LOW CARDIAC-OUTPUT ABOLISHES CARDIOVASCULAR-RESPONSES TO INFRARENAL AORTIC CROSS-CLAMPING IN THE PIG

Citation
H. Seemanlodding et al., LOW CARDIAC-OUTPUT ABOLISHES CARDIOVASCULAR-RESPONSES TO INFRARENAL AORTIC CROSS-CLAMPING IN THE PIG, Acta anaesthesiologica Scandinavica, 41(2), 1997, pp. 232-238
Citations number
27
Categorie Soggetti
Anesthesiology
ISSN journal
00015172
Volume
41
Issue
2
Year of publication
1997
Pages
232 - 238
Database
ISI
SICI code
0001-5172(1997)41:2<232:LCACTI>2.0.ZU;2-A
Abstract
Background: Previous data suggest that preoperative myocardial dysfunc tion is associated with an altered cardiac response to infra-renal aor tic cross-clamping (AXC). This study was designed to further explore h ow acute reductions in stroke volume and cardiac output influence the systemic, preportal and renal circulatory responses to AXC. Methods: I n chloralose-anesthetized normoventilated pigs, graded increases in pe ricardial pressure (P-PERICARD) were obtained by local infusions of de xtran. Measurements included cardiac output (CO, thermodilution), mean blood pressure proximal to the aortic clamping site (MAP(PROX)) and u ltrasonic flowmetry for portal (Q(PORT)) and renal (Q(REN)) blood flow s. In all animals, measurements were made a) prior to AXC, b) at the e nd of a 5 min AXC period and, c) 5 min following declamping. These rec ordings were repeated during control (P-PERiCARD 0 cmH(2)O) and during stages with increased P-PERICARD (4 and 8 cmH(2)O, respectively). Res ults: Pericardial infusions of dextran produced hemodynamic responses that in magnitude were proportional to P-PERICARD levels. Stroke volum e, CO and mean arterial pressure decreased, while systemic vascular re sistance (SVR) increased. In the preportal tissues, vascular resistanc e increased and Q(PORT) decreased. Similarly, in the kidney, vascular resistance and Q(REN) decreased, but only at a P-PERICARD of 8 cmH(2)O . At control, AXC increased SVR, MAP(PROX), Q(PORT) and both renal and preportal vascular resistances. When P-PERICARD was increased to 4 cm H2O, the responses to AXC concerning SVR and MAP(PROX) were not signi ficantly altered, while renal and preportal circulatory responses were blunted. At stages with a P-PERICARD of 8 cmH(2)O, we could not demon strate any circulatory responses to AXC. Conclusions: AXC-induced syst emic, preportal and renal circulatory responses are inhibited during a condition of acutely lowered cardiac output. (C) Acta Anesthesiologic a Scandinavica 41 (1997).