We prospectively evaluated the effects of positive end-expiratory pressure (PEEP) on the respiratory mechanical properties and hemodynamics of 10 postoperative adult cardiac patients undergoing mechanical ventilation while still anesthetized and paralyzed. The respiratory mechanics was evaluated by the inflation inspiratory occlusion method and hemodynamics by conventional methods. Each patient was randomized to a different level of PEEP (5, 10 and 15 cmH 2 O), while zero end-expiratory pressure (ZEEP) was established as control. PEEP of 15-min duration was applied at 20-min intervals. The frequency dependence of resistance and the viscoelastic properties and elastance of the respiratory system were evaluated together with hemodynamic and respiratory indexes. We observed a significant decrease in total airway resistance (13.12 ± 0.79 cmH 2 O l -1 s -1 at ZEEP, 11.94 ± 0.55 cmH 2 O l -1 s -1 (P<0.0197) at 5 cmH 2 O of PEEP, 11.42 ± 0.71 cmH 2 O l -1 s -1 (P<0.0255) at 10 cmH 2 O of PEEP, and 10.32 ± 0.57 cmH 2 O l -1 s -1 (P<0.0002) at 15 cmH 2 O of PEEP). The elastance (E rs ; cmH 2 O/l) was not significantly modified by PEEP from zero (23.49 ± 1.21) to 5 cmH 2 O (21.89 ± 0.70). However, a significant decrease (P<0.0003) at 10 cmH 2 O PEEP (18.86 ± 1.13), as well as (P<0.0001) at 15 cmH 2 O (18.41 ± 0.82) was observed after PEEP application. Volume dependence of viscoelastic properties showed a slight but not significant tendency to increase with PEEP. The significant decreases in cardiac index (l min -1 m -2 ) due to PEEP increments (3.90 ± 0.22 at ZEEP, 3.43 ± 0.17 (P<0.0260) at 5 cmH 2 O of PEEP, 3.31 ± 0.22 (P<0.0260) at 10 cmH 2 O of PEEP, and 3.10 ± 0.22 (P<0.0113) at 15 cmH 2 O of PEEP) were compensated for by an increase in arterial oxygen content owing to shunt fraction reduction (%) from 22.26 ± 2.28 at ZEEP to 11.66 ± 1.24 at PEEP of 15 cmH 2 O (P<0.0007). We conclude that increments in PEEP resulted in a reduction of both airway resistance and respiratory elastance. These results could reflect improvement in respiratory mechanics. However, due to possible hemodynamic instability, PEEP should be carefully applied to postoperative cardiac patients.

The pharmacokinetics of propranolol may be altered by hypothermic cardiopulmonary bypass (CPB), resulting in unpredictable postoperative hemodynamic responses to usual doses. The objective of the present study was to investigate the pharmacokinetics of propranolol in patients undergoing coronary artery bypass grafting (CABG) by CPB under moderate hypothermia. We evaluated 11 patients, 4 women and 7 men (mean age 57 ± 8 years, mean weight 75.4 ± 11.9 kg and mean body surface area 1.83 ± 0.19 m 2 ), receiving propranolol before surgery (80-240 mg a day) and postoperatively (10 mg a day). Plasma propranolol levels were measured before and after CPB by highperformance liquid chromatography. Pharmacokinetic Solutions 2.0 software was used to estimate the pharmacokinetic parameters after administration of the drug pre-and postoperatively. There was an increase of biological half-life from 4.5 (95% CI = 3.9-6.9) to 10.6 h (95% CI = 8.2-14.7; P < 0.01) and an increase in volume of distribution from 4.9 (95% CI = 3.2-14.3) to 8.3 l/kg (95% CI = 6.5-32.1; P < 0.05), while total clearance remained unchanged 9.2 (95% CI = 7.7-24.6) vs 10.7 ml min -1 kg -1 (95% CI = 7.7-26.6; NS) after surgery. In conclusion, increases in drug distribution could be explained in part by hemodilution during CPB. On the other hand, the increase of biological half-life can be attributed to changes in hepatic metabolism induced by CPB under moderate hypothermia. These alterations in the pharmacokinetics of propranolol after CABG with hypothermic CPB might induce a greater myocardial depression in response to propranolol than would be expected with an equivalent dose during the postoperative period.

CCO has a delayed response during acute hemodynamic changes induced by hemorrhage and resuscitation. When sudden changes in mean arterial pressure or in mixed venous oxygen saturation are detected, cardiac output must be estimated by the standard bolus thermodilution technique, not by CCO.