Effect of oxygen administration during sleep on skin surface oxygen and carbon dioxide tensions in patients with chronic lung disease.

Hypoxemia, hypercarbia, and cor pulmonale ultimately occur in most patients with chronic lung disease. Although oxygen therapy may reduce or delay the development of pulmonary hypertension and myocardial failure in these patients, its use is thought to lead to CO2 narcosis and apnea. The effect of O2 administration during sleep has been examined in 12 patients (seven with cystic fibrosis, three with bronchopulmonary dysplasia, one with bronchiolitis obliterans, and one with severe hypersensitivity pneumonitis) using skin surface O2 (Roche) and CO2 (Radiometer) electrodes. Both electrodes were calibrated over wet gas and applied at 44 C. Ten patients had chronic hypercarbia (PaCO2 62 +/- 19 torr; range 46 to 103 torr) when awake. Humidified oxygen was administered by nasal cannula, Venturi mask, or head hood. Oxygen flow was increased every 20 minutes from 80 minutes or until the patient awoke. In eight of ten patients with hypercarbia and in the two normocarbic patients, skin surface carbon dioxide tension (PsCO2) increased by 10% or less as the skin surface oxygen tension (PsO2) was increased. In the remaining two patients with hypercarbia (both had cystic fibrosis) PsCO2 increased 18% and 24% as PsO2 was increased. These last two patients with depressed responsiveness to CO2 could not be separated from the other patients by clinical or laboratory criteria. It is concluded that the skin surface blood gas tensions are a simple and reproducible method for adjusting oxygen therapy in patients with chronic lung disease, and although the response to oxygen varies from patient to patient, most patients with chronic hypercarbia retain their central responsiveness to CO2 during sleep and for them O2 therapy is probably safe.