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Eur J Cardiothorac Surg 1998;13:449-458
© 1998 Elsevier Science NL

Right ventricular function after brain death: Response to an increased afterload¹

^a Department of Cardiac Surgery, University of Heidelberg, Im Neuenheimer Feld 326, 69120 Heidelberg, Germany
^b Department of Cardiac, Thoracic and Vascular Surgery, Hannover Medical School, Hannover, Germany

Received 29 September 1997; received in revised form 29 December 1997; accepted 14 January 1998.

Corresponding author. Tel.: +49 6221 566111; fax: +49 6221 565585; e-mail: szabo@novsrv1.pio1.uni-heidelberg.de

Objective: A major cause of early postoperative morbidity and mortality after cardiac transplantation is right ventricular (RV) failure which is attributed to the inability of the donor’s RV to acutely compensate for the recipient's elevated pulmonary vascular resistance. This study was performed to determine: (1) the acute effects of brain death on the RV function; and (2) the adaptation potential of the RV to a progressive increase in RV afterload. Methods: In 13 anesthetized, open-chest 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), pulmonary arterial pressure (PAP), and cardiac output (CO), and pressure-length loops (sonomicrometry) were recorded. Afterload increase was induced 2 h after brain death induction by constriction of the pulmonary artery with an increase in RVP from 25 to 50 mmHg in 5 mmHg steps. Results: Cushing phenomenon occurred within a few minutes after brain death 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 state. Within 15–60 min, all parameters turned to baseline and remained stable for up to 2 h. When afterload was increased progressively, RVEDP increased 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 the other hand, the increase of peak positive dP/dt was significantly higher 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 contractility remained unchanged in the brain death group in terms of pressure–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 heterometric 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.

Key Words: Brain death • Right ventricle • Contractility • Regulation • Frank-Starling mechanism • Transplantation

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