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

We examined the hypothesis that collateral channels were identical within small airways and ducts, therefore both should respond similarly to chemical and mechanical stresses. A double lumen catheter was wedged into a segmental bronchus of the dog and humidified air or 10% CO2 in air (Vs) flowed at a segmental bronchial pressure (Pb) of 2 cm H2O. A small circular area about 1 cm diameter was peeled from the wedged segment and covered with a capsule glued to the surrounding pleura for measuring either a small airway flow (Vsaw) or capsule pressure (Pcap). Collateral resistance (Rcoll) and small airway resistance (Rsaw) were calculated as Rcoll = Pb/(Vs-Vsaw), Rsaw = (Pb-Pcap)/Vsaw, respectively. Hypocapnia (air) resulted in increases in Rcoll and Rsaw, while hypercapnia (10% CO2) generally had the opposite effect. Gcoll and Gsaw both increased linearly with lung volume (VL). The pattern of the responses of Rsaw closely paralleled those of Rcoll to local hypercapnia and hypocapnia, and to changing VL, implying that the major sites of resistance along collateral channels and along the airways are functionally and structurally similar.
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PMID:Dependence of collateral and small airway resistances of CO2 and volume in dog lobes. 748 Nov 14

Eight morbidly obese patients (body mass index [BMI] = 46) were studied during general anesthesia and controlled mechanical ventilation. To evaluate the effect of large tidal volume ventilation on oxygenation and ventilation, the baseline 13 mL/kg tidal volume (VT) (calculated by the ideal body weight) was increased in 3 mL/kg volume increments to 22 mL/kg, while ventilatory rate (RR) and inspiratory time (TI) were kept constant. Each volume increment was maintained for 15 min. Gas exchange was assessed by measuring the arterial blood oxygen tensions, and calculating the indices of alveolar-arterial oxygen tension difference [P(A-a)O2] and arterial/alveolar oxygen tension ratio (a/A). Peak inspiratory airway pressure (Ppeak), end-inspiratory airway pressure (Pplateau), and compliance of the respiratory system (CRS) were recorded using the Capnomac Ultima (Datex, Helsinki, Finland) on-line respiratory monitor. Increasing tidal volumes to 22 mL/kg increased the recorded Ppeak (26.3 +/- 4.1 vs 37.9 +/- 3.2 cm H2O, P < 0.008), Pplateau (21.5 +/- 3.6 vs 27.7 +/- 4.3 cm H2O, P < 0.01), and CRS (39.8 +/- 7.7 vs 48.5 +/- 8.3 mL/cm H2O) significantly without improving arterial oxygen tension and resulted in severe hypocapnia. Since changes in arterial oxygenation were small and not statistically significant, mechanical ventilation of morbidly obese patients with large VTS seems to offer no advantage to smaller (13 mL/kg ideal body weight) VTS.
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PMID:Large tidal volume ventilation does not improve oxygenation in morbidly obese patients during anesthesia. 761 32

Our goal was to investigate the extent to which thoracotomy for chronic vascular instrumentation alters peripheral airway tone and reactivity. Using the wedged bronchoscope technique to measure peripheral airway resistance (RP), pentobarbital-fentanyl anesthetized, ventilated dogs were studied before and (16 +/- 2 d) after a left thoracotomy for chronic implantation of instrumentation to measure the left pulmonary vascular pressure-flow relationship. A map of the airways was constructed as bronchoscopes were advanced and wedged in the middle lobes of both the left and right lung. This allowed us to measure RP in the same sublobar region of the left and right lung both pre- and postoperatively. At the time of postoperative experimentation, all dogs appeared fully recovered from the surgical procedure. Compared with preoperative values, baseline RP (cm H2O.ml-1.s-1) was selectively increased (p < 0.03) postoperatively in the left (0.41 +/- 0.07 versus 1.27 +/- 0.36) but not in the right (0.29 +/- 0.06 versus 0.35 +/- 0.07) lung. Peripheral airway responses to acetylcholine, histamine, hypocapnia, and dry air challenges were all increased (p < 0.05) in both magnitude and duration in the left but not the right lung postoperatively. Total lung volume (helium dilution technique) was decreased (p < 0.01) by 10 +/- 3% postoperatively. However, similar reductions in lung volume were observed in the left and right lung. These results indicate that left thoracotomy for chronic instrumentation selectively increases left lung peripheral airway tone and reactivity, but has no effect on the right lung.
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PMID:Thoracotomy increases peripheral airway tone and reactivity. 769 29

