SLEEP APNEA

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CHAPTER 16 SLEEP APNEA

The sleeping patient is still a patient. His disease may progress differently in sleep, or disease may originate in sleep. (Eugene Robin, 1958)

Sleep-disordered breathing is the broad term used to describe the endpoint of a number of conditions of diverse etiology that can disrupt breathing during sleep. Apnea is defined as the cessation of breathing for more than 10 seconds. Hypopnea refers to a reduction in tidal volume without total cessation of respiration. Degrees of hypopnea are recognized: either substantial (>50% reduction in airflow) or moderate (<50% reduction in airflow with desaturations of >3%, or electroencephalographic evidence of arousal). Episodes of apnea and hypopnea often, if not always, coexist; apnea represents the more severe end of the spectrum of reduction in tidal volume (Fig. 16-1).

Figure 16-1 Restriction of the airway during an apneic event.

Apneas and hypopneas may develop as a result of lack of drive to breathe, which is a central phenomenon, or as a result of narrowing of the upper airway, which is an obstructive phenomenon. These are considered separately.

Brief episodes of apnea or hypopnea are a feature of normal sleep, occurring most commonly during the transition from wakefulness to sleep when the level of arterial carbon dioxide tension in the body is reset to a level that is higher by approximately 5 mmHg (0.7kPa). Such transitional apneas occur in most individuals but can be very pronounced in patients with frequent arousals during sleep.

In an attempt to differentiate between normal and abnormal frequencies of apneic or hypopneic levels, the apnea-hypopnea index, referring to the number of episodes of apnea and hypopnea per hour of sleep, is used. The upper limit of normal has traditionally been considered to be five events per hour, but some authors have suggested a higher cutoff level, 10 events per hour.

Sleep-disordered breathing is common, and its prevalence increases with age. It is often accompanied by hypoxemia, changes in heart rate and blood pressure, and arousals that may fragment sleep and lead to daytime fatigue and somnolence, as well as cognitive and cardiovascular changes, known as the sleep apnea syndrome. Despite this, most cases remain undiagnosed and untreated.

OBSTRUCTIVE SLEEP APNEA-HYPOPNEA

Epidemiology

Obstructive sleep apnea-hypopnea (OSAH) is an increasingly important disease with numerous clinically relevant consequences, including neurocognitive and cardiovascular sequelae.¹^–³ The prevalence of this disease varies, depending on the definitions (of hypopnea) used. Young and colleagues⁴,⁵ showed that 4% of men and 2% of women in a middle-aged North American population had symptoms of OSAH and an apnea-hypopnea index exceeding 5. However, 24% of men aged 30 to 60 and 9% of women had an abnormal apnea-hypopnea index but without excessive sleepiness, which had been used to define the former statistics. Cardiovascular risk assessments, however, have shown a dose-response relationship between the apnea-hypopnea index and various sequelae; thus, the definition and epidemiology are still evolving (Young, Peppard, Gottlieb 2002).

Pathophysiology

Considerable progress has been made in understanding the genesis of obstructive events. The upper airway is anatomically small, and augmented pharyngeal dilator muscle activation maintains airway patency while the patient is awake but not while asleep, when an increase in upper airway resistance is found. Snoring, an important marker of increased upper airway resistance, is in part genetically determined,⁶ which perhaps reflects anatomical contributions such as a degree of retrognathia or overbite. Racial differences may be explained by this (apnea is more frequent among African Americans).⁷ Airway muscle tone insufficient for the airway size may allow intraluminal negative pressure to collapse the pharyngeal “tube.” Additional anatomical factors include enlarged tonsils or adenoids, vascular perfusion, the posture of the individual (supine versus lateral) and, of importance, fat accumulated in the pads in the lateral pharyngeal wall (Fig. 16-1).⁸

During wakefulness, augmented pharyngeal dilator muscle activity maintains airway potency. At sleep onset and/or during rapid-eye-movement sleep (with active inhibition of muscles), this reflex activity is diminished, and if airway anatomy is abnormal, the airway is compromised, which leads to hypopneas and/or apneas. As a result, hypoxia and hypercapnia occur; ventilation is stimulated, often with arousal from sleep; and airway patency is reestablished. With the return to sleep, the cycle is repeated. It is possible, then, to conceive of a continuum of disordered breathing from snoring alone to an inability to breathe and sleep at the same time. Additional risk factors for OSAH are obesity, male gender, and increasing age. Of patients with OSAH, 70% are obese (pharyngeal size is diminished); sleep laboratories report a fivefold or sixfold increased risk of OSAH in men in comparison with women; and the prevalence increases with age.⁹ An evolving literature¹⁰ also suggests an important concept of snoring-induced traumas causing sensory and/or motor neuronal damage, as well as actual damage to the muscle (Boyd, Petrof, and Hamid, 2004).

Clinical Manifestations/Sequelae

OSAH should be suspected in patients who snore intrusively and who are obese (body mass index > 30) and/or in whom apneas have been witnessed. However, more subtle manifestations can occur (e.g., in the 30% who are not obese); therefore, questioning with regard to daytime sleepiness and sleep quality is mandatory.

Poor sleep quality and daytime sleepiness are largely the results of sleep fragmentation by repetitive arousals. The neurocognitive sequelae of recurrent arousals also include reduced performance in neuropsychological tests, lengthened reaction times, altered quality of life, and an increased risk of vehicular accidents and work-related accidents.¹,⁸ A causal relationship to all is supported by the response to treatment with continuous positive airway pressure (CPAP), which improves these sequelae.¹¹^–¹³ Because of its practical importance, more should be said about sleep apnea and driving.

