Mechanisms of active laryngeal closure during noninvasive intermittent positive pressure ventilation in nonsedated lambs

Abstract

The present study stems from our recent demonstration (Moreau-Bussiere F, Samson N, St-Hilaire M, Reix P, Lafond JR, Nsegbe E, Praud JP. J Appl Physiol 102: 2149-2157, 2007) that a progressive increase in nasal intermittent positive pressure ventilation (nIPPV) leads to active glottal closure in nonsedated, newborn lambs. The aim of the study was to determine whether the mechanisms involved in this glottal narrowing during nIPPV originate from upper airway receptors and/or from bronchopulmonary receptors. Two groups of newborn lambs were chronically instrumented for polysomnographic recording: the first group of five lambs underwent a two-step bilateral thoracic vagotomy using video-assisted thoracoscopic surgery (bilateral vagotomy group), while the second group, composed of six lambs, underwent chronic laryngotracheal separation (isolated upper airway group). A few days later, polysomnographic recordings were performed to assess glottal muscle electromyography during step increases in nIPPV (volume control mode). Results show that active glottal narrowing does not develop when nIPPV is applied on the upper airways only, and that this narrowing is prevented by bilateral vagotomy when nIPPV is applied on intact airways. In conclusion, active glottal narrowing in response to increasing nIPPV originates from bronchopulmonary receptors.

Laryngeal narrowing during nasal ventilation does not originate from bronchopulmonary C-fibers

“…Over the past decade, we have shown in several studies that an active inspiratory narrowing develops against ventilator insufflations during nPSV (15/4 cmH 2 O) in at least two thirds of full-term lambs in quiet sleep and quiet wakefulness (Moreau-Bussière et al, 2007;Roy et al, 2008). These results are in keeping with a recent review suggesting that this active inspiratory laryngeal narrowing can be responsible for significant patient-ventilator asynchrony, patient discomfort and non-invasive ventilation failure.…”

“…This inspiratory laryngeal narrowing can have deleterious consequences, including limitation of lung ventilation (Oppersma et al, 2013) as well as diversion of the insufflated gas into the esophagus. We further showed that this inspiratory laryngeal narrowing during nPSV was reflexively driven by the stimulation of unidentified bronchopulmonary receptors (Roy et al, 2008).…”

“…We previously documented that active inspiratory laryngeal narrowing during nPSV originates from bronchopulmonary receptors (Roy et al, 2008). The short burst of EaTA, disappearing well before the end of the inspiratory pressure plateau in nPSV (see figure 3 in Moreau-Bussière et al, 2007), does not suggest the involvement of SAR.…”

“…Chronic instrumentation was performed under general anesthesia as previously detailed (Roy et al, 2008), in order to measure states of alertness, electrical activity of the thyroarytenoid muscle (EaTA, a glottal constrictor), tracheal PetCO 2 , arterial blood gases and respiratory movements (inductance plethysmography). Two days later, in order to fulfill our first study aim, two polysomnographic recordings during nPSV 15/4 cmH 2 O (Servo-i ventilator; inspiratory pressurization time = 0.12 s) were performed on two consecutive mornings, before (intact CFEs) and after CFE blockade, in non-sedated lambs.…”

“…Over the past few years, we have documented that nasal pressure support ventilation (nPSV) induces an active laryngeal narrowing during inspiration in non-sedated lambs (Moreau-Bussière et al, 2007;Roy et al, 2008). This inspiratory laryngeal narrowing can have deleterious consequences, including limitation of lung ventilation (Oppersma et al, 2013) as well as diversion of the insufflated gas into the esophagus.…”