Chapter 319 - Sleep Apnea

Question 1

Which type of sleep apnea is more common?

Answer 1

Obstructive Sleep Apnea/Hypopnea syndrome.

Question 2

Obstructive Sleep Apnea/Hypopnea syndrome is a major contributor to cardiovascular disease in adults and to behavioral problems in children.
True or False?

Answer 2

True.

Question 3

What are the criteria for Obstructive Sleep Apnea/Hypopnea syndrome (OSAHS)?

Answer 3

(1) either symptoms of nocturnal breathing disturbances (snoring, snorting, gasping, or breathing pauses during sleep) or daytime sleepiness or fatigue that occurs despite sufficient opportunities to sleep and is unexplained by other medical problems; and (2) five or more episodes of obstructive apnea or hypopnea per hour of sleep (the apnea-hypopnea index [AHI], calculated as the number of episodes divided by the number of hours of sleep) documented during a sleep study. OSAHS also may be diagnosed in the absence of symptoms if the AHI is above 15.”

Question 4

How does one define an episode of apnea or hypopnea during sleep?

Answer 4

“Each episode of apnea or hypopnea represents a reduction in breathing for at least 10 sec. OSAHS is often identified when associated with a ≥3% drop in oxygen saturation and/or a brain cortical arousal.”

Question 5

In general terms how does one characterize the severity of Obstructive Sleep Apnea/Hypopnea syndrome (OSAHS)?

Answer 5

“OSAHS severity is based on the frequency of breathing disturbances (AHI), the amount of oxygen desaturation with respiratory events, the duration of apneas and hypopneas, the degree of sleep fragmentation, and the level of daytime sleepiness.”

Question 6

Summarize the pathophysiology of Obstructive Sleep Apnea/Hypopnea syndrome (OSAHS).

Answer 6

“During inspiration, intraluminal pharyngeal pressure becomes increasingly negative, creating a “suctioning” force. Because the pharyngeal airway has no bone or cartilagem, airway patency is dependent on the stabilizing influence of the pharyngeal dilator muscles. Although these muscles are continuously activated during wakefulness, neuromuscular output declines with sleep onset. In patients with a collapsible airway, the reduction in neuromuscular output results in transient episodes of pharyngeal collapse manifesting as an “apnea”) or near collapse (manifesting as a “hypopnea”). The episodes of collapses are terminated when ventillatory reflexes are activated and cause arousal, thus stimulating an increase is neuromuscular activity and opening of the airway.”

Question 7

What is the most common place of airway collapse during sleep apnea?

Answer 7

Soft palate.

Other places of collapse include tongue base, lateral pharyngeal walls, and/or epiglottis.

Question 8

OSAHS is particularly severe during REM sleep and in the supine position.
True or False?

Answer 8

True.

Question 9

Summarize the effect of different anatomic variations over the airways and the predisposition for its collapsibility.

Answer 9

“Individuals with a small pharyngeal lumen require relatively high levels of neuromuscular innervation to maintain patency during wakefulness and thus are predisposed to excessive airway collapsibility during sleep. The airway lumen may be narrowed with enlargement of soft tissue structures (tongue, palate, and uvula) due to fat deposition, increased lymphoid tissue, or genetic variation. Craniofacial factors such as mandibular retroposition or micrognathia, reflecting genetic variation or developmental influences, also can reduce lumen dimensions. In addition, lung volumes influence the caudal traction on the pharynx and consequently the stiffness of the pharyngeal wall. Accordingly, low lung volume in the recumbent position, which is particularly pronounced in the obese, contributes to collapse. A high degree of nasal resistance (e.g., due to nasal septal deviation or polyps) can contribute to airway collapse by increasing the negative intraluminal suction pressure. High-level nasal resistance also may trigger mouth opening during sleep, which breaks the seal between the tongue and the teeth and allows the tongue to fall posteriorly and occlude the airway.”

Question 10

What is the correlation between ventilation and pharingeal muscle activation? How can this relantionship be altered as a predisposition for sleep apnea?

