EFFECTS OF OXYGEN BREATHING ON THE HEART RATE, BLOOD PRESSURE, AND CARDIAC INDEX OF NORMAL MEN—RESTING, WITH REACTIVE HYPEREMIA, AND AFTER ATROPINE*

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Abstract
Oxygen breathing is often used in the treatment of various clinical disorders, yet the hemodynamic effects of hyperoxia in normal man have not been fully defined. Fifteen normal men breathed O2 or air in random sequence. Cardiac index (Indocyanlne green dilution) decreased (3.01[plus or minus]0.53 to 2.67[plus or minus]0.46 L/min/m2 p=0.001) during 02 breathing. Heart rate decreased proportionately and stroke index was unaffected. Mean brachial blood pressure increased (93[plus or minus]9 to 94[plus or minus]8 mm Hg p=0.05), and systemic resistance increased (16.7[plus or minus]3.1 to 18.1[plus or minus]3.1 mmHg/L/minp=0.001). After 2.0 mgm atropine sulfate, cardiac index, heart rate, and total systemic resistance were unaffected by hyperoxic breathing. The same variables were measured before and during the phase of reactive hyperemia following release of arterial thigh tourniquets. Hyperemia increased cardiac index to 4.59 L/min/m2 during air breathing but only to 3.74 L/min/m2 during O2 breathing (p=0.01). The level of inspired O2 at which these changes occur was investigated in 9 normal subjects breathing 7 concentrations of O2 from 15 to 100%. Increasing concentrations of O2 produced proportionately decreasing heart rates over the entire range. Thus, the upper limit of O2 sensitive chemoreceptor activity extends at least to 100% O2 inspired; breathing increased O2 tensions produces a vagus dependent decrease in heart rate and a rate related decrease in cardiac output; this effect persists in situations of altered circulatory demands such as reactive hyperemia. While these effects of O2 breathing are small, they are consistent and should be considered in interpreting the hemodynamic behavior of persons breathing O2.