The effects of left heart assist on right ventricular muscle mechanics and ventricular coupling in the injured heart
Fujita, K.; McGrath, G.E.; Morita, T.; Robinson, B.L.; Davis, J.W.; Morris, J.J.
Journal of Thoracic and Cardiovascular Surgery 108(3): 477-486
1994
ISSN/ISBN: 0022-5223 PMID: 8078340 Document Number: 429480
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 septal-free 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 (M-w) and dimension axis intercept (L-w) of the linear preload recruitable stroke work relationship, and right ventricular isovolumic relaxation by the pressure decay time constant. Ischemia reduced M-w of both the free wall (38.3 +- 16.1 to 16.4 +- 4.2 erg cntdot cm-3 cntdot 10-3, p lt 0.01) and septal free wall (30.2 +- 12.7 to 13.4 +- 4.9 erg cntdot cm-3 cntdot 10-3, p lt 0.01) and shifted L-w rightward (1.3 +- 0.3 to 1.4 +- 0.3 mm, p lt 0.01, and 2.8 +- 0.8 to 3.0 +- 0.9 mm, p lt 0.01), which confirmed myocardial ischemic injury. There were no effects of left heart assist on free wall or septal-free wall systolic contractile performance assessed by M-w and L-w or 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 septal-free 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 lt 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 vermicular systolic pressure generation to preserve beneficial ventricular mechanical coupling.