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J Thorac Cardiovasc Surg 1994;108:477-486
© 1994 Mosby, Inc.
CARDIOPULMONARY BYPASS, |
Rochester, Minn.
From the Division of Cardiovascular and Thoracic Surgery, Mayo Clinic and Foundation, Rochester, Minn.
Received for publication Aug. 10, 1993. Accepted for publication Feb. 4, 1994. Address for reprints: James J. Morris, MD, Division of Cardiovascular and Thoracic Surgery, Mayo Clinic, 200 1st St. S.W. Rochester, MN 55905.
Abstract
So that we could better characterize the effects of left heart assist on right ventricular myocardial muscle mechanics and ventricular mechanical coupling in the injured heart, nine dogs underwent 30 minutes of global cardiac ischemia supported by cardiopulmonary bypass followed by randomly varied levels of left heart assist at 0, 1.0, and 2.0 L/min (0, 37 ± 4, and 74 ± 7 ml/kg per minute). A centrifugal pump with left ventricle-to-aorta bypass was used with the intent to cause left ventricular volume unloading but without complete left ventricular pressure unloading. Right ventricular regional free wall and septalfree wall dimensions were measured by a sonomicrometer and right ventricular pressure by a micromanometer. Pressure and dimension data were acquired over a range of preloads produced by transient vena caval occlusion and at steady state at an initial control point and after ischemia at each level of left heart assist. Right ventricular regional early diastolic function was assessed by percent segmental relaxation during the first third of diastole, end-diastolic compliance by the end-diastolic pressure-dimension relationship, systolic contractile performance by the slope (Mw) and dimension axis intercept (Lw) of the linear preload recruitable stroke work relationship, and right ventricular isovolumic relaxation by the pressure decay time constant. Ischemia reduced Mwof both the free wall (38.3 ± 16.1 to 16.4 ± 4.2 erg·cm -3·103, p< 0.01) and septal free wall (30.2 ± 12.7 to 13.4 ± 4.9 erg·cm-3·103, p< 0.01) and shifted Lwrightward (1.3 ± 0.3 to 1.4 ± 0.3 mm, p< 0.01, and 2.8 ± 0.8 to 3.0 ± 0.9 mm, p< 0.01), which confirmed myocardial ischemic injury. There were no effects of left heart assist on free wall or septalfree wall systolic contractile performance assessed by Mwand Lwor on early diastolic relaxation assessed by percent segmental relaxation during the first third of diastole in either right ventricular region (all p= not significant). There were also no observed characteristic alterations of free wall or septalfree wall end-diastolic pressure-dimension relationships with left heart assist. The pressure decay time constant decreased with increasing levels of left heart assist (51 ± 14, 49 ± 16, and 43 ± 11 msec, p< 0.05), which indicated an improvement in right ventricular isovolumic relaxation attributable to left heart assist. These data demonstrate that mechanical ventricular interactive effects during left heart assist are beneficial, but limited to isovolumic relaxation in the injured heart. The likely optimal method of left heart assist for postcardiotomy support should sufficiently augment cardiac output and arterial pressure but maintain left ventricular systolic pressure generation to preserve beneficial ventricular mechanical coupling. (J THORACCARDIOVASCSURG1994;108:477-86)
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