Pulmonary vascular resistance and right ventricular function in morbid obesity in relation to gastric bypass surgery.

Objective: To investigate right ventricular function (RVF) during gastric bypass surgery in morbidly obese patients. To study the influence of obstructive sleep apnea syndrome on hemodynamics and RVF as a preoperative evaluation in morbidly obese patients.

Methods: Prospective study. Methods: Surgical patients at a university hospital. Methods: 14 morbidly obese patients undergoing gastric bypass surgery. Methods: Hemodynamic changes and RVF were investigated using a thermodilution ejection fraction volumetric catheter and the REF-1 computer.

Results: Hemodynamic parameters and RVF were measured: (1) before induction of anesthesia, awake, (2) after induction of anesthesia, (3) after opening the abdomen, and (4) after closing the abdomen. Esophageal pressure was measured in the midesophagus after induction of anesthesia with a camino catheter and its device. Morbidly obese patients with obstructive sleep apnea syndrome had significantly lower PaO2, higher PaCO2, and higher pulmonary artery (PA) pressure and pulmonary vascular resistance (PVR) compared with patients without sleep apnea (p < 0.05). However, there were no significant differences in heart rate, mean blood pressure, pulmonary capillary wedge pressure (PCWP), right ventricular ejection fraction (RVEF), and right ventricular end-diastolic volume. During gastric bypass procedure, PA pressure, PCWP, and PVR decreased significantly after opening the abdomen (p < 0.05). There were no significant changes in RVEF and cardiac index during gastric bypass procedure.

Conclusions: The presence of chronic hypoxemia and hypercarbia in our morbidly obese patients with obstructive sleep apnea syndrome while awake, causes significant increases in PA pressure and PVR. We also demonstrated that RVEF did not change significantly during gastric bypass procedure despite significant decreases in PA pressure, PCWP, and PVR after opening the abdomen. This decrease in PA pressure and PVR may be caused by decreases in pleural pressure reflected by a concomitant decrease in esophageal pressure.