Abstract
The aim of this study was to determine if resuscitation from hypopnea when breathing oxygen resulted in a slower recovery than that seen when breathing room air. Hyperoxia, in preterm human neonates and lambs, decreases minute ventilation (V̇I), but no study has shown this effect during recovery from apnea or hypopnea, a common clinical setting. Thus, recovery from hypopnea was studied in eight unanesthesized preterm lambs, breathing spontaneously via an endotracheal tube placed into a tracheostomy. Hypopnea, defined here as a decrease in V̇I from baseline greater than 50%, was induced by instillation of distilled water onto the larynx. After a baseline 30 sec when V̇I heart rate, and arterial blood gas were measured, a standard hypopnea stimulus was given over 30 sec. The lambs then breathed air or oxygen during a 2-min recovery period, which started with 15 sec of artifical ventilation. The degree of recovery at 2 min was less in the oxygen (O2) breathing group: V̇I (ml/kg/min) = 381 ± 27 in air and 270 ± 18 in O2, P < 0.01; pH = 7.38 ± 0.005 in air and 7.34 ± 0.008 in O2, P < 0.01; arterial carbon dioxide tension (Pa mrnHg) = 45.0 ± 1.3 in air and 49 ± 1.3 in O2 P < 0.01; base excess = 2.1 ± 0.6 in air and 1.1 ± 0.5 oxygen, P < 0.01. By 2 min a return to baseline values of V̇I, pH, and Pa was noted only in the air breathing group, where the arterial oxygen tension also returned to normal. The heart rate recoveries at 2 min were not different and, in both groups, were less than their baseline values. Resuscitation with O2 in contrast to room air, delays ventilatory recovery from hypopnea. Pediatr Pulmonol 1987; 3:317–323.