Human cardiovascular dose–response to supplemental oxygen

Aim:  The aim of the study was to examine the central and peripheral cardiovascular adaptation and its coupling during increasing levels of hyperoxaemia. We hypothesized a dose‐related effect of hyperoxaemia on left ventricular performance and the vascular properties of the arterial tree. Methods:  Oscillometrically calibrated arterial subclavian pulse trace data were combined with echocardiographic recordings to obtain non‐invasive estimates of left ventricular volumes, aortic root pressure and flow data. For complementary vascular parameters and control purposes whole‐body impedance cardiography was applied. In nine (seven males) supine, resting healthy volunteers, aged 23–48 years, data was collected after 15 min of air breathing and at increasing transcutaneous oxygen tensions (20, 40 and 60 kPa), accomplished by a two group, random order and blinded hyperoxemic protocol. Results:  Left ventricular stroke volume [86 ± 13 to 75 ± 9 mL (mean ± SD)] and end‐diastolic area (19.3 ± 4.4 to 16.8 ± 4.3 cm 2 ) declined ( P  < 0.05), and showed a linear, negative dose–response relationship to increasing arterial oxygen levels in a regression model. Peripheral resistance and characteristic impedance increased in a similar manner. Heart rate, left ventricular fractional area change, end‐systolic area, mean arterial pressure, arterial compliance or carbon dioxide levels did not change. Conclusion:  There is a linear dose–response relationship between arterial oxygen and cardiovascular parameters when the systemic oxygen tension increases above normal. A direct effect of supplemental oxygen on the vessels may therefore not be excluded. Proximal aortic and peripheral resistance increases from hyperoxaemia, but a decrease of venous return implies extra cardiac blood‐pooling and compensatory relaxation of the capacitance vessels.