Pathophysiology of Cardiac Tamponade: Cardiac Responses to Significant Pericardial Compression
Figure 2 schematizes the major hemodynamic events and compensatory mechanisms in uncomplicated cardiac tamponade.
When increasing pericardial contents put the in-trapericardial pressure on the steep portion of its J-shaped pressure-volume curve (Fig 1), the cardiac chambers must operate on parallel steep pressure-volume curves, a form of diastolic dysfunction where, at any diastolic volume, there is necessarily excessive intracardiac pressure. Thus, progressive compression of the atria and ventricles progressively resists cardiac filling, progressively reducing ventricular stroke volume. In intact, unanesthetized, longterm instrumented animals2 compensatory mechanisms maintain arterial pressure until relatively sudden decompensation, as in comparably intact human patients. This is a “last straw”—literally ‘last drop”—phenomenon due to the final increment of pericardial contents. This situation is demonstrated by the reciprocal effect of therapeutic pericardial fluid drainage—the initial decrement usually produces the largest relative hemodynamic improvement by rapidly shifting the stretched pericardium back toward the “flat” portion of its pressure-volume curve with parallel improvement in intracardiac pressure-volume relations and arterial pressures. mycanadianpharmacy
Although the key chambers maintaining cardiac output are the right and left ventricles, within the pathophysiologic continuum of tamponade, the earliest targets of significant compression are the thinner chambers: the right atrium and ventricle, diastolic pressure in which equilibrates with rising pericardial pressure before the left atrial and ventricular pressures do. That right atrial and ventricular pressures are normally somewhat lower than in the corresponding left chambers contributes to their earlier entrainment by inexorably rising pericardial pressure.