Hypercapnia and Sleep O2 Desaturation in Chronic Obstructive Pulmonary Disease

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Abstract
There is a wide clinical spectrum in chronic obstructive pulmonary disease (COPD). The extremes of this spectrum, the “pink puffer” (PP) and “blue bloater” (BB) stereotypes differ in their degree of sleep hypoxemia and pulmonary hypertension. Most patients cannot be characterized as either PP or BE. The data amassed in the recent nocturnal oxygen therapy trial provide an opportunity to see to what extent differences in sleep oxygenation and hemodynamics in a large hypoxemic COPD population are related to awake hypoxemia and hypercapnia. From a large hypoxemic COPD population sleep SaO2 was examined in those with (PaCO2 >44 mm Hg) and without (PaCO2 ≤44 mm Hg) hypercapnia. Hypercapnic patients (mean PaCO2 49.8 mm Hg) had the same PaCO2 and degree of airflow obstruction as normocapnic patients (PaCO2 37.4 mm Hg) but had far greater sleep hypoxemia (measured by mean sleep SaO2 low sleep SaO2, and awake-low sleep SaO2, P < 0.05). In addition, arterial blood gases of the large sleep O2 desaturaters were compared with those of the small desaturaters; PP2 was similar in both groups, whereas PaCO2 was different (p < 0.00. Two common subsets of hypoxemic patients were also compared; one was hypercapnic and overweight, the other normocapnic and hyperinflated. We found that patients in the hypercapnic group had far worse sleep hypoxemia, although they had better lung function. We conclude that hypercapnia is a marker for sleep O2 de saturation in hypoxemic COPD.

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