Effect of Hyperoxia on Ventilation
BECKER, H., POLO, O., MCNAMARA, S.G., BERTHON-JONES, M., & SULLIVAN, C.E. Ventilatory response to isocapnic hyperoxia. J Appl Physiol 78, 696-701, 1995.
Breathing O2 for up to 1 h either does not influence or slightly increases (6-13%) minute ventilation. However, end-tidal PCO2 (PETCO2) was not kept constant in those experiments. In nine men, we studied the ventilatory, blood pressure, and heart rate responses to 30 min of normobaric isocapnic hyperoxia (50% O2). During isocapnic hyperoxia, arterial PO2 and O2 saturation increased but arterial PCO2, pH, blood pressure, and heart rate did not. Hyperoxia increased minute ventilation by 60%, due to an increase in tidal volume.
BECKER, H.F., POLO, O., MCNAMARA, S.G., BERTHON-JONES, M., & SULLIVAN, C.E. Effect of different levels of hyperoxia on breathing in healthy subjects. J Appl Physiol 81, 1683-1690, 1996.
Is the hyperoxia-induced increase in ventilation (see Becker et al, 1985) dose-dependent? And what is the basis for this increase in ventilation? In eight normal subjects, ventilation was measured while they breathed 30 and 75% O2 for 30 min, at constant PETCO2. The 75% O2 experiment was repeated without controlling PETCO2 in 14 subjects. Minute ventilation increased by 21 and 115% with 30 and 75% isocapnic hyperoxia, respectively. When PETCO2 was not controlled during inhalation of 75% O2, ventilation increased only 16%, the increase being buffered by a 3.6 Torr (9%) decrease in PETCO2. Thus, isocapnic hyperoxia stimulates ventilation in a dose-dependent way. Based on the literature, the authors conclude that the [reverse] Haldane effect is the major cause of hyperoxia-induced increase in ventilation.
ISCOE, S. & FISHER, J.A. Hyperoxia-induced hypocapnia: an underappreciated risk. Chest 128, 430-433, 2005.
In this hypothesis paper, the authors contend that hyperoxia can, paradoxically, reduce O2 delivery to tissues because of a hyperoxia-induced increase in ventilation that causes hypocapnia. This hypocapnia causes vasoconstriction which reduces blood flow. Since O2 delivery is the product of arterial O2 content and perfusion, reductions in perfusion can offset any small increases in content, putting tissues at risk. This has implications for the use of O2 in treating, for example, strokes and heart attacks, and probably explains earlier reports of the adverse effects of administering O2.Preventing hypocapnia during administration of O2 is, they suggest, a good idea.