Search

Background: Both preoperative left ventricular dysfunction and postoperative renal function deterioration are associated with increased long-term mortality after cardiac surgery. The influence of preoperative left ventricular dysfunction on postoperative renal dysfunction and long-term mortality is not defined., Methods: We collected data from 641 consecutive patients undergoing coronary bypass surgery with cardiopulmonary bypass in 1991 at our institution. Prospective follow-up was through to July 2004., Results: In-hospital mortality was 2.7% (17 of 641). During follow-up, 248 (40%) patients discharged alive died (5 and 10 yr survival 90% and 70%, respectively). On univariate analysis, preoperative left ventricular dysfunction (ejection fraction <50%) and an increase in serum creatinine > or =25% in the first postoperative week were associated with long-term mortality. The associated mortality risk was additive in predominantly non-overlapping patients groups: the hazard ratio (HR) for renal function deterioration only was 1.41 [95% confidence interval (CI) 0.95-2.32, P=0.083; n=64] and for left ventricular dysfunction only 1.71 (95% CI 1.26-2.95, P=0.0026; n=73). In patients in whom both were present, HR was 3.23 (95% CI 2.52-20.28, P<0.0001; n=20). Although postoperative renal dysfunction was associated with left ventricular dysfunction (P=0.008), both left ventricular dysfunction and postoperative renal function deterioration were independently associated with long-term mortality on multivariate analysis, as were age and the use of venous conduits., Conclusions: Both postoperative renal function deterioration and preoperative left ventricular dysfunction independently identify largely non-overlapping groups of patients with increased long-term mortality after coronary bypass surgery. In the group of patients with both factors present, the mortality risks appear additive.

Background: In cardiac surgery with cardiopulmonary bypass (CPB), corticosteroids are administered to attenuate the physiological changes caused by the systemic inflammatory response. The effects of corticosteroids on CPB-associated renal damage have not been documented. The purpose of this study was to evaluate the effects of dexamethasone on perioperative renal dysfunction in patients undergoing cardiac surgery with CPB., Methods: Renal damage was prospectively studied in 20 patients without concomitant morbidity undergoing coronary artery surgery with CPB. Patients were randomized in a double-blind fashion to receive dexamethasone or placebo. Markers of glomerular function (creatinine clearance) and damage (microalbuminuria), and markers of tubular function (fractional excretion of sodium and free water clearance) and damage (N-acetyl-beta-D glucosaminidase (NAG)) were evaluated in addition to plasma and urinary glucose levels. Plasma and urinary specimens were obtained at the following time periods: (1) baseline, during the 12 h before surgery; (2) skin incision before heparinization; (3) from heparinization until the end of CPB; (4) during the 2 h following weaning from CPB; (5) in the intensive care unit from 2 to 6 h after weaning of CBP; (6) and from 36 to 60 h after weaning of CPB., Results: CPB was associated with an increase in markers in the placebo group, which returned to baseline during the second postoperative day, demonstrating a transient impairment of glomerular and tubular renal function. Similar patterns were observed in patients treated with dexamethasone. While postoperative glycosuria was significantly higher in the dexamethasone-treated group, no other differences between groups were observed., Conclusion: Dexamethasone administration before CPB has no protective effect on perioperative renal dysfunction in low-risk cardiac surgical patients.

Objective: To study the need for suppression of gastric acid secretion for reliable intragastric partial pressure of carbon dioxide (PCO2) tonometry by evaluating the effect of an oral dose of sodium bicarbonate before and after administration of the H2-blocker ranitidine to mimic CO2 generation following the buffering of acid by bicarbonate in patients after cardiac surgery., Design: Prospective, open, non-randomized clinical study., Setting: Cardiothoracic intensive care unit at a university hospital., Patients: 10 patients after elective coronary artery bypass surgery., Interventions: An oral dose of 500 mg sodium bicarbonate before and after acid secretion suppression by 100 mg ranitidine as an intravenous bolus given at approximately 3 h after surgery (day 0) and on the first postoperative day (day 1)., Measurements and Results: Intragastric PCO2 (iPCO2; tonometry), gastric juice pH (aspirate) and arterial blood gas values were measured. On day 0, the iPCO2 was 25 +/- 5 mmHg before and 31 +/- 5 mmHg after the bicarbonate dose, 29 +/- 5 mmHg after ranitidine infusion, and 31 +/- 5 mmHg after the bicarbonate dose following the ranitidine infusion (NS). On day 1, the basal iPCO2 was 32 +/- 4 mmHg and it increased to 56 +/- 25 mmHg following bicarbonate (p < 0.01). After ranitidine, the iPCO2 was 33 +/- 4 mmHg before and 40 +/- 14 mmHg after bicarbonate (NS). Basal gastric juice pH was > 4 in nine of ten patients on day 0 and > 4 in seven of ten patients on day 1., Conclusions: Pharmacological suppression of gastric acid secretion is mandatory for reliable iPCO2 tonometry after cardiopulmonary bypass surgery, even when gastric acid secretion is transiently inhibited. In fact, gastric acid secretion was inhibited immediately after surgery, but returned on the first postoperative day in most patients, as judged from the bicarbonate back titration of gastric acid, even when gastric juice pH was relatively high.