Human error is a major determinant in automobile accidents; inattention, improper lookout, and other perceptual and cognitive errors account for up to 40% of cases. Progressive daytime sleepiness can enhance inattention and thereby increase the risk of accidents in such patients. OSAH is an important cause of daytime sleepiness, along with cognitive impairment, and consequently contributes to the problem of drowsy driving.

The absence of skid marks.

The fact that for 7 seconds, the driver could have clearly seen at the point of runoff or the object hit (which implies prolonged inattention rather than momentary distraction).

Other causes such as mechanical failure are eliminated.

It is appreciated that drivers who are able to respond after these accidents seldom acknowledge having fallen asleep.

A strong association between sleep apnea and the risk of traffic accidents is now well documented. A Spanish study revealed that 102 drivers received emergency treatment after vehicular accidents and were more likely by a factor of 6 to have OSAH. Results of a French study suggested that approximately one half of drivers involved in sleep-related vehicular accidents have sleep disorders and that 31% have clear indications of OSAH. In addition, patients with OSAH in many other studies have been shown to have an increased rate of accidents. It is important to stress, however, that although patients with OSAH as a group are at increased risk, not all patients are at the same risk; results of the largest study to date suggested that increased automobile accidents may be restricted to patients with more severe apnea [age > 40], although sleep-related vehicular accidents are recognized to be multifactorial in origin.

Driver performance can be measured by simulators of varying degrees of sophistication, and some patients with OSAH perform as poorly as subjects intoxicated with alcohol. Beneficial effects of treatment, including CPAP and surgery, have also been shown with these simulators. The U.K. Driver and Vehicle Licensing Agency (DVLA) has a guide for medical practitioners in which it is pointed out that it is the duty of the license holder to notify the DVLA of any medical condition that may affect safe driving. There are some circumstances in which the license holder cannot, or will not, do this. Under these circumstances, the General Medical Council has issued clear guidelines:

Make sure that the patients understand that the condition may impair their ability to drive and explain to the patients they have a legal duty to inform the DVLA. If the patient continues to drive but is not fit to do so, the physician should make every reasonable effort to persuade them to stop. This may include telling their next of kin. If the individuals cannot be persuaded to stop driving, the practitioner should disclose relevant medical information immediately in confidence to the medical adviser of the DVLA, informing the patient of the decision to do so.

Sleep disorders are specifically mentioned under the Respiratory Disorders Section where the Group 1 entitlement states, “driving must cease if continuing to cause excessive awake time sleepiness, but driving will be permitted when satisfactory control of symptoms is achieved,” whilst for Group 2 entitlement, “cease driving on diagnosis. When it is confirmed by specialist assessment that the condition is adequately controlled, driving may be resumed subject to review.”

Readers should consult their national driving agencies for local recommendations or regulations as these may vary between countries.

The cardiovascular sequelae are best considered as immediate and delayed. The immediate response to the obstructed breathing is an increase in negative intrapleural pressure with increased venous return (and increased output of atrial natriuretic peptide and resulting nocturia) and reduced cardiac output (due to the increased afterload).

At the same time, the associated hypoxemia promotes sympathetic activation and circulatory vasoconstriction. With the return of airflow, the augmented preload leads to increases in stroke volume and in systemic blood pressure. This occurs repeatedly, and the normal nocturnal fall in blood pressure may be lost. A delayed effect on diurnal blood pressure may then follow. Indeed, it is appreciated that as much as one third of “essential” hypertension is associated with OSAH.¹⁴,¹⁵ A causal relationship is, again, supported by the response to treatment (with CPAP)¹⁶ (Pepperell, 2002). The combination of immediate and delayed hemodynamic effects in OSAH have been associated with increased risk of myocardial infarction and congestive heart failure, and there is evidence of a link between these and stroke.¹⁷ Additional links have been demonstrated with insulin resistance.¹⁸ The combination of obesity, insulin resistance (with or without diabetes), hypertension, and cardiovascular disease is typical of the metabolic syndrome, or syndrome X. Because these may all be associated with OSAH also, OSAH should obviously be considered as well; some authorities refer to it as syndrome Z.¹⁹

Finally, consideration might be given to the role of chronic hypercapnia in the setting of OSAH. Obesity is complicated in 10% of patients with OSAH by CO₂ retention (in part caused by the increased load on the respiratory system), but OSAH alone may produce this through repeated bouts of CO₂ retention at night, compensatory bicarbonate retention, and a daytime metabolic alkalosis that necessitates compensation. Evidence for this comes, again, from response to treatment with CPAP. One clinical variant of this is the pickwickian syndrome, so named after the “fat boy,” Joe, in Charles Dickens’ “Posthumous Papers of the Pickwick Club” who was, like the patient reported, obese, a snorer, sleepy, and in heart failure (dropsy). All these patients also have CO₂ retention and sleep apnea, usually obstructive.

In the example shown in Figure 16-2, a sleep-onset central apnea is followed by a hypopnea associated with efforts to breathe, registered by abdominal and thoracic impedance plethysmography. The hypopnea in this instance, however, resulted from ineffectual diaphragm contraction, evidenced by the paradoxical inward movement of the abdomen, presumably caused by the excessive abdominal load.