Obesity hypoventilation syndrome (OHS), defined as a PaO2 ≤ 55 mmHg and/or PaCo2 ≥ 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 < 0.0001, and pulmonary artery occlusion pressures (PAOP), p < 0.01. Eighteen OHS patients were restudied 3–9 months after gastric surgery. PaO2 increased from 50 ±; 10 to 69 ±; 14 mmHg, p < 0.0001, and PaCO2 decreased from 52 ±; 7 to 42 ±; 4 mmHg, p < 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 < 0.0001) and PAOP (from 17 ±; 7 to 12 ±; 6 mmHg, p < 0.01). Significant correlations were noted between PAP and PAOP (r = +0.8, p < 0.0001) and PAP and PaO2 (r = −0.6, p < 0.0001). Both left ventricular dysfunction, defined as a PAOP ±; 18 mmHg, as well as pulmonary artery vasoconstriction, defined as PAEDP > 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.