A 50-year-old obese male developed cor pulmonale secondary to repeated obstructive sleep apnea and accompanying marked oxygen desaturation. His ventilatory response to CO2 was depressed in sleep and sleep apnea continued until PaCO2 reached about 60 torr. Huge tonsils also played an important role in obstrucion of his upper airway in sleep apnea. Marked degrees of hypoxemia occurred transiently with each episode of apnea, with SaO2 values falling from 94 to 76%. Bradyarrhythmia (nodal rhythm) appeared and mean pulmonary arterial pressure rose progressively from 15 to 26mmHg with developement of hypoxemia. This pulmonary hypertension was suggested to be a main cause of cor pulmonale in this case.
