• Clinical science

Obstructive sleep apnea

Abstract

Obstructive sleep apnea (OSA) is the most common breathing-related sleep disorder and is typically associated with obesity. It is characterized by obstruction of the upper airways due to the collapse of the pharyngeal muscles. OSA results in multiple episodes of interrupted breathing (apnea and hypopnea) during sleep, leading to alveolar hypoventilation. Patients generally suffer from severe daytime sleepiness and impaired cognitive function (e.g., deficits in attention and/or memory) as a result of sleep disruption. Their partners describe restless sleep associated with irregular snoring, gasping, or choking episodes. Diagnosis is based on the assessment of risk factors and polysomnography. Many patients with OSA (> 50%) are affected by secondary hypertension. The cardiovascular consequences of secondary hypertension reduce life expectancy. However, these effects can be counteracted with weight loss and nightly continuous positive airway pressure (CPAP). Other important aspects of management include avoidance of precipitating factors (e.g., alcohol) and improvement of sleep hygiene.

Definition

  • Obstructive sleep apnea (OSA): breathing-related sleep disorder in which airflow significantly decreases or ceases because of upper airway obstruction (typically the oropharynx)
  • Apnea: respiratory arrests of ≥ 10 seconds
  • Hypopnea: reduction of airflow by ≥ 50% for ≥ 10 seconds in combination with reduction of blood oxygenation by ≥ 3% or EEG arousal
  • Apnea-hypopnea index (AHI)
    • (Hypopnea + apnea events)/hours of sleep
    • OSAH is defined as an AHI of > 15/hours of sleep or > 5/hours of sleep in combination with at least one typical symptom.
  • Respiratory effort-related arousal (RERA): series of breaths (for 10 seconds or more) that lead to arousal due to increased respiratory effort
  • Respiratory disturbance index (RDI) (hypopnea events + apnea events + respiratory effort-related arousal events)/hours of sleep

Severity/
Index

Mild Moderate Severe
AHI 5–15 15–30 > 30
RDI 15–20 20–40 > 40

References:[1]

Epidemiology

  • Sex: > (2:1)
  • Prevalence: ∼ 20–30% in men and 10–15% in women (AHI > 5);∼ 15% in men and 5% in women (AHI ≥ 15 or ≥ 5 plus at least one symptom of disturbed sleep)

References:[1][2][3][4]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

  • Obstruction of the upper airways due to the collapse of the pharyngeal muscles during sleep
  • Risk factors
    • Obesity, especially around the neck (short, wide “bull neck”)
    • Structural abnormalities that impair respiratory flow: tonsillar hyperplasia, nasal septum deviation, enlarged uvula, tongue, or soft palate; nasal polyps; overbite with a small chin; hypertrophied pharyngeal muscles
    • Alcohol consumption before sleep
    • Intake of sedatives and/or beta-blockers before sleep
    • Smoking
    • Family history
    • Hypothyroidism

Obesity is the most important risk factor for OSA.

References:[5][3]

Pathophysiology

References:[6][1][7]

Clinical features

  • Restless sleep with waking, gasping, or choking
  • Loud, irregular snoring with apneic episodes (third-party reports)
  • Excessive daytime sleepiness (e.g., patient falls asleep, microsleep during meetings or while watching TV)
  • Impaired cognitive function; (e.g., impaired concentration, memory loss)
  • Depression, decreased libido

References:[1][3]

Diagnostics

General considerations

  • Initial assessment: standardized questionnaires and third-party reports; (interview sleeping partner regarding snoring and respiratory interruptions)
  • Laboratory tests are not usually considered useful in the diagnosis of OSA, but may help identify underlying conditions or physiological consequences of OSA.

Sleep studies

  • Polysomnography: first-line method
    • Parameters measured in addition to those recorded by polygraphy:
      • Brainwaves via electroencephalography (EEG)
      • Eye movements via electrooculography (EOG) → assess REM phases
      • Muscle activity via electromyography (EMG; e.g., with sensors for movements of legs and chin)
      • Electrocardiography (ECG): often not necessary
    • Classic findings
      • Apnea and hypopnea events (AHI > 15)
      • Oxygen desaturation
      • Arousal events on EEG
      • Bradycardia
      • Fragmentation of sleep with pathological reduction of REM-sleep phases and slow-wave sleep
  • Home sleep apnea testing
    • The following parameters are measured during sleep: respiratory flow, respiratory pauses, saturation of blood with oxygen, heart rate, snoring noises and respiratory movements of the abdomen and thorax. This allows apneas and hypopnea events to be assessed and the AHI to be established.

Obstructive sleep apnea is a very frequent cause of secondary hypertension!

References:[8][9][1]

Differential diagnoses

Central sleep apnea (CSA) (< 10%)

  • Definition: Breathing-related sleep disorder characterized by episodic ventilation and respiratory effort caused by impaired respiratory center stimulation. Airway obstruction is absent.
  • Etiology: idiopathic (primary CSA) or caused by an underlying disorder (secondary (CSA)
  • Risk factors
  • Pathophysiology: lack of stimulation to the respiratory center with patent upper airways → periodic lack of respiratory muscle innervation → interruption of thoracic and/or abdominal respiratory movements
  • Clinical features
    • Morning headaches
    • Repeated waking at night
    • Daytime sleepiness
    • Snoring
    • Association with OSA is very common
  • Diagnosis
  • Treatment
    • Treat underlying disorder (if present)
    • CPAP

Obesity hypoventilation syndrome (Pickwickian syndrome) :

  • Definition: : a breathing disorder that only affects morbidly obese individuals; ; frequently accompanied by OSA, it is characterized by diurnal hypercapnia
  • Etiology: morbid obesity
  • Risk factors: : identical to those of obesity
  • Pathophysiology: ↑ production of CO2; + sleep disordered breathing (e.g., OSA) + failure of ventilatory compensatory mechanisms → alveolar hypoventilation
  • Clinical features
    • Same symptoms as those of OSA
    • Headaches and severe sleepiness
  • Diagnostic criteria
    • BMI ≥ 30 kg/m2
    • Arterial blood gasses showing diurnal hypercapnia (PaCO2 > 45 mm Hg) that cannot not be explained by another condition
    • Polysomnography shows hypoventilation during sleep with or without obstructive apnea events.
  • Treatment
    • Weight loss
    • Nasal intermittent positive pressure ventilation

References:[10][11][12][13]

The differential diagnoses listed here are not exhaustive.

Treatment

Nocturnal positive pressure therapy via CPAP is the therapy of choice in symptomatic OSA. The success of therapy is highly dependent on patient adherence and regular monitoring with sleep studies!
References:[14][15]

Complications

References:[1][16][17][18][19][20]

We list the most important complications. The selection is not exhaustive.

Prognosis

  • The mortality rate is higher in patients with severe OSA who do not receive adequate treatment.
  • CPAP ventilation can significantly lower the risk of mortality in OSA.