Pathophysiology: Hypertensive Urgency and Emergency Management

Hypertensive emergencies are caused by a rapid and severe elevation in blood pressure that exceeds the body’s capacity for autoregulation

Autoregulation maintains stable organ perfusion across a range of blood pressures. This range shifts rightward in chronic hypertension, allowing higher pressures to be tolerated. However, an acute spike in blood pressure can exceed the upper limit of autoregulation.

Hypertensive emergencies lead to episodes of vasoconstriction and vasodilation that disrupt organ perfusion. It also activates RAAS and increases vasoconstrictive peptides like angiotensin II and endothelin.

Further impairs perfusion and causes endothelial damage and platelet aggregation.

Affected organs depend on their autoregulatory capacity and susceptibility to ischemia:

• Brain: Stroke, encephalopathy, hypertensive retinopathy
  • Heart: Myocardial infarction, heart failure
  • Kidneys: Acute kidney injury
  • Eyes: Retinopathy, retinal hemorrhage, papilledema

• Some conditions predispose to acute spikes in blood pressure:
  • Medical (e.g. renal artery stenosis, pheochromocytoma)
  • Pharmacological (e.g. sympathomimetics, withdrawal syndromes)

• Others directly cause endothelial damage:
  • Aortic dissection
  • Thrombotic microangiopathies

In summary, hypertensive emergencies result from an acute rise in blood pressure exceeding the limits of autoregulation and protective mechanisms. This leads to ischemic end-organ damage mediated by disrupted perfusion, endothelial injury, and platelet aggregation. The manifestations depend on the organs affected.