Psychomotor and cardiorespiratory functions during inert gas sedation

Abstract: Relative hypoventilation and bradycardia are commonly observed in both resting and exercising divers. Divers are exposed to a complex environment where there are increases of hydrostatic pressure, gas density and partial pressure of sedating inert gas. The present work addresses the question whether the inert gas sedation contributes to the relative hypoventilation and the bradycardia in hyperbaria. Exercising subjects were studied in 4 different environments (Paper I), which pairwise had the same hydrostatic pressure (1 or 5.5 bar) but where each pair differed with respect to gas density and sedative inert gas partial pressure. This was achieved by administration of normoxic gas mixtures of nitrogen (N2) helium (He), and sulphur hexafluoride (SF6) at normal and increased ambient pressure. It was found that inert gas sedation in combination with raised gas density caused both bradycardia and relative hypoventilation, whereas hydrostatic pressure per se caused additional bradycardia but had no effect on respiration. In order to separate the relative contributions of increased gas density and inert gas sedation on caediorespiratory control, the relative sedative potencies of N2 and SF6 were studied in the ambient pressure range 1-11 bar and compared to nitrous oxide (N2O). The ratios between the sedative potencies of N2, SF6 and N2O were found to be 1:8.5:39 (Papers II, III). In subsequent studies N2O partial pressures up to 0.30-0.39 bar were employed as a model of inert gas sedation in hyperbaria. Respiratory responses to inspiratory loading were found not to be impaired by inert gas sedation (Paper IV). Baroreflex control of heart rate was studied in resting men by means of experimental application of external neck pressure (Paper V) and in exercising men by means of sudden tilts between upright and supine (Paper VI). Steady-state heart rate and blood pressure were not influenced by inert gas sedation. Chronotropic responses to hypotensive carotid stimuli tended to be reduced at rest during N2O inhalation. In exercise, arterial-cardiac chronotropic baroreflex sensitivity during N2O inhalation was reduced by 16 per cent and there was a more than 30 per cent increase of reflex latency. It is concluded that inert gas sedation and increased hydrostatic pressure do not contribute to the hypoventilation observed in hyperbaria. Cardiovascular functions, however, appear to be influenced by both inert gas sedation and hydrostatic pressure. Thus hydrostatic pressure causes a modest relative bradycardia, and inert gas sedation impairs baroreflex control of heart rate. The role of the baroreflex impairment for the bradycardia related to combined inert gas sedation and increased gas density remains unclear.