Mechanisms of hyperbaric bradycardia

Abstract

Relative bradycardias have been reported to occur in humans both at rest and during exercise under a variety of hyperbaric conditions. Review of existing data reveals that there are two major mechanisms operating: one depends on hyperoxia and the other does not. While it is clear that hyperoxia produces bradycardia by a variety of well understood mechanisms, the non-oxygen-dependent causes of hyperbaric bradycardia have not been defined. Experimental results from animals studies have eliminated the involvement of increased ambient pressure and gas density in the development of hyperbaric bradycardia, in all normoxic conditions. This review considers two other possibilities, the altered respiratory pattern which may modify the HR secondarily, and circulatory deconditioning under hyperbaric environments, which masks the hyperbaric bradycardia. We propose that the return of a normal sea level HR following the initial bradycardia represents, in effect, bradycardia which would be seen if cardiovascular deconditioning were not present. It is concluded that hyperoxia is the major factor responsible for initiating and maintaining hyperbaric bradycardia, whereas non-oxygen dependent hyperbaric factors may alter respiratory patterns and secondarily cause a reduction in HR.