Ventilator Liberation in the Pediatric ICU

Abstract

Despite the accepted importance of minimizing time on mechanical ventilation, only limited guidance on weaning and extubation is available from the pediatric literature. A significant proportion of patients being evaluated for weaning are actually ready for extubation, suggesting that weaning is often not considered early enough in the course of ventilation. Indications for extubation are often not clear, although a trial of spontaneous breathing on CPAP without pressure support seems an appropriate prerequisite in many cases. Several indexes have been developed to predict weaning and extubation success, but the available literature suggests they offer little or no improvement over clinical judgment. New techniques for assessing readiness for weaning and predicting extubation success are being developed but are far from general acceptance in pediatric practice. While there have been some excellent physiologic, observational, and even randomized controlled trials on aspects of pediatric ventilator liberation, robust research data are lacking. Given the lack of data in many areas, a determined approach that combines systematic review with consensus opinion of international experts could generate high-quality recommendations and terminology definitions to guide clinical practice and highlight important areas for future research in weaning, extubation readiness, and liberation from mechanical ventilation following pediatric respiratory failure.

Keywords: esophageal pressure measurements; extubation; maximum negative airway pressure; mechanical ventilation; phase angles; pressure rate product; respiratory inductance plethysmography; respiratory support; spontaneous breathing; stridor; weaning.

Fig. 1.

Pressure rate product as a function of pre-extubation support (pressure support 10/PEEP 5 cm H₂O), CPAP 5 cm H₂O, and spontaneous breathing at 5 and 60 min postextubation. Data exclude 107 patients with postextubation upper-airway obstruction, stratified by ETT size. The patterns were the same for ETT size grouping of (A) ≤ 3.5 mm ID, n = 152; (B) 4.0–4.5 mm ID, n = 102; and (C) ≥ 5.0 mm ID, n = 48. Regardless of ETT subgrouping, pressure rate product on pressure support was less than CPAP (log transformed PRP, ANOVA, P < .0001). CPAP pressure rate product was similar to postextubation values (P > .05). ETT = endotracheal tube; ID = inner diameter. From Reference , with permission.

Fig. 2.

Maximum airway pressure during occlusion versus re-intubation. There is a dose-response relationship between lower maximum airway pressure during occlusion and re-intubation (test of trend, P = .01). Those with maximum airway pressure during occlusion of ≤ 30 cm H₂O were a median of 2.8 (interquartile range 1.37–5.69) times more likely to be reintubated than those with a maximum airway pressure during occlusion > 30 cm H₂O. From Reference , with permission.

Fig. 3.

A: Flow-pressure loops using spirometry. The flows are measured with a pneumotachograph (PNT) on the endotracheal tube. The pressure is obtained using an esophageal balloon catheter. B: Flow-pressure loops using respiratory inductance plethysmography (RIP). The flows are obtained from calibrated RIP belts around the thorax and abdomen at the same time as the recordings in (A), and the pressure is obtained using the same esophageal balloon catheter. From Reference , with permission.

Fig. 4.

A: Flow-pressure loops using respiratory inductance plethysmography (RIP) for flow and esophageal manometry while intubated and breathing on CPAP. The loops are narrow and show no evidence of inspiratory flow limitation. B: Inspiratory flow limitation after extubation as subglottic narrowing occurs, as denoted by the flattened flow-pressure limb above the x axis. The pressure rate product has also increased 10-fold. From Reference , with permission.

Fig. 5.

A: Inspiratory flow limitation as denoted by the flattened flow-pressure limb above the x axis, and large negative change in esophageal pressure. B: The loops have narrowed after racemic epinephrine inhalation and show no evidence of inspiratory flow limitation. This is consistent with subglottic edema lessening after epinephrine administration. From Reference , with permission.