Rats were tested in the forced swim test in 35 or 20 cm of water or in an open field to evaluate the effects of different intensities of stress on blood gases, electrolytes, and metabolic indices, compared to nontested controls. Animals tested in the open field did not differ from controls on any measure. Immersion in deep water resulted in a greater mixed metabolic and respiratory acidemia (low pH, low bicarbonate, high pCO2), higher glucose and higher lactate levels than immersion in shallow water which in turn resulted in greater metabolic acidemia (low pH, low bicarbonate), and higher glucose and lactate levels than occurred in open field or control animals. In contrast to immersion in deep water, immersion in shallow water resulted in an initial hypocapnia followed by a hypercapnia. Immersion in deep water also resulted in higher potassium levels, lower bicarbonate and total carbon dioxide levels, and a higher anion gap than immersion in shallow water, testing in the open field, or in controls. In a second study, lactate infusion resulted in a metabolic alkalemia (increased pH and bicarbonate levels) and an increase in total carbon dioxide levels. These results indicate that test parameters from forced swim testing (e.g., water depth) can significantly affect the rat's physiological response to testing. The effects of forced swim testing are not simply due to general stress; and the physiological changes seen in conjunction with forced swim testing (e.g., acidemia) are not due to lactate alone.
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PMID:A further analysis of physiological changes in rats in the forced swim test. 780 Jul 51

To determine the effects of electrical hypoglossal nerve and submental stimulation on upper airway collapsibility, we examined the pressure-volume (P-V) relationships during bilateral supramaximal stimulation of the distal cut hypoglossal nerve ends over a range of frequencies from zero to 100 Hz in the sealed upper airway of 10 anesthetized supine dogs. Animals were artificially ventilated with 50% O2 and maintained under relative hyperoxia and hypocapnia during the study to eliminate the ventilatory drive output. Sealed upper airway pressures were obtained during random injections of different volumes of air from zero to 50 ml with and without hypoglossal nerve stimulation, and the upper airway P-V curves were obtained. The characteristics of the P-V curves were as follows: (1) the upper airway compliance defined as the slope of the regression of P-V curves fell from 4.07 +/- 0.33 ml/cm H2O without stimulation to 3.02 +/- 0.30 ml/cm H2O with stimulation at 50 Hz and plateaued at frequencies greater than 50 Hz, and (2) the volume at a given pressure during stimulation was larger than that without stimulation. The effects of submental stimulation on upper airway collapsibility were similar to those of hypoglossal nerve stimulation. These results suggest that the increase of upper airway muscle tone by hypoglossal nerve or submental stimulation stiffens the upper airway and that increases in muscle tone expand the upper airway.
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PMID:Hypoglossal nerve stimulation affects the pressure-volume behavior of the upper airway. 784 6

Effective gas exchange can be maintained in animals without the need for endotracheal intubation using external chest wall oscillation (ECWO). The clinical application of this technique has been limited by equipment which was either impractical or uncomfortable. We evaluated a prototype of a new oscillator in which an oscillatory profile of negative and positive pressure was imposed on a negative baseline pressure within a cuirass. In seven healthy subjects, we identified an oscillatory cuirass pressure that could effectively ventilate but would not result in severe hypocapnia over 5 min. We then measured the influence of changing the frequency of oscillation (fo) on PaCO2 and spontaneous ventilation. Lastly, we evaluated the capability of this prototype to achieve targeted changes in chamber pressure. Subjects were ventilated with an inspiratory chamber pressure of -20 +/- 4 cm H2O, an expiratory chamber pressure of 5 cm H2O and an inspiratory-expiratory ratio of 1:1 at 9 oscillatory frequencies (fo: 1 to 5 Hz at 0.5-Hz increments). Each subject was ventilated for 5 min with consecutive periods of ECWO being separated from each other by 10 min of unassisted breathing. Oscillatory tidal volume (Vo) was sampled and PaCO2 was determined from the expired carbon dioxide concentration (FECO2) measured at the mouth. The change in PaCO2 (delta PaCO2) was the difference in PaCO2 immediately before and after ECWO. We found that delta PaCO2 and Vo were inversely related to fo. At 1 Hz the delta PaCO2 was -13 +/- 1 mm Hg and Vo was 344 +/- 34 mL in the absence of spontaneous breathing (fb = 0). At 3 Hz and above, at the chamber pressures used, the delta PaCO2 was small (-1 to -2 mm Hg) and the Vo was less than the predicted dead space. Subjects breathed spontaneously but at a frequency below that of their resting fb. With this prototype, chamber pressure changes up to 30 cm H2O could be accurately achieved at 1, 2.5, and 4 Hz. In conclusion, ECWO can provide effective ventilation among healthy adults in the presence or absence of spontaneous breathing, and further studies are warranted to explore its effectiveness in a variety of clinical circumstances.
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PMID:Effect of external chest wall oscillation on gas exchange in healthy subjects. 784 74

