Hämodynamische instabilität nach hirntod I: Auswirkungen der veränderten nachlast

Translated title of the contribution: Impact of altered loading conditions on hemodynamic instability and cardiac dysfunction in the brain dead organ donor

V. Buhmann, T. Hackert, C. Sebening, G. Szabó, C. F. Vahl, S. Hagl

Research output: Contribution to journalArticle

Abstract

Objective: Brain death associated hemodynamic instability in the potential organ donor has become an important topic of transplantation research because the major limiting factor of clinical heart transplantation is the shortage of suitable donor organs. While the underlying mechanisms remain incompletely understood, the clinical relevance of reduced cardiac function in the brain dead donor is the subject of controversial discussion. On the basis of our previous studies (18-19), we hypothesized that altered loading conditions play a key role in the changes of cardiac function after brain death. Methods Brain death was induced by inflation of a subdural balloon catheter. The hearts were investigated in vivo allowing interaction between left ventricular contractility and arterial load. After pericardiotomy and isolation of the great vessels a perivascular electromagnetic flow probe was attached to the ascendent aorta. Aortic pressure and right atrial pressure were monitored by 5F Millar catheter tip manometers. Left ventricular pressure-volume loops were obtained by a combined 6F Millar conductance-pressure catheter and the slope of the endsystolic pressure-volume relationship (Ees), arterial elastance (Ea), stroke work (SW), pressure-volume area (PVA), ventriculo-arterial coupling ratio (VAC) and mechanical efficiency (Eff) were calculated. Results: Brain death induction led to the well-known initial hyperdynamic reaction with a significant increase of most hemodynamic variables except LVEDP and RAP. Immediately after the acute phase AoP, SVR, SW and PVA decreased significantly followed by a slower decrease of LVSP and dP/dtmax. CO returned to baseline level and remained constant. Four hours after induction of brain death Ees (4.07 ± 0.51 vs. 8.06 ± 1.09 mmHg/ml, P < 0.05) and Ea (3.17 ± 0.39 vs. 4.42 ± 0.30 mmHg/ ml, P < 0,05) showed a parallel decrease in comparison to baseline. The ventriculo- arterial coupling ratio (0.78 ± 0.09 vs. 0.65 ± 0.14 n.s.) did not show any significant changes. Similarly, the parallel decrease of SW and PVA resulted in unchanged mechanical efficiency (73.4 ± 2.1% vs. 76.8 ± 3.7% n.s.). Conclusion BD induction leads to an initial hyperdynamic reaction followed by hemodynamic instability. The fact that the ventriculo- arterial coupling ratio and mechanical efficiency remained constant indicates that decreased contractility reflects to decreased arterial elastance after brain death. Therefore, reduced contractile function after brain death at a decreased afterload may contribute to stroke work optimization. If cardiac dysfunction after brain death is related to altered loading conditions and not to neuro-humorally mediated primary cardiomyocyte damage, a part of the rejected donor hearts may be suitable for organ transplantation. Therefore, cardiac function, especially if characterized by load-dependent parameters, should be carefully evaluated. Optimization of donor management may also contribute to unmasking "true" cardiac function (21) and increase the donor heart pool.

Original languageGerman
Pages (from-to)79-85
Number of pages7
JournalZeitschrift fur Herz-, Thorax- und Gefasschirurgie
Volume16
Issue number2
DOIs
Publication statusPublished - May 9 2002

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Keywords

  • Afterload
  • Arterial coupling
  • Brain death
  • Contractility
  • Ventriculo

ASJC Scopus subject areas

  • Surgery
  • Pulmonary and Respiratory Medicine
  • Cardiology and Cardiovascular Medicine

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