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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Positive pressure ventilation, using high inspiratory pressures, often causes lung damage. When associated with hypocapnia, it can produce severe focal alveolar alkalosis and can cause damage in areas of low blood flow. A vein-to-vein extracorporeal membrane oxygenator (ECMO) system was used to control blood gases independently of mechanical ventilation in 12 healthy newborn lambs. After connection to the ECMO system, ventilation was started with a peak inspiratory pressure of 35 cm H2O and a positive end-expiratory pressure of 5 cm H2O; the ventilator rate was 40/min with I:E = 1.5 and FiO2 = 1.0. In 6 of the 12 lambs sweep gases through the silicone membrane were regulated to assure arterial normocapnia. The other 6 were ventilated with the same settings and perfused with the same pump flow, but PaCO2 was allowed to fall to hypocapnic levels. The lambs were ventilated for 4 h. Average pH and PaCO2 were 7.62 +/- 0.14 and 2.11 +/- 0.54 kPa, respectively, in the hypocapnic group and 7.39 +/- 0.11 and 4.79 +/- 0.51 kPa in the normocapnic group. After sacrificing the lambs, the lungs were inspected macroscopically and microscopically by computer-assisted morphometry to assess atelectasis and lung edema. Macroscopically there were no hemorrhages, barotrauma or widespread atelectasis of the lungs in either group. The thickness of interlobular lung septa in the right upper lobe was 32.5 +/- 18.0 microns for the hypocapnic group and 29.7 +/- 12.5 microns for the normocapnic group. The parenchymal-alveolar area ratio in the right upper lobe was 28.4 +/- 5.04 and 24.6 +/- 3.75% in the hypocapnic and normocapnic groups, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of hypocapnia and mechanical pulmonary stress on lung tissue in newborn lambs. 826 May 61

In 5 mechanically ventilated patients with severe neurological injury (SNI), we measured the respiratory system's flow resistance (Rrs) over a range of inspiratory flows between 0.2 to 2 L/s, at inflation volumes (delta V) ranging from 0.1 to 1 L. Under baseline ventilatory conditions (V = 1 L/s; delta V = 0.95 L), we also partitioned Rrs into airway resistance (Raw) and the additional resistance offered by the tissues of the lung and chest wall (delta Rrs). At all inflation volumes, Rrs decreased hyperbolically with increasing flow but was higher than in normal anesthetized paralyzed subjects (N). At V of 1 L/s and delta V of 0.5 L, Rrs was significantly greater in SNI than in N (7.7 +/- 1.5 v 4.2 +/- 0.5 cm H2O/L/s; P < .01). This discrepancy was due to higher Raw in SNI. Indeed, at V of 1 L/s, Raw (mean +/- SEM) was significantly higher in SNI than in N (4.0 +/- 0.9 v 2.4 +/- 0.2 cm H2O/L/s; P < .001), whereas delta Rrs did not differ significantly. The increased Raw in SNI was due to the fact that these patients were therapeutically hyperventilated (PaCO2 = 30.4 +/- 4.2 mm Hg) and as a result their airways were bronchoconstricted. We conclude that in the intensive care unit setting, hyperventilated patients with severe neurological injury can not be considered to be adequate controls in terms of Rrs and Raw, because hypocapnia induces an increase of Raw and consequently also in Rrs (= Raw+delta Rrs).
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PMID:Flow resistance in mechanically ventilated patients with severe neurological injury. 827 57

Intracranial pressure (ICP) has been shown to increase dramatically during desflurane anesthesia, possibly as a result in part of an increase in the rate of cerebrospinal fluid (CSF) formation (Vf) or a decrease in the rate of CSF reabsorption. To examine this phenomenon, I designed a study to measure Vf, resistance to reabsorption of CSF (Ra), brain tissue water content, and the electroencephalographic activity (EEG) during desflurane anesthesia in dogs. Vf and Ra were determined using ventriculocisternal perfusion of mock CSF labeled with blue dextran. EEG activity was determined using aperiodic analysis. At the end of the study, brain tissue water contents of gray and white matter were determined by dry/wet weight ratios. Eighteen dogs were allocated into three groups. Group 1 (n = 6) was examined at five experimental conditions during normocapnia; group 2 (n = 6) was examined at five experimental conditions during hypocapnia. The experimental conditions for groups 1 and 2 were (a) baseline (halothane 0.5-1.0% inspired plus thiopental 12 mg.kg-1 i.v. given over 15 min followed by i.v. infusion at 12 mg.kg-1 x h-1), (b) 0.5 MAC (3.5 +/- 0.1% expired) and (c) 1.0 MAC (7.0 +/- 0.1% expired) desflurane at normal CSF pressure, and (d) and (e) 0.5 and 1.0 MAC desflurane at increased CSF pressure (> 30 cm H2O). Group 3 (n = 6), the control group, was examined over the same time period as groups 1 and 2. In the control group, desflurane was not administered; instead, the baseline condition (i.e., halothane plus thiopental) was maintained throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rate of cerebrospinal fluid formation, resistance to reabsorption of cerebrospinal fluid, brain tissue water content, and electroencephalogram during desflurane anesthesia in dogs. 840 Jul 57

