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Sleep apnea ABCs

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To the Editor: We read with interest the paper by Dr. Reena Mehra,“Sleep apnea ABCs: Airway, breathing, circulation.”1 It was very consistent and informative. However, we feel that some considerations on the pathogenesis warrant more discussion.

The pathophysiologic heterogeneity of sympathetic nervous system activity enhancement is complex and involves both intermittent hypoxia and arousal. We agree with Dr. Mehra about the importance of intermittent hypoxia in sympathetic activation, and we would like to point out the importance of effects of arousal from sleep on autonomic outflow. In some patients with obstructive sleep apnea (OSA) in whom respiratory events are not followed by oxygen desaturation, sympathetic activation cannot be explained by intermittent hypoxia. Arousal has been reported to be associated with an acute increase in sympathetic activity in the absence of hypercapnia or hypoxia.2 Cortical arousals from sleep have been historically assumed to be important in restoring airflow at the end of OSA breathing events.3 Furthermore, arousals often precede upper-airway opening in patients with OSA.4

Reprinted from Mehra R. Sleep apnea ABCs: airway, breathing, circulation. Cleve Clin J Med 2014; 81:479–489.

Figure 1. This polysomnogram of a 2-minute compressed window of time shows repetitive obstructive apneic events and a hypopneic event accompanied by severe oxygen desaturation (nadir, 78%) and arousals detected by encephalography that occur at the termination of the respira-tory events. The patient is lying on his right side and is in N2 and N1 stages of sleep. The red arrow points to the obstructive apnea, the green arrow to the arousal, and the blue arrow to the accompanying oxygen desaturation episode. There is a delay of desaturation due to circulation time. The patient is a 47-year-old man with hypertension, asthma, excessive daytime sleepiness, snoring, witnessed apneic events, and multiple awakenings from sleep caused by cough and shortness of breath. The overall apnea-hypopnea index observed on this polysomnogram was 86 events per hour of sleep. This, along with the severe degree of hypoxia and accompanying symptoms, is consistent with the diagnosis of severe obstructive sleep apnea syndrome. (EEG = electroencephalography; EMG = electromyography)

In Figure 1 of Dr. Mehra’s paper, all the respiratory events were associated with microarousals. According to the conventional definition, cortical arousal is an abrupt shift in the electroencephalogram lasting more than 3 seconds. In Figure 1, the beginning of arousals must be scored a few seconds before breathing recovery, just at the beginning of electroencephalogram acceleration. The second respiratory event was scored as obstructive apnea, or the apnea started out as central apnea, where all respiratory channels are flat and then the chest and abdominal belts start moving, making it look like typical mixed apnea.

In the title of the paper, the “A” of ABCs referred to airway and, more specifically, to the collapse of the upper airway in sleep, which is the cause of OSA. We think that the “A” can be attributed to arousal, which is specific to sleep and contributes to the pathogenesis of OSA.

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  • Letters To The Editor

    In reply: Sleep apnea ABCs

    Whether cortical arousal during sleep is bad or good is controversial.