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.
"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 . "
[Show abstract][Hide abstract] 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.
"The use of a relatively high back-up rate and/or pressure control ventilation may also help to “capture” the patient better . 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” . This effect can be prevented by a simple intervention: decreasing the FİO2 level. "
[Show abstract][Hide abstract] 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.
BMC Pulmonary Medicine 02/2014; 14(1):19. DOI:10.1186/1471-2466-14-19 · 2.40 Impact Factor
" . 2000 ) . Furthermore , normobaric O 2 treatment may even contribute to the morbidity of CO poisoning . Apart from the potential for free radical generation by hyperoxia ( Thom , 1990 ) , there is also the underappreciated effect of hyperoxia as a ventilatory stimulant . Hyperoxia - induced hyperventilation results in some degree of hypocapnia ( Becker et al . 1996 ) , which is associated with a reduction of blood flow in such CO 2 - responsive vascular beds as the coronary ( Case et al . 1975 ) and cerebral circulations . The reduction in cerebral ( Kety & Schmidt , 1948 ) blood flow with hypocapnia occurs even in the presence of increased levels of CO in the blood ( Rucker et al . 2002 ) . In no"
[Show abstract][Hide abstract] ABSTRACT: At the start of the 20th century, CO poisoning was treated by administering a combination of CO(2) and O(2) (carbogen) to stimulate ventilation. This treatment was reported to be highly effective, even reversing the deep coma of severe CO poisoning before patients arrived at the hospital. The efficacy of carbogen in treating CO poisoning was initially attributed to the absorption of CO(2); however, it was eventually realized that the increase in pulmonary ventilation was the predominant factor accelerating clearance of CO from the blood. The inhaled CO(2) in the carbogen stimulated ventilation but prevented hypocapnia and the resulting reductions in cerebral blood flow. By then, however, carbogen treatment for CO poisoning had been abandoned in favour of hyperbaric O(2). Now, a half-century later, there is accumulating evidence that hyperbaric O(2) is not efficacious, most probably because of delays in initiating treatment. We now also know that increases in pulmonary ventilation with O(2)-enriched gas can clear CO from the blood as fast, or very nearly as fast, as hyperbaric O(2). Compared with hyperbaric O(2), the technology for accelerating pulmonary clearance of CO with hyperoxic gas is not only portable and inexpensive, but also may be far more effective because treatment can be initiated sooner. In addition, the technology can be distributed more widely, especially in developing countries where the prevalence of CO poisoning is highest. Finally, early pulmonary CO clearance does not delay or preclude any other treatment, including subsequent treatment with hyperbaric O(2).
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