RECOGNITION AND CONSEQUENCES OF OBSTRUCTIVE SLEEP APNEA HYPOPNEA SYNDROME

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Increasingly, pulmonologists are called on to assist in the evaluation and treatment of patients with suspected sleep apnea hypopnea syndrome (SAHS). In that role, they are asked to communicate with and educate primary care providers and third-party payers, many of whom have little knowledge of sleep disorders medicine, and who seek specific and clear guidelines for screening, diagnosing, and treating the condition. Appropriate identification of high-risk patients requires a broad perspective of risk factors for SAHS in a variety of populations, knowledge of the potential health consequences of untreated SAHS (and of its variability according to individual susceptibility), as well as a healthy appreciation of the limitations of our current knowledge base. In fact, despite considerable clinical experience diagnosing and treating patients with SAHS (often producing “clinical successes” that are among the most remarkable experienced by internal medicine specialists), there is substantial controversy regarding how to best define and identify the syndrome and disagreement regarding which patients with SAHS may best respond to specific therapies. That, to a large extent, has made the management of SAHS more an art than science.

In this article, we first review some of the issues related to identifying individuals with frequent sleep-related respiratory disturbances (referred to as sleep-disordered breathing, SDB), including the limitations of using narrowly defined polysomnographic data for case finding. We then review the distributions of symptoms and physiologic measurements of SDB in the population, and their interrelationships. The epidemiologic data that address risk factors and consequences of SAHS are discussed, with recommendations regarding recognition priorities.

Section snippets

DEFINING THE DISORDER

The International Classification of Sleep Disorders manual35 describes obstructive sleep apnea syndrome as “.… characterized by repetitive episodes of upper airway obstruction that occur during sleep, usually associated with a reduction in blood oxygen saturation….” with associated features of daytime sleepiness and snoring.35 Unfortunately, that definition does not include specific criteria for identifying: (1) the occurrence of upper airway obstruction, (2) the number of obstructive episodes

MONITORING APPROACHES

The standard approach for assessing SDB is with in-laboratory polysomnography. That approach has been used for approximately 25 years. Typically, sleep architecture and arousals are assessed by EEG (from central and sometimes occipital leads), right and left electroculograms, and chin electromyogram (EMG). Breathing is assessed qualitatively, with a measure of airflow, measured with thermocouples or thermistors positioned near the external nares or nares and mouth, or a pressure transducer at

PREVALENCE

The preceding discussion emphasizes that SAHS is characterized by, but not easily defined by, the occurrence of episodes of obstructed breathing that occur during sleep and are associated with oxygen desaturation, sleep fragmentation, and symptoms of disruptive snoring and daytime sleepiness. Variability in measuring and quantifying those parameters limits comparison and interpretation of data from various centers and locales. Furthermore, the prevalence estimates that have been calculated for

SYMPTOMS OF SLEEP APNEA HYPOPNEA SYNDROME

The symptoms used most commonly to characterize, and sometimes to screen for, SAHS can be grouped broadly into the following areas: breathing disturbances occurring during sleep (snoring frequency and intensity, choking or gasping, apneas or pauses); difficulties maintaining sleep (frequent awakenings, restless sleep); daytime sleepiness; fatigue; mood effects (depression and irritability); and general impairment of daily function and quality of life (e.g., problems with performance of daily

RISK FACTORS

Factors that reduce upper airway size or predispose to upper airway collapsibility increase susceptibility to SAHS. The strongest risk factors are obesity and male gender. Obesity, particularly central obesity, may precipitate or exacerbate SAHS by influences related to upper airway fat deposition, which may affect airway patency or compliance, and abdominal mass loading, which may influence breathing pattern (predisposing to hypoventilation) or reduce oxygen stores (predisposing to

CONSEQUENCES OF SLEEP APNEA HYPOPNEA SYNDROME

Patients with SAHS may experience a number of potentially adverse physiologic exposures during sleep, including gas exchange abnormalities and increased sympathetic nervous system activity.128 The latter is probably a response to intermittent hypoxemia and hypercapnia, chemoreflex activation, and the increased central nervous system arousal that occurs with obstructed breathing.9, 43, 67, 97, 128, 130 In addition, large fluctuations in intrathoracic pressure that occur with obstructed breathing

CLINICAL RECOGNITION OF SLEEP DISORDERED BREATHING

Although prevalence estimates vary with differences in the age and underlying morbidity levels of samples studied, and in the specific criteria used for measuring associated attributes and defining disease, it may be estimated that approximately 2% to 5% of the population meet minimal criteria for clinical illness. There are groups with higher prevalences of SDB and groups who may be especially susceptible to adverse health effects associated with SDB.

Despite increasing numbers of epidemiologic

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    Supported in part by the National Heart, Lung and Blood Institute (HL-46380) and a SCOR in Cardiopulmonary Disorders of Sleep (HL-42215), and by the Cleveland Veterans Affairs Medical Center.

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