The currently used coronary artery bypass graft predictive models, although generally accurate, have significant shortcomings and should be used with caution. The predicted mortality rate following coronary artery bypass graft surgery varied by a factor of 3.3 from lowest to highest, making the choice of model a critical factor when assessing outcome. The use of these models for individual patient risk estimations is risky because of the marked discrepancies in individual predictions created by each model.

During the period July 1983 through December 1984, aminoglycoside-resistant Acinetobacter calcoaceticus var anitratus (ACA) were isolated from 98 patients in a university hospital. Eighty-seven percent of patients (85/98) acquired aminoglycoside-resistant ACA in the intensive care unit (ICU) and 92% (90/98) of all initial isolates were from sputum. ICU patients with respiratory colonization/infection with aminoglycoside-resistant ACA were compared with matched ICU controls with other gram-negative rods in sputum. Compared with controls, the duration of ICU stay prior to colonization/infection with aminoglycoside-resistant ACA was significantly longer for cases (14.7 days v 5.9 days, P = 0.002). Although exposures to devices and procedures were not significantly different for the two groups, cases received respiratory therapy significantly longer than did controls (14.7 days v 6.6 days, P = 0.006). Prior to isolation of aminoglycoside-resistant ACA in sputum, cases received more cephalosporins than did controls (1.9 v 1.2, P = 0.018); aminoglycoside usage in the two groups was comparable but cases tended to have received aminoglycoside for longer durations before colonization/infection than had controls (9.0 days v 6.1 days, P = 0.08). Following sputum isolation of ACA, 6 of 22 cases developed ACA bacteremia compared with bacteremia in 2 of 22 controls. We conclude that factors predisposing to colonization/infection with aminoglycoside-resistant ACA were extended ICU care, prolonged respiratory therapy, and prior therapy with cephalosporins and aminoglycoside. In addition, ACA may be a more common cause of secondary bacteremia than previously appreciated.

The simultaneous measurements of mixed venous oxygen saturation (SvO2) and right ventricular ejection fraction (RVEF) have now made it possible to precisely define and correlate the various hemodynamic changes that occur during abdominal aortic operations. Twenty-five patients undergoing infrarenal abdominal aortic aneurysm repair were examined with a pulmonary artery catheter capable of continuously measuring SvO2 and RVEF. With aortic clamping, significant reductions in cardiac index, stroke volume index, and right ventricular end-diastolic volume index (RVEDVI) were noted, while RVEF remained unchanged. Following unclamping of the aorta, a significant reduction in SvO2 occurred, accompanied by an increase in mean pulmonary artery pressure and in pulmonary vascular resistance. Despite the increase in afterload, RVEDVI and RVEF did not change after unclamping. These preliminary data suggest that right ventricular function is preserved during abdominal aortic aneurysm repair.

During the period July 1983 through December 1984, aminoglycoside-resistant Acinetobacter calcoaceticus var anitratus (ACA) were isolated from 98 patients in a university hospital. Eighty-seven percent of patients (85/98) acquired aminoglycoside-resistant ACA in the intensive care unit (ICU) and 92% (90/98) of all initial isolates were from sputum. ICU patients with respiratory colonization/infection with aminoglycoside-resistant ACA were compared with matched ICU controls with other gram-negative rods in sputum. Compared with controls, the duration of ICU stay prior to colonization/infection with aminoglycoside-resistant ACA was significantly longer for cases (14.7 days v 5.9 days, P = 0.002). Although exposures to devices and procedures were not significantly different for the two groups, cases received respiratory therapy significantly longer than did controls (14.7 days v 6.6 days, P = 0.006). Prior to isolation of aminoglycoside-resistant ACA in sputum, cases received more cephalosporins than did controls (1.9 v 1.2, P = 0.018); aminoglycoside usage in the two groups was comparable but cases tended to have received aminoglycoside for longer durations before colonization/infection than had controls (9.0 days v 6.1 days, P = 0.08). Following sputum isolation of ACA, 6 of 22 cases developed ACA bacteremia compared with bacteremia in 2 of 22 controls. We conclude that factors predisposing to colonization/infection with aminoglycoside-resistant ACA were extended ICU care, prolonged respiratory therapy, and prior therapy with cephalosporins and aminoglycoside. In addition, ACA may be a more common cause of secondary bacteremia than previously appreciated.