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Communications to the Editor |

Obstructive Sleep Apnea Treatment Obstructive Sleep Apnea Treatment FREE TO VIEW

Chung-Ming Chu, MB, MSc; Veronica L. Chan, MB
Author and Funding Information

Affiliations: United Christian Hospital, Kowloon, Hong Kong SAR, China ,  Virginia Mason Medical Center, Seattle, WA Mayo Clinic, Rochester, MN Case Western Reserve University, Cleveland, OH University of Pennsylvania, Philadelphia, PA Harvard University, Boston, MA University of Mississippi, Oxford, MS

Correspondence to: Chung-Ming Chu, MB, MSC, Division of Respiratory Medicine, Department of Medicine and Geriatrics, United Christian Hospital, Kowloon, Hong Kong SAR, China; e-mail: nncmchu@netvigator.com



Chest. 1999;116(5):1495-1496. doi:10.1378/chest.116.5.1495
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To the Editor:

We read with interest the article “Indications for Positive Airway Pressure Treatment of Adult Obstructive Sleep Apnea Patients” by Loube and colleagues (March 1999),1 and we offer the following comments.

They suggested that continuous positive airway pressure (CPAP) is indicated for all patients with obstructive sleep apnea (OSA) who have a respiratory disturbance index (RDI) of > 30 events per hour, and they cited Wisconsin sleep cohort data2 for support. However, the Wisconsin study used an apnea-hypopnea index (AHI) rather than an RDI. An RDI also takes respiratory effort-related arousal into account, and measurements using the RDI are usually larger than AHI. Using an RDI of > 30 events per hour seems unwarranted based on the evidence presented.

Loube and colleagues1 also recommended that OSA of a lesser degree also is indicated for treatment if comorbidities, including hypertension, ischemic heart disease, or stroke, are present. However, coexisting COPD was not discussed.

We suggest that patients with both OSA and COPD warrant special consideration. Pulmonary arterial pressure in patients with significant OSA (RDI, > 20 events per hour) has been shown to be correlated with FEV1.3Patients with coexisting OSA and COPD also have been reported to have worse cardiopulmonary dysfunction than those with OSA alone, and tracheostomy improved right ventricular function significantly in these patients.4Sampol and colleagues5 studied 10 male patients with AHIs of 15 to 74 events per hour and treated them with CPAP, oxygen, and suboptimal CPAP and effective CPAP with oxygen on successive nights. Effective CPAP corrected the OSA, but the mean level of arterial oxygen saturation (Sao2) remained at < 90% in all patients. The use of supplemental oxygen with suboptimal CPAP levels produced an increase in apnea frequency and duration. Only an effective CPAP level plus oxygen resulted in the elimination of OSA and produced a mean Sao2 level of > 90% in all patients. From the available evidence, it appears reasonable to offer CPAP with supplemental oxygen to patients with COPD who also have OSA and an AHI of > 15 events per hour.

Notwithstanding these comments, we deeply appreciate the effort of Loube and colleagues in producing a much-needed consensus statement for the management of OSA.

Loube, DI, Gay, PC, Strohl, KP, et al (1999) Indications for positive airway pressure treatment of adult obstructive sleep apnea patients.Chest115,863-866. [PubMed] [CrossRef]
 
Young, T, Peppard, P, Palta, M, et al Population-based study of sleep-disordered breathing as a risk factor for hypertension.Arch Intern Med1997;157,1746-1752. [PubMed]
 
Laks, L, Lehrhaft, B, Grunstein, RR, et al Pulmonary hypertension in obstructive sleep apnoea.Eur Respir J1995;8,537-541. [PubMed]
 
Fletcher, EC, Schaff, JW, Miller, J, et al Long-term cardiopulmonary sequelae in patients with sleep apnea and chronic lung disease.Am Rev Respir Dis1987;135,525-533. [PubMed]
 
Sampol, G, Sagales, MT, Roca, A, et al Nasal continuous positive airway pressure with supplemental oxygen in coexistent sleep apnoea-hypnoea syndrome and severe chronic obstructive pulmonary disease.Eur Respir J1996;9,111-116. [PubMed]
 

Obstructive Sleep Apnea Treatment

To the Editor:

We thank Drs. Chu and Chan for their interest in and thoughtful comments on our consensus statement (March 1999).1

