Effect of different levels of hyperoxia on breathing in healthy subjects

Abstract

We have recently shown that breathing 50% O2 markedly stimulates ventilation in healthy subjects if end-tidal PCO2 (PETCO2) is maintained. The aim of this study was to investigate a possible dose-dependent stimulation of ventilation by O2 and to examine possible mechanisms of hyperoxic hyperventilation. In eight normal subjects ventilation was measured while they were breathing 30 and 75% O2 for 30 min, with PETCO2 being held constant. Acute hypercapnic ventilatory responses were also tested in these subjects. The 75% O2 experiment was repeated without controlling PETCO2 in 14 subjects, and in 6 subjects arterial blood gases were taken at baseline and at the end of the hyperoxia period. Minute ventilation (VI) increased by 21 and 115% with 30 and 75% isocapnic hyperoxia, respectively. The 75% O2 without any control on PETCO2 led to 16% increase in VI, but PETCO2 decreased by 3.6 Torr (9%). There was a linear correlation (r = 0.83) between the hypercapnic and the hyperoxic ventilatory response. In conclusion, isocapnic hyperoxia stimulates ventilation in a dose-dependent way, with VI more than doubling after 30 min of 75% O2. If isocapnia is not maintained, hyperventilation is attenuated by a decrease in arterial PCO2. There is a correlation between hyperoxic and hypercapnic ventilatory responses. On the basis of data from the literature, we concluded that the Haldane effect seems to be the major cause of hyperventilation during both isocapnic and poikilocapnic hyperoxia.

Effects of Peripheral Chemoreceptors Deactivation on Sympathetic Activity in Heart Transplant Recipients

“…20 However, breathing 100% oxygen can also increase ventilation in normal subjects. 39 Central chemoreceptor activation during hyperoxia, known as the Haldane effect, 40 may play a role because oxygenated hemoglobin has a lower transport capacity for tissue CO 2 than does nonoxygenated hemoglobin. Subsequently, an increase of CO 2 in brain tissue may result in stimulation of central chemoreceptors.…”

Treatment of Central Sleep Apnea in US Veterans

“…48 Thus, sustained hyperoxia is a ventilatory stimulant. Specific mechanisms of hyperoxic hyperventilation include increased brain tissue PCO 2 via cerebral vasoconstriction, 49 the Haldane effect, 50 or a direct stimulatory effect on chemosensitive respiratory neurons 51 via production of reactive oxygen species. The net effect of hyperoxia is alveolar hyperventilation, decreased plant gain, and increased CO 2 reserve, thus stabilizing respiration 36 during sleep.…”

Cerebral Perfusion Response to Hyperoxia

“…An increase in the fraction of inspired oxygen leads to an increase in the saturation level of arterial haemoglobin (SaO 2 ), and in the partial pressure of oxygen dissolved in the arterial plasma (PaO 2 ) (Berkowitz, 1997;Johnston et al, 2003b). This results in a multitude of physiologic and biochemical effects (Jensen, 2004;Watson et al, 2000), which alter the acidity of the blood, the binding of carbon dioxide and oxygen with haemoglobin, the partial pressures of oxygen and carbon dioxide in the tissue, plasma and expired gases, as well as changes in ventilation, metabolism, and cerebral blood flow (CBF) (Becker et al, 1996;Bohr et al, 1904;Christiansen et al, 1914;Johnston et al, 2003a, b;Poulin et al, 1998). The exact causes and relationships between these events are quite complicated and not directly essential to the use of hyperoxia as an MRI contrast mechanism.…”

“…A characteristic response to hyperoxia is a reduction in end-tidal PCO 2 (Becker et al, 1996;Floyd et al, 2003;Watson et al, 2000). A decrease in P ET CO 2 is accompanied by vasoconstriction in the arterioles reducing CBF; however, the increase in PaO 2 also has a direct vasoconstrictive effect independently of the P ET CO 2 response (Floyd et al, 2003;Kolbitsch et al, 2002).…”