DISSOCIATION IN THE RESPONSES OF TIDAL VOLUME AND RESPIRATORY FREQUENCY TO HYPOXIA IN PRETERM INFANTS. † 2020

The neonatal ventilatory response to hypoxia is characterized by an initial increase in minute ventilation that is not sustained beyond 1-2 minutes. In animal models hypoxia elicits an initial transient increase in respiratory motor output, accompanied by a decrease in respiratory frequency that appears dependent on both peripheral chemoreceptor input and the ventrolateral pons. We sought to determine whether a similar dissociation between tidal volume and respiratory timing occurs in human infants, and can account for the characteristic biphasic ventilatory response. Six preterm infants (GA 34±1 wk; postnatal age 2.7±.3 wk, Wt 1.8±.1 kg) were exposed to 5 min of 13 or 15% O₂ during quiet sleep. Ventilation was measured via nasal mask pneumotachograph. Hypoxic exposure caused O₂ saturation to fall from 99±1 to 87±6%. This resulted in an initial increase in tidal volume accompanied by a simultaneous decrease in frequency over the first minute. Thereafter, the increase in tidal volume was not sustained and minute ventilation exhibited the characteristic biphasic response that fell below baseline. We conclude that acute hypoxic exposure in the newborn causes rapid dissociation in the responses of tidal volume and respiratory frequency. We speculate that hypoxia-induced peripheral chemoreceptor stimulation serves to simultaneously increase respiratory motor output to enhance alveolar ventilation, and decrease respiratory frequency to conserve energy expenditure. Figure

Figure 1