Both hypoxia and hyperoxia have major effects on cardiovascular function. However, both states affect ventilation and many previous studies have not controlled CO2 tension. We investigated whether hemodynamic effects previously attributed to modified O2 tension were still apparent under isocapnic conditions. In eight healthy men, we studied blood pressure (BP), heart rate (HR), cardiac index (CI), systemic vascular resistance index (SVRI) and arterial stiffness (augmentation index, AI) during 1 h of hyperoxia (mean end-tidal O2 79.6 ± 2.0%) or hypoxia (pulse oximeter oxygen saturation 82.6 ± 0.3%). Hyperoxia increased SVRI (18.9 ± 1.9%; P < 0.001) and reduced HR (−10.3 ± 1.0%; P < 0.001), CI (−10.3 ± 1.7%; P < 0.001), and stroke index (SI) (−7.3 ± 1.3%; P < 0.001) but had no effect on AI, whereas hypoxia reduced SVRI (−15.2 ± 1.2%; P < 0.001) and AI (−10.7 ± 1.1%; P < 0.001) and increased HR (18.2 ± 1.2%; P < 0.001), CI (20.2 ± 1.8%; P < 0.001), and pulse pressure (13.2 ± 2.3%; P = 0.02). The effects of hyperoxia on CI and SVRI, but not the other hemodynamic effects, persisted for up to 1 h after restoration of air breathing. Although increased oxidative stress has been proposed as a cause of the cardiovascular response to altered oxygenation, we found no significant changes in venous antioxidant or 8-iso-prostaglandin F2α levels. We conclude that both hyperoxia and hypoxia, when present during isocapnia, cause similar changes in cardiovascular function to those described with poikilocapnic conditions.
Acute and short-term hemodynamic effects of partial left ventriculectomy analyzed by pressure-volume loops