Changes in body fluid homeostasis during acute hypoxaemia suggest a crucial role of renal function in acclimatization processes. Hypoxaemia stimulates sympathetic nervous activity, and also the cardiovascular system is affected with increases in heart rate and cardiac output. In most subjects, a hypoxic ventilatory response produces hypocapnia and respiratory alkalosis. Acute hypoxaemia depresses aldosterone secretion secondary to a direct effect on adrenal cells. Also plasma renin is decreased in resting hypoxaemic conditions, but the mechanism remains unknown. These hormonal changes may have the advantage of opposing excessive sodium and water retention, which characterizes acute mountain sickness. Short-term isocapnic or hypocapnic hypoxaemia in spontaneously breathing humans causes moderate if any increases in renal blood flow and only minor changes in GFR. In contrast, renal blood flow and GFR decreases during hypercapnic hypoxaemia. Renal clearance studies in humans after 24-48 hours in altitude hypoxia (4,350 m) demonstrate that glomerular and tubular function is only slightly changed in spite of marked depression of the renin-aldosterone system and increased plasma levels of norepinephrine. However, renal vascular tone may increase most probably secondary to the increased adrenosympathetic activity. In the first hours, acute hypoxaemia may induce an increased excretion of sodium and water. Previous studies suggest that the natriuretic response is caused by decreased reabsorption of sodium and bicarbonate in the proximal tubules secondary to the associated hyperventilation and hypocapnia. After 6 hours, sodium and water excretion is normalized or even depressed, dependent on the severity of acute mountain sickness. In view of the prompt increase in sodium and water excretion found during short-term hypoxaemia, the absence of such a response to more prolonged hypoxaemia suggests an adaptive time-dependent course of renal functional changes in hypoxaemia. Taken together, previous studies suggest that effects of acute hypoxaemia on renal haemodynamics are minor compared with effects on cerebral and coronary circulation. This might be the result of an appropriate resetting of autoregulatory mechanisms that would maintain the role of the kidney as a major sense organ to hypoxaemia and, subsequently, as a mediator of plasma volume regulation and erythropoietin synthesis.
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PMID:Effect of hypoxaemia on water and sodium homeostatic hormones and renal function. 859 71

Hypoxia lowers the basic thermoregulatory responses of animals and humans. In cold-exposed animals, hypoxia increases core temperature (Tco) cooling rate and suppresses shivering thermogenesis. In humans, the experimental effects of hypoxia on thermoregulation are equivocal. Also, the effect of hypoxia has not been separated from that of hypocapnia consequent to hypoxic hyperventilation. To determine the isolated effects of hypoxia on warm and cold thermoregulatory responses and core cooling during mild cold stress, we examined the Tco thresholds for sweating, vasoconstriction, and shivering as well as the core cooling rates of eight subjects immersed in 28 degrees C water under eucapnic conditions. On 2 separate days, subjects exercised on an underwater cycle ergometer to elevate Tco above the sweating threshold. They then rested and cooled until they shivered vigorously. Subjects inspired humidified room air during the control trial. For the eucapnic hypoxia trial, they inspired 12% O2-balance N2 with CO2 added to maintain eucapnia. Eucapnic hypoxia lowered the Tco thresholds for vasoconstriction and shivering by 0.14 and 0.19 degrees C, respectively, and increased core cooling rate by 33% (1.83 vs. 1.38 degrees C/h). These results demonstrate that eucapnic hypoxia enhances the core cooling rate in humans during mild cold stress. This may be attributed in part to a delay in the onset of vasoconstriction and shivering as well as increased respiratory heat loss during hypoxic hyperventilation.
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PMID:Eucapnic hypoxia lowers human cold thermoregulatory response thresholds and accelerates core cooling. 892 79

