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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study extension of O2 tolerance by interruption of hyperoxic exposure, as compared to previous studies of continuous oxygen exposure, five healthy volunteers were exposed to oxygen at 2 ATA on an intermittent schedule of 20 min breathing O2, alternating with 5 min on a normoxic N2-O2 mixture. The cycle was repeated until symptoms or signs of O2 toxicity caused cessation of the experiment. Tracheal irritation and burning on inspiration occurred after 6-9 "oxygen hours" of exposure and progressed to severe tracheobronchial burning sensation, chest pain, and dyspnea after 11-15 h of O2. Average duration of exposure was 13.7 O2 h, inducing a mean vital capacity decrease of 10.3%. The decrease began soon after onset of symptoms. With intermittent O2 administration, nearly a doubling of the average duration of actual oxygen breathing was required to induce marked vital capacity change (greater than 10%) as compared to the previous studies of continuous O2 exposure. The increased duration of tolerable O2 exposure in man resembles the extension of O2 tolerance known to occur in animals exposed to intermittent hyperoxia.
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PMID:Extension of pulmonary O2 tolerance in man at 2 ATA by intermittent O2 exposure. 86 21

Exercise capacity in patients with stable heart failure may be influenced by prolonged drug treatment or exercise training, but acute interventions are generally thought to have little effect. Cardiorespiratory responses to exercise were studied in 12 consecutive patients with chronic congestive heart failure who underwent serial submaximal and maximal exercise tests at inspired oxygen concentrations of 21% (room air), 30%, and 50%. Mean (SD) exercise duration during progressive testing to maximum exercise capacity was prolonged from 548 (276) s on room air to 632 (285) s on 50% oxygen (p = 0.012). During steady-state exercise at 45 W, oxygen enrichment to 50% was associated with significantly increased arterial oxygen saturation (94.6 [1.9]% to 97.5 [1.3]%), and significantly reduced minute ventilation (36.1 [8.6] l/min to 28.1 [5.9] l/min), cardiac output (7.5 [2.3] l/min to 6.5 [1.9] l/min), and subjective scores for fatigue and breathlessness (13.9 [3.1] to 11.5 [3.5]) compared with room air intermediate changes were observed with 30% inspired oxygen. Increased inspired oxygen concentrations can improve exercise performance acutely and modify the ventilatory response to exercise in patients with heart failure. Hyperoxia reduces ventilatory response and circulatory demand while maintaining oxygen delivery at a given workload. The potential benefits of increased inspired oxygen concentrations in the treatment of chronic heart failure merit further assessment.
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PMID:Effects of increased inspired oxygen concentrations on exercise performance in chronic heart failure. 135 2

Respiration is automatically regulated via chemo- and mechanoreceptors existing in and outside the lungs, but it is also controlled voluntarily by behavioral factors. Voluntary increase in ventilation accentuates dyspnea and the sensory intensity at a given ventilation does not differ from that of exercise-induced hyperventilation, but it is significantly smaller than that during hypercapnia or hypoxia. Voluntary constraint of ventilation augments dyspnea in proportion to the degree of constraint even under isocapnic hyperoxia, and the respiratory sensation during constrained breathing is qualitatively more discomfortable than that during hyperventilation. Changes in the level and pattern of breathing under constant levels of chemical stimuli increase respiratory sensations and the intensity of dyspnea is minimal near the spontaneous levels, which supports the hypothesis that breathing is behaviorally regulated in part to minimize dyspnea. The system of behavioral control of breathing appears to be involved in the maintenance of body homeostasis by modifying the respiratory output through respiratory sensations.
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PMID:[Dyspnea and behavioral control]. 140 64

