BRAIN-DEATH ALTERS CARDIOPULMONARY HEMODYNAMICS AND IMPAIRS RIGHT-VENTRICULAR POWER RESERVE AGAINST AN ELEVATION OF PULMONARY VASCULAR-RESISTANCE

Citation
Hb. Bittner et al., BRAIN-DEATH ALTERS CARDIOPULMONARY HEMODYNAMICS AND IMPAIRS RIGHT-VENTRICULAR POWER RESERVE AGAINST AN ELEVATION OF PULMONARY VASCULAR-RESISTANCE, Chest, 111(3), 1997, pp. 706-711
Citations number
22
Categorie Soggetti
Respiratory System
Journal title
ChestACNP
ISSN journal
00123692
Volume
111
Issue
3
Year of publication
1997
Pages
706 - 711
Database
ISI
SICI code
0012-3692(1997)111:3<706:BACHAI>2.0.ZU;2-D
Abstract
Right ventricular (RV) failure, which is a leading cause of early morb idity and mortality following cardiac transplantation, is attributed t o the inability of the donor RV to acutely compensate for the recipien t's elevated pulmonary vascular resistance (PVR). Furthermore, the eff ect of donor brain death (BD) on RV function is unclear. The purpose o f this study was to investigate the effects of donor BD on RV function in the setting of elevated PVR. The interactions of the RV and its af terload, the pulmonary vasculature, and left atrial pressure were asse ssed. by measurements of pulmonary vascular energetics and their oscil latory nature using proximal ultrasonic pulmonary artery (PA) flow pro be and micromanometers in the proximal and distal PA in 20 mongrel dog s (25.8 +/- 0.4 kg, five control animals). A band was placed around th e distal PA (PA-systolic gradient >15 mm Hg). BD was induced by rising intracranial pressure and was validated neuropathologically. Data wer e collected at 0, 2, 4, and 6 h after BD in both banded and control an imals. Fourier analysis was used to calculate RV oscillatory power, me an power, and total power (TP). Comparison of changes due to handing w ere made to baseline measurements using multivariate analysis and pair ed Student's t test (p < 0.05). A significant twofold to fourfold incr ease in pulmonary impedance and PVR occurred with an acute rise in PA gradient. Control animals tolerated acute increases in PVR without sig nificant changes in TP. There was a significant increase of RV TP from 73 (+/- 11) to 98 (+/- 10) mW at baseline after the acute rise in PVR and impedance. After BD, the response to increased PVR and impedance was abolished significantly compared with baseline and control animals , suggesting a significant loss of compensatory TP to sustain pulmonar y vascular blood flow. The data indicate that BD is detrimental to RV mechanical function.