Types of Apnea

Fig. 101.43 - Different types of breathing patterns. A = Normal, B = Upper airway obstructive apnea, C = Central apnea, D = Mixed apnea, E = Paradoxical breathing, F = Cheyne-Stokes respiration. (Bradley and Daroff's Neurology in Clinical Practice)

1. Obstructive Apnea (OSA)

• Mechanism: The upper airway collapses during sleep. Airflow ceases despite continued - and increasingly forceful - thoracic and abdominal respiratory effort.
• Key feature on polysomnography: Airflow absent, but chest wall effort persists (see panel B in the diagram above).
• Pathophysiology: Chest wall restriction, upper airway narrowing, increased upper airway compliance, and impaired compensation for increased upper airway resistance. During REM sleep, descending neural inhibition of accessory ventilatory and upper airway muscles worsens obstruction.
• Clinical features: Loud chronic snoring, witnessed choking/gasping, excessive daytime somnolence (~50% of patients), morning headache, dry mouth, nocturia, mood disorders, and neurocognitive deficits.
• Cardiovascular consequences: Each obstructive event increases left and right ventricular afterload, decreases left ventricular compliance, raises pulmonary artery pressure, decreases coronary blood flow, and increases myocardial oxygen demand. The termination of each event causes a spike in heart rate and systemic blood pressure.
• Diagnosis: Apnea-Hypopnea Index (AHI) ≥5 events/hour on polysomnography (clinically significant cutoff, interpreted in context of symptoms and comorbidities).

2. Central Apnea (CSA)

• Mechanism: Absent or reduced respiratory effort from the brainstem - airflow and effort both disappear (see panel C in diagram).
• Key feature: PaCO2 falls to or below the apnea threshold during sleep, removing the chemical drive to breathe. Either PaCO2 falls too low, or the apnea threshold rises.
• Two major subtypes (classified by CO2 level):

A. Hypercapnic CSA

B. Non-hypercapnic CSA

• Cheyne-Stokes Respiration (CSR): The most clinically important form of non-hypercapnic CSA. Characterized by a waxing-waning (crescendo-decrescendo) breathing pattern separated by central apneas or hypopneas (see panel F in diagram). Most commonly associated with heart failure, where altered circulatory timing and augmented ventilatory responses to CO2 drive oscillation between apnea and hyperpnea. Associated with increased mortality.
• Complex/Treatment-emergent CSA: CSA that arises after CPAP treatment of OSA, or persists after treating a combination of obstructive, mixed, and central events.

3. Mixed Apnea

• Mechanism: Begins as a central apnea (no effort), followed by resumed respiratory effort against an obstructed airway (obstructive component). An initial central apnea followed by obstructive apnea (see panel D in diagram).
• Common in end-stage kidney disease, where the distribution of all three types (obstructive, central, mixed) is broader than in the general population.

4. Neonatal Apnea

• Apnea of prematurity: Occurs in most infants born at <28 weeks' gestation, ~20% born at 34 weeks, and <10% beyond 34 weeks. Usually resolves by 34-36 weeks postmenstrual age but may persist past term in those born at <25 weeks.
• Common causes: CNS abnormalities (seizures, meningitis, IVH), metabolic disturbances, sepsis, anemia, patent ductus arteriosus, reflux, thermal instability.
• Treatment: Caffeine (loading dose 5-6 mg/kg IV, maintenance 1-2 mg/kg/dose Q6-8h), CPAP, or mechanical ventilation.

5. Posthyperventilation Apnea

Special Neurological Breathing Patterns Related to Apnea

Summary Table

• Bradley and Daroff's Neurology in Clinical Practice, Section 101
• Murray & Nadel's Textbook of Respiratory Medicine, Chapter 121 (CSA) and Chapter 120 (OSA)
• Goldman-Cecil Medicine, Chapter 374
• The Harriet Lane Handbook, 23rd ed., Chapter 18