Previous studies suggest that desflurane may increase cerebrospinal fluid (CSF) formation rate (Vf) and volume, particularly during conditions of hypocapnia combined with elevated CSF pressure. The present study was designed to determine whether treatments routinely used in patients during anesthesia for neurological surgery would decrease Vf during desflurane anesthesia in rabbits. Three groups of six rabbits each were examined at four experimental conditions. Condition 1 was the combination of isoflurane, normocapnia, and normal CSF pressure (baseline, all groups). Condition 2 was the combination of isoflurane (group 1) or desflurane (groups 2 and 3), hypocapnia, and elevated CSF pressure (27 and 33 cm H2O). Conditions 3 and 4 were the same as condition 2 with the addition of furosemide, dexamethasone, mannitol, or fentanyl in groups 2 and 3. Vf, resistance to reabsorption of CSF (Ra), and systemic values were determined at each experimental condition, and brain water content was determined at the end of the study. Mean baseline Vf was 9.8 +/- 2.6 microliters.min-1. During the combination of desflurane, hypocapnia, and elevated CSF pressure, furosemide decreased Vf to 3.2 +/- 1.7 microliters.min-1, mannitol increased plasma osmolality and decreased plasma sodium concentration, and fentanyl decreased heart rate and increased plasma potassium concentration. Values for Ra and brain water content did not differ between groups. Of the four treatments examined, only furosemide decreased Vf during the combination of desflurane, hypocapnia, and elevated CSF pressure.
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PMID:Furosemide decreases cerebrospinal fluid formation during desflurane anesthesia in rabbits. 910 Jan 89

This study was carried out on seven chloralose-anesthetized sheep and was designed to investigate the role of muscular afferent fiber stimulation on the duration of reflex apnea triggered by laryngeal stimulation (LS). In six animals, injection of distilled water onto the laryngeal mucosa provoked a 15.7 +/- 1.0 s (mean +/- SE) apnea associated with a rise in systemic blood pressure (+7 +/- 0.8 Torr). Electrically induced contractions (EIC) of the hindlimb muscles doubled the metabolic rate and ventilation and reduced the duration of the apnea produced by LS to 7.4 +/- 1.0 s (P < 0.01). Apnea duration was still reduced during the first minute after the cessation of EIC (7.2 +/- 1.1 s, P < 0.01) but returned to control after a 5-min recovery period (16.7 +/- 1.6 s). The apnea triggered by LS was also reduced during EIC when the venous return was impeded by occluding the inferior vena cava (5.2 +/- 1.1 s, P < 0.01), despite a profound hypocapnia (20.7 +/- 0.3 Torr). The duration of apnea was not significantly affected (14.2 +/- 1.4 s) by breathing a 6% CO2-14% O2 in N2 gas mixture that roughly mimicked the alveolar gas composition when the apnea turned off. These results suggest that chemical drive has a negligible role in the fast reinitiation of breathing after LS during muscular stimulation. Stimulation of muscle afferent fibers does, however, appear to be a potent source of ventilatory reflexes capable of counteracting the inhibition of breathing resulting from laryngeal stimulation. Conversely, it is postulated that any reduction in somatic afferent traffic during this type of reflex apnea, including that resulting from the LS-induced systemic vasoconstriction, may delay the termination of apnea.
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PMID:Laryngeal reflex apnea is blunted during and after hindlimb muscle contraction in sheep. 912 82

