MECHANISMS FOR EPISODES OF HYPOXEMIA IN PRETERM INFANTS UNDERGOING MECHANICAL VENTILATION

Citation
Jm. Bolivar et al., MECHANISMS FOR EPISODES OF HYPOXEMIA IN PRETERM INFANTS UNDERGOING MECHANICAL VENTILATION, The Journal of pediatrics, 127(5), 1995, pp. 767-773
Citations number
30
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00223476
Volume
127
Issue
5
Year of publication
1995
Pages
767 - 773
Database
ISI
SICI code
0022-3476(1995)127:5<767:MFEOHI>2.0.ZU;2-X
Abstract
Objective: To ascertain possible mechanisms implicated in the developm ent of transient episodes of hypoxemia (oxygen saturation <85%) freque ntly observed in preterm infants undergoing mechanical ventilation, ev en after the acute phase of respiratory failure has passed. Study desi gn: Tidal flow, airway and esophageal pressure, and oxygen saturation were continuously recorded in 10 infants (mean +/- SD, birth weight 73 3 +/- 149 gm, gestational age 25.5 +/- 2.2 weeks, age 26.3 +/- 11.9 da ys) who had repeated episodes of hypoxemia without any evident cause. Measurements of minute ventilation (V-E), inspiratory compliance (C-i) , and inspiratory resistance (R(i)) were compared before and during ep isodes of hypoxemia. Results: All episodes of hypoxemia were preceded by an active exhalation that produced a mean decrease in end-expirator y lung volume of 6.4 +/- 2.8 ml/kg. The reduction in lung volume was i mmediately followed by a sudden decrease in tidal flow and volume, des pite continuation of mechanical ventilation at the same rate and peak pressure. The resulting hypoventilation was associated with a drop in Ci to approximately one half and an increase in R(i) to more than doub le the baseline values. Approximately 30 seconds after the beginning o f hypoventilation, the arterial oxygen saturation reached a hypoxemic level (oxygen saturation <85%). Conclusion: Most hypoxemic episodes we re triggered by an expiratory effort that produced a large decrease in lung volume. This reduction in lung volume probably leads to closure of small airways and the development of intrapulmonary shunts, which w ould explain the rapid development of hypoxemia.