Medical Grand Rounds

Sleep apnea ABCs: Airway, breathing, circulation

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ABSTRACTObstructive sleep apnea (OSA) is increasingly common but largely underrecognized. Untreated, it is associated with heart disease, stroke, and sudden nocturnal death. Simple clinical assessments can determine if a patient is likely to have OSA and is a candidate for diagnostic polysomnography. Continuous positive airway pressure (CPAP) is the mainstay of treatment and ameliorates symptoms as well as long-term sequelae. Patient education and effective troubleshooting and evaluation of CPAP adherence issues increase successful adjustment to therapy. Alternative treatments can be considered in those whose OSA does not respond to standard CPAP therapy.


  • Although obesity and snoring are common features of OSA, they are not always present.
  • Home sleep testing is appropriate for those highly likely to have sleep apnea and without other significant sleep or cardiovascular, respiratory, or neurologic disorders.
  • Upper-airway surgery has a limited role—it is indicated primarily for those unable to tolerate CPAP.
  • Risk of motor vehicle accidents is dramatically increased in untreated sleep apnea; patients should be counseled on the dangers of drowsy driving.



Obstructive sleep apnea (OSA) is common and poorly recognized and, if untreated, leads to serious health consequences. This article discusses the epidemiology of OSA, describes common presenting signs and symptoms, and reviews diagnostic testing and treatment options. Adverse health effects related to untreated sleep apnea are also discussed.


OSA is very common in the general population and is associated with substantial morbidity and mortality. An estimated 17% of the general adult population has OSA, and the numbers are increasing with the obesity epidemic. Nearly 1 in 15 adults has at least moderate sleep apnea,1,2 and approximately 85% of cases are estimated to be undiagnosed.3 A 1999 study estimated that untreated OSA resulted in approximately $3.4 billion in additional medical costs per year in the United States,4 a figure that is likely to be higher now, given the rising prevalence of OSA. The prevalence of OSA in primary care and subspecialty clinics is even higher than in the community, as more than half of patients who have diabetes or hypertension and 30% to 40% of patients with coronary artery disease are estimated to have OSA.5–7


During sleep, parasympathetic activity is enhanced and the muscle tone of the upper airway is decreased, particularly in the pharyngeal dilator muscles. Still, even in the supine position, a healthy person maintains patency of the airway and adequate airflow during sleep.

OSA is characterized by repetitive complete or partial collapse of the upper airway during sleep, resulting in an apneic or hypopneic event, respectively, and often causing snoring from upper-airway tissue vibration.

People who are susceptible to OSA typically have a smaller, more collapsible airway that is often less distensible and has a higher critical closing pressure. Radiographic and physiologic data have shown that the airway dimensions of patients with OSA are smaller than in those without OSA. The shape of the airway of a patient with OSA is often elliptical, given the extrinsic compression of the lateral aspects of the airway by increased size of the parapharyngeal fat pads. OSA episodes are characterized by closure of the upper airway and by progressively increasing respiratory efforts driven by chemoreceptor and mechanoreceptor stimuli, culminating in an arousal from sleep and a reopening of the airway.

The disease-defining metric used for assessing OSA severity is the apnea-hypopnea index, ie, the number of apneas and hypopneas that occur per hour of sleep.8 An apneic or hypopneic event is identified during polysomnography by the complete cessation of airflow or by a reduction in airflow for 10 seconds or longer (Figure 1).

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 respiratory 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


Untreated sleep apnea causes numerous pathophysiologic perturbations, including chronic intermittent hypoxia, ventilatory overshoot hyperoxia, increased sympathetic nervous system activity, intrathoracic pressure swings, hypercapnea, sleep fragmentation, increased arousals, reduced sleep duration, and fragmentation of rapid-eye-movement sleep.

Intermittent hypoxia activates the sympathetic nervous system and causes pulmonary vasoconstriction, with increases in pulmonary arterial pressures and myocardial workload. Sympathetic activation, ascertained by peroneal microneurography, has been shown to be increased not only during sleep but also persisting during wakefulness in patients with untreated OSA vs those without OSA.9 Autonomic nervous system fluctuations accompany apneic episodes, resulting in enhanced parasympathetic tone and sympathetic activation associated with a rise in blood pressure and heart rate that occur after the respiratory event.

Intermediate pathways that link the negative pathophysiologic effects of OSA with adverse health outcomes include increased systemic inflammation, increased oxidative stress, metabolic dysfunction, insulin resistance, hypercoagulability, endothelial dysfunction, and autonomic dysfunction.

As a result, a variety of adverse clinical outcomes are associated with untreated OSA, including systemic hypertension, ischemic heart disease and atherosclerosis, diastolic dysfunction, congestive heart failure, cardiac arrhythmias, stroke, increased risk of death, and sudden death, as well as noncardiovascular outcomes such as gout, neurocognitive deficits, and mood disorders.10


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  • Letters To The Editor

    Sleep apnea ABCs

    We believe that arousal contribute to the pathophysiology of obstructive sleep apnea.

  • Letters To The Editor

    In reply: Sleep apnea ABCs

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