Non-invasive ventilation in neonates: the lungs don’t like it!

Nasal intermittent positive pressure ventilation (nIPPV) is a non-invasive modality of ventilatory support that is frequently used for a number of clinical conditions. Suggested applications for nIPPV include the treatment of respiratory distress and apnea of prematurity, sleep apnea syndromes, COPD, and as a bridge between mechanical ventilation and unassisted breathing (1, 5). Its appeal derives largely from its non-invasive nature: portability, the avoidance of acute and chronic damage to the airways during intubation, and minimization of mechanical ventilation-induced lung injury (baro- and volotrauma). In the special case of premature infants, nIPPV prevents subglottic stenosis and is associated with a lower incidence of extubation failure and of bronchopulmonary dysplasia (2, 5). The benefits of nIPPV come with an unexpected problem: it causes reflexive inspiratory contraction of the thyroarytenoid muscle, a glottal constrictor, narrowing the glottis and increasing airway resistance (4). Since non-invasive ventilation requires low-resistance airways throughout the respiratory system, this reflex creates a limitation to airflow of sufficient magnitude to ultimately impair gas exchange (3). Moreover, it is not immediately clear where in the respiratory system such a reflex would be triggered. The paper by Roy et al. in this issue of the Journal presents a clever study that demonstrates that inspiratory activation of glottal constrictors during nIPPV is most likely mediated by bronchopulmonar