Answer 10

“A build in CO2 during sleep activates both the diaphragm and the pharyngeal muscles, which stiffen the upper airway and can counteract inspiratory suction pressures and maintain airway patency to an extent that depends on the anatomic predisposition to collapse. However, pharyngeal collapse can occur when the ventilatory control system is overly sensitive to CO2, with resultant wide fluctuations in ventilation and ventilatory drive and in upper airway instability. Moreover, increasing levels of CO2 during sleep result in central nervous system arousal, causing the individual to move from a deeper to a lighter level of sleep or to awaken. Alow arousal threshold (i.e., awaken to a low level of CO2 or ventilatory drive) can preempt the CO2-mediated process of pharyngeal muscle compensation and prevent airway stabilization. A high arousal threshold, conversely, may prevent appropriate termination of apenas, prolonging apnea duration and oxyhemoglobin desaturation severity.”

Question 11

Name the risk factors for OSAHS.

Answer 11

“The major risk factors for OSAHS are obesity and male sex. Additional risk factors include mandibular retrognathia and micrognatia, a positive family history of OSAHS, genetic syndromes that reduce upper airway patency (e.g., Down syndrome, Treacher-Colling syndrome), menopause (in women), and various endocrine syndromes (e.g., acromegaly, hypothyroidism).”

Question 12

How many cases of OSAHS are due to obesity?

Answer 12

40-60%.

Question 13

A 10% weight is associated with an increased of apnea-hypopnea index in what percentage?

Answer 13

> 30%.

Question 14

What is the physiopathology of sleep apnea in most obese patients?

Answer 14

“Obesity predisposes to OSAHS through the narrowing effects of upper airway fat on the pharyngeal lumen. Obesity also reduces chest wall compliance and decreases lung volumes, resuling in a loss of caudal traction on upper airway structures.

Question 15

What is the risk of developping SAHOS in an obese patient in comparison to a normal-weight individual?

Answer 15

Fourfold increase.

Question 16

Summarize the epidemiology of SAHOS regarding differences between sex.

Answer 16

“The prevalence of OSAHS is two- to fourfold higher among men than among women. Factors that predispose men to OSAHS include android patterns of obesity (resulting in upper-airway fat deposition) and relatively great pharyngeal lenght, which exacerbates collapsibility. Premenopausal women are relatively protected from OSAHS by the influence of sex hormones on ventilatory drive. The decline in sex differences in older age is associated with an increased OSAHS prevalence in women after menopause.”

Question 17

For a first-degree relative of a patient with OSAHS, the odds ratio of having OSAHS is approximately twofold higher than that for someone without an affected relative.
True or False?

Answer 17

True.

Question 18

Summarize the epidemiology of SAHOS regarding the age groups and etiologies.

Answer 18

“OSAHS prevalence varies with age, from 2-15% among middle-aged adults to >20% among elderly individuals. There is a peak due to lymphoid hypertrophy among children between the ages of 3 and 8 years; with airway growth and lymphoid tissue regression during later childhood, prevalence declines. Then, as obesity prevalence increases in middle life and women enter menopause, OSAHS again increases.”

Question 19

From the following group of patients, select those in greater risk of developping SAHOS: obese vs non-obese; 3-8 years old vs young adult; diabetic hypertensive patient vs nondiabetic normotensive; asians versus europeans; afroamerican vs caucasian children/young adults.

Answer 19

• Obesity
• 3-8 years old
• Diabetes and hypertension
• Asians
• Afroamerican children and young adults.

Question 20

How does one explain the greater propensity of asian population to develop SAHOS with lower mass body index?

Answer 20

This probably might be due to craniofacial risk factors that narrow the nasopharynx.

Question 21

OSAHS is undiagnosed in a majority of adults.

True or False?

Answer 21

True.

Question 22

Name the main nocturnal differential diagnosis for sleep apnea and which features help differentiate them.