We agree that data from prior obstructive sleep apnea (OSA) syndrome outcome studies were based on nocturnal obstructive respiratory events for which airflow was measured by oronasal thermistor. However, the detection of airflow by these thermal sensors provides qualitative information that is not well correlated with breath amplitude. Thermistors have been shown to have poor accuracy in recording hypopneas in awake subjects under ideal conditions.2Due to the inadequate nature of the signal, it is unlikely that any further research on thermal sensors would yield acceptable data on accuracy or precision. Hence, alternative techniques, including esophageal and pleural pressure (Pes) manometry,3nasal pressure transduction,4or quantitative respiratory inductive plethysmography,5are advocated to aid in the detection of nocturnal obstructive respiratory events. Because of the decreased sensitivity of the oronasal thermistor in measuring airflow to detect events, compared to some of these other methods,6 the term respiratory effort-related arousal (RERA) was developed.

A RERA is an event that is characterized by increasing respiratory effort for ≥ 10 s leading to an arousal from sleep, but that does not fulfill the criteria for a hypopnea or an apnea.7At the present time, the recommendations are that there is no added clinical value in differentiating apneas from hypopneas, because they have similar pathophysiology and usually end in arousal, and often in desaturation.8Similarly, with the exception of the number of apneas and hypopneas measured by thermistor, respiratory parameters evaluated by standard 12-channel polysomnography with the addition of Pes manometry recently were demonstrated to be the same for upper airway resistance syndrome patients and OSA patients when body mass index and gender were controlled for.9 These findings suggest that the inclusion of apneas, hypopneas, and RERAs in a single index is appropriate and that these events likely do not differ with respect to the potential for causing the consequences of untreated OSA. Thus, we still believe that positive airway pressure treatment is warranted for a patient with a respiratory disturbance index (RDI) of> 30 events per hour, with the inclusion of apneas, hypopneas, and RERAs in the RDI.

We also agree with Drs. Chu and Chan that patients with both OSA and COPD warrant special consideration. It was an oversight not to state that some studies suggest that there is an additive risk for mortality when OSA and COPD occur concomitantly in individual patients.1011 We purposely did not discuss the therapy of nocturnal breathing disorders in COPD patients as this is addressed in another recent consensus statement that was prepared with that specific objective.12 However, we did recommend that “a trial of bilevel positive airway pressure may be indicated for OSA patients with concomitant nocturnal breathing disorders including COPD.”1

References
Loube, DI, Gay, P, Strohl, KP, Pack, A, White, DP, Collop, NJ Indications for positive airway pressure treatment of adult obstructive sleep apnea syndrome.Chest1999;115,863-866. [PubMed] [CrossRef]
 
Berg, S, Haight, JSJ, Yap, V, et al Comparison of direct and indirect measurements of respiratory airflow: implications for hypopneas.Sleep1997;20,60-64. [PubMed]
 
Zamagni, M, Sforza, E, Boudewijns, A, et al Respiratory effort. A factor contributing to sleep propensity in patients with obstructive sleep apnea.Chest1996;109,651-658. [PubMed]
 
Hosselet, JJ, Norman, RG, Ayappa, I, et al Detection of flow limitation with a nasal cannula/pressure transducer system.Am J Respir Crit Care Med1998;157,1461-1467. [PubMed]
 
Loube, DI, Andrada, TF Upper airway resistance syndrome: detection with respiratory inductive plethysmography.Chest1999;115,1333-1337. [PubMed]
 
Clark, SA, Wilson, CR, Satoh, M, et al Assessment of inspiratory flow limitation invasively and noninvasively during sleep.Am J Respir Crit Care Med1999;158,713-722
 
American Sleep Disorders Association Task Force. The Chicago criteria for measurements, definitions, and severity of sleep related breathing disorders in adults. Presented at: The Association of Professional Sleep Societies Conference; June 20, 1998; New Orleans, LA.
 
