In their article regarding the effects of hyperoxia on tissue perfusion, Forkner et al.  1conclusively stated that administration of high oxygen concentration augments tissue oxygenation and produces no adverse effects on tissue oxygenation.

Forkner et al.  tried to convince readers that Iscoe et al. ’s position2that the hyperventilation induced by hyperoxia as a result of the Haldane effect would lead to arterial hypocapnia and, hence, vasoconstriction in certain vascular beds, including those in brain, is not correct. Based on findings of very old studies, Forkner et al.  also argued that during hyperoxia blood flow is not reduced enough to offset the higher oxygen content, and oxygen delivery is enhanced. This argument is not correct. A previous human study has shown that the magnitude of a decrease in cerebral blood flow is much more profound than that of an increase in arterial oxygen content.3In that study, for example, the arterial oxygen content was 18 ml/dl and cerebral blood flow was 54 ml · 100 g−1· min−1(the cerebral oxygen delivery was 9.7 ml · 100 g−1· min−1) at baseline, and after breathing 100% oxygen at 1 atmosphere absolute, the arterial oxygen content increased by 13.4% but the cerebral blood flow decreased by 33%, so the cerebral oxygen delivery decreased to 7.3 ml · 100 g−1· min−1(20.7 ml/dl oxygen content × 36 ml · 100 g−1· min−1), a 25% decrease in cerebral oxygen delivery. In addition, the partial pressure of arterial carbon dioxide decreased by 3 Torr with the administration of 100% oxygen. When hypocapnia was corrected by adding carbon dioxide to 100% oxygen, decreased cerebral blood flow was restored by only 8%. Although the role of hyperoxia-induced hypocapnia on decreases in cerebral blood flow may not be great, the independent cerebral vasoconstrictive effect of hyperoxia is too great in magnitude to be ignored. A hyperoxia-induced decrease in cerebral blood flow would cause a rightward shift of cerebral blood flow-perfusion pressure relationship line, so that cerebral blood flow would be much lower at a given perfusion pressure.

By employing laser Doppler velocimetry for the measurement of retinal blood velocity and fundus imaging with the Zeiss retinal vessel analyzer for the assessment of retinal vessel diameter, another previous human study4showed that hyperoxia by breathing greater than 92% oxygen decreases retinal blood velocity and retinal blood flow by 60% each and decreases retinal vessel diameter by 15%, suggesting that the decrease in retinal blood flow is mainly the result of decreased cerebral blood flow rather than the retinal vessel vasoconstriction. The decrease in retinal blood flow during hyperoxia could contribute to ischemic retinopathy when combined with increased intraocular pressure5during prone spine surgery.

A clinical study has shown that breathing 100% oxygen reduces coronary blood flow velocity by 20% and increases coronary vascular resistance by 23% in patients with coronary artery disease and that vitamin C reverses this effect, suggesting that these changes are mediated by an oxidative stressor acting on the coronary microcirculation.6A hyperoxia-induced decrease in coronary microcirculatory blood flow in patients with coronary artery stenosis can be detrimental.

To determine whether the routine use of high inspired oxygen concentration during the perioperative period alters the incidence of surgical site infection in a general surgical population, a double-blind, randomized controlled trial was conducted.7The incidence of surgical site infection was significantly higher (25%) in the group receiving inspired oxygen concentration of 80% than in the group with inspired oxygen concentration of 35% (11.3%). This is further evidence that does not support the argument of Forkner et al. 

Supplemental oxygen benefits patients who would otherwise suffer hypoxia while breathing room air. However, in this situation, supplemental oxygen would not induce hyperoxia. Forkner et al.  made no distinction between supplemental oxygenation and the administration of high oxygen concentration.

The effect of hyperoxia-induced hypocapnia on decreases in cerebral blood flow or other organ flow may not be great and is unlikely to be of clinical significance. However, the independent vasoconstricitive effect of hyperoxia is too great in magnitude to be ignored. One cannot say that hyperoxia is harmless.

New York Medical College, Valhalla, New York.

Forkner IF, Piantadosi CA, Scafetta N, Moon RE: Hyperoxia-induced tissue hypoxia: A danger? Anesthesiology 2007; 106:1051–5
Iscoe S, Fisher JA: Hyperoxia-induced hypocapnia: An underappreciated risk. Chest 2005; 128:430–3
Floyd TF, Clark JM, Gelfand R, Detre JA, Ratcliffe S, Guvakov D, Lambertsen CJ, Eckenhoff RG: Independent cerebral vasoconstrictive effects of hyperoxia and accompanying arterial hypocapnia at 1 ATA. J Appl Physiol 2003; 95:2453–61
Luksch A, Garhöfer G, Imhof A, Polak K, Polska E, Dorner GT, Anzenhofer S, Wolzt M, Schmetterer L: Effect of inhalation of different mixtures of O2and CO2on retinal blood flow. Br J Ophthalmol 2002; 86:1143–7
Cheng MA, Todorov A, Tempelhoff R, McHugh T, Crowder CM, Lauryssen C: The effect of prone positioning on intraocular pressure in anesthetized patients. Anesthesiology 2001; 95:1351–5
McNulty PH, Robertson BJ, Tulli MA, Hess J, Harach LA, Scott S, Sinoway LI: Effect of hyperoxia and vitamin C on coronary blood blow in patients with ischemic heart disease. J Appl Physiol 2007; 102:2040–5
Pryor KO, Fahey IIITJ Lien CA Goldstein PA: Surgical site infection and the routine use of perioperative hyperoxia in a general surgical population: A randomized controlled trial. JAMA 2004; 291:79–87