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

Because of the close anatomic and physiologic relationship between the heart and lungs, patients with chronic obstructive lung disease are at special risk of arrhythmias. Effective therapy hinges on identifying the mechanisms of the arrhythmias--hemodynamic, metabolic, or drug-induced. Impulsive use of antiarrhythmic agents may result only in a more complex and dangerous rhythm disorder. Extremes of pH are a major cause of arrhythmias in these patients. Respiratory alkalemia usually originates with inappropriate ventilation, often during mechanical respiration, while metabolic alkalemia generally can be traced to diuretic or bicarbonate therapy. Lidocaine or diphenylhydantoin are of little use, since the alkaline pH inside and outside heart muscle cells hampers drug distribution and activity. At the other extreme, the arrhythmias of acidemia strike patients who have severe respiratory failure with carbon dioxide retention or severe cardiac failure with shock and lactic acidemia. Arrhythmias may develop if vagal restraint is lost, which is especially likely in patients with potassium depletion. Irritant receptors along the bronchopulmonary tree can trigger arrhythmias if stimulated by cough, microembolism, or mechanical irritation, which is a hazard with endotracheal or tracheostomy tubes.
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PMID:Mechanisms of arrhythmias in chronic obstructive lung disease. 1 Feb 30

In order to test the relationship between changes in plasma potassium concentration and pH changes of respiratory origin, we produced hypercapnia (mean PaCO2 71 mmHg = 9.5 kPa) in a group of 17 patients and hypocapnia (mean PaCO2 21 mmHg = 2.8 kPa) in another 20 patients during neurolept analgesia and intraabdominal operations. A control group of 19 patients was studied under normocapnia but otherwise identical conditions. During hypercapnia, serum potassium rose, deltaK/deltapH amounting to -0.82, -1.05 and -1.34 after 30, 60 and 90 min, respectively. During hypocapnia, serum potassium decreased, deltaK/deltapH being a little more negative than during hypercapnia (mean values -1.62, -2.44 and -1.60). Red cell potassium concentration decreased in all three groups to a similar extent. Blood lactate levels during hypercapnia decreased to 75% of control and during hypocapnia rose to a maximum of 186% of control. In order to obtain reasonable values for base excess in primarily respiratory acid-base disorders, it is necessary to use nomograms based on in vivo ECF-CO2-titration curves. With this premise, hypercapnia or hypocapnia in our patients was not associated with significant changes in base excess.
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PMID:Effects of acute hypercapnia and hypocapnia on plasma and red cell potassium, blood lactate and base excess in man during anesthesia. 3 56

The interconnections between EEG, intermediary and energy metabolism of the brain cortex and CSF potassium level are studied during severe hypercapnia in anaesthetized, artificially ventilated cats. Hypercapnic animals were ventilated with 40 to 50% to CO2 in oxygen. During severe hypercapnia the EEG becomes isoelectric. The CSF potassium concentration is raised and the changes in metabolism suggest an acidosis-induced inhibition of phosphofructokinase and, probably, of hexokinase. The energy charge potential remains unchanged whereas the cortical ATP concentration increases slightly. It is assumed that the changes in P-creatine and creatine levels are related to the pH-dependency of creatine phosphokinase. Recovery animals were ventilated with 40% CO2 in O2 and subsequently with room air. After termination of CO2 inhalation the EEG reappears, the CSF potassium concentration normalizes, and the inhibition of the glycolytic enzymes disappears. The energy charge potential shows a small decrease. It is not possible to trace back the disappearance of the EEG to only one of the recorded parameters. Cortical P-creatine levels, CSF potassium concentration, changes in membrane permeability and cortical amino acid concentrations are considered in this context.
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PMID:Influence of severe hypercapnia upon cerebral cortical metabolism, CSF electrolyte concentrations and EEG in the cat. 13 59

Studies in patients undergoing peritoneal laparoscopy, in which carbon dioxide was used as insufflating gas, showed that artificial hyperventilation was an effective means of preventing serious hypercapnia. The hypercapnia caused a rapid hyperkalaemia and there was a linear relationship between the two. Reversal of the hypercapnia caused the serum potassium to fall towards normal but the speed of this fall did not match the speed of reduction in Paco2. It is suggested that the changes in serum potassium following changes in Paco2 may have some clinical relevance in potassium-depicted patients.
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PMID:Hypercapnia and hyperkalaemia. 16 Nov 43

Rats with dietary potassium (K) depletion have an altered breathing pattern compared to age matched control rats. The K depleted rats also have a decreased body weight gain, basal metabolic rate and body temperature. In this study, age matched controls are underfed (UFC) to match for body weight gain and metabolic rate and controls are exposed to different ambient temperatures to alter metabolism and body temperature. Compared to UFC rats with the same body weight and basal metabolic rate the K depleted rats breathe slower and with a larger tidal volume in the basal state and in response to hypercapnia and hypoxia. With heat stress body temperature is increased in K depleted rats as is metabolic rate. While frequency is increased it is still slower than in controls at the same ambient and body temperatures. We conclude that the low metabolic rate and body temperature of K depleted rats is not the cause of the altered breathing pattern. In addition, it is shown that the hypothermia of K depletion is present only at ambient temperatures below the thermoneutral zone and that is is apparently due to an inability of the K depleted rat to increase metabolic heat production with cold stress.
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PMID:Breathing in the potassium depleted rat: the role of metabolic rate and body temperature. 50 31

