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Hypertension is extremely common in the United States, requiring some form of treatment in more than 50 million Americans.

Hypertensive emergencies will occur in approximately 1% of these individuals. Hypertensive urgencies and emergencies account for approximately 2-3% of all ED visits annually, with urgencies being more common than emergencies (70% vs 30%, respectively). Several risk factors increase the likelihood of developing a hypertensive emergency. Preexisting hypertension appears to be the most common risk factor, occurring in approximately 75-90% of patients diagnosed with a hypertensive emergency. In one case series, hypertensive emergencies were found to occur more often in older black or Hispanic males with known hypertension who had previously been on antihypertensive therapy. Similarly, another case control study found hypertensive emergencies were more common among patients without a primary care physician and those who did not comply with antihypertensive treatment. A retrospective study of 100 patients with severe hypertension admitted to a large urban hospital (of whom two thirds had end-organ damage) showed that less effective outpatient systolic blood pressure control was an independent risk factor for developing a hypertensive emergency.
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Finally, data from the Framingham Heart Study also confirmed that appropriate, monitored, long14

term treatment of hypertension lowers the incidence of hypertensive complications.

Etiology/Pathophysiology
The pathophysiology of hypertensive emergencies has not been fully delineated. It is generally agreed that an abrupt rise in blood pressure initiates a series of vascular events that eventually manifest as end-organ dysfunction. Two theories presently define the debate: the pressure hypothesis and the humoral hypothesis. The pressure hypothesis posits that, as blood pressure rises, mechanical stress causes damage to the vascular endothelium, focal vasodilatation, and leakage of plasma proteins and fibrinogen. This eventually leads to fibrinoid necrosis of the vessel wall and proliferative endarteritis. The humoral hypothesis proposes that hypertensive emergencies occur as a result of an imbalance in the action of the renin-angiotensin system and other local mediators on the vasculature. The vasodilators nitric oxide and prostacyclin largely balance the effects of the vasoconstrictors angiotensin II, norepinephrine, and vasopressin. However, when a critical pressure is reached, there is a loss of sodium and water through a pressure natriuresis. The resulting relative hypovolemia causes local vascular mediators to be activated, leading to vasoconstriction and increased vascular permeability. This results in myointimal proliferation and fibrinoid necrosis of the endothelium, and a vicious cycle ensues.
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It is likely that the vascular and end-organ changes that define hypertensive emergencies represent a combination of these 2 theories working in concert. The concept of autoregulation is central to effective management of hypertensive emergencies and urgencies. Autoregulation functions to maintain constant blood flow and perfusion pressure to so-called target organs (brain, kidneys, heart, large arteries) even in the presence of large variations in blood pressure. As blood flow is equal to pressure divided by resistance, changes in blood pressure will not affect flow, as long as a parallel change in resistance via either vasoconstriction or vasodilation occurs. The most widely studied system of autoregulation involves the cerebral circulation. Cerebral blood flow in normotensive individuals is maintained via vasoconstriction and vasodilation when the mean arterial pressure (MAP) is between 70 and 120 mmHg. MAP is Diastolic Blood Pressure (DBP) + 1/3 [Systolic Blood Pressure (SBP) - DBP]. In this MAP range the cerebral perfusion pressure remains relatively constant. Beyond this range of autoregulation, no further vasodilation or vasoconstriction can occur, and further changes in blood pressure lead to either hypoperfusion or hyperperfusion, respectively. In hypertensive individuals, the range of autoregulation has been shown to shift to the right, so that higher BPs are better tolerated and lower BPs more poorly tolerated. This is a result of the arteriolar hypertrophy that accompanies chronic hypertension, causing the arteries to lose their ability to adequately vasodilate. Thus, in chronically hypertensive individuals, the lower limit of MAP is 100-120 mmHg and the upper limit is 150-160 mmHg.
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An understanding of the pathophysiology provides the basis for management recommendations in hypertensive emergencies initially blood pressure should be lowered by no more than 25% of the initial MAP. A marked BP drop in a right-shifted autoregulation curve causes hypoperfusion and relative brain ischemia.
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(See Figure 1.)