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

In this study cerebral oxygenation was measured using the NIRO 300 and the INVOS 5100 spectrophotometers in 10 healthy adult volunteers, exposed to varying degrees of hyperoxia and hypoxia. The results showed similar baseline values for tissue oxygenation index and regional cerebral oxygen saturation with mean (SD) values being 64.9% (5.1) and 62.3% (6.0), respectively. The overall bias was -2.1%, with the INVOS 5100 under-reading cerebral oxygenation compared to the NIRO 300, with limits of agreement of +/-14.7%. Both monitors demonstrated similar changes in response to hyperoxia and hypocapnia (coefficient of variance for FIo2 0.45 = 10.0%, FIo2 1.0 = 10.1%, hypocapnia = 14.5%). The reasons for the bias and variability may relate to differences in the methodological approaches of the two monitors. The correlation between the monitors in response to changes in cerebral oxygenation implies that they may be useful as trend monitors in clinical practice.
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PMID:A comparison of cerebral oxygenation as measured by the NIRO 300 and the INVOS 5100 Near-Infrared Spectrophotometers. 1235 58

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

We determined the effects on breathing of transient ventilatory overshoots and concomitant hypocapnia, as produced by pressure support mechanical ventilation (PSV), in intact and carotid body chemoreceptor denervated (CBX) sleeping dogs. In the intact dog, PSV-induced transient increases in tidal volume and hypocapnia caused apnea within 10-11 s, followed by repetitive two-breath clusters separated by apneas, i.e., periodic breathing (PB). After CBX, significant expiratory time prolongation did not occur until after 30 s of PSV-induced hypocapnia, and PB never occurred. Average apneas of 8.4 +/- 1-s duration after a ventilatory overshoot required a decrease below eupnea of end-tidal Pco(2) 5.1 +/- 0.4 Torr below eupnea in the intact animal and 10.1 +/- 2 Torr in the CBX dog, where the former reflected peripheral and the latter central dynamic CO(2) chemoresponsiveness, as tested in the absence of peripheral chemoreceptor input. Hyperoxia when the dogs were intact shortened PSV-induced apneas and reduced PB but did not mimic the effects of CBX. We conclude that, during non-rapid eye movement sleep, carotid chemoreceptors are required to produce apneas that normally occur after a transient ventilatory overshoot and for PB.
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PMID:Carotid body denervation eliminates apnea in response to transient hypocapnia. 1239 Oct 82

We measured ventilation, arterial O2 saturation, end-tidal CO2 (PET,CO2), blood pressure (intra-arterial catheter or photoelectric plethysmograph), and flow velocity in the middle cerebral artery (CFV) (pulsed Doppler ultrasound) in 17 healthy awake subjects while they performed 20 s breath holds under control conditions and during ganglionic blockade (intravenous trimethaphan, 4.4 +/- 1.1 mg min-1 (mean +/- S.D.)). Under control conditions, breath holding caused increases in PET,CO2 (7 +/- 1 mmHg) and in mean arterial pressure (MAP) (15 +/- 2 mmHg). A transient hyperventilation (PET,CO2 -7 +/- 1 mmHg vs. baseline) occurred post-apnoea. CFV increased during apnoeas (by 42 +/- 3 %) and decreased below baseline (by 20 +/- 2 %) during post-apnoea hyperventilation. In the post-apnoea recovery period, CFV returned to baseline in 45 +/- 4 s. The post-apnoea decrease in CFV did not occur when hyperventilation was prevented. During ganglionic blockade, which abolished the increase in MAP, apnoea-induced increases in CFV were partially attenuated (by 26 +/- 2 %). Increases in PET,CO2 and decreases in oxyhaemoglobin saturation (Sa,O2) (by 2 +/- 1 %) during breath holds were identical in the intact and blocked conditions. Ganglionic blockade had no effect on the slope of the CFV response to hypocapnia but it reduced the CFV response to hypercapnia (by 17 +/- 5 %). We attribute this effect to abolition of the hypercapnia-induced increase in MAP. Peak increases in CFV during 20 s Mueller manoeuvres (40 +/- 3 %) were the same as control breath holds, despite a 15 mmHg initial, transient decrease in MAP. Hyperoxia also had no effect on the apnoea-induced increase in CFV (40 +/- 4 %). We conclude that apnoea-induced fluctuations in CFV were caused primarily by increases and decreases in arterial partial pressure of CO2 (Pa,CO2) and that sympathetic nervous system activity was not required for either the initiation or the maintenance of the cerebrovascular response to hyper- and hypocapnia. Increased MAP or other unknown influences of autonomic activation on the cerebral circulation played a smaller but significant role in the apnoea-induced increase in CFV; however, negative intrathoracic pressure and the small amount of oxyhaemoglobin desaturation caused by 20 s apnoea did not affect CFV.
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PMID:Mechanisms of the cerebrovascular response to apnoea in humans. 1258 94

