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European Journal of Cardio-Thoracic Surgery, Vol 11, 609-615, Copyright © 1997 by European Association for Cardio-thoracic Surgery

ARTICLES

Right ventricular function in the donor heart

SW Kendall, HB Bittner, DS Peterseim, KA Campbell and P Van Trigt
Department of General and Cardiothoracic Surgery, Duke University Medical Center, Durham, NC 27710, USA.

OBJECTIVES: Early morbidity and mortality post cardiac transplantation is frequently caused by right ventricular failure; this is usually attributed to an elevated pulmonary vascular resistance in the recipient. Brain death in the donor is recognised as causing left ventricular dysfunction, but its effects on the right ventricle have not previously been studied. The aim of this study was to investigate right ventricular function following brain death, using a canine model. METHODS: The hearts of 33 dogs were instrumented with micromanometers, flow probes and dimension transducers to measure minor/major axes, and right and left ventricular free wall to septal distances. Left ventricular volume was calculated according to the prolate ellipsoid model and right ventricular volume was calculated according to the shell subtraction method. Systolic function for left and right ventricles was analysed by plotting ventricular stroke work vs. end- diastolic volume during a caval occlusion (preload-independent recruitable stroke work PRSW). Brain death was instigated by inflation of a subdurally placed intracranial balloon; subsequently blood pressure was maintained with intravenous fluid whilst no inotropic medications were given. Data were collected at baseline, and at 2 and 4 h thereafter. A two-tailed paired Student's t-test was applied to compare post-brain death data with baseline measurements. RESULTS: All animals had an initial hyperdynamic response post brain death ensued by the development of diabetes insipidus. Brain stem death was validated by neuropathological examination at the termination of the experiments. Right and left ventricular systolic function had deteriorated significantly 2 h post brain death by 34.4% (+/- 5.1%, P < 0.001) and 20.4% (+/- 3.4%, P < 0.001), respectively, from baseline PRSW [RV = 23.6 erg.10(3) (+/- 1.5), LV = 76.2 erg.10(3) (+/- 3.5)]. This deterioration remained at 4 h post brain death (29.4% (+/- 4.9%, P < 0.001) and 21.2% (+/- 4.3%, P < 0.001), respectively). (The results are expressed as mean and S.E.M.). CONCLUSIONS: Brain death causes a significant decrease in left and right ventricular function. The injury to the right ventricle is more prominent than the left ventricle, and at 2 h post brain death it is significantly greater. Failure of the right ventricle post transplantation in clinical practice may be related to this brain death induced injury. Further studies are required to investigate the mechanisms of this injury.

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