Effect of different levels of hyperoxia on breathing in healthy subjects

David Read Laboratory, Department of Medicine, University of Sydney, New South Wales, Australia.
Journal of Applied Physiology (Impact Factor: 3.06). 11/1996; 81(4):1683-90.
Source: PubMed


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.

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    • " Numerous studies completed in the last two decades have repeatedly shown that administration of high dose oxygen will precipitate a transient hyperpnea with a secondary reduction in arterial carbon dioxide (PaCO 2 ) concentrations. While the phenomena is common, the exact mechanism of hyperoxic hyperpnea is not well understood. Becker et al. (1996) suggested " that the hyperventilation caused by hyperoxia is caused by hypercapnia in the central chemoreceptors. " This central effect is thought to be secondary to the decreased CO 2 carrying capacity of the blood in the face of high PaO 2 and HbO 2 saturation (the Haldane effect) (Rangel-Castilla et al., 2010). While understanding th"
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    ABSTRACT: The first descriptions of carbon monoxide (CO) and its toxic nature appeared in the literature over 100 years ago in separate publications by Drs. Douglas and Haldane. Both men ascribed the deleterious effects of this newly discovered gas to its strong interaction with hemoglobin. Since then the adverse sequelae of CO poisoning has been almost universally attributed to hypoxic injury secondary to CO occupation of oxygen binding sites on hemoglobin. Despite a mounting body of literature suggesting other mechanisms of injury, this pathophysiology and its associated oxygen centric therapies persists. This review attempts to elucidate the remarkably complex nature of CO as a gasotransmitter. While CO's affinity for hemoglobin remains undisputed, new research suggests that its role in nitric oxide release, reactive oxygen species formation, and its direct action on ion channels is much more significant. In the course of understanding the multifaceted character of this simple molecule it becomes apparent that current oxygen based therapies meant to displace CO from hemoglobin may be insufficient and possibly harmful. Approaching CO as a complex gasotransmitter will help guide understanding of the complex and poorly understood sequelae and illuminate potentials for new treatment modalities. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Full-text · Article · May 2015 · Toxicology
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    • "Then resting and exercise data were collected. This might have had a large influence on results, since some minutes of exposure to hyperoxia have a secondary effect on chemoreflex function [122–124] presumably due to production of reactive oxygen species [119, 125]. This was observed in the context of carotid chemoreceptors contribution during exercise in normoxia, when hyperoxia administration started during exercise and resumed during 2 min [116]. "
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    ABSTRACT: During dynamic exercise, mechanisms controlling the cardiovascular apparatus operate to provide adequate oxygen to fulfill metabolic demand of exercising muscles and to guarantee metabolic end-products washout. Moreover, arterial blood pressure is regulated to maintain adequate perfusion of the vital organs without excessive pressure variations. The autonomic nervous system adjustments are characterized by a parasympathetic withdrawal and a sympathetic activation. In this review, we briefly summarize neural reflexes operating during dynamic exercise. The main focus of the present review will be on the central command, the arterial baroreflex and chemoreflex, and the exercise pressure reflex. The regulation and integration of these reflexes operating during dynamic exercise and their possible role in the pathophysiology of some cardiovascular diseases are also discussed.
    Full-text · Article · Apr 2014
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    • "The use of a relatively high back-up rate and/or pressure control ventilation may also help to “capture” the patient better [26]. Another key factor in patients with HES is the rebound effect of high-fractionated oxygen (FİO2) on the PaCO2 and pH, known as the “Haldane effect” [27]. This effect can be prevented by a simple intervention: decreasing the FİO2 level. "
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    ABSTRACT: Identifying the predictors of noninvasive ventilation (NIV) failure has attracted significant interest because of the strong link between failure and poor outcomes. However, very little attention has been paid to the timing of the failure. This narrative review focuses on the causes of NIV failure and risk factors and potential remedies for NIV failure, based on the timing factor. The possible causes of immediate failure (within minutes to <1 h) are a weak cough reflex, excessive secretions, hypercapnic encephalopathy, intolerance, agitation, and patient-ventilator asynchrony. The major potential interventions include chest physiotherapeutic techniques, early fiberoptic bronchoscopy, changing ventilator settings, and judicious sedation. The risk factors for early failure (within 1 to 48 h) may differ for hypercapnic and hypoxemic respiratory failure. However, most cases of early failure are due to poor arterial blood gas (ABGs) and an inability to promptly correct them, increased severity of illness, and the persistence of a high respiratory rate. Despite a satisfactory initial response, late failure (48 h after NIV) can occur and may be related to sleep disturbance. Every clinician dealing with NIV should be aware of these risk factors and the predicted parameters of NIV failure that may change during the application of NIV. Close monitoring is required to detect early and late signs of deterioration, thereby preventing unavoidable delays in intubation.
    Full-text · Article · Feb 2014 · BMC Pulmonary Medicine
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