The Gasthmatic System is a new method for monitoring transcutaneously pO2 and pCO2 changes prior to, during and after bronchial provocation. Unlike normals, asthmatic and atopic subjects reproduce the same gas patterns: immediate transient hypocapnia, during inhalation of ultrasonically nebulised distilled water (UNDW) (dead space effect) and delayed more persistent hypoxia, after end of UNDW exposure. This pattern is suggestive of an uneven distribution of the alveolar ventilation and ventilation/perfusion ratio and is noted both in asymptomatic asthmatics and in nonasthmatic atopic rhinitis subjects FEV1-non-responders to UNDW. This distributional pattern, therefore, appears to be able to screen very early stages of airway disease, when conventional parameters of lung volumes and mechanics fail to reveal any significant changes in hyper-reactive response. The Gasthmatic model is simple, painless, effortless, and allows transcutaneous measurements during all the phases of the hyperreactivity test, including the actual stimulation phases. It proves, therefore, to be particularly useful for children too young to cooperate with common lung function tests.
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PMID:[The use of the Gasthmatic System in studying bronchial hyperreactivity]. 788 59

Desflurane-induced increase of intracranial pressure (ICP) does not appear to be completely explained by desflurane-induced changes in cerebral blood flow, cerebrospinal fluid (CSF) formation and reabsorption, or brain tissue water content. The present study was designed to determine whether desflurane alters intracranial volume/pressure relationships sufficiently to account for desflurane-induced increase of ICP. In 24 dogs, infusions of mock CSF were used to determine the CSF pressure increase due to increase of CSF volume, and the capacity of CSF pressure to return to baseline after a CSF pressure increase (CSF pressure normalization). CSF pressure increase was assessed by determining (a) CSF pressure prior to volume infusion (P(o)), (b) peak CSF pressure (Pp) caused by volume injection, (c) intracranial compliance (C, calculated as the ratio of change of intracranial volume [delta V] to change of CSF pressure [delta P]), (d) the volume pressure response (VPR, a measure of elastance, calculated as the ratio of delta P to delta V, (e) the pressure/volume index (PVI, calculated as the ratio of delta V to log Pp/P(o)), and (f) estimated intracranial compliance (C(e), calculated from PVI as 0.4343PVI/P(o)). CSF pressure normalization was assessed by determining the first (S1) and second (S2) phase slopes of decrease of CSF pressure from Pp, the duration of S1 (DS1), and the intersection of extrapolated S2 with the P(o) to Pp slope (delta Ps). During normocapnia (Group 1, n = 6) and hypocapnia (Group 2, n = 6), two infusions were made at each of four experimental conditions: 0.5 minimum alveolar anesthetic concentration (MAC) desflurane and normal or increased CSF pressure, and 1.0 MAC desflurane and normal or increased CSF pressure. For comparison to these two desflurane-anesthetized groups, intracranial volume/pressure values were determined at the same experimental conditions during 0.5 MAC isoflurane (Group 3, n = 6) and in controls (Group 4, n = 6) anesthetized with thiopental 12 mg/kg then 12 mg.kg-1.h-1 intravenously combined with halothane 0.5% inspired. In comparison to controls, both desflurane and isoflurane decreased Ce at normal CSF pressure but not at increased CSF pressure. However, desflurane and isoflurane had no consistent effect on the other measures of CSF pressure increase caused by increase of CSF volume. Isoflurane also decreased the capacity for CSF pressure normalization at normal CSF pressure as indicated by decreased S1 and increased delta Ps. It is concluded that, under conditions of normal ICP, desflurane may decrease Ce, favoring an increase of ICP.
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PMID:Intracranial volume/pressure relationship during desflurane anesthesia in dogs: comparison with isoflurane and thiopental/halothane. 794 87

