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Ann Thorac Surg 1997;64:1723-1724
© 1997 The Society of Thoracic Surgeons
Price Institute of Surgical Research, Division of Thoracic and Cardiovascular Surgery, University of Louisville, Louisville, KY 40292
Darrah and colleagues present an interesting way to potentially treat patients with acute right ventricular pressure overload failure. In sheep, they created acute right ventricular failure by obstructing right ventricular outflow. This resulted in an increase in right ventricular systolic pressure and a severe decrease in cardiac output and systemic pressure. Perfusion blood flow to the right ventricle was maintained, but left ventricular perfusion blood flow was compromised. In this setting, increasing systemic pressure with an intraaortic balloon pump increased aortic pressure as expected. However, this also increased left ventricular perfusion, which, in turn, resulted in an increase in right ventricular ejection fraction and an increase in cardiac output.
The early experimental studies attributed right ventricular pressure overload failure primarily to inadequate right ventricular myocardial blood flow. Increasing myocardial blood flow helped to restore or maintain function. However, most studies raised flow by increasing aortic and thus left ventricular pressure. More recent studies suggest that, independent of blood flow, reestablishing systemic blood pressure by ligating the descending aorta, administering norepinephrine, or, as in Darrah and colleagues' study, intraaortic balloon pumping can restore right ventricular function.
These results are probably best explained by ventricular interdependence. My colleagues and I and others have shown that both the diastolic and systolic function of the right ventricle are highly dependent on left ventricular function. Thus, via ventricular interdependence, the decrease in left ventricular systolic function decreases left ventricular assistance to right ventricular function. This sets up a positive feedback mechanism: the decreased left ventricular assistance reduces right ventricular systolic pressure and stroke volume, which decreases left ventricular filling, leading to a decrease in left ventricular systolic pressure. This leads to a further decrease in left ventricular assistance and right ventricular systolic pressure and stroke volume. This ventricular interdependencepositive feedback mechanism is partially responsible for the circulatory failure. A corollary of the ventricular interdependence mechanism is that if left ventricular systolic function (and its assistance to the right ventricle) could be maintained, then the right ventricle could reach greater systolic pressure levels before circulatory failure occurs.
Darrah and colleagues provide a new approach to treating patients with acute right ventricular pressure overload that is firmly based in sound physiologic principles.
Related Article
Ann. Thorac. Surg. 1997 64: 1718-1723.
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