The purpose of the present study was to investigate the effect of exercise induced hyperventilation and hypocapnia on airway resistance (Raw), and to try to answer the question whether a reduction of Raw is a mechanism contributing to the increase of endurance time associated with a reduction of exercise induced hyperventilation as for example has been observed after respiratory training. Eight healthy volunteers of both sexes participated in the study. Cycling endurance tests (CET) at 223 (SD 47) W, i.e. at 74 (SD 5)% of the subject's peak exercise intensity, breathing endurance tests and body plethysmograph measurements of pre- and postexercise Raw were carried out before and after a 4-week period of respiratory training. In one of the two CET before the respiratory training CO2 was added to the inspired air to keep its end-tidal concentration at 5.4% to avoid hyperventilatory hypocapnia (CO2-test); the other test was the control. The pre-exercise values of specific expiratory Raw were 8.1 (SD 2.8), 6.8 (SD 2.6) and 8.0 (SD 2.1) cm H2O.s and the postexercise values were 8.5 (SD 2.6), 7.4 (SD 1.9) and 8.0 (SD 2.7) cm H2O.s for control CET, CO2-CET and CET after respiratory training, respectively, all differences between these tests being nonsignificant. The respiratory training significantly increased the respiratory endurance time during breathing of 70% of maximal voluntary ventilation from 5.8 (SD 2.9) min to 26.7 (SD 12.5) min. Mean values of the cycling endurance time (tcend) were 22.7 (SD 6.5) min in the control, 19.4 (SD 5.4) min in the CO2-test and 18.4 (SD 6.0) min after respiratory training. Mean values of ventilation (VE) during the last 3 min of CET were 123 (SD 35.8) l.min-1 in the control, 133.5 (SD 35.1) l.min-1 in the CO2-test and 130.9 (SD 29.1) l.min-1 after respiratory training. In fact, six subjects ventilated more and cycled for a shorter time, whereas two subjects ventilated less and cycled for a longer time after the respiratory training than in the control CET. In general, the subjects cycled longer the lower the VE, if all three CET are compared. It is concluded that Raw measured immediately after exercise is independent of exercise-induced hyperventilation and hypocapnia and is probably not involved in limiting tcend, and that tcend at a given exercise intensity is shorter when VE is higher, no matter whether the higher VE occurs before or after respiratory training or after CO2 inhalation.
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PMID:Effect of exercise-induced hyperventilation on airway resistance and cycling endurance. 913 61

The respiratory response to CO2 during pressure-support ventilation (PSV) was studied in 16 conscious normal humans. The subjects breathed through a mouthpiece connected to a ventilator in PSV mode, with pressure set to the highest comfortable level for each subject (10.1 +/- 0.6 cm H2O, mean +/- SE). Compared with breathing spontaneously through the ventilator (CPAP mode with zero positive end-expiratory pressure), with PSV, tidal volume (VT) increased significantly (1.16 +/- 0.1 versus 0.85 +/- 0.04 L), whereas breathing frequency (f) remained stable (16.0 +/- 0.9 versus 15.6 +/- 1.1 breaths/min). As a result, the subjects hyperventilated, decreasing significantly end-tidal PCO2 (PETCO2, 23.5 +/- 1.2 versus 35.5 +/- 1.1 mm Hg). Fraction of inspired CO2 (FICO2) was then increased in steps, and changes in respiratory motor output were quantitated from changes in f, VT, ventilation (VI), peak inspiratory flow (Vpeak), and muscle pressure (Pmus). Pmus was calculated by the equation of motion, based on respiratory system mechanics, which were measured previously by airway occlusion at end-inspiration, VT, VI, and Pmus increased significantly with increasing PETCO2, and the response was detectable even below eupneic levels; f remained relatively stable over a wide range of PETCO2 (23 to 45 mm Hg) and increase significantly only when PETCO2 approached 50 mm Hg. These results indicate that in conscious normal humans during PSV, CO2 responsiveness extends well into hypocapnia and is expressed principally as an increase in intensity of respiratory motor output with little change in respiratory rate.
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PMID:Respiratory response to CO2 during pressure-support ventilation in conscious normal humans. 923 Jul 39

We have shown that tracheal and tongue displacement represent two basic mechanisms by which upper airway collapsibility can be altered. In this study, we investigated whether hypercapnia, which activates upper airway muscles, alters upper airway collapsibility by a mechanism similar to tracheal or tongue displacement. To answer this question, we utilized a feline isolated upper airway preparation in which maximal inspiratory airflow (Vimax), the pharyngeal critical pressure (Pcrit) and the nasal resistance (Rn) upstream to the flow-limiting site (FLS) were measured. In protocol #1, upper airway airflow dynamics were studied at two levels of trachea displacement under either hypo- or hypercapnic conditions. We found that the increase in Vimax with 1 cm of caudal tracheal displacement was attenuated by hypercapnia (44 +/- 12 ml/s versus 81 +/- 7 ml/s during hypocapnia, p = 0.048), as was the decrease in Pcrit (-2.4 +/- 1.1 cm H2O versus -5.2 +/- 1.1 cm H2O, p = 0.001). In protocol #2, we investigated the effect of transecting the cervical strap muscles and hypoglossal nerves on airflow dynamics during hypercapnia. Vimax, Pcrit, and Rn did not change after transecting either the strap muscles or the hypoglossal nerves. We conclude that the primary mechanism for changes in Pcrit during hypercapnia is similar to trachea displacement and is mediated by muscles other than the straps or tongue.
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PMID:Neuromuscular activity and upper airway collapsibility. Mechanisms of action in the decerebrate cat. 927 33


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