Patient with sleep apnea will present as → a 49-year-old man who is brought to your office by his partner, who is concerned about his daytime sleepiness. Last week, the patient fell asleep while stopped at a red light. She says that he snores loudly and sometimes stops breathing for a few seconds while sleeping. His past medical history is significant for hypertension. He has a 20-pack-year history of smoking. His temperature is 98.6 F, heart rate is 86/min, blood pressure is 148/98 mm Hg, and respiratory rate is 12/min. On physical exam, he is obese. His lungs are clear, and his lower extremity exam is within normal limits.
Patient with obesity hypoventilation syndrome will present as → a 52-year-old male with a history of severe obesity (BMI of 42 kg/m²) presents with chronic daytime sleepiness and fatigue. He reports a long-standing history of snoring, and recently, his wife noticed episodes of apnea during sleep. He also complains of morning headaches and shortness of breath with minimal exertion. On examination, he is noted to have an increased neck circumference and a BMI consistent with severe obesity. His oxygen saturation is 88% on room air, and he exhibits shallow, rapid breathing. Arterial blood gas analysis reveals chronic respiratory acidosis with elevated bicarbonate levels, suggesting chronic hypoventilation. A sleep study confirms the diagnosis of obesity hypoventilation syndrome with concomitant obstructive sleep apnea. The patient is started on positive airway pressure therapy at night and is counseled extensively on weight loss strategies, including dietary changes and exercise. Referral to a pulmonologist and a bariatric specialist is made for further management.
Intermittent obstruction of the airflow (typically at the level of the oropharynx) produces periods of apnea during sleep
- Each apneic period is usually 20 to 30 seconds long (but may be longer) and results in hypoxia, which arouses the patient from sleep. This occurs multiple (sometimes hundreds of) times overnight.
Risk factors
- Obesity (especially around the neck): nonobese patients can also have OSA
- Structural abnormalities: enlarged tonsils, uvula, soft palate; nasal polyps; hypertrophy of muscles in the pharynx; deviated septum; deep overbite with a small chin
- Family history
- Alcohol and sedatives worsen the condition
- Hypothyroidism (multifactorial)
Presents as:
- Snoring and daytime sleepiness due to disrupted nocturnal sleep
- Personality changes, decreased intellectual function, decreased libido, morning headaches, polycythemia
- Repeated oxygen desaturation and hypoxemia can lead to systemic and pulmonary HTN as well as cardiac arrhythmias
Obesity-hypoventilation syndrome (OHS) (historically described as the Pickwickian syndrome)
- Consists of the triad of obesity (BMI > 30), sleep-disordered breathing, and chronic hypercapnia (PaCO2 ≥45 mmHg) during wakefulness in the absence of other known causes of hypercapnia
- Signs and symptoms of obesity hypoventilation syndrome (OHS) are essentially the same as OSA. These two diseases are often concurrent.
Polysomnography (overnight sleep study in a sleep laboratory) confirms the diagnosis of obstructive sleep apnea and can distinguish OSA from CSA
- Home sleep apnea testing (HSAT) may be an acceptable alternative for patients who are strongly suspected of having OSA and who do not have medical comorbidities (eg, heart failure or lung disease)
In adults, a diagnosis of OSA is defined by either of the following:
Five or more predominantly obstructive respiratory events per hour of sleep (for polysomnography) or recording time (for HSAT) in a patient with one or more of the following:
- Sleepiness, nonrestorative sleep, fatigue, or insomnia symptoms
- Waking up with breath-holding, gasping, or choking
- Habitual snoring, breathing interruptions, or both noted by a bed partner or other observer
- Hypertension, mood disorder, cognitive dysfunction, coronary artery disease, stroke, congestive heart failure, atrial fibrillation, or type 2 diabetes mellitus
Fifteen or more predominantly obstructive respiratory events per hour of sleep (for polysomnography) or recording time (for HSAT), regardless of the presence of associated symptoms or comorbidities
Obesity-hypoventilation syndrome (OHS) is a diagnosis of exclusion that can be made when the following criteria are met:
- Obesity (body mass index [BMI] >30 kg/m2)
- Awake alveolar hypoventilation as indicated by a partial arterial pressure of carbon dioxide ≥45 mmHg
- Alternative causes of hypercapnia and hypoventilation have been excluded