Gould, GA, Whyte, KF, Rhind, GB, et al The sleep hypopnea syndrome.Am Rev Respir Dis1988;137,895-898. [PubMed]
 
Loube, DI, Andrada, TF Comparison of nocturnal respiratory parameters in upper airway resistance and obstructive sleep apnea syndrome patients.Chest1999;115,1519-1524. [PubMed]
 
Lavie, P, Herer, P, Peled, R, et al Mortality in sleep apnea patients: a multivariate analysis of risk factors.Sleep1995;18,149-157. [PubMed]
 
Fletcher, EC, Schaff, JW, Miller, J, et al Long-term cardiopulmonary sequelae in patients with sleep apnea and chronic lung disease.Am Rev Respir Dis1987;135,525-533. [PubMed]
 
Clinical indications for noninvasive positive pressure ventilation in chronic respiratory failure due to restrictive lung disease, COPD, and nocturnal hypoventilation: a consensus conference report. Chest 1999; 116:521–534.
 

Figures

Tables

References

Loube, DI, Gay, PC, Strohl, KP, et al (1999) Indications for positive airway pressure treatment of adult obstructive sleep apnea patients.Chest115,863-866. [PubMed] [CrossRef]
 
Young, T, Peppard, P, Palta, M, et al Population-based study of sleep-disordered breathing as a risk factor for hypertension.Arch Intern Med1997;157,1746-1752. [PubMed]
 
Laks, L, Lehrhaft, B, Grunstein, RR, et al Pulmonary hypertension in obstructive sleep apnoea.Eur Respir J1995;8,537-541. [PubMed]
 
Fletcher, EC, Schaff, JW, Miller, J, et al Long-term cardiopulmonary sequelae in patients with sleep apnea and chronic lung disease.Am Rev Respir Dis1987;135,525-533. [PubMed]
 
Sampol, G, Sagales, MT, Roca, A, et al Nasal continuous positive airway pressure with supplemental oxygen in coexistent sleep apnoea-hypnoea syndrome and severe chronic obstructive pulmonary disease.Eur Respir J1996;9,111-116. [PubMed]
 
Loube, DI, Gay, P, Strohl, KP, Pack, A, White, DP, Collop, NJ Indications for positive airway pressure treatment of adult obstructive sleep apnea syndrome.Chest1999;115,863-866. [PubMed] [CrossRef]
 
Berg, S, Haight, JSJ, Yap, V, et al Comparison of direct and indirect measurements of respiratory airflow: implications for hypopneas.Sleep1997;20,60-64. [PubMed]
 
Zamagni, M, Sforza, E, Boudewijns, A, et al Respiratory effort. A factor contributing to sleep propensity in patients with obstructive sleep apnea.Chest1996;109,651-658. [PubMed]
 
Hosselet, JJ, Norman, RG, Ayappa, I, et al Detection of flow limitation with a nasal cannula/pressure transducer system.Am J Respir Crit Care Med1998;157,1461-1467. [PubMed]
 
Loube, DI, Andrada, TF Upper airway resistance syndrome: detection with respiratory inductive plethysmography.Chest1999;115,1333-1337. [PubMed]
 
Clark, SA, Wilson, CR, Satoh, M, et al Assessment of inspiratory flow limitation invasively and noninvasively during sleep.Am J Respir Crit Care Med1999;158,713-722
 
American Sleep Disorders Association Task Force. The Chicago criteria for measurements, definitions, and severity of sleep related breathing disorders in adults. Presented at: The Association of Professional Sleep Societies Conference; June 20, 1998; New Orleans, LA.
 
Gould, GA, Whyte, KF, Rhind, GB, et al The sleep hypopnea syndrome.Am Rev Respir Dis1988;137,895-898. [PubMed]
 
Loube, DI, Andrada, TF Comparison of nocturnal respiratory parameters in upper airway resistance and obstructive sleep apnea syndrome patients.Chest1999;115,1519-1524. [PubMed]
 
Lavie, P, Herer, P, Peled, R, et al Mortality in sleep apnea patients: a multivariate analysis of risk factors.Sleep1995;18,149-157. [PubMed]
 
Fletcher, EC, Schaff, JW, Miller, J, et al Long-term cardiopulmonary sequelae in patients with sleep apnea and chronic lung disease.Am Rev Respir Dis1987;135,525-533. [PubMed]
 
Clinical indications for noninvasive positive pressure ventilation in chronic respiratory failure due to restrictive lung disease, COPD, and nocturnal hypoventilation: a consensus conference report. Chest 1999; 116:521–534.
 
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