LARYNGEAL RESPONSE TO PASSIVELY INDUCED HYPOCAPNIA DURING NREM SLEEP IN NORMAL ADULT HUMANS

Passively induced hypocapnia in animals activates vocal cord adductor muscles and decreases the glottic aperture. The purpose of this study was to determine if passively induced hypocapnia has similar effects i n normal adult humans in stage 3/4 non-rapid-eye-movement (NREM) sleep . Hypocapnia was induced by hyperventilating the subjects with a posit ive-pressure ventilator via a nose mask. At hypocapnic levels below th e CO2 apneic threshold, abrupt cessation of mechanical ventilation was followed by an apnea. In protocol 1, intramuscular electromyographic recordings of intrinsic laryngeal muscles were obtained in nine subjec ts. Activity of the posterior cricoarytenoid muscle, a vocal cord abdu ctor, disappeared during passive hyperventilation. The muscle remained electrically silent during an apnea, but phasic inspiratory activity reappeared with the first respiratory effort. The thyroarytenoid and a rytenoideus muscles, both vocal cord adductors, were electrically sile nt during spontaneous breathing in NREM sleep. Hypocapnia was frequent ly associated with activation of both adductor muscles. Once activated , the adductor muscles remained tonically active during an ensuing apn ea. In protocol 2, a fiber-optic scope was advanced transnasally into the hypopharynx to determine glottic aperture size during passively in duced hypocapnic apnea. In the seven subjects who achieved stable NREM sleep, the glottic aperture during an apnea was smaller than at any t ime throughout the respiratory cycle during spontaneous breathing just before positive-pressure ventilation. The results suggest that the de crease in glottic aperture observed during an induced hypocapnic apnea is due to suppression of the posterior cricoarytenoid muscle and/or a ctivation of vocal cord adductor muscles.