Effects of nasal intermittent positive pressure hyperventilation on
the glottis in normal awake subjects.
Jounieaux, V., G. Aubert, M. Dury, P. Delguste, and D. O. Rodenstein.
Pneumology and EEG Units, Cliniques Universitaires Saint Luc,
Universit[acute]e Catholique de Louvain, 1200 Brussels, Belgium.
APStracts 2:0083A, 1995.
We have recently observed glottic narrowing during nasal intermittent
positive pressure ventilation (nIPPV) and suggested that it was due
to hypocapnia-induced glottic closure. To confirm this hypothesis, we
have studied seven healthy subjects and submitted them to nIPPV while
their glottis was continuously monitored through a fiberoptic
bronchoscope. During wakefulness, we measured breath by breath the
widest inspiratory angle formed by the vocal cords at the anterior
commissure, the corresponding actual tidal volume (VT, with
inductance plethysmography), end-tidal carbon dioxide concentration
(PetCO2) and several other indices (see below). Mechanical
ventilation was progressively increased up to 30 l/min. In addition,
in three subjects, the glottis was monitored during spontaneous
breathing and in three others CO2 was added to the inspired gas
during nIPPV. We have observed, in the absence of diaphragmatic
activity during nIPPV, that increase in delivered minute ventilation
resulted in progressive narrowing of the vocal cords, with increase
in inspiratory resistance and progressive reduction in the percentage
of the delivered tidal volume effectively reaching the lungs. Adding
CO2 to the inspired gas led to partial widening of the glottis in two
out of three subjects. Moreover, glottic width was narrower during
nIPPV than during inspiration in spontaneous breathing and the
activation of the diaphragmatic muscle was always associated with a
significant inspiratory abduction of the vocal cords. Sporadically,
during passive hyperventilation, complete adduction of the vocal
cords was directly responsible for obstructive laryngeal apneas and
cyclic changes in the glottic aperture resulted in waxing and waning
of VT. We conclude that in awake humans, passive ventilation with
nIPPV results in vocal cords adduction. This vocal cords adduction
depends partly on PetCO2, but our results suggest that other factors
may also influence glottic width.
Received 17 May 1994; accepted in final form 16 February 1995.
APS Manuscript Number A473-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 March 1995.