Webcast CME

Obstructive Sleep Apnea



A 54-year-old male presents with fatigue, morning headaches, and excessive sleepiness. His medical history is significant for diabetes, hypertension, hypercholesterolemia, advanced heart failure (New York Heart Association, NYHA class IV) and a 20-pack year tobacco history. Medications include daily carvedilol, spironolactone, metformin, and simvastatin. His wife reports loud snoring that can be heard outside the bedroom on a nightly basis. The patient sometimes wakes up with a choking sensation and his wife has heard him stop breathing in his sleep on a couple of occasions. He wakes up feeling unrefreshed with a dry mouth and sore throat almost every morning. He prefers to sleep on his side with one pillow under his head, and snoring is loudest when he sleeps supine. The patient reports excessive daytime sleepiness, with an Epworth Sleepiness Scale (ESS) score of 16/24. His bedtime is 9 pm. He falls asleep within 5 minutes, wakes up twice a night briefly to use the restroom, and wakes up in the morning at 5:30 am. He does not nap during the day. He reports drinking one cup of coffee in the morning and two glasses of wine each night. He denies symptoms of restless legs syndrome, abnormal behaviors at night, cataplexy, sleep-related hallucinations and sleep paralysis.

This patient’s presentation is most suggestive of:

  1. Idiopathic hypersomnia
  2. Narcolepsy type without cataplexy
  3. Obstructive sleep apnea
  4. Central sleep apnea
  5. Obesity hypoventilation

Correct! Answer:



Rationale

Obstructive sleep apnea (OSA) is a sleep-related breathing disorder characterized by episodes of partial and complete collapse of the upper airway during sleep, that result from anatomical and functional disturbances, such as craniofacial features, soft tissue changes, and obesity.1,2 It is a common cause of excessive sleepiness and is associated with non-restorative sleep, frequent awakenings, morning headaches, and affective and cognitive symptoms. OSA increases the risk of systemic hypertension, cardiovascular risk, and metabolic disorders.3–5 While the patient has significant daytime sleepiness, narcolepsy, and idiopathic hypersomnia would not be considered highly likely in the setting of untreated OSA. Central sleep apnea and obesity hypoventilation, independently would not produce the presentation of snoring and witnessed apnea. The diagnostic criteria of OSA are shown in Table 1.

Table 1

  Diagnostic Criteria for Obstructive Sleep Apnea Syndrome

Criteria (A and B) or C have to be met
  1. The presence of 1 or more of the following:
        1. Complaints of sleepiness, nonrestorative sleep, fatigue, or insomnia
        2. Complaints of waking up with breath holding, gasping, or choking
        3. An observer reports habitual snoring, breathing interruptions, or both during sleep
        4. Hypertension, mood disorder, cognitive dysfunction, coronary artery disease, stroke, congestive heart failure, atrial fibrillation, or type 2 diabetes mellitus
  1. Polysomnography or home sleep apnea test demonstrates:

Predominantly obstructive sleep disordered breathing events occurring ≥ 5 times per hour
  1. Polysomnography or home sleep apnea test demonstrates:

Predominantly obstructive sleep disordered breathing events occurring ≥ 15 times per hour

Adapted from: The AASM International Classification of Sleep Disorders – Third Edition, Text Revision (ICSD-3-TR)6

Case Continued

The patient’s physical examination revealed a blood pressure of 140/80 mmHg, heart rate 71 bpm, respiratory rate 18/min, neck circumference of 45 cm, and body mass index (BMI) of 30 kg/m2. The oropharyngeal exam was notable for Friedman tongue position class III. Chest examination demonstrated bilateral basilar inspiratory crackles with normal heart sounds. Neurologic examination was unremarkable save for hyperreflexia (deep tendon reflexes 3+), including normal muscle tone and strength, intact fine touch, vibration, and proprioception, normal gait, and no rigidity or tremor.

