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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of nebulisers was assessed in four hospitals. Nebulisers were checked in use and medical and nursing staff were interviewed. All but one nebuliser was driven by 100% oxygen and only 3 of 111 interviewees preferred air for patients with hypercapnia. In 5 of 44 nebulisers in use, water was used as the dilutant. The calculated times for complete nebulisation of the solutions ranged from 3.5 to 117 min. The results of this survey illustrate a need for better education concerning the use of nebulisers in hospitals.
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PMID:Audit of nebuliser use. 409 48

Previously we have demonstrated that continuous positive pressure breathing (PB) depresses diaphragm activity and excites expiratory activity in the abdominal muscle (AMR) via vagal proprioceptive impulses. During prolonged PB the AMR persists at a constant level whereas inhibition of the diaphragm wanes, possibly as a result of CO2 retention. This study measures CO2 retention during PB and compares the responses of the abdominal muscle and diaphragm to chemostimulation alone and to chemostimulation and PB in combination. Continuous recordings of minute ventilation, integrated EMGs of the diaphragm and abdominal muscle, and mass spectrometer analysis of airway gases were obtained during PB on air, 5.25 percent CO2 and 12.4 percent O2 in eight Dial-anaesthetized cats. Between 0 and 15 cm H2O the steady-state end-tidal CO2 rises about 0.6 mm Hg/km H2O, diaphragm activity decreases and AMR increases exponentially with each increment in PB. When 5.25 percent CO2 is inspired, diaphragm activity is augmented at every pressure suggesting algebraic summation of proprioceptive and chemoreceptive effects at the respiratory centre. In contrast, the AMR is not significantly altered by hypercapnia. The absence of all abdominal muscle expiratory activity after bilateral vagotomy suggests that the role of active expiration is to regulate thoracic-lung volume, not blood gases.
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PMID:Comparative influence of proprioceptors and chemoreceptors in the control of respiratory muscles. 426 86

The response to a standard water load (20 ml/kg body weight) was studied in 20 patients with chronic obstructive airways disease and in 13 healthy subjects. The percentage of the water load excreted in four hours was significantly lower in the patients (mean 51%) than in the controls (mean 106%). The maximum urine flow, osmolar clearance, free water clearance, and creatinine clearance were also significantly reduced in the patients. There was a significant inverse correlation between the percentage of load passed and the arterial PCO(2) (r = -0.798). Among the several possible causes of the reduced excretion of water which are discussed is a direct effect of hypercapnia.
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PMID:Impaired water handling in chronic obstructive airways disease. 557 93

During a ten-year period, 22 children from our 170 cases of acute epiglottitis had reliable records of arterial blood gas data. The arterial/alveolar (a/A) oxygen tension ratios were calculated, with a value less than 0.75 representing abnormal gas exchange. The mean a/A ratio for the whole group, 17 of whom already had an artificial airway, was 0.59 (range, 0.29 to 0.83). A subgroup of five children with blood samples taken during conservative treatment or before airway insertion had a mean a/A ratio of 0.62 (range, 0.49 to 0.77) without hypercapnia (mean Paco2, 32 mm Hg; range, 29 to 39 mm Hg), which seemed to be a late feature. Thirty-three percent of initial chest roentgenograms were abnormal, with the major disorder being atelectasis and/or consolidation. We propose that the radiologic and gas exchange abnormalities result from the common pathophysiologic mechanism of increased lung water.
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PMID:Respiratory status of children with epiglottitis with and without an artificial airway. 640 84