Answer 22

“Dyspnea is unusual, and its absence generally distinguishes OSAHS from paroxysmal nocturnal dyspnea, nocturnal asthma, and acid reflux with laryngospasm.”

Question 23

Awakening or sleep diruption are more frequent among women and older adults.
True or False?

Answer 23

True.

Question 24

Name all the symptoms associated with obstructive sleep apnea/hypopnea syndrome.

Answer 24

• Snoring, gasping or snorting.
• Awakening or sleep diruption
• Sleepiness
• Dry mouth, nocturnal heartburn, diaphoresis of the chest and neck, nocturia, morning headaches, trouble concentrating, irratability, and mood disturbances.

Question 25

How does one quantify the severity of OSAHS?

Answer 25

Mild OSAHS: AHI 5-14events/h
Moderate OSAHS: AHI 15-29 events/h
Severe OSAHS: AHI ≥30 events/h

Question 26

Heart failure patients are at increase risk for both OSAHS and CSA.
True or False?

Answer 26

True.

Question 27

Home study may yield a false-negative reuslt if sleep time is not accurately estimated.
True or False?

Answer 27

True.

Question 28

What are the key physiological information that one collects during a sleep study?

Answer 28

“The key physiological information collected during a sleep study for OSAHS assessment includes measurement of breathing (changes in airflow, respiratory excursion), oxygenation (hemoglobin oxygen saturation), body position, and cardiac rhythm. In addition, PSGs and some home sleep studies measure sleep continuity and sleep stages (by electroencephalogray, chin electromyography, and electro-oculography), limb movements (by leg sensors), and snoring intensity. This information is used to quantify the frequency and subtyps of abnormal respiratory events during sleep as well as associated changes in oxygen saturation, arousals, and sleep stage distributions. (…) Reports may also include the respiratory disturbance index, which includes the number of respiratory effort-related arousals in addition to the number of apneas plus hypopneas. In-laboratory PSG also quantifies sleep latency (time from “lights off” to first sleep onset), sleep efficiency (percentage of time asleep relative to time in bed), arousal index (number of cortical arousals per hour of sleep), time in each sleep stage, and periodic limb movement index. OSAHS severity can be further characterized according to the degree of sleep fragmentation associated with respiratory disturbances. Relevant metric include the frequency of cortical micro-arousals or awakenings per sleep hour, reduction in sleep continuity (low sleep efficiency), reduction of time in deeper stages of sleep (stage N3 and REM sleep) and increases in light sleep (stage N1). The detection of autonomic arousals, such as surges in blood pressure, changes in heart rate, and abnormalities in cardiac rhythm, also provides relevante information on OSAHs severity.”

Question 29

How does one define apnea, hypopnea and RERAs?

Answer 29

• Apnea: Cessation of airflow for 10 seconds or more during sleep, accompaied by persistent respiratory effort (if obstructive apnea) or absence of respiratory effort (if central apnea;
• Hypopnea: a 30% or more reduction in airflow for at least 10 sec during sleep that is accompanied by either a 3% or more desaturation or an arousal;
• Respiratory effort-related arousal (RERA): a partially obstructed breath that does not meet the criteria for hypopnea but provides evidence of increasing inspiratory effort (usually trough pleural pressure monitoring) punctuated by an arousal.

Question 30

What is the usuall blood pressure pattern during the night on a patient with OSAHS?

Answer 30

Non-dipper (absencwe of the typical 10-mmHg fall during sleep).

Question 31

Which tests might be useful in the differential diagnosis of OSAHS and narcolepsy?

Answer 31

Multiple sleep latency test or maintenance of wakefulness test.

Question 32

Summarize the comorbid conditions and consequences associated with OSAHS.

