Several well controlled epidemiologic and hemodynamic studies suggest that about 20% of
sleep apnea syndrome (SAS) patients will have
chronic obstructive pulmonary disease (
COPD), and the majority of these patients (with combined diseases) will have
pulmonary hypertension. Indeed it has been suggested that only patients with underlying
hypoxemia, such as that from
COPD, will develop right
heart failure in the OSA setting. Experience shows that
apnea/
COPD patients will have severe
hypersomnolence associated with the OSA,
cough and
dyspnea with the airways disease, and
edema and plethora related to chronic
hypoxemia. Many patients present with
respiratory failure and are diagnosed at the time of initial intubation and
mechanical ventilation. Episodic nocturnal
hypoxemia may be worsened by a steeper rate of desaturation due to lower alveolar and blood
oxygen stores, and longer
apneas perhaps contributed to by depressed chemosensitivity. Daytime
hypoxemia may also add to the severe hemodynamic disturbances. Since
COPD cannot be cured, aggressive treatment of SAS is critical. Past studies have shown that
tracheostomy or nasal CPAP in this setting not only leads to resolution of episodic nocturnal desaturation but may lead to rapid improvement in daytime oxygenation in many patients.
Pulmonary hypertension and other measures of cardiopulmonary function improve when
apnea is cured. Elimination of the SAS may disclose nonapneic REM related desaturation that could require supplemental
oxygen therapy in addition to
tracheostomy or nasal CPAP. Pulmonary function testing in SAS patients with smoking histories, followed by aggressive treatment of SAS, is recommended.