Pathophysiology of Cardiac Tamponade: Influence of State of Hydration
The progressively increasing diastolic chamber pressures ultimately equilibrate (averaged over the respiratory cycle) throughout the heart. The typical range of 15 to 30 mm Hg applies mainly to euv-olemic patients and animals. All physiologic phenomena in tamponade occur earlier and at lower pressures in hypovolemic patients and later and at higher pressures in hypervolemic than in euv-olemic patients. Indeed, significantly hypovolemic patients can have tamponade at average diastolic pressures as low as 6 mm Hg, a form of low-pressure tamponade. (This can be difficult to recognize clinically particularly in patients treated with diuretics.)
Coronary Blood Flow
With normal coronary arteries, coronary blood flow is reduced but remains adequate to support aerobic metabolism. This is due to a proportionate reduction in cardiac work, because the ventricles are underloaded—“underafterloaded” as well as “underpreloaded.”’ Even coronary vasodilatory reserve, capacitance, and resistance are not reduced sufficiently to add a measurable ischemic burden. sildenafil citrate pink
In otherwise normal hearts, gross systolic function remains intact and the ventricles support stroke volume by an increased ejection fraction (often visibly striking during echocardiography). In contrast, previously diseased or injured hearts may not maintain cardiac output and arterial pressure as well, and tamponade decompensates earlier.
Compensatory Responses: Decompensated Tamponade
In addition to time-dependent blood volume expansion, pericardial stretch, and increased ejection fraction, compensatory mechanisms for tamponade include tachycardia and peripheral vasoconstriction due to intense adrenergic stimulation evoked by the falling cardiac output. Rising right atrial pressure reflexly contributes to the tachycardia that enhances the minute cardiac output (stroke volumeXheart rate) in the face of the falling stroke volume (Fig 2).
Adrenergic stimulation, both alpha and beta, and including increased serum catecholamines, is a principal compensatory response to the reduced cardiac output (Fig 2) with four major effects: (1) (3-adrenergic contribution to heart rate increases; (2) (3-adrenergic-dependent augmentation of diastolic relaxation; (3) a-adrenergically increased peripheral resistance to maintain central blood pressure and support the gradient for coronary flow; and (4) increased inotropy to minimize ventricular end-systolic volume via increased ejection fraction which, as already noted, is normal to high in tamponade in the absence of cardiac disease.