VENTILATORY INSTABILITY IN PATIENTS WITH CONGESTIVE-HEART-FAILURE ANDNOCTURNAL CHEYNE-STOKES BREATHING

Many of the factors that appear to cause Cheyne-Stokes Breathing (CSB) in sleeping patients with congestive heart failure (CHF) are present during wakefulness. We studied the stability of ventilatory pattern in nine awake CHF patients (left ventricular ejection fraction 9-48%) wh o demonstrated CSB only while asleep and compared results with 13 age- matched normals. The test involved brief (30-50-second) exposure to hy poxia (end-tidal PO2 = 55 Torr) followed by breathing pure oxygen. Dur ing hypoxia, ventilation increased about 40% above air breathing contr ol in both groups, whereas end-tidal CO2 declined to 92% of control in both groups. During hyperoxia, however, breathing pattern differed be tween groups. In the normals, ventilation gradually declined to air-br eathing levels and did not significantly undershoot. In the patients, ventilation dropped more rapidly to baseline and an overshoot was pres ent with ventilation being 72% and air-breathing control at 45 seconds of hyperoxia. Circulatory delay was calculated from the time interval between alveolar hypoxia and in increase in ventilation, and when cor rections for circulatory delay were applied to ventilation during hype roxia the differences between groups increased in that the patients' v entilation was less than baseline immediately after the delay. In the normals, the gradual decline in hyperoxic ventilation probably represe nts the decay of short-term potentiation (STP) activated by hypoxic hy perventilation. Results in the patients were compatible with absence o f such STP decay, but could also have been due to a reduction in venti latory drive early in hyperoxia related to prolonged circulation times . In either case, awake patients with CHF and nocturnal CSB demonstrat ed decreased ventilatory stability in response to transient hypoxia, w hich may relate to their abnormal breathing at night.