Management of obstructive sleep apnea
Behavior/lifestyle modification for ALL patients who have OSA and a modifiable risk factor
- This includes weight loss and exercise, avoiding alcohol and sedatives, smoking cessation, and sleeping in a non-supine position
Mild to moderate OSA:
- Positive airway pressure therapy
- If the patient refuses or there are issues with compliance, an oral appliance can be offered
Severe OSA:
- Continuous positive airway pressure (CPAP) provides positive pressure, thus preventing occlusion of the upper pharynx. This is the preferred therapy for the majority of patients because it is noninvasive and has proven efficacy. It is poorly tolerated by some due to noise and discomfort
- Uvulopalatopharyngoplasty—removal of redundant tissue in the oropharynx to allow more airflow
- Tracheostomy is a last resort for those in whom all other therapies have failed or who have life-threatening OSA (severe hypoxemia or arrhythmias)
Management of obesity hypoventilation syndrome
- Positive airway pressure (PAP) at night — CPAP is first-line for most patients, who have coexisting severe OSA — plus sustained weight loss
- For patients with OHS who fail or do not tolerate first-line therapies in whom aggressive attempts have been made to optimize PAP therapy, options include tracheostomy for the treatment of sleep-disordered breathing and bariatric surgery or rarely medication for weight loss
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Picmonic
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Obstructive sleep apnea (OSA) is caused by narrowing or obstruction of the airway during sleep. A patient diagnosed with this disorder will experience five or more episodes of apnea per hour. When a patient becomes hypercapnic due to periods of apnea, they will experience a startle response, in the form of a snort or a gasp, which allows the tongue and soft palate to fall forward, thereby reopening the patient’s airway. Loud, frequent snoring, daytime sleepiness, and headaches are also common clinical manifestations in those with OSA. Complications of untreated sleep apnea include hypertension, right-sided heart failure from pulmonary hypertension, and cardiac dysrhythmias. Interventions to treat obstructive sleep apnea include changing the patient’s sleeping position, use of an oral appliance such as a mouth guard, CPAP, BiPAP, or surgical interventions. Patients with OSA should be encouraged to lose weight, as being overweight or obese worsens sleep apnea.
Play Video + QuizQuestion 1 |
A 47-year-old man is evaluated for loud snoring and witnessed pauses in breathing during sleep. His BMI is 36 kg/m², neck circumference is 45 cm (17.7 in), and oropharyngeal examination shows a crowded airway with an enlarged uvula. Polysomnography shows repeated 20-second episodes of absent airflow with continued chest and abdominal respiratory effort. Which of the following is the most likely mechanism of these events?
Absent central respiratory drive from the brainstem Hint: Loss of central drive causes central sleep apnea, in which respiratory effort stops along with airflow. This patient keeps breathing against a closed airway. | |
Bronchospasm of the small airways Hint: Bronchospasm causes wheezing and obstructive spirometry while awake; it does not cause sleep-related cessation of airflow with continued effort. | |
Collapse of the pharyngeal airway during sleep | |
Diaphragmatic weakness from phrenic nerve injury Hint: Diaphragmatic weakness causes orthopnea and reduced effort, not complete airflow cessation with preserved chest and abdominal effort. | |
Reduced pulmonary diffusing capacity Hint: A reduced diffusing capacity lowers oxygen transfer but does not stop airflow at the level of the upper airway. |
Question 1 Explanation:
In obstructive sleep apnea, upper-airway dilator muscle tone (especially the genioglossus) falls during sleep, so the pharyngeal walls collapse and airflow stops even though the patient keeps trying to breathe. Continued chest and abdominal effort during the apnea is what separates obstructive sleep apnea from central sleep apnea, where the brainstem stops sending the signal to breathe. Obesity, a large neck, and a crowded oropharynx all narrow the airway and make collapse more likely.
Question 2 |
A 50-year-old man comes to the office because his wife reports loud snoring and pauses in his breathing during sleep. He has daytime sleepiness and hypertension. BMI is 33 kg/m². He has no heart failure, lung disease, or neuromuscular disease. Which of the following is the most appropriate next step to confirm the diagnosis?
