Lt Col Dara D. Regn, USAF, MC, FSa; Lt Col Anh H. Davis, USAF, MC, FSb; Lt Col William D. Smith, USAF, MC, FSa; Maj Catherine J. Blasser, USAF, MC, FSa; Lt Col Caelan M. Ford, USAF, MC, FSa
Correspondence: Dara Regn (drregn@hotmail.com)
aUnited States Air Force School of Aerospace Medicine, Wright-Patterson Air Force Base, Ohio
bDepartment of Aerospace Medicine, McConnell Air Force Base, Kansas
Author disclosures
The authors report no actual or potential conflicts of interest or outside sources of funding with regard to this article.
Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the US Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.
CSA also is highly prevalent in neuromuscular conditions, such as amyotrophic lateral sclerosis, Duchenne muscular dystrophy, myotonic dystrophy, advanced multiple sclerosis, and acid maltase deficiency. There is reduced respiratory muscle strength and tone in these disorders, resulting in alveolar hypoventilation with hypercapnia. Given the hypercapnia, NIV/BiPAP is the first-line treatment to improve survival, gas exchange, symptom burden, and quality of life.
Stroke-Induced CSA
Extensive cerebrovascular events commonly precipitate sleep-related breathing disorders. The incidence increases in the acute phase of stroke and decreases 3 to 6 months poststroke; however, incidence also depends on the severity of the stroke.7,39,40 Stroke also has been shown to be a predictor of CSA (odds ratio, 1.65; 95% CI, 1.50-1.82; P < .001) in a retrospective analysis of a large cohort of US veterans.2 The location of the lesion often determines whether normocapnic or hypercapnic CSA will predominate, based on ventilatory instability resulting in normocapnia or reduced ventilatory drive resulting in hypercapnic CSA. PSG results and blood gases direct the treatment options. CSA with normocapnia is treated with ASV, and patients with hypercapnia/REM sleep hypoventilation are treated with NIV/BiPAP.
Conclusions
While much has been learned about CSA in recent decades, more evidence needs to be gathered to determine optimal treatment strategies and the impact on patient prognosis. The identification of CSA can lead to the diagnosis of previously unrecognized medical conditions. With proper diagnosis and treatment, we can optimize clinical management and improve patients’ prognosis and quality of life.
Acknowledgments
The authors thank the librarians of the Franzello Aeromedical Library in particular Sara Craycraft, Catherine Stahl, Kristen Young and Elizabeth Irvine for their support of this publication.
