Harrison’s Manual of Medicine



Hypoventilation Syndromes
Sleep Apnea

ALVEOLAR HYPOVENTILATION   Exists when arterial PCO2 increases above the normal 37–43 mmHg. In most clinically important chronic hypoventilation syndromes, PaCO2 is 50–80 mmHg.
Cause   Alveolar hypoventilation always is (1) a defect in the metabolic respiratory control system, (2) a defect in the respiratory neuromuscular system, or (3) a defect in the ventilatory apparatus (Table 135-1).

Table 135-1 Chronic Hypoventilation Syndromes

Disorders associated with impaired respiratory drive, defects in respiratory neuromuscular system, and upper airway obstruction produce an increase in PaCO2, despite normal lungs, because of a decrease in overall minute ventilation.
Disorders of chest wall, lower airways, and lungs produce an increase in PaCO2, despite a normal or increased minute ventilation.
Increased PaCO2 leads to respiratory acidosis, compensatory increase in HCO3–, and decrease in PaO2.
Hypoxemia may induce secondary polycythemia, pulmonary hypertension, right heart failure. Gas exchange worsens during sleep, resulting in morning headache, impaired sleep quality, fatigue, daytime somnolence, mental confusion (Fig. 135-1).

FIGURE 135-1. Physiologic and clinical features of alveolar hypoventilation. PACO2 alveolar PCO2 (After EA Phillipson: HPIM-15.)

Hypoventilation Syndromes
PRIMARY ALVEOLAR   Cause unknown; rare; thought to arise from defect in metabolic respiratory control system; key diagnostic finding is chronic respiratory acidosis without respiratory muscle weakness or impaired ventilatory mechanics. Some pts respond to respiratory stimulants and supplemental O2.
RESPIRATORY NEUROMUSCULAR   Several primary neuromuscular disorders produce chronic hypoventilation (Table 135-1). Hypoventilation usually develops gradually, but acute, superimposed respiratory loads (e.g., viral bronchitis with airways obstruction) may precipitate respiratory failure. Diaphragm weakness is a common feature, with orthopnea and paradoxical abdominal movement in supine posture. Testing reveals low maximum voluntary ventilation and reduced maximal inspiratory and expiratory pressures. Therapy involves treatment of underlying condition. Many pts benefit from mechanical ventilatory assistance at night (often through nasal mask) or the entire day (typically through tracheostomy).
OBESITY-HYPOVENTILATION   Massive obesity imposes a mechanical load on the respiratory system. Small percentage of morbidly obese pts develop hypercapnia, hypoxemia, and ultimately polycythemia, pulmonary hypertension, and right heart failure. Most pts have mild to moderate airflow obstruction. Treatment includes weight loss, smoking cessation, and pharmacologic respiratory stimulants such as progesterone.
Sleep Apnea
By convention, apnea is defined as cessation of airflow for >10 s. Hypopnea is defined as reduction in airflow resulting in arousal from sleep or oxygen desaturation. Minimum number of events per night for diagnosis is uncertain, but most pts have at least 10–15/h of sleep. Prevalence estimates vary depending on threshold for diagnosis (events/h) and on definition of hypopnea (degree of desaturation required), but conservative figures are 10% of working-age men & 4% of women. Some pts have central apnea with transient loss of neural drive to respiratory muscles during sleep. Vast majority have primarily obstructive apnea with occlusion in the upper airway. Sleep plays a permissive role in collapse of upper airway. Alcohol and sedatives exacerbate the condition. Most pts have structural narrowing of upper airway. Obesity is frequent, but many pts have normal body habitus. Most pts have obstruction at nasal or palatal level. Mandibular deformities (retrognathia) also predispose. Symptoms include snoring, excessive daytime sleepiness, memory loss, and impotence. Sleepiness increases risk of automobile accidents. Nocturnal hypoxia, a consequence of apnea, may contribute to systemic hypertension, arrhythmias, and right ventricular hypertrophy. Sleep apnea, in the absence of co-morbidity causing daytime hypoxia, is not a cause of substantial pulmonary hypertension or right heart failure.
Diagnosis   This requires overnight observation of the pt. The definitive test for obstructive sleep apnea is overnight polysomnography, including sleep staging and respiratory monitoring.

(See Table 135-2) Therapy is directed at increasing upper airway size, increasing upper airway tone, and minimizing upper airway collapsing pressures. Weight loss often reduces disease severity. Majority of pts with severe sleep apnea require nasal continuous positive airway pressure (nasal C-PAP). Mandibular positioning device (dental) may treat pts with mild or moderate disease. Surgery (uvulopalatopharyngoplasty) is usually reserved for pts who fail other therapies, as failure rate is high (>50%) and surgery may compromise later therapy with CPAP.

Table 135-2 Management of Obstructive Sleep Apnea (OSA)

Increased ventilation, causing PaCO2 <37 mmHg. Causes include lesions of the CNS, metabolic acidosis, anxiety, drugs (e.g., salicylates), hypoxemia, hypoglycemia, hepatic coma, and sepsis. Hyperventilation may also occur with some types of lung disease, particularly interstitial disease and pulmonary edema.

For a more detailed discussion, see Phillipson EA: Disorders of Ventilation, Chap. 263, p. 1517, and Sleep Apnea, Chap. 264, p. 1520, in HPIM-15.



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