Cardio-metabolic correlates of sleep disordered breathing in Andean highlanders

Globally, approximately 150 million people live at altitudes >2500 m. Ambient hypoxia makes highlanders chronically hypoxaemic, which further worsens during sleep. Hypoxia causes increases in ventilatory chemo-sensitivity, which predisposes to central sleep apnoea with intermittent nocturnal oxyhaemoglobin desaturations. Ambient hypoxia further amplifies sleep-related decreases and swings in nocturnal

oxyhaemoglobin saturation since oxygenation lies on the steep rather than flat portion of the oxyhaemoglobin dissociation curve. Thus, altitude may represent a “perfect storm” for sleep disordered breathing (SDB), exposing highlanders to uncommon degrees of sleep apnoea and nocturnal oxyhaemoglobin de-saturation, and related cardiometabolic sequelae. Nevertheless, the effects of chronic and intermittent nocturnal hypoxaemia have not been well characterised in highlanders.

It is well recognised that chronic nocturnal hypoxaemia is associated with pulmonary hypertension, cor pulmonale and mortality. In patients with severe chronic obstructive pulmonary disease, nocturnal hypoxaemia is a predictor of pulmonary hypertension and mortality. Oxygen treatment trials in patients with sustained nocturnal hypoxaemia have, however, yielded equivocal haemodynamic responses and no improvements in

mortality. In morbid obesity, chronic nocturnal hypoxaemia has also been associated with elevations in pulmonary artery pressure, secondary polycythaemia and frank cor pulmonale [9]. Nevertheless, clinical comorbidities in these patients may confound the effects of chronic nocturnal hypoxaemia on pulmonary haemodynamics and overall morbidity and mortality. At high altitude, a similar constellation of clinical

findings can develop in normal highlanders, without co-morbid obesity or lung disease.

Cardiometabolic correlates of SDB in Andean highlanders.pdf

Download PDF • 625KB