Affiliations: Denver, CO ,
Dr. Zwillich is Staff Physician, Denver Veterans Affairs Medical Center, and Professor of Medicine, University of Colorado at Denver Health Sciences Center, Denver Veterans Affairs Medical Center, Denver, CO. Dr. Welsh is Staff Physician, Denver Veterans Affairs Medical Center, and Professor of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado at Denver Health Sciences Center.
Correspondence to: Clifford Zwillich, MD, Denver Veterans Affairs Medical Center, 1055 Clermont St, Denver, CO 80220; e-mail: Clifford.email@example.com
Hypercapnia during wakefulness is a marker of disease severity in patients with sleep apnea. These patients are often very obese, have long apnea events with marked oxygen desaturation, evidence of pulmonary hypertension, and right-heart failure. Without appropriate treatment, such patients require frequent hospital admission1and have alarming mortality rates.2Fortunately, following the successful application of continuous positive airway pressure (CPAP) or bilevel ventilation, daytime hypercapnia often improves3 and recurrent hospital admission rates decrease.1
Unfortunately, clinicians may underestimate the severity of illness of these patients and often miss an opportunity to intervene. Presenting symptoms are nonspecific and include fatigue, sleepiness, subtle changes in mental status, and headaches. Since there is often no increase in respiratory rate or use of accessory muscles to breathe, their tenuous status is not fully appreciated. Even the underlying obstructive sleep apnea (OSA) as well as the hypoventilation in these patients is often missed. When oxyhemoglobin desaturation and right-heart failure are detected, supplemental oxygen is often provided without the knowledge of arterial blood gas abnormalities. Therefore, these hypercapnic patients often go unrecognized and undertreated with high risk for recurrent hospitalization and even early death.2
Published case series usually demonstrate that patients with this disorder exhibit a body mass index > 35 kg/m2, and have restrictive pulmonary function but no other cause for hypoventilation such as airflow obstruction, thyroid failure, or neuromuscular disease. Interestingly, prior older studies in a small number of patients demonstrated that the respiratory restriction and hypercapnia were linked to the degree of obesity,4and this association has been verified by recent reports of successful weight loss and improved Paco2 in larger numbers of patients following bariatric surgery.5
With the worldwide increasing incidence of obesity, it is likely that this form of severe apnea will become more common. When first described, the Pickwickian syndrome was thought to be rare. However, most modern series of consecutive patients with OSA estimate that approximately 10% have hypercapnia. The large series6 published in this issue of CHEST (see page 1832) reports that 14% of Japanese patients referred to an academic sleep center for sleep apnea symptoms had daytime hypercapnia. However, it is possible that the illness among Japanese patients is somewhat different than that seen in white patients because the current series does not report more frequent restrictive pulmonary physiology among those with hypercapnia. Nonetheless, if approximately 5% of adult men have OSA syndrome and if 10 to 15% of these have hypercapnia, hundreds of thousands of increasingly obese Americans are at risk for severe disease, associated hospitalizations, and possibly premature death.
What explains hypercapnia in only some individuals with OSA and severe obesity? The fact that normal Paco2 can be achieved without weight loss in some after initiation of CPAP or bilevel ventilation suggests that resetting attenuated ventilatory drive might play a role.7Although improved sleep architecture or less sleep hypoxemic ventilatory depression are plausible explanations, there is at best conflicting data to support this possibility. Improved respiratory mechanics during therapy probably does not alone explain normalization of Paco2 because untreated patients usually demonstrate reasonable respiratory muscle strength and can voluntarily hyperventilate effectively.8
It is not clear how to best manage patients with hypercapnia complicating OSA. Airflow limitation and thyroid insufficiency should be sought and treated. We know of no randomized studies evaluating usual therapy (CPAP or bilevel) compared to more invasive measures such as bariatric surgery and/or tracheostomy. Our experience with CPAP and bilevel ventilation is that compliance is poor, as it is in many with uncomplicated OSA; however, the impact of incompletely treated disease is likely to be worse. If future prospective studies verify the poor prognosis of those with hypercapnic OSA, trials comparing usual CPAP/bilevel therapy to a more aggressive approach of bariatric surgery after initiation of CPAP would be justified. Finally, when severe hypercapnic OSA patients are started on CPAP/bilevel and fail, as we believe is common because of mask discomfort, or other complaints, is early tracheostomy the best means to achieve stability such that the next phase of therapy (bariatric surgery) can be more safely initiated?
Dr. Zwillich is a shareholder in ResMed, a manufacturer of devices used to treat sleep apnea. Dr. Welsh has no personal or financial conflicts associated with this article.
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