Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical experience of 661 children with bronchiolitis is reported in four-years period to gain a better understanding of diagnosis and pathogenesis of bronchiolitis. Upper airways infections, expiratory dyspnea, clear sound by chest percussion, vesicular rales and whistling by chest auscultation, air trapping on the chest radiography were considered as essential data of diagnosis. It was found in 595 patients: expiratory dyspnea, air trapping, vesicular r. and whistling in 85% and whistling only in 15%; hypoxemia in 20% combined with hypercapnic acidosis in 10%; normoxemia in 80% combined with hypocapnia in 54%; hyperlactemia in 64% combined with an increment in the serum of CPK in 50% and of GPT in 30%; virus were cultured in 27%, adenovirus and RSV were identified in 90%. Instead it was found in 66 patients: air trapping but no difficult breath, with normal chest auscultation; crisis of cyanosis or paleness-cyanosis chilly sweat in 80% were motive of admission. The clinical and/or radiological features of "air trapping" were considered as essential symptoms and signs of bronchiolitis. The insufficient systemic perfusion was considered as a frequent occurrence and as cause for sudden respiratory and circulatory emergency.
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PMID:[Bronchiolitis. Our clinical experience in the 4 years from 1981 to 1984]. 383 40

Previous studies from this laboratory have demonstrated that the decreased renal bicarbonate reabsorption prevailing during chronic hypocapnia is not mediated by the alkalemia that normally accompanies this acid-base disturbance but by some direct consequence of the change in PaCO2 itself. Based on the reasonable expectation that the mechanisms underlying the kidney's response to primary respiratory disturbances would be similar over the entire spectrum of physiologic carbon dioxide tensions, the present study was designed to assess whether an acidic change in systemic pH is a critical factor in the renal response to chronic hypercapnia. For this purpose, the plasma and renal responses to chronic respiratory acidosis in normal dogs were compared to those in dogs chronically fed a large hydrochloric acid (HCl) load (7 mmoles/kg/day). Exposure to 6% carbon dioxide for 7 days in a large environmental chamber induced a stable increment in PaCO2 which averaged 17 +/- 0.5 and 22 +/- 1.3 mm Hg in normal and HCl-fed animals, respectively. Steady-state plasma bicarbonate concentration rose from 22.0 +/- 0.4 to 27.1 +/- 0.5 mEq/liter in normals and from 14.7 +/- 0.7 to 24.2 +/- 0.8 mEq/liter in the HCl-fed group. As a result of these changes in PaCO2 and plasma bicarbonate, steady-state plasma hydrogen ion concentration rose in normals from 41 +/- 0.8 to 49 +/- 0.9 nEq/liter (pH 7.39 +/- 0.01 vs. 7.31 +/- 0.01) but did not change significantly in the HCl-fed group (55 +/- 1.4 vs. 56 +/- 1.4 nEq/liter; pH 7.26 +/- 0.01 vs. 7.25 +/- 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of acid-base equilibrium in chronic hypercapnia. 399 41

We studied the effects of acute changes in the partial pressure of arterial carbon dioxide on diaphragmatic contractility and performance in four normal men. To study contractility we measured the ability of the diaphragm to generate pressure at a given level of excitation by determining the relation between the electrical activity of the diaphragm and transdiaphragmatic pressure during a voluntary quasi-isometric inspiratory effort carried out at different levels of end-tidal carbon dioxide. Our results show that contractility was reduced with hypercapnia (when end-tidal carbon dioxide was 7.5 per cent or higher), although hypocapnia (end-tidal carbon dioxide, 3 per cent) had no effect on diaphragmatic contractility. We also studied the development of diaphragmatic fatigue before and during carbon dioxide breathing. Subjects were studied at the same diaphragmatic tension-time index, a value analogous to the more familiar myocardial tension-time index, while the same inspiratory flow was maintained. Electromyographic signs of fatigue appeared at a lower tension-time index during hypercapnia than during normocapnia, indicating that endurance is diminished during hypercapnia. These findings show that acute respiratory acidosis equivalent to an arterial carbon dioxide tension of about 54 mm Hg decreases the contractility and endurance time of the diaphragm in human beings.
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PMID:Effect of carbon dioxide on diaphragmatic function in human beings. 642 98