In 16 experiments male subjects, age 22.4 +/- 0.5 (SE) yr, inspired CO2 for 15 min (8% end-tidal CO2) or hyperventilated for 30 min (2.5% end-tidal CO2). Osmolality (Osm) and acid-base status of arterialized venous blood were determined at short intervals until 30 min after hypo- and hypercapnia, respectively. During hypocapnia [CO2 partial pressure (PCO2) -2.31 +/- 0.32 kPa (-17.4 Torr), pH + 0.19 units], Osm decreased by 3.9 +/- 0.3 mosmol/kg H2O; during hypercapnia [PCO2 + 2.10 +/- 0.28 kPa (+15.8 Torr), pH -0.12 units], Osm increased by 5.8 +/- 0.7 mosmol/kg H2O. Presentation of the data in Osm-PCO2 or Osm-pH diagrams yields hysteresis loops probably caused by exchange between blood and tissues. The dependence of Osm on PCO2 must result mainly from CO2 buffering and therefore from the formation of bicarbonate. In spite of the different buffer capacities in various body compartments, water exchange allows rapid restoration of osmotic equilibrium throughout the organism. Thus delta Osm/delta pH during a PCO2 jump largely depends on the mean buffer capacity of the whole body. The high estimated buffer value during hypercapnia (38 mmol/kg H2O) compared with hypocapnia (19 mmol/kg H2O) seems to result from very strong muscle buffering during moderate acidosis.
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PMID:Blood osmolality during in vivo changes of CO2 pressure. 640 68

Although it is known that hypercarbia increases and benzodiazepines decrease cerebral blood flow (CBF), the effects of benzodiazepines on CBF responsiveness to CO2 are not well documented. The influence on CBF and CBF-CO2 sensitivity of placebo or midazolam, which is a new water-soluble benzodiazepine, was measured in eight healthy volunteers using the noninvasive 133Xe inhalation method for CBF determination. Under normocarbia, midazolam decreased CBF from 40.6 +/- 3.2 to 27.0 +/- 5.0 ml 100 g-1 min-1 (means +/- SD). At a later session under hypercarbia, CBF was 58.8 +/- 4.4 ml 100 g-1 min-1 after administration of placebo, and 49.1 +/- 10.2 ml 100 g-1 min-1 after midazolam. The mean of the slopes correlating PaCO2 and CBF was significantly steeper with midazolam (2.5 +/- 1.2 ml 100 g-1 min-1 mm Hg-1) than with placebo (1.5 +/- 0.4 ml 100 g-1 min-1 mm Hg-1). Our results suggest that midazolam may be a safe agent to use in patients with intracranial hypertension, since it decreases CBF and thus cerebral blood volume; however, it should be administered with caution in nonventilated patients with increased intracranial pressure, since its beneficial effects on cerebrovascular tone can be readily counteracted by the increase in arterial CO2 tension induced by this drug.
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PMID:Effects of midazolam on cerebral hemodynamics and cerebral vasomotor responsiveness to carbon dioxide. 640 14

In healthy subjects, patterns of inhalation and exhalation durations during growing hypercapnia were studied in free breathing and under the effect of resistive inspiratory resistance 20 and 35 cm H2O/1/sec. Pattern of the inhalation duration was divided into two ranges: the inhalation elongated in the first range and shortened in the second one. The border between these ranges corresponded in free breathing to CO2 tension of exhalation terminal portion (PETCO2)--47.2 +/- 1.0 mm Hg (M +/- m). The 1st range was found in 2/3 of cases in the exhalation duration pattern. Under the effect of additional inspiratory resistance, the border between the two ranges of inhalation pattern shifted towards greater PETCO2 values and was 51.0 +/- 1.0 mm Hg for the greater resistance. The 1st range was found in 1/3 of cases in the exhalation duration dynamics. The shift of the border between the ranges of the inhalation duration pattern occurring in breathing with a resistive load in the course of growing hypercapnia seems to result from an augmentation of cortical effects upon breathing and/or weakening of afferent influences from the lung stretch receptors under these conditions.
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PMID:[Duration of inhalation and exhalation in increasing hypercapnia and the effect of additional resistive inspiratory resistance]. 640 79

