Hemodynamics in Hypertension at Rest and During Exercise

Summary: The results of the last 20 years have shown that the hemodynamic mechanisms behind the increased blood pressure in essential hypertension differ widely and depend at least on the age of the patients and the stage of the hypertensive disorder. The cardinal hemodynamic disturbance is increased vascular resistance seen in most vascular beds, but to a different extent in various other areas. Even in relatively young subjects (20–40 years) with mild hypertension, where the typical hemodynamic pattern is an increased cardiac index during rest with almost “normal” total peripheral resistance, exercise studies show that total peripheral resistance does not fall as in normotensive age-matched controls. The heart pump function is slightly reduced (subnormal stroke index and cardiac index during exercise). When hypertension is left untreated, the hemodynamic pattern changes over time, toward the “low cardiac output-high resistance” pattern—associated with reduced left ventricular compliance—and left ventricular hypertrophy in a large fraction of the patients. Blood flow to such vital organs as the brain, the kidneys, and the myocardium diminishes. The initiating and maintaining mechanisms responsible for the high blood pressure include disturbances in the central nervous system, in the catecholamines, in the various vasoactive peptides, reduced compliance of the venous system, and probably an inborn tendency to structural changes and increased stiffness in the heart as well as in the major vessels. These are the changes we would like to prevent or reverse with our antihypertensive treatment. Our presently available antihypertensive drugs lower blood pressure through widely different mechanisms, interfering with intravascular volume, ion composition, calcium and sodium transport through membranes, the renin-angiotension system, and blockade or stimulation of α or β receptors. Over the years we have studied the immediate and chronic hemodynamic effects of most of the commonly used antihypertensive agents in about 400 patients with mild to moderate hypertension. Although the effect on blood pressure may be similar, the hemodynamic mechanisms differ widely. In general, β-blockers tend to induce a chronic depression in cardiac output, particularly during exercise, and sometimes induce chronic reduction of physical endurance during severe work loads. In contrast, α-receptor blockers, calcium antagonists, and angiotensin converting enzyme inhibitors all induce reduction in vascular resistance without fall in blood flow, but sometimes with immediate but temporary counteracting reflex tachycardia and increase in cardiac output. In general, the combination of drugs or the use of drugs with such multiple actions as combined α- and β-blockade (labetalol) or β-blockade plus direct vasodilation (prizidolol or carvedilol) induce better blood pressure control at rest as well as during exercise, with relatively little disturbance in blood flow. More interest should be directed to normalizing blood pressure physiologically than to just achieving a certain reduction in blood pressure in millimeters of mercury, recorded by the cuff method during rest.