Abstract
Obesity hypoventilation syndrome (OHS), defined as a PaO2 less than or equal to 55 mmHg and/or PaCo2 greater than or equal to 47 mmHg, was found in approximately 8% of morbidly obese patients undergoing gastric surgery for morbid obesity and was frequently associated with clinically significant pulmonary hypertension and cardiac dysfunction. Forty-six morbidly obese patients, 26 with and 20 without OHS, underwent preoperative pulmonary artery catheterization. Although the two groups had similar values for percent ideal body weight, blood pressure, and cardiac index, the OHS patients had significantly higher mean pulmonary artery pressures (PAP), p less than 0.0001, and pulmonary artery occlusion pressures (PAOP), p less than 0.01. Eighteen OHS patients were restudied 3-9 months after gastric surgery. PaO2 increased from 50 +/- 10 to 69 +/- 14 mmHg, p less than 0.0001, and PaCO2 decreased from 52 +/- 7 to 42 +/- 4 mmHg, p less than 0.0001), after the loss of 42 +/- 19% excess weight. These changes were associated with significant decreases in PAP (from 36 +/- 14 to 23 +/- 7 mmHg, p less than 0.0001) and PAOP (from 17 +/- 7 to 12 +/- 6 mmHg, p less than 0.01). Significant correlations were noted between PAP and PAOP (r = +0.8, p less than 0.0001) and PAP and PaO2 (r = -0.6, p less than 0.0001). Both left ventricular dysfunction, defined as a PAOP greater than or equal to 18 mmHg, as well as pulmonary artery vasoconstriction, defined as PAEDP greater than 5 mmHg above PAOP, contributed to pulmonary hypertension in OHS patients. In conclusion, weight loss after gastric surgery for morbid obesity significantly improved arterial blood gases and hemodynamic function in OHS patients.