Friedman Tongue Position (FTP) III allows the visualization of:

  1. Only the hard palate
  2. Some of the soft palate, but the distal soft palate is eclipsed
  3. The uvula but the tonsils are only partially seen
  4. The entire uvula and tonsils or pillars

Correct! Answer:



Rationale

FTP is one of two scales that assess the oropharynx in the evaluation of OSA.7 It is performed with the mouth wide open and the tongue resting inside the mouth in the normal position. The tongue position relative to the palate and the tonsils is graded and the posterior pharyngeal space is staged based on the combination of findings. In contrast, the Mallampati test assesses oropharyngeal airway crowding by grading visibility of the soft palate, uvula, and tonsillar pillars with the mouth open and tongue protruded.8 In a meta-analysis, both the Mallampati and FTP techniques predicted OSA severity as determined by the apnea-hypopnea index (AHI), however the FTP showed an increased strength of correlation.9

Friedman tongue position grading:

FTP I: The entire uvula and tonsils or pillars are visualized.
FTP II: The uvula is visualized, but the tonsils are only partially seen.
FTP III: Some of the soft palate is visualized, but the distal soft palate is eclipsed.
FTP IV: Only the hard palate is visualized.

Case Continued

Which of the following renders home sleep apnea testing (HSAT) an inappropriate diagnostic study in this case?

  1. Severe excessive daytime sleepiness
  2. Loud snoring with witnessed apneas
  3. Advanced heart failure (NYHA class IV)
  4. Positional worsening of symptoms

Correct! Answer:



Rationale

Home sleep apnea testing is recommended for patients with a high pretest probability of moderate-to-severe OSA without significant comorbid medical or sleep disorders that would render polysomnography (PSG) more appropriate. Due to the absence of electroencephalography (EEG), the severity of OSA measured by the HSAT respiratory event index (REI) assumes all of monitoring time to be sleep time, underestimating disease severity.10,11 If a single HSAT is negative, inconclusive, or technically inadequate, PSG should be performed if clinical suspicion for OSA is high.10 Given our patient has severe cardiac disease, HSAT is not the optimal diagnostic assessment. Excessive daytime sleepiness, snoring and witnessed apnea and their worsening in the supine position are typical in OSA.

Polysomnography is recommended to confirm the diagnosis of OSA when significant comorbidities render HSAT insufficient (Table 2). This includes significant cardiorespiratory disease, neuromuscular disease, awake hypoventilation or suspicion of sleep-related hypoventilation, chronic opioid medication use, history of stroke, or severe insomnia (8). PSG diagnosis of OSA is based on an obstructive respiratory disturbance index (RDI) that includes apneas, hypopneas, and respiratory event-related arousals (RERAs) or the apnea-hypopnea index (AHI) ≥ 5 events/h associated with symptoms or comorbidities or an obstructive RDI or AHI ≥ 15 events/h.6

Table 2. Comorbid conditions that warrant in-laboratory PSG
  • Body mass index (BMI) >50 kg/m<sup>2 </sup>
  • Obesity-hypoventilation syndrome (PaCO2 awake >45 mmHg and BMI >30 kg/m<sup>2</sup>)
  • Chronic obstructive pulmonary disease (COPD) with a forced expiratory volume in 1 second (FEV1) of <60%
  • Moderate to severe cardiac disease (New York Heart Association, NYHA, class III or IV)
  • Moderate to severe neuromuscular disease (FEV1 < 60-80% of predicted)
  • Documented pulmonary hypertension >40 mmHg
  • Hypoxia and/or hypercapnia at rest, or oxygen dependent for any reason
  • Chronic nightly narcotic use
  • Violent behaviors during sleep, REM sleep behavior disorder, atypical parasomnias, sleep-related epilepsy
  • Inability to understand instructions
  • History of central sleep apnea
  • Inadequate HSAT results after ≥2 attempts
  • Unsuitable home environment (noise level, partner/family interactions, distance from sleep laboratory)
  • Severe intellectual, physical, and/or psychiatric disability with inadequate caregiver attendance
  • Second opinion where symptoms/results of previous testing do not equate with the clinical impression, the original diagnosis is uncertain, and/ or serious medical legal consequences may be relevant
  • Sleep duration typically <4 h per night

Clinical Practice Guideline for Diagnostic Testing for Adult Obstructive Sleep Apnea: An American Academy of Sleep Medicine Clinical Practice Guideline12

Case Continued

Polysomnography revealed an AHI ≥ 15 events/h, a minimum oxygen saturation of 87%, mean end-tidal CO2 during wake of 40 mmHg and during sleep of 45 mmHg, without positional or sleep stage dependency.

