Transient blood pressure (BP) elevations at presentation are common in stroke patients (both hemorrhagic and ischemic). Indeed, in this analysis of 334 cases of confirmed strokes showed transient BP elevation in 84% cases. Most other studies show 70-80% stroke cases associated with initial high BP at admission. In a few instances of hypertensive urgencies on patient admissions, I have either correctly suspected atypical strokes or at least keep them high on the differentials – but is there a real evidence based approach & significance to this ? What piqued my interest in this was recent news about a atypical stroke with diagnostic delay that won US $13.5 million in malpractice award for a patient in Idaho !
Functionally it makes sense to me for BP elevation in acute ischemic strokes being an attempt to improve perfusion to stroke-affected areas of the brain. Another study published in 1991 found BP spikes common in 843 stroke patients and that previous hypertension and hemorrhage were strong predictors for BP elevation at admission, however it concluded that mental stress was a major factor for acute BP elevation in stroke. That is plausible, except we now that BP elevation on stroke presentation seems to correlate to stroke pathology.
A 2015 study showed BP elevations, especially systolic, strongly correlated with lacunar strokes compared to non-lacunar for similar severity of strokes. Cardioembolic strokes on the other hand tend to actually have lower BPs or impaired BP elevation on admission , as shown in studies published in 2006 & 2009. A more recent study published in 2020 found that having normal BPs on acute stroke presetation was actually predictive of cardio-embolic etiology – systolic BP < 130 was 85% specific for a cardioembolic stroke. Diastolic BP ? …not so much. We already covered an easy way to recall various pathologic mechanisms of a stroke earlier.
💡 Take home points:
– Keep stroke in your list of differential diagnosis for acute BP elevations
– However normal systolic BP in an acute stroke can occur AND should make you strongly suspect cardioembolic pathology and look for source ( A-fib, PFO, Cardiac thrombus / Myocardial infarction , valve vegetations, etc.) to consider anticoagulation for secondary prevention