Arterial blood gas Hint: An arterial blood gas can show daytime hypercapnia in obesity hypoventilation syndrome but cannot diagnose obstructive sleep apnea. | |
Chest radiograph Hint: A chest radiograph does not detect apneas during sleep. | |
Echocardiogram Hint: Echocardiography can show complications such as pulmonary hypertension but does not diagnose sleep apnea. | |
Pulmonary function testing Hint: Pulmonary function tests assess lung disease while awake and do not detect sleep-related airway collapse. | |
Sleep study (polysomnography or home sleep apnea test) |
Question 2 Explanation:
A sleep study confirms obstructive sleep apnea. In-lab polysomnography is the gold standard and also separates obstructive from central sleep apnea. A home sleep apnea test is an acceptable alternative for uncomplicated adults with a high pretest probability of moderate-to-severe OSA and no significant heart, lung, or neuromuscular disease, like this patient. OSA is diagnosed with an apnea-hypopnea index of 5 or more events per hour plus symptoms or related conditions (such as hypertension), or 15 or more events per hour regardless of symptoms.
Question 3 |
A 52-year-old man with hypertension comes to the office because of loud snoring, witnessed pauses in breathing, and excessive daytime sleepiness. BMI is 34 kg/m². Polysomnography shows an apnea-hypopnea index of 38 events per hour with oxygen desaturation to 82%. He has already started a weight-loss program and stopped drinking alcohol. Which of the following is the most appropriate next step in treatment?
Alprazolam Hint: Benzodiazepines relax the upper-airway muscles and depress breathing, worsening obstructive sleep apnea; they should be avoided. | |
Continuous positive airway pressure (CPAP) | |
Nortriptyline Hint: Antidepressants are not recommended as treatment for obstructive sleep apnea. | |
Tracheostomy Hint: Tracheostomy is a last resort for severe, life-threatening sleep apnea when all other therapies fail. | |
Uvulopalatopharyngoplasty Hint: Upper-airway surgery is reserved for selected patients who cannot tolerate CPAP or have a correctable anatomic obstruction. |
Question 3 Explanation:
Continuous positive airway pressure (CPAP) is the first-line treatment for obstructive sleep apnea, together with weight loss and avoidance of alcohol and sedatives. Alternatives for patients who cannot tolerate CPAP include an oral (mandibular advancement) appliance and upper-airway surgery such as uvulopalatopharyngoplasty (UPP) or hypoglossal nerve stimulation. Tracheostomy is a last resort for severe, life-threatening OSA. Antidepressants such as protriptyline or SSRIs are not recommended to treat OSA, and nortriptyline has no role. Benzodiazepines such as alprazolam can worsen upper-airway collapse and respiratory depression, so they should be avoided.
Question 4 |
A 58-year-old man comes to the office because his wife reports loud snoring and pauses in his breathing at night. He feels tired during the day and has fallen asleep while driving. BMI is 35 kg/m² and blood pressure is 154/94 mmHg. Polysomnography shows an apnea-hypopnea index of 42 events per hour with oxygen desaturation to 80%. He declines treatment. If his condition remains untreated, he is at greatest risk of developing which of the following?
Atrial fibrillation | |
Bronchiectasis Hint: Bronchiectasis results from recurrent airway infection and inflammation, not from sleep-disordered breathing. | |
Hypothyroidism Hint: Hypothyroidism can contribute to obstructive sleep apnea, but sleep apnea does not cause hypothyroidism. | |
Pneumothorax Hint: Pneumothorax is linked to blebs, emphysema, and trauma, not to obstructive sleep apnea. | |
Pulmonary fibrosis Hint: Pulmonary fibrosis is an interstitial lung disease unrelated to upper-airway collapse during sleep. |
Question 4 Explanation:
Untreated moderate-to-severe obstructive sleep apnea causes repeated nighttime hypoxemia and surges in sympathetic tone. Over time this leads to systemic hypertension (often resistant), atrial fibrillation and other arrhythmias, pulmonary hypertension, heart failure, stroke, and motor-vehicle crashes from daytime sleepiness. Continuous positive airway pressure is first-line treatment and helps control blood pressure and reduce atrial fibrillation recurrence.
Question 5 |
A 45-year-old man with mild obstructive sleep apnea asks how to reduce his nighttime symptoms. He has a BMI of 31 kg/m², drinks 3 glasses of wine every evening shortly before bed, and takes no medications. He usually sleeps on his back. Which of the following habits is most likely to be worsening his sleep apnea?
