Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied the problem of pulmonary capillary-alveolar CO2 exchange in the cat during acute hypercapnia. Three cats, anesthetized with xylazine and pentobarbital sodium and prepared with acute tracheostomy and femoral arterial catheter, and three awake cats, prepared with a small tracheal catheter and femoral arterial catheter, were subjected to acute hypercapnia (FICO2 = 0.00, 0.06, and 0.08). During steady states, end tidal PCO2 was determined with an infrared analyzer, and arterial PCO2 was measured with a Radiometer ABL-2 analyzer in simultaneously drawn samples. In vitro studies indicated that our blood sampling techniques resulted in a 6% reduction in PCO2. Blood PCO2 readings were corrected for (1) non-ideal performance of the analyzer as determined by tonometry, (2) 6% reduction due to sampling, and (3) differences between electrode and rectal temperature. Mean arterial-end tidal PCO2 differences were not significantly different from zero in any condition in either group (except for 0.08 CO2 in the awake group when the difference was 2.0 Torr). These findings in the cat agree with the classical view that PCO2 in pulmonary capillary blood approaches PCO2 in alveolar gas. Further, our findings provide evidence that CO2 loss from blood samples is an important technical factor which can cause systematic underestimation of blood PCO2 and, hence, contribute to the observation of negative PCO2 gradients.
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PMID:Arterial-end tidal PCO2 equilibration in the cat during acute hypercapnia. 313 49

The hemoglobin-oxygen dissociation curve and the relationships between the parameters of tension, saturation, capacity, affinity and concentration of oxygen in the course of respiratory failure in chronic obstructive lung diseases (COLD) were studied. The study included 141 patients divided into four basic groups according to the value of pO2 (a): patients with normoxia, mild, moderate and severe arterial hypoxia. The blood-gas status was determined using the ABL-330 and OSM-3 analyzers (Radiometer A/S, Denmark). It is concluded that: 1. Presence of normoxia (pO2 and sO2 in norm) in COLD patients does not exclude abnormalities in their arterial blood oxygen transport and increased risk of tissue hypoxia. 2. Total oxygen concentration in respiratory failure is relatively stable and "independent" from the stepwise decrease of the arterial pO2, which results from the compensatory increase of the total and effective hemoglobin. 3. There are phase fluctuations of the ctO2/pO2 dissociation curve in the reference interval, expressed in the "lowering" of P50 and p90 in mild hypoxia and the "centering" or "raising" of their values in severe hypoxia. Such fluctuations are more pronounced in the p90 than in the p50. 4. The oxygen extraction tension lowers progressively (without reaching the anaerobic threshold) and the oxygen compensation factor elevates with the pO2 (a) reduction and the arising of hypercapnia and acidemia. 5. The calculated 2,3-diphosphoglycerate (2,3-DPG) concentration values are significantly higher in hypercapnics with COHb > 1% than in those with COHb < 1%. The relationships between hypoxia, oxygen affinity, hemoglobinemia and oxygen affinity as well as the dissociation curve properties in chronic respiratory failure are discussed.
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PMID:Relationships between blood oxygen parameters in patients with chronic obstructive lung disease. 819 1