ABSTRACT

At altitude, hypoxia immediately triggers carotid body (CB) hypertrophy with new glomus cells, which hypersensitizes the hypoxic ventilatory response (HVR) and mediates much of the time-dependent ventilatory acclimatization to high altitude. This minimizes the reduction in partial pressure of oxygen (PO2) at altitude. Failure to acclimate, at times from ascending to altitude too rapidly, may lead to acute mountain sickness.

In addition, in hypoxia, the CB increases its response to carbon dioxide (CO2). The increased HVR, and hypercarbic ventilatory response in the hypoxia of altitude immediately increase ventilatory loop gain favoring periodic breathing. Insomnia may result, but also hypertension and other consequences of sympathetic activation are potential results of the intermittent hypoxemia of central sleep apnea (CSA). Supplemental nocturnal oxygen will eliminate periodic breathing. Acetazolamide (ACZ) may help treat both acute mountain sickness and periodic breathing at altitude.

Patients with obstructive sleep apnea (OSA) traveling to altitude or living at altitude may be affected by central apneas and central hypopneas adding into their mixture of respiratory events and may develop complex sleep apnea on continuous positive airway pressure (CPAP). For complex sleep apnea at altitude, the addition of in line oxygen, or for the traveler, adding ACZ, may be helpful.