Nine anesthetized dogs breathed against an expiratory threshold load (ETL) applied by switching the expiratory circuit into a column of H2O to a depth of 20-30 cm. Arterial blood gas tensions were maintained in the normal range by placing the dogs under arteriovenous bypass to avoid any uncontrolled chemostimulation. There was an increase in integrated electromyogram activity of the diaphragm with the ETL. This was rarely observed after cold block of the vagus nerves which also reduced the evoked expiratory activity. The ventilatory response to hypercapnia was greatly depressed under loaded breathing whether vagal afferents were intact or blocked by cold. Both inspiratory drive and ventilatory timing were affected, suggesting that the central integration of chemosensitive afferents was altered. Proof of supraspinal projections of proprioceptive inputs from abdominal muscles was provided by the demonstration of changes in ventilatory timing during selective activation of muscle spindles in abdominal muscles by high-frequency mechanical vibration applied to the linea alba. Thus these observations suggest that during ETL breathing, a possible interaction exists between chemoreflex drive and proprioceptive afferents.
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PMID:Expiratory threshold load under extracorporeal circulation: effects of vagal afferents. 641 63

The aquatic urodeles Ambystoma tigrinum and Necturus maculosus responded to hypercapnia quite differently. A. tigrinum, after 2-h exposure to 22 Torr partial pressure of CO2 (PCO2), decreased arterial pH (pHa) from 7.85 to 7.32 and increased arterial pressure of CO2 (PaCO2) to 26 Torr. Plasma [HCO-3] [( HCO-3]pl) remained constant at about 17 mM. Prolonged exposure (24 h) led to a 26% extracellular compensation as pHa rose to 7.46 while [HCO-3]pl increased to 24 mM. Plasma [K+] increased and [Cl-] decreased while [Na+] remained unchanged. Recovery in normocapnic water reversed these changes. N. maculosus did not display similar compensatory changes. Two-hour exposure to 17 Torr PCO2 resulted in a decline of pHa from 7.66 to 7.24, which was not compensated (pHa = 7.19) after 24 h. There were no significant changes in plasma [Na+], [K+], [Cl-], or [HCO-3]. The pHa decline reversed after recovery in normocapnic water, however. The fact that compensation for hypercapnic in A. tigrinum was accompanied by changes in Cl- and K+ concentrations may indicate the participation of epithelial transport mechanisms involving these ions in acid-base balance.
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PMID:Acid-base and ionic balance in Ambystoma tigrinum and Necturus maculosus during hypercapnia. 641 88

The effect of acute changes in arterial PCO2 on absolute proximal reabsorption of bicarbonate, chloride, and water has not been systematically studied. In the present free-flow micropuncture studies in Munich-Wistar rats, arterial PCO2 was increased or decreased by 20 mmHg. Under conditions of stable SNGFR, proximal and whole kidney electrolyte reabsorption was measured. Acute hypocapnia decreased absolute proximal bicarbonate reabsorption by 23% (from 1,008 +/- 38 to 773 +/- 36 pmol/min). Proximal volume reabsorption also decreased. Although bicarbonate delivery out of the superficial proximal convoluted tubule did not exceed normal levels, bicarbonaturia developed, suggesting an additional suppression of acidification by distal and/or juxtamedullary nephron segments. Acute hypercapnia increased absolute proximal bicarbonate reabsorption by only 10% in chronically alkalotic animals (from 1,050 +/- 68 to 1,176 +/- 77 pmol/min). In acutely alkalotic animals, hypercapnia caused no significant increment in the higher basal level of absolute proximal bicarbonate reabsorption (from 1,158 +/- 120 to 1,234 +/- 97 pmol/min). Whole kidney bicarbonate reabsorption rose, again suggesting a distal and/or juxtamedullary effect. Hypercapnia inhibited proximal chloride reabsorption and caused a chloruresis. In conclusion, acute hypo- and hypercapnia caused alterations in proximal bicarbonate, chloride, and sodium transport that may participate, at least in part, in the changes in whole kidney electrolyte reabsorption observed in these conditions. Distal and/or juxtamedullary nephrons also appeared to contribute to the changes in renal acidification induced by alterations in systemic PCO2.
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PMID:Effects of acute alterations in PCO2 on proximal HCO-3, Cl-, and H2O reabsorption. 642 Nov 73


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