Positive airway pressure therapy was initiated, and the patient was counseled on its evidence-based benefits. Which of the following statements regarding PAP therapy for OSA is not supported by current evidence:

  1. PAP therapy is associated with reductions in blood pressure.
  2. PAP therapy reduces the risk of cardiovascular outcomes and death.
  3. PAP therapy improves quality of life (QoL).
  4. PAP therapy improves cognitive performance

Correct! Answer:



Rationale

Positive airway pressure therapy is the first-line treatment for moderate to severe OSA and is often preferred as initial therapy for mild disease severity.11,13 Pressure generated by the device is delivered via an interface worn over the nose, in the nares, or over both nose and mouth. Pressure may be delivered as a preset single pressure (CPAP), different inspiratory and expiratory pressures (Bilevel PAP), or variable over a pre-determined range (Auto CPAP, Auto Bilevel).11 In patients with OSA, CPAP is associated with a reduction in systolic blood pressure of 2.5 mmHg (95% CI, 1.5 to 3.5 mmHg; p<0.001) and diastolic blood pressure of 2.0 mmHg (95% CI, 1.3 to 2.7 mmHg; p<0.0013,14 being more effective in resistant hypertension than nonresistant hypertension.15 Moreover, CPAP therapy improves QoL (0.20; 95%CI = 0.04, 0.35), specifically physical symptoms based on a meta-analysis pooling the physical subscales of the SF-36, Nottingham Health Profile, EuroQoL, Calgary Sleep Apnea Quality of Life Index, and Functional Outcomes of Sleep Questionnaire.16 CPAP therapy also improves cognitive impairment in patients OSA, including those with mild cognitive impairment and some aspects of cognition in Alzheimer’s disease17. Despite these beneficial effects18, recent meta-analyses showed no association of PAP therapy and reduced risk of cardiovascular outcomes or death in patients with OSA.7,19,20 Experts believe this to be due to study limitations including poor PAP adherence and small sample size.

Table 3. Predictors of PAP Adherence


Good Adherence to PAP

Poor Adherence to PAP
  • Presence of daytime sleepiness
  • Strong perceived benefit
  • Good early adherence
  • Oxygen desaturations
  • Increasing age
  • Lack of daytime symptoms
  • High mask leak
  • Race (African American)
  • Lower socioeconomic group
  • Small nasal airway
  • Mask related discomfort

Adapted from: Kasetti et al., “Personality Traits and Pre-Treatment Beliefs and Cognitions Predicting Patient Adherence to Continuous Positive Airway Pressure.”
Dielesen et al., “Six Early CPAP-Usage Behavioral Patterns Determine Peak CPAP Adherence and Permit Tailored Intervention, in Patients with Obstructive Sleep Apnea.”
Chai-Coetzer et al., “Predictors of Long-Term Adherence to Continuous Positive Airway Pressure Therapy in Patients with Obstructive Sleep Apnea and Cardiovascular Disease in the SAVE Study.

Case Continued

The patient returned after six months of regular auto-CPAP use and reported dissatisfaction with PAP therapy. He asked about PAP therapy alternatives.

All the following meet eligibility for hypoglossal nerve stimulation (HNS) therapy consideration except:

  1. Body mass index >35 kg/m2
  2. Apnea-hypopnea index >15 events/h
  3. Nonconcentric collapse of the retropalatal airway on drug-induced sleep endoscopy (DISE)
  4. Intolerance to PAP therapy for at least 3 months

Correct! Answer:



Rationale

Hypoglossal nerve stimulation is a surgical treatment for OSA that functions as a closed-loop system, consisting of an implanted pulse generator, a stimulation lead placed around the distal hypoglossal nerve, and a sensing lead in the intercostal space to detect respiration. Therapy reduces airway obstruction by physically increasing muscle tone to selected upper airway muscles innervated by the hypoglossal nerve.20 It is approved by the FDA for treatment of OSA in patients with a BMI <32 kg/m2, AHI 15-65 and <25% of central apneas, absence of concentric collapse of the retropalatal airway on drug induced sleep endoscopy (DISE), and PAP failure or intolerance over 3 months.1,21,22 A recent systematic review and meta-analysis found HNS therapy significantly improved AHI, and sleep-related functional outcomes in both the short term (less than a year) and long term (more than a year).23 Serious adverse events are rare and consist of pain, tongue abrasion and internal/external device malfunction.23

Case Continued

The patient underwent HNS implantation. One month later, the device was activated during an office visit and the patient instructed to use it at night at home. Two months later, he underwent an overnight PSG to determine the optimal stimulation parameter settings. The patient’s treatment AHI was reduced to five events/h in the presence of both supine sleep and REM sleep at the default electrode configuration with a therapeutic range of 1.9 to 2.3 volts.

