Pathophysiological events leading to the end-organ effects of acute hypertension.

The term "hypertensive crisis" refers to a group of acute hypertensive disorders that have, in common, evidence of end-organ dysfunction. From a pathophysiological viewpoint, these disorders may be classified into two major categories. In primary hypertensive disorders, the predominant pathophysiological events and subsequent end-organ failure are directly attributable to the uncontrolled hypertension. Secondary hypertensive crises have many similar features; however, the ultimate progression from onset of hypertension to end-organ failure tends to be modified by concurrent target-organ disease. The chain of events leading to the progression from benign to malignant hypertension centers around two general theories--the pressure hypothesis and the humoral hypothesis--both of which suggest that when a critical imbalance of pressure and/or humoral factors occurs, depending variously on etiological factors, rapidity, and degree and duration of blood pressure elevation, a series of pathological events ensue leading to myointimal proliferation and fibrinoid necrosis. The primary target-organ effects of severe hypertension generally affect the central nervous, renal, and cardiovascular systems and occur when the normal compensatory mechanisms are exceeded either by a breakthrough in autoregulation, as in the central nervous system, or by an imbalance in myocardial supply and demand. To a certain extent the pathophysiological events and target-organ susceptibility will determine the manner in which the hypertensive event presents. Although effective therapy is optimally tailored to the specific underlying disease process, in the acute setting, where important clinical data may be lacking, an appreciation of these underlying mechanisms will aid in the selection of a regimen that is both safe and effective.