understood. However, several studies have investigated the relationship between blood pressure and ischemic stroke:

• Elevated blood pressure is present in more than 60% of patients with acute stroke, and moderate to severe hypertension affects stroke outcomes 2.
• High blood pressure is seen in 75% of patients with acute ischemic stroke and is independently associated with poor functional outcome 3.
• Both high and low systolic blood pressures have a detrimental effect on the neurologic outcome, and blood pressure fluctuation early in the course of ischemic stroke is a proven independent predictor of morbidity and mortality 4.

Management of Hypertension in Acute Ischemic Stroke

The management of hypertension in acute ischemic stroke is a topic of ongoing debate:

• Current guidelines support permissive hypertension in the early course of acute ischemic stroke, with antihypertensive treatment warranted in patients with systolic blood pressure greater than 220 mm Hg, receiving thrombolytic therapy, or with concomitant medical issues 5, 4.
• The use of predictable and titratable medications that judiciously reduce (approximately 10% to 15%) the initial presenting mean arterial pressure is recommended in these situations 5.
• Aggressive blood pressure reduction in patients presenting with acute ischemic stroke is currently not recommended due to the potential deleterious effect of lowering blood pressure observed in some clinical trials 3.

Blood Pressure Goals and Treatment

The optimal blood pressure goals and treatment strategies for patients with acute ischemic stroke are not well established:

• A reasonable goal would be to lower blood pressure by 15% during the first 24 hours after onset of stroke, but the level of blood pressure that would mandate such treatment is not known 4.
• The first-line drugs for lowering of blood pressure remain labetalol, nicardipine, and sodium nitroprusside, but these recommendations are based on consensus rather than evidence 4.
• Comorbid conditions such as myocardial infarction, left ventricular failure, aortic dissection, preeclampsia, or eclampsia would override the guidelines for permissive hypertension, and a lower blood pressure would be preferred in these conditions 4.