We examined the effects of different levels of inspired CO2 on ventilation and the pattern of breathing in healthy adults during the awake and the stage II quiet-sleep states. During both states, subjects were studied supine with their heads enclosed in a canopy. Tidal volume (VT) was determined from quantitative measurements of abdominal and rib cage excursions with magnetometers. Inspired CO2 was raised by blending CO2-enriched gas into the airflow, which continuously flushed the canopy. During sleep, while room air was breathed, VT decreased significantly from 410 to 360 ml, and respiratory rate also fell from 17 to 16 breaths/min. As a consequence, ventilation was significantly reduced from 6.5 to 5.8 l/min, and end-tidal CO2 partial pressure (PCO2) rose from 39.1 to 42.5 Torr. Ventilatory responses to CO2 were reduced, on the average, during sleep to 79% of waking levels. The change in average inspiratory flow produced by CO2 was also less during sleep. Waking and sleeping ventilatory responses to CO2 correlated inversely with the rise in end-tidal PCO2 when room air was breathed during sleep. At all levels of VT, the rib cage contribution to VT was greater during quiet sleep than during wakefulness. These findings suggest that quiet sleep, in addition to depressing ventilation and the response to CO2 alters the manner in which VT is attained by rib cage and abdominal displacements.
Can an initial end-tidal CO2 <1.33 kPa predict lack of return of spontaneous circulation during pre-hospital cardiac arrest?