All the following are demonstrated outcomes of HNS therapy except:

  1. Quality of life improvement
  2. Reduction in ESS score
  3. Reduction in AHI
  4. Reduction in tongue strength and fatigability

Correct! Answer:



Rationale

The ESS is a self-administered questionnaire that measures a person’s subjective level of daytime sleepiness across eight common situations, with total scores ranging from 0 to 24. An ESS score ≥10 is generally considered abnormal and indicative of clinically significant excessive daytime sleepiness.24

In a multicenter prospective HNS cohort, treatment after five years was associated with improvement in AHI response rate (AHI <20 events/h and >50% reduction), daytime sleepiness measured by the ESS, and quality of life25. Similar findings were found in the Acute Decompensated Heart Failure National Registry (ADHERE), with a reduction in the median AHI (34 to 7 events/h) and ESS (12 to 7)26. Moreover, after 1.5 years of HNS therapy, tongue strength and fatigability were not affected27.

Case Continued

Which of the following statements best summarizes the effects of exercise and dietary interventions in patients with OSA?

  1. Exercise and dietary interventions improve OSA by reducing the AHI to <5.
  2. Exercise and dietary interventions significantly reduce AHI and improve functional status but typically do not eliminate OSA.
  3. Dietary quality has no measurable association with OSA severity or BMI.
  4. Caffeine and tobacco cessation are associated with a decreased risk of OSA.

Correct! Answer:



Rationale

A systematic review and meta-analysis of randomized controlled trials found both exercise and dietary interventions reduced the AHI (−8.09 events/h, 95% CI: −11.94 to −4.25), but not enough to resolve OSA (mean baseline and post‐intervention AHI 27.9 ± 4.0 and 23.8 ± 3.9 events/h, respectively).28 In a randomized clinical trial, exercise improved NYHA functional class distribution in patients with OSA, classes II and III moved into class I (P < .05).29 In the Multi-Ethnic Study of Atherosclerosis, subjects with moderate to severe OSA had poorer Alternative Healthy Eating Index – 2010 (AHEI-10), a dietary quality tool, because of reduced whole grain intake (β = −0.200, SE = 0.072, p < 0.01) and increased red/processed meat consumption (β = −0.440, SE = 0.136, p < 0.01)30. Diet reduces BMI and disease severity (BMI, −2.41 kg/m2, 95% CI: −4.09 to −0.73) in patients with OSA.28

A meta-analysis of the association between OSA, alcohol, caffeine and tobacco found alcohol increases the risk for OSA (OR 1.33 95% [CI]; 1.10‐1.62), while insufficient data exits for caffeine and tobacco use31.

Case Continued

Which of the following best characterizes the mechanism and clinical impact of tirzepatide in adults with obesity and OSA?

  1. Tirzepatide improves OSA primarily through direct stimulation of upper-airway dilator muscle tone independent of weight loss.
  2. Tirzepatide produces modest weight loss without meaningful change in AHI or OSA remission rates.
  3. Tirzepatide leads to significant reduction in AHI and higher rates of OSA remission, with benefits largely mediated by weight reduction rather than direct airway effects.
  4. Tirzepatide replaces PAP as first-line therapy for patients with moderate-to-severe OSA regardless of BMI.

Correct! Answer:



Rationale

Tirzepatide, a dual glucose-dependent insulinotropic polypeptide (GIP) and GLP-1 receptor agonist, was recently approved by the FDA for the treatment of moderate-to-severe OSA in adults with obesity, to be used in combination with a reduced-calorie diet and increased physical activity. In the phase 3 SURMOUNT-OSA studies, participants receiving Tirzepatide had statistically significant reductions in AHI compared with placebo over 52 weeks, and a substantially higher proportion of patients achieved remission or mild OSA (e.g., AHI < 5 or reduced symptoms) than those on placebo. These benefits are thought to be mediated primarily through weight loss and reduction in fat burden around the upper airway, rather than direct effects on airway mechanics.32

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