Mechanisms of apnea

Abstract

This paper focuses on the underlying mechanisms contributing to sleep-disordered breathing. Obstructive sleep apnea (OSA) is the most common sleep-related breathing disorder and is characterized by repetitive narrowing or collapse of the pharyngeal airway during sleep. Conversely, central sleep apnea (CSA), highly prevalent in congestive heart failure, is distinguished by a lack of drive to breathe during sleep, resulting in repetitive periods of insufficient ventilation. Both lead to compromised gas exchange, impaired sleep continuity, and catecholamine surges and are associated with major comorbidities including excessive daytime sleepiness and increased risk of cardiovascular disease. Although OSA and CSA exist on a spectrum of sleep-disordered breathing, the 2 entities may overlap in their underlying pathophysiologies. This brief review summarizes the etiology and current understanding of OSA and CSA pathophysiology and the role that the cardiovascular system may play in contributing to disease pathology and highlights the likely substantial overlap that exists between the various forms of sleep-disordered breathing.

Figures

Figure 1. Obstructive Sleep Apnea

Polysomnographic example of obstructive sleep apnea from an experimental study in a patient with severe disease (apnea/hypopnea index= 75 events per hour). Repeated oxygen desaturations occu due to an absence of airflow (apnea) despite continual breathing efforts (Pepi). Note the associated surges in heart rate that occur with apnea termination and arousal from stage 1 sleep (grey boxes). EEG= electroencephalogram (C3-A2), HR= heart rate, EKG= Electrocardiogram, Pepi= pressure at the level of the epiglottis (as a measure of respiratory effort), Flow measured via nasal mask and pneumotachograph, SaO2= Arterial blood oxygen saturation.

Figure 2. Reduced Central Respiratory Drive May Lead to Both Central Apnea and Upper Airway Closure

Schematic demonstrating one of the possible links between central sleep apnea and airway obstruction. In the left hand diagram respiratory pattern generator output to both the diaphragm and upper airway dilator muscles are reduced resulting in central apnea and airway closure. In the example on the right, respiratory pattern generator output to both muscles is increased resulting in sufficient ventilation. Note than in obstructive sleep apnea a mismatch between the respiratory pattern generator output to the diaphragm versus the upper airway dilator muscles may contribute to airway collapse.

Figure 3. Cheyne-Stokes Breathing

A polysomnographic example of a patient with heart failure experiencing Cheyne-Stokes breathing during sleep. EEG= electroencephalography, SaO2= arterial blood oxygen saturation. Note that arousal occurs at the peak of the crescendo (highlighted in grey on the EEG tracing) and that each oxygen desaturation (highlighted in grey on the SaO2 tracing) corresponds to the previous apnea due to prolonged circulatory delay. Adapted with permission from reference (47).

Figure 4. The Spectrum of Disease

Schematic of the disease spectrum from OSA to CSA and some of the various perpetuating factors that likely influence where a particular patient lies (grey dashed arrows). A proposed example of complex apnea whereby a patient diagnosed with OSA at baseline switches to the CSA side of the disease spectrum upon commencement of CPAP due to currently unknown mechanisms is also depicted. Refer to the text for further detail.