THE MECHANICAL INFLUENCE OF THE PERICARDIUM UPON CARDIAC FUNCTION

Abstract

From 28 experiments on cats with open chests under artificial respiration it appears that opening the pericardium is without effect upon either arterial or venous pressures. Gradual compression of the pulmonary artery results in a slow fall in arterial pressure and a corresponding rise in venous pressure. Opening the pericardium when cardiac decompensation has been produced by compression of the pulmonary artery or aorta is without significant effect on the elevated venous pressure or the low arterial pressure. Tight closure of the pericardium with sutures produces cardiac tamponade with a fall in arterial and a rise in venous pressures. On opening the pericardium again, the pressures return to their former level. When the pericardium has been closed with the production of cardiac tamponade and partial obstruction of the pulmonary artery superimposed, opening the pericardium causes a rise in the carotid pressure and a fall in the superior caval pressure. By exercising care the pericardium may be closed with sutures without affecting either venous or arterial pressures. Subsequent opening is similarly without effect on pressure levels. When the pericardium has been snugly closed by sutures without affecting either arterial or venous pressures and cardiac decompensation produced by compression of the pulmonary artery, opening the pericardium causes a rise in arterial pressure and a fall in venous pressure. In none of the 28 experiments performed was the removal of the pericardium detrimental to the circulation, even when signs of cardiac decompensation had been experimentally produced. Increased work is accomplished by increase in the diastolic size of the heart. Removal of a pericardium which limits this normal cardiac dilatation materially lessens the degree of cardiac decompensation.