[Lung inflation or mechanical ventilation in extracorporeal circulation?]

Extracorporeal circulation (ECC), with its shock-like pulmonary perfusion, leads to pathomorphologic and functional pulmonary changes, the postperfusion syndrome. This study investigated the effects of different types of ventilation during ECC on postoperative pulmonary function and the resulting pulmonary blood gas changes. METHOD. Thirty patients scheduled for aortocoronary bypass surgery were studied. Patients with pre-operative left ventricular end-diastolic pressures exceeding 15 mmHg or signs of right ventricular failure, pulmonary hypertension, or pre-existing pulmonary disease were excluded. The patients were randomly assigned to one of the following three groups: Group 1 (n = 10): static pulmonary inflation during ECC, PEEP 5-10 cm H2O, F1O2 1.0; Group 2 (n = 10): low-frequency ventilation during ECC, rate 10/min, PEEP 5 cm 5H2O, F1O2 1.0; Group 3 (n = 10): medium-frequency ventilation during ECC, rate 120/min, PEEP 5 cm 5H2O, F1O2 1.0. The measurements were made under relative steady-state conditions before the start of surgery and postoperatively after an equilibrium phase of at least 15 min. During ECC using a bubble oxygenator (Bentley BOS 10 S) in moderate hypothermia, blood was aspirated from the pulmonary artery during inflation of the wedge balloon and blood gases were analyzed. Postoperative changes in pulmonary function were evaluated by venous admixture (QVA/Qt); changes in pulmonary vascular resistance after ECC were determined using the pulmonary pressure-flow relationship. RESULTS. In group 1, QVA/Qt rose significantly from 9.6 +/- 2.9% preoperatively to 13.6 +/- 3.5% postoperatively (P less than 0.05, t-test for paired samples). In groups 2 and 3, postoperative QVA/Qt was significantly lower than preoperative QVA/Qt (P less than 0.05; group 2: preoperative 11.9 +/- 3.5%, postoperative 8.1 +/- 2.6%; group 3: preoperative 11.9 +/- 3.0%, postoperative 7.8 +/- 3.2%; Fig. 1). The postoperative pulmonary pressure-flow relationship changed similarly in all three groups (Fig. 2). During ECC, blood aspirated from the pulmonary artery during inflation of the wedge balloon was fully oxygenated with a hematocrit approximating that of arterial blood. In ventilated patients, pO2 during ECC was higher in pulmonary arterial blood than in arterial blood. Pulmonary ventilation during ECC did not lead to pulmonary arterial alkalosis. CONCLUSIONS. Pulmonary ventilation during ECC can prevent a post-operative increase in venous admixture. ECC-related pulmonary vascular changes were not affected by ventilation. Middle-frequency ventilation offers no advantage over low-frequency ventilation during ECC, except that the operating field is more quiet.