The infrared CO2 analyzer continuously monitors the CO2 tension in exhaled air at end-tidal expiration. In experimental animals, we found a consistent relationship between PaCO2 and end-tidal CO2 (ET.CO2) in the normal steady state, and in acid-base disturbances (respiratory acidosis and alkalosis, and hypoperfusion acidosis). Paired data analyses of PaCO2 (X) and ET.CO2 (Y) yielded correlation coefficients of r = 0.98 (Y = 0.96X + 4.43) during progressive hypercarbia (PaCO2: 32----110 torr), and r = 0.93 (Y = 0.89X + 0.93) during hyperventilation hypocapnia (PaCO2: 41----14 torr). The relationship between PaCO2 and ET.CO2 was seen during hypovolemic shock if pulmonary perfusion was maintained uniform in all areas of lung. The ability of the ET.CO2 sensor to predict instantaneously the PaCO2 makes it attractive enough to be used in conjunction with the subcutaneous tissue pH(pHe) sensor in the management of acid-base disturbances. After hypercarbia (FiCO2 0.15 X 40 min; PaCO2/ET.CO2: 100/101 torr), when the dogs were returned to room air, abruptly both the ET.CO2 and pHe sensors were sensitive to the changes in Fi.CO2. But the response of the ET.CO2 was swifter. The advent of transcutaneous gas monitors has shown that intermittent blood gas analyses, however frequent, are inadequate for the monitoring of the rapidly altering blood gas status in the acutely ill. The ability of the pHe sensor to identify whole-body acidosis and alkalosis combined with the speed and ease of the ET.CO2 monitor in pinpointing hypercarbic and hypocarbic states makes this two-parameter system suitable for the continuous, noninvasive monitoring of the critically ill.
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PMID:End-tidal CO2 and tissue pH in the monitoring of acid-base changes: a composite technique for continuous, minimally invasive monitoring. 644 Sep 69

On day 16 of the chick embryo, a catheter was implanted in the allantoic vein carrying arterialized blood, and a syringe was attached to the blunt end of the shell connecting to the air cell. This technique allowed for repetitive sampling and analysis of air cell gas and arterialized blood when these eggs were exposed to a He-O2 or SF6-O2 atmosphere. Exposure to He-O2 reduced the arterial CO2 tension(PaCO2) from 36 to 17 Torr and increased pH by 0.17 units; exposure to SF6-O2 increased PaCO2 from 37 to 62 Torr and reduced the pH by 0.14 units. These responses were brought about by changes in the gas conductance of the shell, resulting in a diffusive hypocapnia and respiratory alkalosis in He-O2 and a diffusive hypercapnia and respiratory acidosis in SF6-O2. During a 4-h exposure to these foreign gases the observed pH changes were smaller than predicted because of marked shifts of HCO3- into the blood (SF6-O2) or out of the blood (He-O2).
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PMID:Changes in acid-base balance of chick embryos exposed to a He or SF6 atmosphere. 679 Apr 88

