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 in normal adult humans in stage 3/4 non-rapid-eye-movement (NREM) sleep. Hypocapnia was induced by hyperventilating the subjects with a positive-pressure ventilator via a nose mask. At hypocapnic levels below the 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 subjects. Activity of the posterior cricoarytenoid muscle, a vocal cord abductor, 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 arytenoideus muscles, both vocal cord adductors, were electrically silent during spontaneous breathing in NREM sleep. Hypocapnia was frequently associated with activation of both adductor muscles. Once activated, the adductor muscles remained tonically active during an ensuing apnea. In protocol 2, a fiber-optic scope was advanced transnasally into the hypopharynx to determine glottic aperture size during passively induced hypocapnic apnea. In the seven subjects who achieved stable NREM sleep, the glottic aperture during an apnea was smaller than at any time throughout the respiratory cycle during spontaneous breathing just before positive-pressure ventilation. The results suggest that the decrease in glottic aperture observed during an induced hypocapnic apnea is due to suppression of the posterior cricoarytenoid muscle and/or activation of vocal cord adductor muscles.