Many patients with chronic obstructive pulmonary disease (COPD) experience severe arterial oxygen desaturation during REM sleep. Studies of arterial blood gas changes during these times of desaturation indicate both alveolar hypoventilation and worsening ventilation-perfusion abnormalities likely play a role in the desaturation. To date, no studies have clarified the specific mechanism(s) of this arterial oxygen desaturation. We have shown that COPD patients who desaturate during REM sleep, in contradistinction to those who do not desaturate, have 1) long episodes of hypopneic breathing, 2) a large increase in airflow resistance without a decrease in dynamic compliance, findings suggesting changes are in the upper airway, and, 3) a decrease in lung volume, all occurring concurrent with desaturation. Reversal of these changes occurs within one breath, suggesting the respiratory muscles per se can function appropriately if driven. We hypothesize: sleep desaturation in COPD is due to a global depression of the controls of respiratory muscle tone and inspiratory activity during REM sleep. Decreased tone would contribute to decreased lung volume and increased resistance of th supralaryngeal airway. Decreased inspiratory activity and the increased airflow resistance would cause hypopnea. Thus, our findings of hypoventilation and a decrease in lung volume resulting in maldistribution of ventilation, would be compatible with the arterial blood gas studies. We plan to test our hypothesis by examining the effect of oxygen and stimulation of the potentially depressed ventilatory drive system with doxapram hydrochloride. We will examine the changes in ventilation, the mechanical properties of the respiratory system, resistance of the supralaryngeal airway, inspiratory muscle activity and oxygenation under these test circumstances compared to control variables during the same REM period. Specificity of effect will be addressed by putting non-desaturating COPD patients through the same protocol. An inductance vest will be used to measure tidal volume, a differentiated flow signal, and changes in end-expiratory lung volume. Lateral supralaryngeal pressure will be measured with a catheter, the tip of which is located just above the larynx. Transpulmonary pressure will be measured with an esophogeal balloon. In our experience, patients are able to sleep satisfactorily with this instrumentation. If hypoxemia per se causes inspiratory muscle dysfunction, oxygen administration should reverse the abnormalities described above. If doxapram is effective, ventilatory drives may be implicated as the cause of decreased inspiratory muscle activity. Determination of the specific mechanism(s) of arterial oxygen desaturation in these patients should lead to specific and more effective therapy for hypoxemia, an important complication of COPD.
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