The modifications of systemic hemodynamics, oxygen transport and tissular oxygenation in mechanically-ventilated critical ARF (acute respiratory failure) patients, after the correction of its hypocapnia by addition of dead space (VD) are determined. The prospective and randomized study was carried out in a multidisciplinary ICU. Fifteen ARF patients were studied within the first 48 hours of evolution. All the patients were intubated and mechanically ventilated. Three stages were delimited: I) 30 min after the beginning of anesthesia; II) 30 min after adding 30 cm of VD; III) 30 min after replacing the previous VD with a VD of 60 cm. Similar steady states had been reached when the measurements were taken. Ventilation parameters and FiO2 were kept stable. In stage I the patients presented a pure respiratory alkalosis and, with respect to hemodynamics, a hyperdynamic situation. In stage II the acid-base balance was normalized with a continuation of the hyperdynamic situation and an increase in mixed venous oxygen tension and saturation (PvO2 and SvO2) (p < 0.001). Stage III was characterized by a pure hypercapnic acidosis and an increase in capillary wedge pressure (CWP) (p < 0.05), right atrial pressure (RAP) (p < 0.001) and cardiac output (Qt) (p < 0.001); simultaneously, the systemic vascular resistances (SVR) decreased (p < 0.01), the PvO2, SvO2 and oxygen delivery (DO2) increased (p < 0.001); oxygen utilization coefficient (OUC) decreased (p < 0.01). The results suggest that the variations in PvO2 and SvO2 are a direct consequence of the modifications in blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modifications of tissular oxygenation and systemic hemodynamics after the correction of hypocapnia induced by mechanical ventilation. 799 35

Quantitative electroencephalography was assessed in 6 dogs anesthetized with 1.8% end-tidal halothane, under conditions of eucapnia, hypocapnia, and hypercapnia. Ventilation was controlled in each condition. Heart rate, arterial blood pressure, core body temperature, arterial pH, blood gas tensions, end-tidal CO2 tension, and end-tidal halothane concentration were monitored throughout the study. A 21-lead linked-ear montage was used for recording the EEG. Quantitative electroencephalographic data were stored on an optical disk for analysis at a later date. Values for absolute power of the EEG were determined for delta, theta, alpha, and beta frequencies. Hypocapnia was achieved by hyperventilation. Hypercapnia was achieved by titration of 5% CO2 to the inspired gas mixture. Hypercapnia was associated with an increase in the absolute power of the delta band. Hypocapnia caused an increase in the absolute power of delta, theta, and alpha frequencies. Quantitative electroencephalographic data appear to be altered by abnormalities in arterial carbon dioxide tension. Respiratory acidosis or alkalosis in halothane-anesthetized dogs may obscure or mimic electroencephalographic abnormalities caused by intracranial disease.
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PMID:Effects of altered arterial carbon dioxide tension on quantitative electroencephalography in halothane-anesthetized dogs. 801 90

We studied the effect of respiratory acidosis and respiratory alkalosis on acid-base composition and on microdissected renal adenosinetriphosphatase (ATPase) enzymes. Rats were subjected to hypercapnia or hypocapnia of 6, 24, and 72 h duration. After 6 h of hypercapnia, collecting tubule (CT) ATPases were not changed. At 24 h, plasma bicarbonate was 35 +/- 1 meq/l (P < 0.01) and CT H-ATPase and H-K-ATPase activities were 90% greater than controls (P < 0.01). By 72 h, plasma bicarbonate was 37 +/- 1 meq/l (P < 0.005 vs. control) and CT enzyme activity had increased even more, averaging approximately 130% of control (P < 0.05). Significant increases in enzyme activities were also observed in the proximal convoluted tubule and medullary thick ascending limb. Plasma aldosterone was three to four times that of control at all three time periods. In hormone-replete adrenalectomized rats, acid-base parameters and ATPase activities were the same as those seen in adrenal intact animals. After 6 h of hypocapnia, plasma bicarbonate was not significantly changed, but H-ATPase and Na-K-ATPase activities were decreased by 35% along the entire nephron (P < 0.05). H-K-ATPase activity in CT also decreased by 35%. At 24 h, plasma bicarbonate was 20.5 +/- 0.5 meq/l (P < 0.05 vs. control) and CT H-ATPase and H-K-ATPase activities were 60% less than control (P < 0.01). By 72 h, plasma bicarbonate was 18.5 +/- 0.5 meq/l (P < 0.05); however, only CT H-ATPase activity continued to fall, averaging 75% less than control (P < 0.005). Hypocapnia had no effect on plasma aldosterone or potassium. These results demonstrate that chronic, but not acute, respiratory acidosis stimulates activity of both renal proton ATPases. By contrast, both acute and chronic respiratory alkalosis decrease the two renal proton pumps. The stimulatory effect of hypercapnia and the inhibitory effect of hypocapnia on the renal ATPases appear to be potassium and aldosterone independent. Although the precise mechanisms for these results are not known, a direct effect of PCO2, pH, or changes in bicarbonate delivery may be involved.
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PMID:Effect of respiratory acidosis and respiratory alkalosis on renal transport enzymes. 809 53