We examined, in 32 normal adults, the effect of hypoxia on the sensation of dyspnea during hypercapnic ventilatory response (HCVR). The tests were conducted under two different levels of inspiratory O2 content, either hyperoxia (PETO2 greater than 150 Torr) or hypoxia (PETO2 50-55 Torr), with simultaneous assessment of dyspnea sensation by visual analogue scaling (VAS). The sensation was evaluated either in relation to VE standardized by predicted MVV (the slope of VAS-VE regression line or VAS at VE 40%) or in relation to PETCO2 (the slope of VAS-PETCO2 line or VAS at PETCO2 55 Torr). Concomitant hypoxia significantly enhanced both the mean value of delta VE/delta PETCO2 and that of delta P0.1/delta PETCO2. The sensation of dyspnea did not differ between the two conditions when it was evaluated in relation to ventilation, whereas it was markedly greater during hypoxic HCVR when it was evaluated in relation to PETCO2. The hypoxic augmentation of the sensation, compared at PETCO2 55 Torr, could be explained by increase of the motor output from the respiratory center, since it was positively correlated with the relative change of VE, VTTI, and delta P0.1/delta PETCO2 (r = 0.70, p less than 0.0001; r = 0.63, p less than 0.0001; r = 0.40, p less than 0.05, respectively). From these findings, we conclude that hypoxia does not have a direct dyspnogenic effect, at least in normal subjects.
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PMID:[Effect of hypoxia on the sensation of dyspnea during hypercapnic ventilatory response in normal subjects]. 140 97

1. Respiratory sensation during exercise is generally considered to be related to respiratory mechanical factors which may be manifest as an abnormal relationship between the force applied to the lungs and chest wall and the resulting motion (if any); that is, a 'length-tension' inappropriateness (Campbell & Howell, 1963). This suggests that there should be a direct correlation between ventilation (VE) and the associated intensity of the perceived sensation, such that the sensation associated with a particular level of VE should remain essentially constant regardless of the source of respiratory stimulation. 2. In order to establish whether certain respiratory stimuli might be 'dyspnoeagenic' (i.e. capable of evoking an intensity of respiratory sensation out of proportion to their influence on VE), we investigated the influence of both peripheral chemoreflex activation (induced by isocapnic hypoxia) and central chemoreflex activation (induced by hypercapnic hyperoxia) on the intensity of respiratory sensation in seven healthy adults during moderate cycle ergometer exercise (i.e. below the lactate threshold, theta 1ac). 3. In each test, an 'isopnoea' was established for which a particular level of VE was sustained over a prolonged period (approximately 30 min) while the proportional contributions to the ventilatory drive from either exercise and the peripheral chemoreflex or from exercise and the central chemoreflex were slowly altered to new stable levels, without the subject's knowledge, VE, tidal volume, inspiratory and expiratory durations, mean inspiratory flow, and end-tidal PCO2 and PO2 (PET,CO2, PET,O2) were monitored breath-by-breath. The intensity of respiratory sensation was rated with a visual analogue scale. 4. Isopnoeic ratings of respiratory sensation were systematically greater for peripheral chemoreflex activation by isocapnic hypoxia during exercise at 50% theta 1ac (for which the degree of peripheral chemoreflex activation, estimated by hyperoxic transition or 'Dejours' testing, averaged approximately 23% of the total VE), compared to 90% theta 1ac during isocapnic hyperoxia. Ratings during exercise at 50% theta 1ac for central chemoreflex activation by hypercapnic hyperoxia were not systematically different from 90% theta 1ac during isocapnic hyperoxia, however. 5. As VE was stable throughout each isopnoea and the MVV (maximum voluntary ventilation) was uninfluenced by the test condition, the dyspnoea index (VE x 100/MVV) was not affected. Breathing pattern was also unaffected. 6. We conclude that in normal subjects exercising moderately, activation of the peripheral chemoreceptors by isocapnic hypoxia evokes an intensity of respiratory sensation which is out of proportion to that evoked by an isopnoeic stimulation of the central chemoreceptors with hypercapnic hyperoxia at the same level of exercise.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of peripheral and central chemoreflex activation on the isopnoeic rating of breathing in exercising humans. 251 73