We have previously shown that hypocapnia triggers Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in patients with congestive heart failure (CHF). Nasal continuous positive airway pressure (NCPAP) may attenuate CSR-CSA in patients with CHF and CSR-CSA. Accordingly, we hypothesized that attenuation of CSR-CSA by NCPAP would be related to an increase in PCO2. Therefore, we examined the effect of NCPAP on the frequency of apneas and hypopneas, transcutaneous PCO2 (PtcCO2), and minute volume of ventilation (VI) in 12 consecutive patients with CHF and CSR-CSA during stage 2 sleep. A control group of six patients, who did not receive NCPAP, was also studied. In the control group, there were no changes from baseline to 1 mo in the frequency of central apneas and hypopneas, mean PtcCO2, mean VI, or mean SaO2 during stage 2 sleep. In contrast, from baseline to 1 mo the NCPAP group experienced a decrease in the frequency of apneas and hypopneas (58.7 +/- 5.2 to 23.2 +/- 6.0/h of sleep, p < 0.001), an increase in mean PtcCO2 (34.6 +/- 1.4 to 40.8 +/- 1.1 mm Hg, p < 0.001), a reduction in mean VI (8.1 +/- 1.0 to 5.2 +/- 0.5 L/min, p < 0.01) and an increase in mean SaO2 (91.6 +/- 1.1 to 95.0 +/- 0.5%, p < 0.025) during stage 2 sleep while on 10.2 +/- 0.5 cm H2O nasal CPAP. We conclude that likely mechanisms through which NCPAP reduces CSR-CSA are by increasing SaO2 and raising PaCO2 during sleep toward or above the apneic threshold.
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PMID:Effect of continuous positive airway pressure on central sleep apnea and nocturnal PCO2 in heart failure. 795 21

Previous studies to determine whether desflurane increases cerebrospinal fluid (CSF) pressure are inconclusive because none have included all of the following: multiple doses of desflurane, administration for at least several hours, examination at normo- and hypocapnia, a concurrent comparison group, direct measurement of both intra- and extracranial CSF pressures, and measurement of venous pressures that influence CSF pressure. The present study was designed to determine whether CSF pressure increases during 4.0 h desflurane anesthesia using a study design that included the above elements. Catheters were placed in the lateral cerebral ventricle, cisterna magna, sagittal sinus, and jugular vein of 12 dogs anesthetized with thiopental 12 mg.kg-1.h-1 and halothane 0.5 to 0.8%. Catheter pressures were measured, and the CSF-sagittal sinus pressure gradient and slope of the gradient to CSF pressure relationship were determined during control conditions. Then, 6 dogs were anesthetized with desflurane and 6 dogs were anesthetized with isoflurane, and the same values were determined for 1.0 h at each of four experimental conditions: 0.5 and 1.0 minimum alveolar concentration (MAC) during normocapnia (PaCO2 35-39 mm Hg) and 0.5 and 1.0 MAC during hypocapnia (PaCO2 20-24 mm Hg). CSF and sagittal sinus pressures, but not jugular venous pressure, increased with both desflurane and isoflurane. The greater increase of CSF pressure with 4.0 h desflurane (to 40.2 +/- 12.7 cm H2O) than with 4.0 h isoflurane (to 26.2 +/- 11.5 cm H2O) was attributable to an increase of CSF pressure that was greater during 2.0 h desflurane and normocapnia than during 2.0 h isoflurane and normocapnia, and to an increase of CSF pressure during 2.0 h desflurane and hypocapnia that was similar to that during 2.0 h isoflurane and hypocapnia. The greater increase of CSF pressure during desflurane may have resulted, in part, from increased CSF volume as indicated by a positive CSF-sagittal sinus pressure gradient (in contrast, there was little or no CSF-sagittal sinus pressure gradient during isoflurane) and a steeper slope of the gradient to CSF pressure relationship.
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PMID:CSF, sagittal sinus, and jugular venous pressures during desflurane or isoflurane anesthesia in dogs. 800 Jan 96


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