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Effects of short-term isocapnic hyperoxia and hypoxia on cardiovascular function

¹Department of Anaesthesia, Critical Care and Pain Medicine, Royal Infirmary, and ²Clinical Pharmacology Unit, Centre for Cardiovascular Science, Queen’s Medical Research Institute, The University of Edinburgh, Royal Infirmary of Edinburgh, Edinburgh, United Kingdom

Submitted 19 September 2005 ; accepted in final form 1 May 2006

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 F₂ levels. We conclude that both hyperoxia and hypoxia, when present during isocapnia, cause similar changes in cardiovascular function to those described with poikilocapnic conditions.

arterial stiffness; vascular resistance; cardiac output; carbon dioxide