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)

Plasma renin activity (PRA) and plasma angiotensin II (PAT II) level were determined with the method of radioimmunoassay in 55 patients with advanced chronic obstructive pulmonary disease (COPD) and chronic cor pulmonale (41 of them had respiratory failure) and 12 healthy aged persons. The results showed that PRA and PAT II levels were significantly elevated in the presence of such factors as severe hypoxia and hypercapnia (PaO2 less than or equal to 45 mmHg, mean 40 mmHg, PaCO2 greater than or equal to 65 mmHg), right heart failure, acidosis, hyponatremia and hypochloremia. It is shown that the prognosis would be poor when the patient's PRA level is significantly elevated.
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PMID:[Influence of acute respiratory failure on plasma renin activity and plasma angiotensin II level in advanced chronic obstructive pulmonary disease and chronic cor pulmonale]. 268 74

To determine the relative contribution of sudden death as a cause of late inpatient mortality in newborns after prolonged mechanical ventilation, we reviewed the charts of 348 patients who received ventilation assistance and who were admitted to the neonatal intensive care unit during a 26-month period. The overall mortality rate for these patients was 25%, with 88% (77/88) of these deaths occurring within 30 days of birth. Eleven infants died after more than 60 days of mechanical ventilation. Seven of these late deaths were sudden, unexpected in-hospital deaths. Sudden deaths occurred at a mean (uncorrected) age of 12 months (range, 4 to 27 months), during periods when infants appeared to be stable or clinically improving, were unrelated to recent respiratory exacerbations, and occurred despite prompt resuscitative efforts. Four infants still required mechanical ventilation, and 4 had tracheostomies at the time of death. All of the infants had chronic hypercarbia (greater than 50 mm Hg) and an elevated serum bicarbonate level (greater than 30 mmol/L), but not hyponatremia, hypochloremia (less than 80 mmol/L), or alkalemia. Left and right ventricular hypertrophy, multiple drug therapy, recurrent cyanotic episodes, and frequent unexplained fevers were common. In comparison with 17 bronchopulmonary dysplasia survivors who required longer than 60 days of ventilation therapy, the late deaths group more frequently had left ventricular hypertrophy and received prolonged combination theophylline anhydrous and beta-adrenergic agonist therapy. We report that sudden death can occur in infants with severe bronchopulmonary dysplasia despite in-hospital cardiopulmonary monitoring and the rapid institution of cardiopulmonary resuscitation, and is a significant cause of late mortality in infants who receive ventilation therapy for longer than 2 months.
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PMID:Late sudden unexpected deaths in hospitalized infants with bronchopulmonary dysplasia. 274 53

In metabolic alkalosis, a compensatory decrease in alveolar ventilation with hypercapnia has been noted only rarely. We recently managed a patient with gastric outlet obstruction from a duodenal ulcer who survived after arriving in the emergency room comatose with severe hypochloremic metabolic alkalosis, compensatory hypoventilation, and hypercapnia. We know of no report in the English literature of a patient with gastric outlet obstruction having a respiratory acidosis or hypochloremia as severe as that in our patient. Proper understanding of the pathophysiology of primary metabolic alkalosis due to gastric losses is necessary to correct the acid-base abnormalities quickly and to restore normal alveolar ventilation.
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PMID:Marked hypochloremic metabolic alkalosis with severe compensatory hypoventilation. 376 30

The metabolic contributions to chronic acid-base changes were examined in the plasma of arterial blood in patients with chronic obstructive pulmonary disease (COPD) and chronic hypercapnia, by a quantitative physical-chemical analysis. Patients were stratified into three groups: group 1 (Paco2 less than 40 mmHg; 1 mmHg = 133.3 Pa), group 2 (Paco2 between 40 and 50 mmHg), and group 3 (Paco2 higher than 50 mmHg). With the development of hypercapnia (Paco2 from 38.2 +/- 1.6 to 53.8 +/- 0.6 mmHg) and hypoxemia (Pao2 from 73.6 +/- 2.5 to 62.1 +/- 2.1 mmHg), blood pH decreased slightly (from 7.405 +/- 0.007 to 7.372 +/- 0.009). The strong ion difference ([SID]) increased in the hypercapnic group (from 39.7 +/- 1.7 to 46.2 +/- 2.9 mequiv.L-1) parallel to the increase in [HCO3-] (from 23.8 +/- 0.5 to 30.8 +/- 0.8 mequiv.L-1). The change in [SID] was quantitatively similar to the [HCO3-] change, thus reflecting a metabolic compensation of chronic respiratory acidosis. [SID] increase was mainly accounted for by changes in the [Na+]/[Cl-] ratio due to a significant decrease in plasma [Cl-]. Other ions measured as well as the weak acid buffers ([ATOT]) remained constant. From the present results, we suggest the usefulness of the physical chemical approach in the characterization of acid-base disturbances due to chronic hypercapnia when water retention or protein depletion are expected further to hypochloremia, as can be the case in severe COPD patients.
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PMID:A physical-chemical analysis of the acid-base response to chronic obstructive pulmonary disease. 902 82

Rainbow trout were experimentally infected with the causative agent of bacterial gill disease (BGD) (Flavobacterium branchiophilum) via bath challenge. All fish were cannulated with dorsal aortic catheters, had nasogastric tubes sutured in place for feeding, and were maintained individually, in plexiglass boxes with a flow-through water system. Fish were either fed, or unfed during the trial. Acute changes in blood gas, serum biochemistry and clinical parameters were monitored. By 24h post-challenge, BGD-infected trout that had been fed had significant hypoxemia, hypercapnia, increased blood ammonia, hypoosmolality, hyponatremia, hypochloremia, and increased cough and respiratory rates when compared to control levels. Unfed BGD-infected trout had similar, but less severe blood gas and clinical changes, and no electrolyte disturbances. The BGD-induced hypoxemia is likely exacerbated by increased oxygen demands brought on by feeding. It is not known what association feeding has with the development of low serum ion levels in BGD-infected trout. This is the first study to report the use of fed fish, as opposed to unfed or starved trout, in obtaining blood chemistry values from indisturbed and cannulated animals.
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PMID:Blood chemistry and acid-base balance in rainbow trout Oncorhynchus mykiss with experimentally-induced acute bacterial gill disease. 2419 47