The Bottom Line: Most authorities have defined hypertensive crises or emergencies as a sudden increase in systolic and diastolic blood pressures associated with ‘acute end-organ damage’ (i.e. cardiovascular, renal, central nervous system) that requires immediate management. On the other hand, the term ‘hypertensive urgency’ has been used for patients with severely elevated blood pressure without acute end-organ damage. It is important to emphasize that the clinical distinction between hypertensive emergencies (crises) and hypertensive urgencies depends on the presence of acute target organ damage, rather than the absolute level of blood pressure.
Reference: Varon J, Marik PE. Clinical review: The management of hypertensive crises. Critical Care 2003; 7(5):374-384. doi:10.1186/cc2351.
Summary: The symptoms and signs of hypertensive crises vary from patient to patient. Headache, altered level of consciousness, and/or focal neurologic signs are seen in patients with hypertensive encephalopathy. On physical examination, these patients may have retinopathy with arteriolar changes, hemorrhages and exudates, as well as papilledema. In other patients, the cardiovascular manifestations of hypertensive crises may predominate, with angina, acute myocardial infarction, or acute left ventricular failure. In some patients, severe injury to the kidneys may lead to acute renal failure with oliguria and/or hematuria.
The risks for developing malignant hypertension are related to the severity of the underlying hypertension, and therefore the role of mechanical stress on the vessel wall appears to be critical in its pathogenesis. The release of humoral vasoconstrictor substances from the stressed vessel wall is thought to be responsible for the initiation and perpetuation of the hypertensive crisis. Increased blood pressure results in endothelial damage, with local intravascular activation of the clotting cascade, fibrinoid necrosis of small blood vessels, and release of vasoconstrictor substances. This leads to a vicious cycle of further vascular injury, tissue ischemia, and release of vasoconstrictor substances. The volume depletion that results from pressure natriuresis further simulates the release of vasoconstrictor substances from the kidney. The release of vasoconstrictor substances from the kidney has long been postulated to play a central role in the pathophysiology of malignant hypertension. Activation of the renin–angiotensin system has been strongly implicated in the initiation and perpetuation of the vascular injury associated with malignant hypertension. In addition to activation of the renin–angiotensin system vasopressin, endothelin and catecholamines are postulated to play important roles in the pathophysiology of hypertensive emergencies.
Unfortunately, hypertensive emergencies and urgencies are among the most misunderstood and mismanaged of acute medical problems seen today. Indeed, the reflex of rapidly lowering an elevated blood pressure is associated with significant morbidity and death. Clinicians dealing with hypertensive emergencies and urgencies should be familiar with the pathophysiology of the disease and the principles of treatment. This article reviews current concepts, and common misconceptions and pitfalls in the diagnosis and management of patients with severe hypertension.