RIGHT-VENTRICULAR FUNCTION AFTER BRAIN-DEATH - RESPONSE TO AN INCREASED AFTERLOAD

Objective: A major cause of early postoperative morbidity and mortalit y after cardiac transplantation is right ventricular (RV) failure whic h is attributed to the inability of the donor's RV to acutely compensa te for the recipient's elevated pulmonary vascular resistance. This st udy was performed to determine: (1) the acute effects of brain death o n the RV function; and (2) the adaptation potential of the RV to a pro gressive increase in RV afterload. Methods: In 13 anesthetized, open-c hest dogs (eight with brain death vs. five control with sham operation ), brain death was induced by inflation of a subdural balloon catheter . Heart rate, RV systolic and end-diastolic pressure (RVSP, RVEDP), pu lmonary arterial pressure (PAP), and cardiac output (CO), and pressure -length loops (sonomicrometry) were recorded. Afterload increase was i nduced 2 h after brain death induction by constriction of the pulmonar y artery with an increase in KVP from 25 to 50 mmHg in 5 mmHg steps. R esults: Gushing phenomenon occurred within a few minutes after brain d eath induction, with a significant increase of HR (229 +/- 10 vs. 89 /- 6 min (-1), P < 0.001), CO (3.2 +/- 0.2 vs. 1.7 +/- 0.1 l/min, P < 0.001), PAP (30.4 +/- 2.5 vs. 15.5 +/- 1.3 mmHg, P(0.01), RVSP (55 +/- 5 vs. 23 +/- 2 mmHg, P < 0.001) and RVEDP (7.4 +/- 0.9 vs. 3.3 +/- 0. 6 mmHg, P < 0.001). All these values were also significantly (P < 0.01 ) higher than the time corresponding values of the control group. The analysis of the pressure-length loops showed a hypercontractile slate. Within 15-60 min, all parameters turned to baseline and remained stab le for up to 2 h. When afterload was increased progressively, RVEDP in creased markedly in the brain death and slightly in the control group (9.4 +/- 0.7 vs. 4.2 +/- 1.1 mmHg, P < 0.01, at RVSP = 50 mmHg). On th e other hand, the increase of peak positive dP/dt was significantly hi gher in the control group (430 +/- 37 vs. 644 +/- 55 mmHg/s, P < 0.01, at RVP = 50 mmHg). However, global RV pump function characterized by CO and stroke work was similar in both groups. While regional RV contr actility remained unchanged in the brain death group in terms of press ure-length relationships, RV contractility significantly increased in the control group. Conclusion: (1) Brain death per se does not result in an acute impairment of RV function. (2) While control animals adapt to an increased afterload by the homeometric, as well as the heterome tric regulation, after brain death, an increase in RV preload follows elevations in RV afterload by the Frank-Starling mechanism subserving the increased stroke work required to ensure unchanged pump function. (C) 1998 Elsevier Science B.V. All rights reserved.