Determinants of Cardiovascular Stability During Abdominal Aortic Aneurysmectomy (AAA)

Abstract
Patients undergoing abdominal aortic aneurysmectomy (AAA) develop depressed cardiac function during aortic clamping. The importance of volume status and thromboxane (Tx) mediated declines in cardiac contractility in determining this event was studied. In a blinded fashion, patients received the cyclo-oxy-genase inhibitor ibuprofen 12 mg/kg by mouth (n = 11) or a placebo (n = 15), 1.5 hours prior to surgery. In the placebo group levels of 6-keto-PGF]a, the hydrolysis product of pros-tacyclin (PGI2) rose from 20 ± 10 to 1170 + 80 pg/ml (p < 0.05) soon after incision. Concentrations of TxB2, the stable hydrolysis product of TxA2, were unchanged until 30 minutes after the aorta was clamped when arterial TxB2 concentrations rose from 90 ± 20 to 230 ± 30 pg/ml (mean ± SEM) (p < 0,05). A pulmonary source for PGI2 and TxA2 was indicated by the observation that arterial 6-keto-PGF1(, and TxB2 levels exceeded those in pulmonary arterial blood by 180 ± 50 and 110 + 30 pg/ml, respectively (p < 0.05). Levels of TxB2 in circulating platelets remained unchanged from baseline in the placebo group. During aortic clamping, cardiac index (CI) fell 0.7 ± 0.2 1/min m2 (p < 0.05) in placebo treated patients, and there was a 6% decline in plasma contractility as bioassayed with a rat papillary muscle (p < 0.05). Placebo patients entered surgery with a PAWP ≥10 mmHg (mean 13 mm). Ibuprofen suppressed production of TxB2, such that 30 minutes after aortic clamping TxB2 was 70 ± 30 pg/ml, a value lower than control patients (p < 0.05). Further, plasma no longer depressed contractility of the papillary muscle. Five patients given ibuprofen had an initial pulmonary arterial wedge pressure (PAWP) of 10 mmHg or greater (mean 12 mmHg). During aortic clamping there was an insignificant decrease in CI of 0.2 ± 0.11/min m2. This was in contrast to the CI decrease in six other ibuprofen treated patients of 0.9 ± 0.2 1/min m2 whose PAWP at the start of surgery was <10 mmHg (mean 6 mmHg) (p < 0.05), and to placebo patients whose initial PAWP was ≥10 (p < 0.05). Platelet counts fell from 185,000 to 121,000/mm3 in placebo patients (p < 0.05), but did not fall when ibuprofen was given. Creatinine concentrations were unaffected by ibuprofen. Blood replacement in placebo and ibuprofen patients was similar, 1.90 ± 0.20 and 0.65 ± 0.15 1, respectively. Results indicate that CI