Mechanical ventilation causing hypocapnia or hyperoxia carries a risk for the pre-term infant. The aim was to improve blood gas control in our unit. A guideline was written, and all personnel were motivated concerning blood gas control. Case records of all mechanically ventilated premature infants were examined during two 3-month periods, before and after intervention. The hours spent with hypocapnia (pCO2 < 4 kPa) or hyperoxia (PO2 > 12 kPa) were recorded. Case records of 31 infants were examined for a total of 1358 h of mechanical ventilation, 641 h before and 717 h after the intervention. The percentage time of hypocapnia before intervention (7.0%) was reduced significantly (P = 0.044) to less than half (2.9%) after intervention. Hyperoxia was reduced from 14.5% to 8.7% (P = 0.072). Blood gas control of mechanically ventilated premature infants could be improved with little effort, but hyperoxia is too frequent.
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PMID:Improving blood gas control in mechanically ventilated, premature infants through monitoring and evaluation of clinical practice. 1475 66

The blood oxygenation level-dependent (BOLD) responses to visual stimuli, using both a 1-s long single trial stimulus and a 20-s long block stimulus, were measured in a 4-T magnetic field both before and immediately after a 200-mg caffeine dose. In addition, resting levels of cerebral blood flow (CBF) were measured using arterial spin labeling. For the single trial stimulus, the caffeine dose significantly (p<0.05) reduced the time to peak (TTP), the time after the peak at which the response returned to 50% of the peak amplitude (TA50), and the amplitude of the poststimulus undershoot in all subjects (N=5). Other parameters, such as the full-width half-maximum (FWHM) and the peak amplitude, also showed significant changes in the majority of subjects. For the block stimulus, the TTP, TA50, and the time for the response to reach 50% of the peak amplitude (T50) were significantly reduced. In some subjects, oscillations were observed in the poststimulus portion of the response with median peak periods of 9.1 and 9.5 s for the single trial and block responses, respectively. Resting CBF was reduced by an average of 24%. The reproducibility of the results was verified in one subject who was scanned on 3 different days. The dynamic changes are similar to those previously reported for baseline CBF reductions induced by hypocapnia and hyperoxia.
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PMID:Caffeine alters the temporal dynamics of the visual BOLD response. 1558 4

To investigate the contribution of the peripheral chemoreceptors to the susceptibility to posthyperventilation apnea, we evaluated the time course and magnitude of hypocapnia required to produce apnea at different levels of peripheral chemoreceptor activation produced by exposure to three levels of inspired P(O2). We measured the apneic threshold and the apnea latency in nine normal sleeping subjects in response to augmented breaths during normoxia (room air), hypoxia (arterial O2 saturation = 78-80%), and hyperoxia (inspired O2 fraction = 50-52%). Pressure support mechanical ventilation in the assist mode was employed to introduce a single or multiple numbers of consecutive, sigh-like breaths to cause apnea. The apnea latency was measured from the end inspiration of the first augmented breath to the onset of apnea. It was 12.2 +/- 1.1 s during normoxia, which was similar to the lung-to-ear circulation delay of 11.7 s in these subjects. Hypoxia shortened the apnea latency (6.3 +/- 0.8 s; P < 0.05), whereas hyperoxia prolonged it (71.5 +/- 13.8 s; P < 0.01). The apneic threshold end-tidal P(CO2) (Pet(CO2)) was defined as the Pet(CO2)) at the onset of apnea. During hypoxia, the apneic threshold Pet(CO2) was higher (38.9 +/- 1.7 Torr; P < 0.01) compared with normoxia (35.8 +/- 1.1; Torr); during hyperoxia, it was lower (33.0 +/- 0.8 Torr; P < 0.05). Furthermore, the difference between the eupneic Pet(CO2) and apneic threshold Pet(CO2) was smaller during hypoxia (3.0 +/- 1.0 Torr P < 001) and greater during hyperoxia (10.6 +/- 0.8 Torr; P < 0.05) compared with normoxia (8.0 +/- 0.6 Torr). Correspondingly, the hypocapnic ventilatory response to CO2 below the eupneic Pet(CO2) was increased by hypoxia (3.44 +/- 0.63 l.min(-1).Torr(-1); P < 0.05) and decreased by hyperoxia (0.63 +/- 0.04 l.min(-1).Torr(-1); P < 0.05) compared with normoxia (0.79 +/- 0.05 l.min(-1).Torr(-1)). These findings indicate that posthyperventilation apnea is initiated by the peripheral chemoreceptors and that the varying susceptibility to apnea during hypoxia vs. hyperoxia is influenced by the relative activity of these receptors.
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PMID:Influence of arterial O2 on the susceptibility to posthyperventilation apnea during sleep. 1617