Most survivors of ARDS have persistent mild reductions of TLCO even as long as a year after their episode. The lung volumes and flows return to normal in most instances, although a subset of patients will have persistent impairment. Both obstructive and restrictive deficits may be seen. This group may be predicted by the degree of acute lung injury assessed by the level of FIO2, PEEP, and gas exchange abnormality that exists in the first few days. In the first year after ARDS most physiological abnormalities will improve, but if deficits persist at one year further improvement is unlikely. Although many patients report dyspnoea following ARDS, the symptom does not correlate with abnormalities of pulmonary function. The possibility that conventional management may augment the degree of acute injury and worsen outcome must be considered. The effects of chronic hyperoxia in humans with acute lung injury or those of high levels of PEEP compared with low levels are not known. Exploring new ventilator management strategies while we await more specific treatment directed at the primary problem of acute lung inflammation will hopefully reduce acute mortality as well as acute and chronic morbidity.
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PMID:Sequelae of the adult respiratory distress syndrome. 815 46

To examine possible genetic influence on the sensation of dyspnea and on load compensation, we conducted a twin study using healthy adult pairs (10 monozygotes, MZ, and 9 dizygotes, DZ). The ventilatory response to progressive hypercapnia (HCVR) was examined under three different conditions: hyperoxia (PETO2 > 150 mm Hg), hypoxia (PETO2 maintained at 50 to 55 mm Hg), and hyperoxia with an inspiratory flow-resistive load (17 mm H2O/L/s), with simultaneous assessment of the dyspnea sensation by visual analog scale (VAS). Although the VDZ/VMZ ratio (VMZ and VDZ are within-pair variances in MZ and DZ, respectively) for the slope value of the minute ventilation-PETCO2 regression line was not different from 1 in hyperoxia either with or without an inspiratory load, it was significantly larger than 1 in hypoxia (F = 5.17, p < 0.05), suggesting that a genetic influence on HCVR existed only in the presence of hypoxia. During 3% CO2 inhalation, the VDZ/VMZ ratio for the tidal volume (VT) was larger than 1 in hyperoxic HCVR with loading (F = 7.89, p < 0.01), and that for respiratory frequency (f) was larger than 1 only in hypoxic HCVR (F = 3.59, p < 0.05). At a PETCO2 of 55 mm Hg, the VT ratio was larger than 1 under all conditions (F = 5.91, p < 0.05; F = 6.99, p < 0.05; F = 3.75, p < 0.05; respectively), and the f ratio was significantly larger than 1 again only in hypoxic HCVR (F = 3.48, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dyspnea sensation and chemical control of breathing in adult twins. 848 30

The mechanisms of exertional dyspnea relief in response to supplemental oxygen (O2) in chronic airflow limitation (CAL) are not precisely known and are likely multifactorial. To explore factors contributing to the relief of dyspnea after oxygen administration, 11 patients with severe CAL (FEV1.0 = 39 +/- 3% predicted, mean +/- SEM) and mild hypoxemia (resting PaO2 = 74 +/- 2 mm Hg) breathed room air (RA) and 60% O2 during exercise at approximately 50% of their maximal incremental exercise capacity. Breathlessness ratings (Borg scale), endurance time, respiratory drive (change in mouth occlusion pressure over the first 0.1 s of inspiration, P0.1), ventilation (VE), breathing pattern, operational lung volumes, gas exchange, and metabolic parameters were compared during RA and 60% O2. PaO2 at exercise cessation during RA and 60% O2 was 65 +/- 3 mm Hg and 226 +/- 12 mm Hg, respectively (p < 0.001). With 60% O2, the mean of individual Borg/time slopes fell significantly (p < 0.05) by 23 +/- 12% and was associated with a 35 +/- 11% increase (p < 0.01) in endurance time (r = -0.64, p < 0.05). During 60% O2, slopes of P0.1 and lactate over time also fell significantly (p < 0.05), whereas delta PaCO2/time did not change significantly. At a standardized time near end-exercise, Borg, VE, and P0.1 changed during 60% O2 by -0.8 +/- 0.3 (p < 0.05), -4.1 +/- 2.0 L/min (p = 0.07), and -1.3 +/- 0.5 cm H2O/s (p < 0.05), respectively. Slopes of Borg/VE, Borg/lactate, and VE/lactate were essentially superimposable during tests on RA and O2: Borg, lactate, and VE all fell proportionally during hyperoxia. In patients with CAL and mild exercise hypoxemia, relief of exertional breathlessness during hyperoxia is explained by reduced ventilatory demand in association with reduced blood lactate levels.
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PMID:Factors contributing to relief of exertional breathlessness during hyperoxia in chronic airflow limitation. 903 90

