The role of right ventricular systolic dysfunction and elevated intrapericardial pressure in the genesis of low output in experimental right ventricular infarction.

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Abstract
To elucidate the pathophysiology of severe right ventricular infarction (RVI), isolated RVI was produced in 15 dogs with the pericardium intact or open. After RVI in dogs with the pericardium intact, RV systolic pressure decreased by 27%, aortic pressure by 29% and cardiac output by 34%. RV transmural pressure, RV end-diastolic size and intrapericardial pressure increased, left ventricular transmural pressure and end-diastolic size decreased and the diastolic pressures equalized. Pericardiotomy after RVI resulted in increased ventricular transmural pressures and diastolic size, improved cardiac output and resolution of equalized diastolic pressures. RVI in dogs with the pericardium open resulted in similar changes, but of lesser magnitude and without equalization of diastolic pressures. These results indicate that reduced left ventricular preload due to impaired RV systolic function contributes to low cardiac output in RVI. Elevated intra-pericardial pressure further reduced left ventricular preload and produces equal diastolic pressures.