Biology of the neonate · 2005
Postnatal changes in pulmonary mechanics and energetics of infants with respiratory distress syndrome following surfactant treatment.
Клиническое исследованиеСтатьяМногоцентровое исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Bhutani Vinod K, Bowen Frank W, Sivieri Emidio M
Аннотация
BACKGROUND: Postnatal alterations in pulmonary mechanics, energetics and functional residual capacity (FRC) describe the structural maturation of the preterm respiratory system.
OBJECTIVE: To evaluate longitudinal changes in pulmonary function in infants with respiratory distress syndrome (RDS) treated with oxygen, positive pressure ventilation and synthetic surfactant (Exosurf).
METHODS: Serial pulmonary function tests were performed in surfactant-treated infants [mean +/- SD birth weight (BW) = 1,112 +/- 276 g, gestational age (GA) = 29 +/- 3 weeks] at postnatal ages: <3 days, 1, 2, 3, 4 and 6-8 weeks until term postmenstrual age (PMA). Tidal volume, pulmonary compliance (C(L)), pulmonary resistance (R(T)) and flow-resistive work were analyzed following simultaneous measurements of airflow and transpulmonary pressure signals. Serial FRC measurements were made in a randomly selected group.
RESULTS: Prior to 28 weeks' PMA, C(L) was unchanged irrespective of GA. At age 1 week the likelihood ratio (LR) for bronchopulmonary dysplasia (BPD) based on C(L), R(T) and GA was predicted to be >90% for those with BW <750 g (LR >100) as compared to <10% probability (LR = 0.3) for infants >1,500 g. Significant linear increase in C(L) to PMA was evident >28 weeks' PMA (r = 0.86, p < 0.01) at 0.17 ml/cm H2O/kg/week. By term PMA, mean C(L) was 2.60 +/- 0.07 ml/cm H2O. Improvements in FRC of preterm infants with RDS who recovered occur at a more rapid rate ( approximately 25 ml/kg) compared to those who developed BPD ( approximately 20 ml/kg).
CONCLUSIONS: Slow but incremental postnatal pulmonary improvement, minimal <28 weeks' PMA, were comparable for all infants. Along with diminished FRC, these changes reflect persistent deleterious effects of positive pressure ventilation, alveolar hyperoxia and unrecognized pulmonary overdistension.
OBJECTIVE: To evaluate longitudinal changes in pulmonary function in infants with respiratory distress syndrome (RDS) treated with oxygen, positive pressure ventilation and synthetic surfactant (Exosurf).
METHODS: Serial pulmonary function tests were performed in surfactant-treated infants [mean +/- SD birth weight (BW) = 1,112 +/- 276 g, gestational age (GA) = 29 +/- 3 weeks] at postnatal ages: <3 days, 1, 2, 3, 4 and 6-8 weeks until term postmenstrual age (PMA). Tidal volume, pulmonary compliance (C(L)), pulmonary resistance (R(T)) and flow-resistive work were analyzed following simultaneous measurements of airflow and transpulmonary pressure signals. Serial FRC measurements were made in a randomly selected group.
RESULTS: Prior to 28 weeks' PMA, C(L) was unchanged irrespective of GA. At age 1 week the likelihood ratio (LR) for bronchopulmonary dysplasia (BPD) based on C(L), R(T) and GA was predicted to be >90% for those with BW <750 g (LR >100) as compared to <10% probability (LR = 0.3) for infants >1,500 g. Significant linear increase in C(L) to PMA was evident >28 weeks' PMA (r = 0.86, p < 0.01) at 0.17 ml/cm H2O/kg/week. By term PMA, mean C(L) was 2.60 +/- 0.07 ml/cm H2O. Improvements in FRC of preterm infants with RDS who recovered occur at a more rapid rate ( approximately 25 ml/kg) compared to those who developed BPD ( approximately 20 ml/kg).
CONCLUSIONS: Slow but incremental postnatal pulmonary improvement, minimal <28 weeks' PMA, were comparable for all infants. Along with diminished FRC, these changes reflect persistent deleterious effects of positive pressure ventilation, alveolar hyperoxia and unrecognized pulmonary overdistension.