In physiological conditions, the regulation of acid-base balance in brain maintains a noteworthy stability of cerebral pH. During systemic metabolic acid-base imbalances cerebral pH is well controlled as the blood/brain barrier is slowly and poorly permeable to electrolytes (HCO3- and H+). Cerebral pH is regulated by a modulation of the respiratory drive, triggered by the early alterations of interstitial fluid pH, close to medullary chemoreceptors. As blood/brain barrier is highly permeable to Co2, CSF pH is corrected in a few hours, even in case of severe metabolic acidosis and alkalosis. Conversely, during ventilatory acidosis and alkalosis the cerebral pH varies in the same direction and in the same range than blood pH. Therefore, the brain is better protected against metabolic than ventilatory acid-base imbalances. Ventilatory acidosis and alkalosis are able to impair cerebral blood flow and brain activity through interstitial pH alterations. During respiratory acidosis, [HCO3-] increases in extracellular fluids to control cerebral pH by two main ways: a carbonic anhydrase activation at the blood/brain and blood/CSF barriers level and an increase in chloride shift in glial cells (HCO3- exchanged for Cl-). During respiratory alkalosis, [HCO3-] decreases in extracellular fluids by the opposite changes in HCO3- transport and by an increase in lactic acid synthesis by cerebral cells. The treatment of metabolic acidosis with bicarbonates may induce a cerebral acidosis and worsen a cerebral oedema during ketoacidosis. Moderate hypocapnia carried out to treat intracranial hypertension is mainly effective when cerebral blood flow is high and vascular CO2 reactivity maintained. Hypocapnia may restore an altered cerebral blood flow autoregulation. Instrumental hypocapnia requires a control of cerebral perfusion pressure and cerebral arteriovenous difference for oxygen, to select patients for whom this kind of treatment may be of benefit, to choose the optimal level of hypocapnia and to avoid any deleterious effect. If hypocapnia is maintained over several days, an adaptation of CSF pH may limit the therapeutic effect on the cerebral blood flow and the intracranial pressure.
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PMID:[Acid-base equilibrium and the brain]. 809 67

1. Plasma concentrations of noradrenaline and adrenaline were measured in 11 anaesthetized patients during normocapnia, hypocapnia and hypercapnia. Hypocapnia was produced by deliberate hyperventilation and hypercapnia by adding carbon dioxide to the inspired gas mixture. 2. With a median (range) arterial partial pressure of carbon dioxide of 4.7 (4.2-5.2) kPa, the median (range) plasma concentration of noradrenaline was 0.41 (0.12-0.94) nmol/l and of adrenaline was 0.15 (0.05-0.31) nmol/l. 3. With an arterial partial pressure of carbon dioxide of 2.6 (2.2-3.3) kPa, there was no change in the plasma concentration of noradrenaline [0.37 (0.12-0.86) nmol/l] or that of adrenaline [0.16 (0.05-0.32) nmol/l]. 4. However, with an arterial partial pressure of carbon dioxide of 10.4 (7.6-13.2) kPa, there were significant increases in the plasma concentrations of both noradrenaline [1.13 (0.79-2.05) nmol/l, P < 0.01] and adrenaline [0.67 (0.20-2.92) nmol/l, P < 0.05]. 5. This is the first demonstration in man that respiratory acidosis causes an increase in plasma concentrations of catecholamines.
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PMID:Effect of respiratory acidosis and alkalosis on plasma catecholamine concentrations in anaesthetized man. 838 37


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