Evening alcohol intake | |
Exercising in the morning Hint: Regular exercise helps with weight loss and modestly improves sleep apnea severity. | |
Sleeping with the head of the bed elevated Hint: Elevating the head of the bed can reduce airway collapse in some patients; it does not worsen sleep apnea. | |
Taking a nasal saline spray at bedtime Hint: Nasal saline improves nasal patency and does not worsen upper-airway collapse. | |
Using a side-sleeping pillow Hint: Side (lateral) sleeping keeps the tongue from falling back and reduces apneas compared with sleeping supine. |
Question 5 Explanation:
Alcohol and sedating drugs (benzodiazepines, opioids, sedating antihistamines) relax the upper-airway dilator muscles and blunt the arousal response, so the airway collapses more often and apneas last longer. Patients with obstructive sleep apnea should avoid alcohol and sedatives, especially near bedtime. Other risk factors include obesity, male sex, older age, a large neck, craniofacial abnormalities (retrognathia), tonsillar hypertrophy, hypothyroidism, and acromegaly. Supine sleeping also worsens apneas, so positional therapy is often recommended.
Question 6 |
A 54-year-old woman comes to the office because of daytime sleepiness, morning headaches, and loud snoring. She has never smoked. BMI is 44 kg/m². Lungs are clear. Awake arterial blood gas on room air shows pH 7.37, PaCO2 52 mmHg, PaO2 62 mmHg, and HCO3− 30 mEq/L. Chest radiograph and spirometry are normal. Which of the following is the most likely diagnosis?
Chronic obstructive pulmonary disease Hint: COPD can cause chronic hypercapnia, but this patient has never smoked and has normal spirometry. | |
Obesity hypoventilation syndrome | |
Panic disorder Hint: Panic attacks cause hyperventilation with a low PaCO2 and acute respiratory alkalosis, the opposite of this ABG. | |
Pulmonary embolism Hint: Pulmonary embolism typically causes hypoxemia with a low PaCO2 from tachypnea. | |
Salicylate toxicity Hint: Salicylate toxicity causes a mixed respiratory alkalosis and anion-gap metabolic acidosis, not chronic hypercapnia. |
Question 6 Explanation:
Obesity hypoventilation syndrome is defined by obesity (BMI ≥30 kg/m²) plus awake daytime hypercapnia (PaCO2 ≥45 mmHg) after other causes of hypoventilation are excluded. Chronic CO2 retention is compensated by the kidneys, so the ABG shows a near-normal pH with an elevated bicarbonate. About 90% of patients also have obstructive sleep apnea, which explains her snoring and sleepiness. Treatment is positive airway pressure at night plus sustained weight loss.
Question 7 |
A 50-year-old woman comes to the office for evaluation of her snoring. Her husband reports that she snores loudly most nights and wakes up frequently during the night, but he has not observed her choking, gasping, or stopping breathing while asleep. The patient reports no morning headaches, memory loss, or excessive daytime sleepiness. She drinks one glass of wine with dinner daily. Vital signs are normal. BMI is 27 kg/m² and neck circumference is 38 cm (15 in). Oropharyngeal examination is normal. Cardiac examination reveals normal heart sounds. Lung fields are clear bilaterally. Which of the following is the best next step in management of this patient?
Advise weight loss and alcohol cessation | |
Refer for polysomnography Hint: Polysomnography (sleep study) is indicated for diagnosing OSA, particularly if there are symptoms such as witnessed apneas, excessive daytime sleepiness, or other signs of sleep-disordered breathing. In this case, the absence of these symptoms makes immediate referral for polysomnography less necessary. | |
Prescribe a mandibular advancement device Hint: Mandibular advancement devices are used to treat mild to moderate OSA and significant snoring. Without evidence of OSA or a trial of conservative measures, it is premature to prescribe such a device. | |
Recommend nasal continuous positive airway pressure (CPAP) Hint: CPAP is the treatment of choice for moderate to severe OSA. This patient does not have symptoms suggestive of OSA, making CPAP inappropriate at this stage. | |
Schedule a follow-up in six months Hint: While follow-up is important, immediate lifestyle interventions should be recommended to address the patient’s snoring. Waiting six months without intervention may lead to continued symptoms and potential progression of any underlying issues. |
Question 7 Explanation:
The best next step in the management of this patient is to advise weight loss and alcohol cessation. Weight loss can help reduce the severity of snoring and improve overall health, while avoiding alcohol before bedtime can decrease snoring by reducing airway muscle tone. Given that the patient has no observed apneas or other symptoms of obstructive sleep apnea (OSA), conservative measures such as these are appropriate initial steps.
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References: Merck Manual · UpToDate