This article reviews the basic properties of breath-holding in humans and the possible causes of the breath at breakpoint. The simplest objective measure of breath-holding is its duration, but even this is highly variable. Breath-holding is a voluntary act, but normal subjects appear unable to breath-hold to unconsciousness. A powerful involuntary mechanism normally overrides voluntary breath-holding and causes the breath that defines the breakpoint. The occurrence of the breakpoint breath does not appear to be caused solely by a mechanism involving lung or chest shrinkage, partial pressures of blood gases or the carotid arterial chemoreceptors. This is despite the well-known properties of breath-hold duration being prolonged by large lung inflations, hyperoxia and hypocapnia and being shortened by the converse manoeuvres and by increased metabolic rate. Breath-holding has, however, two much less well-known but important properties. First, the central respiratory rhythm appears to continue throughout breath-holding. Humans cannot therefore stop their central respiratory rhythm voluntarily. Instead, they merely suppress expression of their central respiratory rhythm and voluntarily 'hold' the chest at a chosen volume, possibly assisted by some tonic diaphragm activity. Second, breath-hold duration is prolonged by bilateral paralysis of the phrenic or vagus nerves. Possibly the contribution to the breakpoint from stimulation of diaphragm muscle chemoreceptors is greater than has previously been considered. At present there is no simple explanation for the breakpoint that encompasses all these properties.
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PMID:Breath-holding and its breakpoint. 1627 64

This study examined the time course of early scotopic threshold sensitivity during dark adaptation under mild to moderate hypoxia, moderate hypocapnia and hyperoxia, measuring detection time displacement relative to normoxia. Cone rod inflection and early rod adaptation were highlighted using progressively dimmer green flash stimuli. Early scotopic sensitivity was significantly delayed by hypoxia and hastened by hypocapnia and hyperoxia. Effects of respiratory disturbance on dark adaptation include temporal shifts of early scotopic sensitivity while human rod photoreceptors appear functionally hypoxic when breathing air at one atmosphere. At night, supplementary oxygen may benefit aircrew visual sensitivity, even at ground level.
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PMID:Aviation-related respiratory gas disturbances affect dark adaptation: a reappraisal. 1637 44

To test our hypothesis that resuscitation with 21% and 40% oxygen (O2) would shorten time to onset of respiratory activity when compared with resuscitation with 100% O2, diaphragmatic electromyogram (EMG) electrodes were inserted in Sprague-Dawley rat pups, age 8-10 d before intubation and mechanical ventilation with 5% O2 to induce cessation of respiratory activity. Each animal was then resuscitated with 100% and 21% O2 (n = 10) or 100% and 40% O2 (n = 11) for 30 s before the ventilator was disconnected. Recovery of diaphragm activity was compared between resuscitation groups. Blood gas status and heart rate data were characterized in additional rat pups. Time to first respiratory effort was 36 +/- 21 s (mean +/- SD) for room air resuscitation and 72 +/- 22 s for 100% O2, (p = 0.002). In contrast, there was no difference in time to onset of diaphragm activity when resuscitation with 40% O2 was compared with 100% O2: 84 +/- 27 s versus 76 +/- 23 s, respectively (p > 0.05). Resuscitation with 100% and 40% O2 both resulted in hyperoxia and hypocapnia when compared with room air, without effect on heart rate. Our findings indicate that even modest hyperoxic resuscitation will result in a delayed onset of respiration compared with normoxic gas, via a mechanism that may involve both hyperoxemic and hypocapnic inhibition of chemoreceptors.
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PMID:Effect of supplemental oxygen on reinitiation of breathing after neonatal resuscitation in rat pups. 1742 59


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