Answer 32

“OSAHS is a major contributor to cardiac, cerebrovascular, and metabolic disorders as well as to premature death. It is the most common medical cause of daytime sleepiness and negatively influences quality of life. This broad range of health effects is attributable to the impact of sleep fragmentation, cortical arousal, and itnermittent hypoxemia on vascular, cardiac, metabolic and neurologic functions. OSAHS-related respiratory events stimulate sympathetic overactivity, leading to acute blood pressure surges during sleep, endothelial adamage, and nocturnal as well as daytime hupertension. OSAHS-related hypoxemia also stimulates release of acute-phase proteins and reactive oxygen species that exacerbate insulin resistance and lipolysis and cause an augmenet prothrombotic and proinflammatory state. Inspiratory effort against an occluded airway causes large intrathoracic negative pressure swings, altering cardiac preload and afterload and resulting in cardiac remodeling and reduced cardiac function. Hypoxemia and sympathetic-parasympathetic imbalance also may cause electrical remodeling of the heart and myocyte injury.”

Question 33

What are the consequences of OSAHS over the blood pressure? How can one reduce these consequences?

Answer 33

“OSAHS can raise blood pressure to prehypertensive and hypertensive ranges, incrase the prevalence of a non-dipping overnight blood pressure pattern, and increase the risk of resistant hypertension. Elevations in blood pressure are due to augmented sympathetic nervous system activation as well as alterations in the rennin-angiotensin-aldosterone system and fluid balance. Treatment has been shown to reduce 24-h ambulatory blood pressure. Although the overall impact of CPAP on blood pressure levels is relatively modest (averaging 2-4 mmHg), larger improvements are observed among patients with high AHIs and sleepiness.”

Question 34

Summarize the correlation between OSAHS en cardiovascular, cererebrovascular, and metabolic diseases.

Answer 34

“Among the most serious health consequences of OSAHS is its impact on cardiac and metabolic functions. Strong epidemiologic evidence indicates that OSAHS significantly increases the risk of coronary artery disease, heart failure with and without reduced ejection fraction, atrial and ventricular arrhythmias, atherosclerosis and coronary artery disease, stroke, and diabetes. Treatment of OSAHS has been shown to reduce several markers of cardiovascular risk, improve insulin resistance, decrease the recurrence rate of atrial fibrillation, and improve various outcomes in patients with active cardiovascular disease. Large-scale trials are under way to evalute the role of OSAHS treatment in reducing cardiac event rates and in prolonging the survival of patients with cardiac disease.”

Question 35

What are the consequences of sleepiness due to OSAHS? How can we prevent this consequence?

Answer 35

“More than 50% of patients with moderate to severe OSAHS report daytime sleepiness. Patients with OSAHS symptoms have a twofold increased risk of occupational accidedents. Individuals with elevated aHIs are involved in motor vehicle crashes as much as seven times more often than persons with normal AHIs. Randomized controlled trials have shown that treatment of OSAHS with nasal CPAP therapy alleviates sleepiness as measured by either questionnaire or objective testing.”

Question 36

Name the factors that might explain residual sleepiness after CPAP treatment in OSAHS patients.

Answer 36

“Residual sleepiness may be due to several factors, including suboptimal treatment adherence, insufficient sleep time, other sleep disorders, or prior hypoxic-mediated damage in brain areas involved in alertness. Visceral adipose tissue, whose amounts are increased in patients with OSAHS, release smnogenic cytokines that may contribute to sleepiness.”

Question 37

What components of quality of life are most affected due to OSAHS?

Answer 37

Physical and vitality subscales.

Question 38

Depression, in particular symptoms of somatic depression (irritability, fatigue, lack of energy) is commonly reported in OSAHS.
True or False?

Answer 38

True.

Question 39

Explain the general treatments for OSAHS and its comorbid conditions.

Answer 39

“The clinician should seek to identify and address lifestyle and behavioral factors as well as comorbidities that may be exacerbating OSAHS. As appropriate, treatment should aim to reduce weight; optimize sleep duration (7-9 hours); regulate sleep schedules (with similar bedtimes and wake times across the week); encourage the patient to avoid sleepin in the supine position; treat nasal allergies; increase physical activity; eliminate alcohol ingestion within 3 h of bedtime; and minimize use of sedating medications. Patients should be counseled to avoid drowsy driving.”

