Abstract
Any increase in arterial pressure is the result of either an increase in cardiac output, an increase in total peripheral resistance or a combination of the two. Hypertension is not a homogeneous disease, however, and different mechanisms may be operative during the life span of the patient. Hypertension in the young, nonobese patient is usually hemodynamically characterized by high cardiac output, normal to slightly contracted intravascular volume and numerically normal total peripheral resistance. In contrast, hypertension in the middle-aged or elderly patient is usually hemodynamically characterized by normal to low cardiac output, contracted intravascular volume and high total peripheral resistance. Two further subgroups of hypertensive patients can be identified: obese patients, whose hypertension is characterized by high cardiac output, expanded intravascular volume and normal or low total peripheral resistance, and black patients, whose hemodynamic and fluid volume findings are similar to those of their white counterparts, but who tend to have lower heart rates and greater responsiveness to intravascular volume depletion than white hypertensive subjects. A rational therapeutic approach to essential hypertension should take into account these variable pathophysiologic features. Thiazide diuretics continue to be appropriate and generally well-tolerated choices for initial antihypertensive therapy in obese or in black patients. Many obese patients or black patients, however, are likely to develop early left ventricular (LV) hypertrophy. Patients with electrocardiographic or echocardiographic evidence of LV hypertrophy have been shown to have a higher prevalence of ventricular ectopic activity and to be at higher risk of sudden death than patients without evidence of LV hypertrophy. Some studies have shown that obese patients and black patients are at higher risk of developing LV hypertrophy. Thiazide diuretic-induced hypokalemia may exacerbate ventricular ectopic activity and cause more serious arrhythmias. Potassium depletion should, therefore, be prevented in patients with evidence of the LV hypertrophy. If thiazide diuretics are used in this context, the addition of a potassium sparing agent, such as amiloride, is recommended.
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