A Study on Pericarditis

Abstract

Pericardial heart disease is one of the more infrequent cardiac diseases, however, there is higher incidence in unrecognized pericarditis associated with collagen disease, uremia, or myocardial infarction. Since numerous hemodynamic studies of constrictive pericarditis and cardiac tamponade have appeared in the literature, it is surprising that many of the mechanisms responsible for the cardinal clinical features remain obscure. For evaluating the hemodynamic changes in acute cardiac compression, an experimental study was carried out with 23 open chest dogs under constant heart rate. The pressures were recorded from the left and/or right ventricle, right atrium, superior vena cava and intra-pericardial space, using a cathetertip manometer or water-filled catheter. Saline solution (37°C) was progressively infused into the intrapericardial space. Cardiac output was measured by the dye-dilution method and the peak dp/ dt of left ventricular pressure of postextrasystolic potentiation was examined as a parameter of myocardial contractility. The results of infusing the fluid into the pericardial space were proportional decrease in cardiac output, decrese in left ventricular pressure and decrease in the maximum velocity of left ventricular pressure rise. On further infusion of the fluid, these parameters decrased markedly. With the aspiration of the fluid from the pericardial cavity, the values returned to the control levels, before all fluid was withdrawn. This hysteresis was demonstrated during infusion and aspiration of the fluid from the pericardial cavity, and is considered to be due to the character of pericardium itself, judging from the pericardial pressure-volume relationship, using the sacrificed dogs. The mechanisms of the deterioration of hemodynamics during intrapericardial infusion was determined in the following order, 1) decrease in veno-atrial pressure gradient, 2) decreased srtroke volume, 3) impairment of atrial inflow during ventricular systole, and 4) domino effect of 1-3. In cardiac tamponade, the hypothesis on impairment of ventricular contactility caused by the reduction of coronary flow, was denied. It was reported that heart failure augmented postextrasystolic potentiation. In this experiment, however, there was no augmentation of postextrasystolic potentiation. So, conclusively, it may be derived that cardiac tamponade does not impair myocardial contractility.