Myocardial Stress: Exercise versus Sleep in Patients with COPD

Abstract

Epidemiologic investigation has revealed that patients with pulmonary disease are at increased risk of dying during the early morning hours. To provide a pathophysiologic explanation for these excessive nocturnal mortality statistics, we tested the hypothesis that episodes of arterial O2 desaturation during sleep can produce as severe a stress on the maintenance of myocardial O2 balance as maximal exercise in patients with chronic obstructive pulmonary disease (COPD). Thirty-one subjects with COPD underwent both overnight sleep and treadmill exercise study to their dyspnea-limited maximum. During both activities, systemic blood pressure was directly recorded and myocardial oxygen consumption (MVO2) estimated from the pulse rate (HR) - systolic blood pressure (SBP) product. Arterial O2 content (CaO2) was calculated from hemoglobin concentration and arterial O2 saturation (SaO2) measured by ear oximetry. Using these data and the Fick principle, myocardial blood flow (MBF) was continuously estimated during both exercise and sleep. During sleep, mean SaO2 was 88 +/- 7 percent while the average of the lowest SaO2 recorded for each subject was 71 +/- 14 percent. Episodes of nocturnal oxyhemoglobin desaturation produced consistent elevations in SBP frequently accompanied by an increase in HR. Because this hemodynamic response resulted in increased MVO2 at precisely the times when arterial O2 contents were low, high demands for MBF were generated. The average of the highest individual values for MBF during sleep was 244 +/- 144 (ml/100 g LV/min). This value was not significantly different from the value of MBF = 281 +/- 91 (ml/100 g LV/min) determined for maximal exercise. This finding suggests that the demand for coronary blood flow during episodes of nocturnal hypoxemia can be transiently as great as during maximal exercise in patients with COPD.