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(Chest. 2001;120:894-899.)
© 2001 American College of Chest Physicians

Nocturnal Hypoxemia Is Common in Primary Pulmonary Hypertension*

Albert L. Rafanan, MD; Joseph A. Golish, MD, FCCP; Dudley S. Dinner, MD; L. Kathleen Hague, RN and Alejandro C. Arroliga, MD, FCCP

* From St. Vincent Mercy Medical Center Hospital and the Medical College of Ohio (Dr. Rafanan), Toledo, OH; and the Departments of Pulmonary and Critical Care Medicine (Drs. Golish and Arroliga, and Ms. Hague), and Neurology (Dr. Dinner), The Cleveland Clinic Foundation, Cleveland, OH.

Correspondence to: Alejandro C. Arroliga, MD, FCCP, Head, Section of Critical Care Medicine, Department of Pulmonary and Critical Care Medicine, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195-0001; e-mail: arrolia{at}ccf.org

Study objective: Unsuspected sleep-related respiratory events are common in patients with severe pulmonary disease. Sleep in patients with primary pulmonary hypertension (PPH) has not been studied (to our knowledge). The purpose of this study was to measure the prevalence of respiratory disturbances and nocturnal hypoxemia during the sleep of patients with PPH.

Setting: Tertiary-care referral hospital.

Design: Retrospective review.

Patients: Thirteen patients with PPH.

Measurements: All patients underwent a single-night comprehensive polysomnogram study. Patients who spent > 10% of the total sleep time with oxygen saturation by pulse oximetry (SpO2) at < 90% or who needed oxygen to maintain their SpO2 level at > 90% were classified as nocturnal desaturators. Analysis was performed to determine which clinical variables (ie, demographics, body mass index, spirometry, diffusion capacity, right heart catheterization pressures, 6-min walk test, arterial blood gas levels, resting and walking SpO2 levels, and polysomnogram variables) would predict nocturnal desaturation. Statistical significance was considered when p values were < 0.05.

Results: Of the 13 patients in the study, 10 (77%) were nocturnal desaturators. All patients had normal apnea indexes, but two had mild elevations of the hypopnea index (< 15 episodes per hour). Nocturnal desaturations occurred independently of apneas or hypopneas. Six patients who did not have O2 titration during sleep spent > 25% of sleep time with SpO2 < 90%. The mean (± SD) variables that were significantly different between desaturators (10 patients) and nondesaturators (3 patients) were FEV1 (70.1 ± 9.1% predicted vs 98.1 ± 15.1% predicted, respectively; p = 0.002), resting PaO2 (61.8 ± 16.1 vs 90.3 ± 2.3 mm Hg, respectively; p = 0.001), alveolar-arterial oxygen pressure difference (P[A-a]O2) (40.5 ± 20.5 vs 12.2 ± 7.2 mm Hg, respectively; p = 0.048), resting SpO2 (91.6 ± 5.4% vs 98.7 ± 2.3%, respectively; p = 0.038), and walking SpO2 (83.8 ± 9.3% vs 95.3 ± 1.2%, respectively; p = 0.002). The mean hemoglobin level was higher in the group of nocturnal desaturators than in the group of nondesaturators (10.43 ± 0.31 vs 13.95 ± 0.98 g/dL, respectively; p < 0.0001).

Conclusion: Seventy-seven percent of patients with PPH have significant nocturnal hypoxemia that is unrelated to apneas and hypopneas. Nocturnal desaturation occurs more frequently in patients with higher P(A-a)O2 values and lower FEV1 values, resting arterial PaO2 and SpO2 values, and walking SpO2 values.

Key Words: nocturnal hypoventilation • obstructive sleep apnea • oxygen therapy • pulmonary hypertension • sleep




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