We studied interrelationships between exercise endurance, ventilatory demand, operational lung volumes, and dyspnea during acute hyperoxia in ventilatory-limited patients with advanced chronic obstructive pulmonary disease (COPD). Eleven patients with COPD (FEV(1.0) = 31 +/- 3% predicted, mean +/- SEM) and chronic respiratory failure (Pa(O(2)) 52 +/- 2 mm Hg, Pa(CO(2 ))48 +/- 2 mm Hg) breathed room air (RA) or 60% O(2) during two cycle exercise tests at 50% of their maximal exercise capacity, in randomized order. Endurance time (T(lim)), dyspnea intensity (Borg Scale), ventilation (V E), breathing pattern, dynamic inspiratory capacity (IC(dyn)), and gas exchange were compared. Pa(O(2)) at end-exercise was 46 +/- 3 and 245 +/- 10 mm Hg during RA and O(2), respectively. During O(2), T(lim) increased 4.7 +/- 1.4 min (p < 0.001); slopes of Borg, V E, V CO(2), and lactate over time fell (p < 0.05); slopes of Borg-V E, V E-V CO(2), V E-lactate were unchanged. At a standardized time near end-exercise, O(2) reduced dyspnea 2.0 +/- 0.5 Borg units, V CO(2) 0.06 +/- 0.03 L/min, V E 2.8 +/- 1.0 L/min, and breathing frequency 4.4 +/- 1.1 breaths/min (p < 0.05 each). IC(dyn) and inspiratory reserve volume (IRV) increased throughout exercise with O(2) (p < 0.05). Increased IC(dyn) was explained by the combination of increased resting IRV and decreased exercise breathing frequency (r(2) = 0.83, p < 0.0005). In conclusion, improved exercise endurance during hyperoxia was explained, in part, by a combination of reduced ventilatory demand, improved operational lung volumes, and dyspnea alleviation.
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PMID:Effects of hyperoxia on ventilatory limitation during exercise in advanced chronic obstructive pulmonary disease. 1128 62

Anecdotal observations suggest that hypoxia does not elicit dyspnea. An opposing view is that any stimulus to medullary respiratory centers generates dyspnea via "corollary discharge" to higher centers; absence of dyspnea during low inspired Po(2) may result from increased ventilation and hypocapnia. We hypothesized that, with fixed ventilation, hypoxia and hypercapnia generate equal dyspnea when matched by ventilatory drive. Steady-state levels of hypoxic normocapnia (end-tidal Po(2) = 60-40 Torr) and hypercapnic hyperoxia (end-tidal Pco(2) = 40-50 Torr) were induced in naive subjects when they were free breathing and during fixed mechanical ventilation. In a separate experiment, normocapnic hypoxia and normoxic hypercapnia, "matched" by ventilation in free-breathing trials, were presented to experienced subjects breathing with constrained rate and tidal volume. "Air hunger" was rated every 30 s on a visual analog scale. Air hunger-Pet(O(2)) curves rose sharply at Pet(O(2)) <50 Torr. Air hunger was not different between matched stimuli (P > 0.05). Hypercapnia had unpleasant nonrespiratory effects but was otherwise perceptually indistinguishable from hypoxia. We conclude that hypoxia and hypercapnia have equal potency for air hunger when matched by ventilatory drive. Air hunger may, therefore, arise via brain stem respiratory drive.
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PMID:Hypoxic and hypercapnic drives to breathe generate equivalent levels of air hunger in humans. 1239 Oct 41


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