A mountaineer ascending to 5000m altitude experiences periodic Cheyne-Stokes breathing during sleep. The mechanism is best explained by:

• A Increased respiratory muscle fatigue during sleep causing periodic apnea
• B Altitude-induced pulmonary hypertension reducing cardiac output, slowing CO2 delivery to chemoreceptors and increasing oscillatory instability
• C Decreased hypoxic ventilatory response at altitude, causing inadequate ventilation and periodic CO2 accumulation
• D Hypoxia-driven hyperventilation causing hypocapnia; PaCO2 falls below the apneic threshold; brief apnea allows PaCO2 to rise; then hypoxia restimulates breathing — a cycle caused by increased chemoreceptor sensitivity at altitude and prolonged circulatory delay ✓

Explanation

At altitude, chronic hypoxia drives hyperventilation (hypoxic ventilatory response via peripheral chemoreceptors), reducing PaCO2 below normal and respiratory alkalosis develops. This hypocapnia brings PaCO2 close to or below the apneic threshold (PaCO2 below which respiratory center ceases firing). During sleep (when cortical drive is reduced), this balance is disrupted, causing apneas. During apnea, PaCO2 rises and hypoxia worsens; hypoxia then restimulates breathing (waxing phase). Additionally, prolonged circulatory time at altitude (from reduced cardiac output and increased blood volume) amplifies the oscillatory response by delaying chemoreceptor feedback. Cheyne-Stokes is also seen in heart failure for the same circulation-time reason.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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