The effect of high ambient pressure, raised respired gas density and increased partial pressure of oxygen on the carotid sinus baroreceptor control of heart rate in man
Experiments were performed to elucidate the mechanisms contributing to the hyperbaric bradycardia. Ethical approval was obtained and all subjects gave written and informed consent. Heart rate, arterial blood pressure, respiratory activity and carotid sinus baroreceptor reflexes were monitored non-invasively. Four healthy male saturation divers were compressed to 46ATA. Significant reductions in resting heart rate, mean arterial pressure, systolic blood pressure and diastolic blood pressure were observed. Baroreceptor sensitivity was significantly increased at 46ATA. A separate series of investigations determined the effects of breathing an increased gas density and an increased partial pressure of oxygen (P02) on arterial blood pressure, heart rate and baroreceptor sensitivity at 1ATA. Two groups of 6 healthy male subjects participated in the experiments. No significant changes in resting heart rate, arterial blood pressure, respiratory rate, tidal volume or baroreceptor sensitivity were observed breathing an increased gas density up to 5.47gl-1. Raising the inspired P02 to 0.5bar at 1ATA resulted in a significant reduction in resting heart rate and a significant increase in carotid sinus baroreceptor sensitivity. Respiratory sinus arrhythmia (RSA) was used as a non-invasive estimate of vagal tone to determine whether the hyperbaric bradycardia is associated with changes in vagal autonomic control. No changes in the overall magnitude of RSA were observed over a range of respiratory rates at high pressure compared to controls at 1ATA. These results suggest that increased gas density is not a contributing factor but increased P02 may play a role in the development of hyperbaric bradycardia.