Pressure support ventilation, sigh adjunct to pressure support ventilation, and neurally adjusted ventilatory assist in infants after cardiac surgery: A physiologic crossover randomized study.

OBJECTIVES: We sought to compare gas exchange, respiratory mechanics, and asynchronies during pressure support ventilation (PSV), sigh adjunct to PSV (PSV SIGH), and neurally adjusted ventilatory assist (NAVA) in hypoxemic infants after cardiac surgery. DESIGN: Prospective, single-center, crossover, randomized physiologic study. SETTING: Tertiary-care pediatric intensive care unit. PATIENTS: Fourteen hypoxemic infants (median age 11.5 days [8.7-74]). INTERVENTIONS: The protocol begins with a 1 hour step of PSV, followed by two consecutive steps in PSV SIGH and NAVA in random order, with a washout period of 30 minutes (PSV) between them. MAIN RESULTS: Three infants presented an irregular Eadi signal because of diaphragmatic paralysis and were excluded from analysis. For the remaining 11 infants, PaO2 /FiO 2 and oxygenation index improved in PSV SIGH compared with PSV (P < 0.05) but not in NAVA compared with PSV. PSV SIGH showed increased tidal volumes and lower respiratory rate than PSV (P < 0.05), as well as a significant improvement in compliance with respiratory system indexed to body weight when compared with both PSV and NAVA (P < 0.01). No changes in mean airway pressure was registered among steps. Inspiratory time resulted prolonged for both PSV SIGH and NAVA than PSV (P < 0.05). NAVA showed the higher coefficient of variability in respiratory parameters and a significative decrease in asynchrony index when compared with both PSV and PSV SIGH (P < 0.01). CONCLUSIONS: The adjunct of one SIGH per minute to PSV improved oxygenation and lung mechanics while NAVA provided the best patient-ventilator synchrony in infants after cardiac surgery.

Sevoflurane improves respiratory mechanics and gas exchange in a case series of infants with severe bronchiolitis-induced acute respiratory distress syndrome.

This report describes the successful use of a new intervention to improve respiratory mechanics and gas exchange in a relatively homogeneous group of infants with severe bronchiolitis-induced PARDS after failure of conventional treatment. These results may open a new interesting area of research and management for PARDS patients.

The effects of anesthesia, muscle paralysis, and ventilation on the lung evaluated by lung diffusion for carbon monoxide and pulmonary surfactant protein B.

BACKGROUND: An increased alveolar-arterial oxygen tension difference is frequent in anesthetized patients. In this study, we evaluated the effect on the lung of anesthesia, muscle paralysis, and a brief course of mechanical ventilation. METHODS: Lung diffusion for carbon monoxide (DLCO), including pulmonary capillary blood volume (Vc) and conductance of the alveolar-capillary membrane (DM), and pulmonary surfactant protein type B (a marker of alveolar damage) were measured in 45 patients without pulmonary disease undergoing extrathoracic surgery. RESULTS: Anesthesia, muscle paralysis, and mechanical ventilation led to impairment of gas exchange, with a reduction of DLCO values immediately after anesthetic induction due to a concomitant reduction of both DM and Vc. While changes in DM were due to the reduction of lung volume, changes in Vc were not limited to volume loss, since the Vc/alveolar volume ratio decreased significantly. Although DLCO and its components decreased immediately after induction, none of the values decreased further at 1 and 3 hours. Surfactant protein type B, however, was unchanged immediately after anesthesia but increased at 1 hour after induction and further increased after 3 hours of anesthesia. The level of alveolar damage correlated with the reduction of lung perfusion and lung dynamic strain (i.e., ratio between tidal volume and end-expiratory lung volume). CONCLUSIONS: A brief course of anesthesia and controlled ventilation leads to: (1) alveolar damage, which is correlated with lung strain and perfusion, and (2) impaired gas exchange mainly due to volume loss but also to reduced aerated lung perfusion.