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J Thorac Cardiovasc Surg 2002;123:72-80
© 2002 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Determinants of maximal right ventricular function: Role of septal shift

From the Departments of Surgery^a (Division of Cardiac Surgery) and Medicine^b (Cardiac Unit), Massachusetts General Hospital and Harvard Medical School, Boston, Mass.

Supported in part by a research grant from the Max Kade Foundation, Inc, New York, NY.

Received for publication March 22, 2001. Revisions requested April 26, 2001; revisions received June 22, 2001. Accepted for publication July 11, 2001. Address for reprints: Gus J. Vlahakes, MD, Division of Cardiac Surgery, Massachusetts General Hospital, 55 Fruit St, BUL119, Boston, MA 02114-2696 (E-mail: vlahakes.gus{at}mgh.harvard.edu).

Background: Right heart failure can occur after orthotopic heart transplantation and can complicate implantation of left ventricular assist devices. The functional codeterminants of right ventricular function are not fully understood. We investigated the effects of left ventricular preload and afterload, systemic pressure, and the contribution of the interventricular septum to right ventricular function.
Methods and Results: In vivo studies were conducted in 12 dogs by using a highly defined, isovolumic right heart preparation. At any given arterial pressure, maximal right ventricular developed pressure was not influenced by left heart output; however, right ventricular volumes at which peak right ventricular developed pressure occurred differed significantly between the volume-loaded versus the unloaded left ventricle (P < .05). A correlation was found between peak right ventricular developed pressure and mean arterial pressure. The shift of the interventricular septum toward the left ventricle is delayed under the influence of left ventricular volume load, but the maximal interventricular septal deformation does not differ at maximal right ventricular developed pressure. There was a substantial and significant decrease in peak right ventricular developed pressure when the interventricular septum was inactivated (P < .05).
Conclusions: Right ventricular function has multiple determinants, including the right ventricular free wall, the left ventricle, and the interventricular septum. Changes in right ventricular performance caused by alterations in left ventricular volume load and mean arterial pressure are mediated partially through the interventricular septum, as well as through perfusion of the right ventricular free wall; inactivation of the interventricular septum leads to a significant decrease in right ventricular function. Maintaining left ventricular developed pressure and hence the contribution of the interventricular septum to right ventricular function may be important in the management of right ventricular failure.

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