With the aid of potassium-sensitive microelectrodes reinforced by bitumen (tip diameter, 1.5 micrometer), extracellular potassium activity ([K+]e) and DC potential were measured in the cat's carotid body. Under normoxic and normocapnic conditions, potassium values of 1--16 mM (mean value 7.2 mM, standard deviation 3.8 mM) and DC potential values of -11 mV to + 13 mV were recorded. With hypoxia, [K+5e increased by between 1 mM and 9 mM; DC potential was reduced by between 0.5 and 3 mV. With hypercapnia, [K+]e decreased by between 1 mM and 5 mM changes in DC potential were variable. The results suggest that, during hypoxia potassium influences the nervous structures in the carotid body whereas this influence is absent during hypercapnia.
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PMID:Measurements of potassium changes in the cat carotid body under hypoxia and hypercapnia. 56 90

Seventeen male patients with chronic obstructive airways disease in remission were separated into two groups according to arterial carbon dioxide tensions. Hypercapnia was associated significantly with hypoxia and increased red cell volume whereas normocapnia was not. Normocapnic patients were significantly lighter than those with hypercapnia. Total body potassium (TBK) measured by the whole body monitor was significantly low in two of the patients studied (P less than 0.005). The mean value for TBK for the normocapnic group as a whole was significantly low (P less than 0.005), but the mean value for the hypercapnic group was not. Serum potassium and erythrocyte potassium concentrations were normal even when TBK was low, and diuretics had no apparent influence on these potassium values. Of four patients (two in the series and two others) who had TBK measured after a recent episode of cor pulmonale, three had significantly low values. The only previous studies using a whole body monitor to measure TBK in chronic obstructive airways disease found no such low values, though other workers estimating exchangeable potassium by isotope dilution techniques had found evidence of gross potassium depletion. It is concluded that low TBK does indeed occur in patients with chronic obstructive airways disease and that gross depletion is more likely to follow an episode of cor pulmonale.
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PMID:Potassium studies in chronic obstructive airways disease. 74 98

During acute asphyxia in pentobarbital-narcotized cats, the elevation in plasma potassium level was parallel to that of PCO2. From the time when PO2 reached its minimum, the elevation in serum potassium was higher than that of plasma potassium. The increase of the difference between serum and plasma potassium values seems therefore to be more related to hypoxia than hypercapnia; it could be due to membrane alteration of blood cells.
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PMID:Differences between elevations of plasma and serum potassium in pentobarbital-narcotized cats during asphyxia. 99 Mar 78

The role of the skeleton in electrolyte equilibrium, well known for various diseases, remains difficult to understand during chronic hypercapnia. An experimental study of normoxic (O2:21%) hypercapnia (CO2:8 +/- 1%) was carried out for two, four and six weeks, followed by a systematic quantitative determination, in thigh-bone samples of Na+, K+, Ca++, PO4--, N2 and CO2 in 72 rats, and of total H2O and extracellular H2O (H2Oe) in 129 rats. Considering the mean values of groups (from 16 to 42 subjects for each group), at various times of hypercapnia, bone K+ was increased during hypercapnia (+3 to 4 X 10(-3) mEq/g fresh tissue), Ca++ diminished (--12.5 to 15.4 mEq). PO4-- and Na+ temporarily decreased at two and four weeks of hypercapnia. On account of the scatter of individual results, only the variation of K+ was statistically significant (at two weeks). This increase in bone K+, accompanying a partially compensated acidaemia, is to compare with the significant hyperkaliemia observed at two and four weeks, whereas this period is characterized by a decrease in K+ in skeletal muscle, as shown in a previous work. In a group of 72 rats, the analysis of correspondances and correlations points out the bone CO2 as a very significant variable, opposite to the variable H2Oe. PO4--is positively correlated to Na+. The complexity of the results does not permit a decisive interpretation of the phenomenon. On the other hand, this study corroborates the bone calcium loss and reveals the gain in bone potassium during hypercapnia.
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PMID:[Bone electrolytes in experimental chronic hypercapnia (author's transl)]. 101 78

The bile acid-base parameters are analyzed in 42 male Wistar rats under pentobarbital anaesthesia, in normal conditions of blood acid-base equilibrium. The reproducibility of the results is emphasized. In acute hypercapnia (FICO2 : 0.12 for 15 min) without hypoxia, and for the same increase in PCO2, and pH variation is lesser in bile than in blood, thus showing an high buffer capacity. In vitro and in vivo comparative studies show that bile buffer capacity is about five times higher in vivo, independently of a possible increase in choleresis. Comparative studies of bile-acid-base equilibrium are effected during perfusions of dehydrocholate, sodium taurocholate, secretin and acetazolamide. Sodium and chlorine remain stable during hypercapnia both in blood and in bile ; potassium concentration is increased in the two media. To explain these results, the role of the liver is still to specify.
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PMID:[Acute hypercapnia and bile. Experimental studies in the rat (author's transl)]. 101 82


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