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Review
. 2017 Jan;124(1):179-191.
doi: 10.1213/ANE.0000000000001546.

Understanding Phenotypes of Obstructive Sleep Apnea: Applications in Anesthesia, Surgery, and Perioperative Medicine

Affiliations
Review

Understanding Phenotypes of Obstructive Sleep Apnea: Applications in Anesthesia, Surgery, and Perioperative Medicine

Yamini Subramani et al. Anesth Analg. 2017 Jan.

Abstract

Obstructive sleep apnea (OSA) is a prevalent sleep-disordered breathing with potential long-term major neurocognitive and cardiovascular sequelae. The pathophysiology of OSA varies between individuals and is composed of different underlying mechanisms. Several components including the upper airway anatomy, effectiveness of the upper airway dilator muscles such as the genioglossus, arousal threshold of the individual, and inherent stability of the respiratory control system determine the pathogenesis of OSA. Their recognition may have implications for the perioperative health care team. For example, OSA patients with a high arousal threshold are likely to be sensitive to sedatives and narcotics with a higher risk of respiratory arrest in the perioperative period. Supplemental oxygen therapy can help to stabilize breathing in OSA patients with inherent respiratory instability. Avoidance of supine position can minimize airway obstruction in patients with a predisposition to upper airway collapse in this posture. In this review, the clinically relevant endotypes and phenotypes of OSA are described. Continuous positive airway pressure (CPAP) therapy is the treatment of choice for most patients with OSA but tolerance and adherence can be a problem. Patient-centered individualized approaches to OSA management will be the focus of future research into developing potential treatment options that will help decrease the disease burden and improve treatment effectiveness.

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Conflict of interest statement

Disclosures: Conflicts of Interest: Yamini Subramani declares no Conflicts of interest.

Mandeep Singh declares no Conflicts of interest.

Jean Wong declares no Conflicts of interest.

Clete A. Kushida declares no Conflicts of interest.

Atul Malhotra declares no Conflicts of interest.

Frances Chung, MBBS, FRCPC. STOP Bang tool is proprietary to University Health Network. Royalties from UpToDate. Research grants from ResMed Foundation and Acadia Pharma.

Figures

Figure 1
Figure 1
Risk factors, pathogenic mechanisms, and treatments for obstructive sleep apnoea. Specific pathogenetic mechanisms of the various risk factors of OSA have recently been recognized. This paves the way for novel therapeutic approaches targeting individual pathogenic mechanisms, as possible successful alternatives to CPAP, which is the current universal treatment of choice. Reprinted with permission from Jordan et al. Adult obstructive sleep apnoea. Lancet. 2014;383:736–747. CPAP, indicates continuous positive airway pressure; HGNS, hypoglossal nerve stimulation; MAD, mandibular advancement device; O2, oxygen; UPPP, uvulopalatopharyngoplasty.
Figure 2
Figure 2
A schematic representation of the interaction between soft tissue and the upper airway bony enclosure and their combined effect on airway size. Reprinted with permission from Watanabe et al; Am J Respir Crit Care Med. 2002; 165:260–265. Ptissue – pressure exerted by soft tissue on upper airway. Ptissue is determined by the balance between the amount of soft material inside the enclosure and the size of the surrounding rigid box. Obesity leads to an excess of soft material inside the rigid box. In contrast, a small bony enclosure reduces the size of the rigid box. Accordingly, an imbalance between body habitus and craniofacial abnormalities may result in increased tissue pressure surrounding the pharyngeal airway, leading to closure of this airway.
Figure 3
Figure 3
PSG tracings of an obstructive sleep apnea event in a patient with severe OSA. There was increased EMG activity of the genioglossus muscle during the apneic event, although it was not significant enough to restore flow without arousal. The arousal threshold is characterized using Pepi, which is the epiglottic pressure immediately preceding arousal and there is a large ventilatory response following arousal. Reprinted with permission from Campana et al; Indian J Med Res. 2010;131:176–187. EEG indicates electroencephalogram (C3-A2); EMGgg, electromyogram of the genioglossus muscle (intramuscular); Pepi, pressure at the level of the epiglottis; Pmask, pressure measured via nasal mask; Vt, tidal volume.

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