Long-Term Effects of Treatment with Nasal Continuous Positive Airway Pressure on Lung Function in Patients with Overlap Syndrome

Abstract

We assessed the effects of chronic nasal continuous positive airway pressure (CPAP) therapy on lung function in a series of unselected patients with overlap syndrome, and we determined whether there were differences in the response induced by CPAP between hypercapnic (PaCO2 > or =45 mm Hg) and eucapnic patients with overlap syndrome. The study population included 55 unselected patients (48 men, mean age of 58.5 +/- 10.5 years) with a concurrent diagnosis of chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea-hypopnea syndrome (OSAHS) who had been referred to the Department of Pulmonology of our hospital over 2 consecutive years and in whom work-up studies resulted in the prescription of nasal CPAP therapy. An apnea-hypopnea index (AHI) greater than or equal to 10 in the cardiorespiratory polygraphy was required for the diagnosis of OSAHS. A forced expiratory volume in one second (FEV1) less than 80% and FEV1-forced vital capacity (FVC) ratio less than 70% of the reference values were required for the diagnosis of COPD. Control lung function studies and arterial blood gas measurements were performed at 6 and 18 months of CPAP therapy. These patients with overlap syndrome accounted for 28.5% of all patients with OSAHS treated with CPAP during the study period. The mean AHI was 37.3 +/- 26.1 and the mean CPAP level 7.3 +/- 1.3 cm H2O. Thirty-three patients were hypercapnic (PaCO2 > or = 45 mm Hg) and 22 eucapnic. The hypercapnic group had higher AHI value (44.3 +/- 26.9) than the eucapnic group (28.6 +/- 21.9) (P < 0.05). After 6 months of CPAP therapy, there were statistically significant increases in PaO2, FEV1, and FVC, accompanied by significant decreases in PaCO2, serum bicarbonate levels, and alveolar-arterial oxygen difference. Response of overlap syndrome patients to CPAP therapy was superior in the hypercapnic group, particularly in relation to improvement of arterial blood gases. However, statistically significant differences in all parameters for the comparison between 6 and 18 months were not recorded.

CPAP and survival in moderate-to-severe obstructive sleep apnoea syndrome and hypoxaemic COPD

“…Previous studies have shown that the use of CPAP improves lung function, gas exchange and respiratory muscle function, and decreases the risk of hospitalisations in patients with COPD plus OSAS [13,14]. It is also possible that CPAP protects against cardiovascular disease, particularly since it has been shown that CPAP reduced cardiovascular mortality in a population of OSAS patients referred for CPAP treatment [18].…”

“…Treatment with continuous positive airway pressure (CPAP) improves pulmonary function and gas exchange in patients with overlap OSAS/ COPD [13,14]. CPAP treatment may also reduce mortality in patients with OSAS who do not have clinically evident COPD [15][16][17][18].…”

Sleep Disorders in Chronic Obstructive Pulmonary Disease: Etiology, Impact, and Management

“…112 Indeed, apart from the expected improvement in sleep, spirometric parameters (FEV1, FVC) and gas exchange (PaO 2 , PaCO 2 ) appear to improve with CPAP treatment of patients with OSA and COPD. 141 CPAP treatment for OSA also reduces the number of COPD-related severe exacerbations and hospital admissions.…”

Noninvasive Positive-Pressure Ventilation Therapy in Patients with COPD

“…NPPV effectively unloads the respiratory muscles by increasing tidal volume, decreasing the respiratory rate, and decreasing the diaphragmatic work of breathing, which translates into an improvement in oxygenation, a reduction in hypercapnia, and an improvement in dyspnea. NPPV treatment counterbalances auto-PEEP, assists inspiration, reduces transdiaphragmatic pressure, lowers respiratory rate, rests the accessory muscles, increases functional residual capacity, decreases respiratory load and work of breathing and leads to favorable changes in the ventilation/perfusion ratio as well as the respiratory center and the sensivity of chemoreceptors (Mansfield & Naughton 1999;de Miguel et al 2002). Expiration positive airway pressure (EPAP) counterbalances intrinsic PEEP.…”