Question 40

Name the side effects of CPAP treatment and how can one prevent/treat them.

Answer 40

• Nasal congestion: provide heated humidification, administer saline/steroid nasal sparys;
• Claustrophobia: change mask inferface, promote habituation;
• Difficulty exhaling: temporarily reduce pressure or BiPAP
• Bruised nasal ridge: change mask interface, provide protective padding;
• Aerophagia: administer antacids.

Question 41

What are the advantages of using CPAP for OSAHS?

Answer 41

Although average rates of adherence aren’t optimal (average, 50-80%), “controlled studies have demonstrated its beneficial effects on blood pressure, alertness, mood, and insulin sensitivity. Uncontrolled studies also indicate a favorable effect on cardiovascular outcomes, cardiac ejection fraction, atrial fibrillation recurrence, and mortality risk.”

Question 42

Oral applications might have a higher adherence than CPAP and some studies indicate that these devices can reduce AHI by ≥50% in two-thirds of individuals, although these data are based largely on mild OSAHS.
True or False?

Answer 42

True.

Question 43

Name the different surgeries available for OSAHS treatment. What are their advantages and limitations? Is there any indicators for patient selection?

Answer 43

“Upper airway sugery for OSAHS is less effective than CPAP and is mostly reserved for the treatment of patients who snore, have mild OSAHS, and cannot tolerate CPAP. Uvulopalatopharyngoplasty (removal of the uvula and the margin of the soft palate) is the most common surgery and, although results vary greatly, has a success rate similar to or slighly lower than treatment with oral applicances. Upper airway sugery is less effective in severe OSAHS and in obese patients. Success rates may be higher for multilevel surgery (involving more than one site/structure) performed by an experience surgeon, but the selection of patients is an important factor and relies on careful targeting of culprit areas for surgical resection. Bariatric surgery is an option for obese patients with OSAHS and can improve not only OSAHS but also other obesity-associated health conditions. Other procedures that can decrease snoring but have minimal effects on OSAHS include injection of the soft palate (resulting in stiffening), radiofrequency ablation, laser-assisted uvulopalatoplasty, and palatal implants.”

Question 44

Supplemental oxygen can improve oxygen saturation, but there is little evidence that it improves OSAHS symptoms or the AHI.
True or False?

Answer 44

True.

Question 45

Explain the pathophysiology of central sleep apnea (CSA).

Answer 45

“CSA, whi is less cmmon than OSAHS, may occur in isolation or, more often, in combination with obstructive events in the form of “mixed” apneas. CSA is often caused by an increased sensitivy to pCO2, which leads to an unstable breathing pattern that manifests as hyperventilation alternating with apnea. A prolonged circulation delay between the pulmonary capillaries and carotid chemoreceptrs is also a contributing cause; thus individuals with congestive heart failure are at risk for CSA. With prolonged circulation delay, there is a crescendo-decrescendo breathing pattern known as Cheyne-Stokes respiration.”

Question 46

Besides heart failure, what other risk factors are associated with central sleep apnea?

Answer 46

Opioid medication (which appear to have a dose-dependent effect on CSA) and hypoxia.

Question 47

How do you describge complex sleep apnea?

Answer 47

Central apneas induced by CPAP, particularly at high pressures.

Question 48

Compare the use of oxygen in OSAHS versus CSA.

Answer 48

There is no evidence of efficacy of oxygen suplementation in the first. In the latter, it “can reduce the frequency of central apneas, particularly in patients with hyopxemia.”

Question 49

How should one treat Cheyne-Stokes respiration?

Answer 49

“Cheyne-Stokes respiration is treated by optimizing therapy for heart failure and, in some cases, using CPAP with or without supplemental oxygen. Adaptive seroventilation, a form of ventilatory support that dynamically changes inspiratory support levels across periods of apnea and hypopnea, can minimize large fluctuations in PCO2 that produce central apnea and can be effective for the treatment of CSA.”