Figure 823

Pathogenesis of acute hypertensive heart failure. Both malignant hypertension and severe benign hypertension can be complicated by acute pulmonary edema caused by isolated diastolic dysfunction. In acute hypertensive heart failure the compromise of left ventricular (LV) diastolic function occurs as a result of a decrease in LV compliance caused by an increased workload imposed on the heart by the marked elevation in systemic vascular resistance. Illustrated are the hemody-namic derangements in acute hypertensive heart failure in a study that compared five patients with severe essential hypertension complicated by acute pulmonary edema with a control group of five patients with equally severe hypertension but no pulmonary edema [28]. Patients in both groups had electrocardiographic evidence of LV hypertrophy caused by long-standing hypertension.

A, Baseline hemodynamic measurements before treatment revealed that the following measurements were the same in both groups: mean arterial pressure (MAP), heart rate, cardiac index, systemic vascular resistance, and stroke work index. Likewise, the LV end-diastolic volume (LVEDV) was similar in both groups. In fact, the only hemodynamic difference between the groups was a significant elevation of LV filling pressure (LVFP) (pulmonary capillary wedge pressure) in the group with pulmonary edema. In acute hypertensive heart failure the finding of elevated LV end-diastolic pressures (LVEDPs), despite normal ejection fraction and cardiac index, implies the presence of isolated diastolic dysfunction. The increased LV end-diastolic pressure (LVEDP), despite similar LVEDV, can only be explained by a decrease in LV compliance in patients with acute hypertensive heart failure. B, The importance of an acute decrease in LV compliance in the pathogenesis of acute hypertensive heart failure (AHHF) was confirmed in these patients by the hemodynamic response to vasodilator therapy. Sodium nitroprusside infusion resulted in prompt resolution of pulmonary edema in the group having AHHF, with the LVEDP decreasing from a mean of 43 to 18 mm Hg. C, The decrease in filling pressure during nitroprusside therapy in patients with AHHF was not caused by venodilation with decreased venous return because the LVEDV actually increased during nitroprusside infusion. Thus, the response to sodium nitroprusside therapy was mediated through a decrease in systemic vascular resistance that led to an immediate improvement in LV compliance and reduction in wedge pressure despite an increase in LVEDV. These findings suggest that the proximate cause of AHHF is an elevation of the systemic vascular resistance that precipitates acute diastolic dysfunction (decreased LV compliance) with elevated pulmonary capillary wedge pressure, resulting in pulmonary edema. NS— not significant. (Adapted from Cohn and coworkers [28]; with permission.)

Left ventricular end-diastolic volume, mL/m2
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