Author + information
- Received March 14, 1983
- Revision received September 28, 1983
- Accepted October 21, 1983
- Published online April 1, 1984.
- Otto A. Smiseth, MD, PhD,
- Helge Refsum, MD, PhDb,
- Michael Junemann, MD,
- Richard E. Sievers, BSc,
- Martin J. Lipton, MD, FACCc,
- Erik Carlsson, MD, PhD and
- John V. Tyberg, MD, PhD, FACCa
- ↵aPresent address and address for reprints: John V. Tyberg, MD, Department of Medicine and Medical Physiology, University of Calgary, 3330 Hospital Drive, N.W., Calgary, Alberta, T2N 4N1, Canada.
Ischemic left ventricular failure was produced in eight acutely instrumented, anesthetized dogs to study the contribution of changing myocardial compliance and pericardial pressure to shifts in right and left ventricular diastolic pressure-volume relations. Right and left ventricular and pericardial volumes were measured by ungated computed tomography. Cardiac volumes were manipulated by infusion of saline solution, hemorrhage, phenylephrine infusion and, during failure only, nitroglycerin administration. During both control and failure periods, these interventions shifted the left and right ventricular pressure-volume relations by changing pericardial pressure only; that is, these interventions caused no change in the ventricular transmural pressure-volume relation. The induction of failure as such increased pericardial pressure only minimally and did not change the left ventricular or right ventricular transmural pressurevolume relations significantly. Volume loading during the control period caused an apparent pericardial creep which attenuated the pericardial effect on ventricular pressure-volume relations. During failure, volume loading caused an increase of right ventricular volume, but tended to decrease left ventricular volume; this was associated with a leftward displacement of the interventricular septum.
In conclusion, in the presence of ischemic left ventricular failure as well as normally, changes in preload, afterload and circulating blood volume shift ventricular diastolic pressure-volume relations by stretching or relaxing the pericardium, thus changing pericardial pressure. In these circumstances, there were no consistent changes in myocardial compliance.
↵b Dr. Refsum was a recipient of a Fogarty International Fellowship from the U.S. Public Health Service, Bethesda, Maryland.
↵c Dr. Lipton was the recipient of Research Career Development Award HL 00360 from the National Heart, Lung, and Blood Institute, Bethesda. Maryland.
This work was supported in part by Program Project Grant HL 06285, and Grant-in-Aid 79-791 and 79-827 from the American Heart Association, Dallas, Texas, by the Norwegian Research Council for Science and the Humanities, Oslo, and by the Norwegian Council on Cardiovascular Disease, Oslo.
- Received March 14, 1983.
- Revision received September 28, 1983.
- Accepted October 21, 1983.
- American College of Cardiology Foundation