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Hyperoxia-induced tissue hypoxia: a danger?
| Content Provider | Semantic Scholar |
|---|---|
| Author | Forkner, Ivy F. Piantadosi, Claude A. Scafetta, Nicola Moon, Richard E. |
| Copyright Year | 2007 |
| Abstract | OXYGEN supplementation has traditionally been believed to increase blood and tissue oxygenation. However, hyperoxia induces bradycardia and a reduction in cardiac output, which partly offsets the otherwise increased oxygen delivery. Recently, an additional mechanism that could further reduce tissue oxygen delivery has been propounded. Experiments in animals and normal humans have suggested that breathing very high concentrations of oxygen can cause an increase in ventilation. Proposed mechanisms for this include increased production of reactive oxygen species directly stimulating brain stem carbon dioxide chemoreceptors, oxygen disinhibition of an inhibitory input present during normoxia, and increased brainstem partial pressure of carbon dioxide (PCO2) secondary to the Haldane effect. As a result of the observed ventilatory effects of oxygen, it has been speculated that hypocapnia ensuing from hyperoxia-induced hyperventilation can reduce organ blood flow sufficiently to cause hypoxia. This notion is now being used by some clinicians for clinical decision making and has been published in the clinical literature. During hyperoxia, the solubility of carbon dioxide in blood is reduced. This is known as the Haldane effect and is a result of the displacement of carbon dioxide from hemoglobin by oxygen. As a result, it has been argued that this decrease in carbon dioxide solubility causes PCO2 in both venous blood and tissue to increase. Hyperventilation should ensue due to increased PCO2 and proton accumulation in the brainstem, causing stimulation of the central chemoreceptors. It has been hypothesized that this hyperventilation would lead to arterial hypocapnia, and hence vasoconstriction in certain vascular beds, including those in the brain. This hypothesis has been used to suggest that oxygen supplementation can, through reduced tissue blood flow, create tissue hypoxia. There are multiple flaws in this argument. First, during hyperoxia blood flow is not reduced enough to offset the higher oxygen content, and oxygen delivery is enhanced. Second, if carbon dioxide accumulates in tissue, the resulting acidosis would tend to offset vasoconstriction. Third, although the Haldane effect might be responsible for clinically significant changes in PCO2 under hypoxic conditions, in normoxia and hyperoxia modeling shows that it accounts for only very small changes in PCO2 (fig. 1). Fourth, although several investigators have observed that hyperoxia can lead to hyperventilation, the evidence is not at all compelling that this hyperventilation leads to significant arterial hypocapnia as has been suggested. In only one study cited in the development of this hypothesis was arterial PCO2 (PaCO2) actually measured. In that study, oxygen breathing was associated with a decrease in PaCO2 in five of six subjects, although the effect was small (mean decrease 2.5 mmHg). In several other published studies, 87–100% O2 administration caused no significant change in arterial PCO2 by direct measurement. 9–21 Even 100% O2 administration up to 3 atmospheres absolute (ATA) does not cause arterial hypocapnia. In a study of normal volunteers studied while breathing room air at 1 ATA and 100% O2 at 3 ATA, PaCO2 was 37 2.9 and 36 2.6 mmHg (mean SD), respectively. In other studies at 3.5 ATA, mild hypocapnia (mean decrease 5 mmHg) has been observed; however, at such extreme oxygen partial pressure (PO2) values (approximately 2,100 mmHg), hyperventilation due to direct toxic effects is likely. The evidence for oxygen-induced hypocapnia is based either on observations of increased ventilation only, or on reduced end-tidal PCO2 (PETCO2). 1,4 There are plausible mechanisms that account for these findings that involve the lung directly. For instance, exposure to high oxygen concentrations causes atelectasis, which could cause a decrease in lung compliance and a reflex increase in * Medical Student, Department of Anesthesiology, Center for Hyperbaric Medicine and Environmental Physiology, † Professor, Department of Medicine, and Director, Center for Hyperbaric Medicine and Environmental Physiology, ‡ Research Scientist, Department of Physics, Center for Hyperbaric Medicine and Environmental Physiology, § Professor of Anesthesiology, Associate Professor of Medicine, and Medical Director, Center for Hyperbaric Medicine and Environmental Physiology, Duke University Medical Center. |
| Starting Page | 386 |
| Ending Page | 425 |
| Page Count | 40 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://anesthesiology.pubs.asahq.org/pdfaccess.ashx?url=/data/journals/jasa/931063/0000542-200705000-00025.pdf |
| PubMed reference number | 17457139v1 |
| Volume Number | 106 |
| Issue Number | 5 |
| Journal | Anesthesiology |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Absolute neutrophil count Acidosis Anesthesiology Arterial Occlusive Diseases Atelectasis Atmosphere, planetary Beds Bradycardia Brain Stem Carbon dioxide measurement, partial pressure Cardiac Output Cell Respiration Chemoreceptor Cells Compliance:Compli:Pt:Lung:Qn Decision Making Hyperoxia Hypoxia Intracranial Hypertension Medical Specialities Oxygen content level PO-2 Protons Psychologic Displacement Reactive Oxygen Species Scientific Publication Social disinhibition Stimulation (motivation) Structure of parenchyma of lung Vascular constriction (function) physiological aspects torr |
| Content Type | Text |
| Resource Type | Article |
