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)

Hypercapnia due to respiratory failure can be more severe when accompanied by coexistent metabolic alkalosis. We therefore tested the hypothesis that hydrochloric acid (HCl) infusion could improve PaCO2 in 15 critically ill patients admitted with mixed respiratory acidosis and metabolic alkalosis, and a pH of between 7.35 and 7.45. HCl was infused at a constant rate of 25 mmol/h until the bicarbonate concentration decreased less than 26 mmol/L, or until the pH decreased less than 7.35 (initial pH greater than 7.40) or 7.30 (initial pH less than 7.40). Administration of 170 +/- 53 mmol of HCl decreased the bicarbonate concentration from 34 +/- 3 to 25 +/- 2 mmol/L (p less than .001), the pH from 7.41 +/- 0.03 to 7.33 +/- 0.02 (p less than .001), and the PaCO2 from 54 +/- 8 to 48 +/- 8 torr (p less than .001). Postinfusion PaCO2 could be predicted accurately from the initial status of the patients (r = .95, p less than .001) except in one patient with fixed hypercapnia. PaCO2 increased from 77 +/- 19 to 94 +/- 24 torr (p less than .001) and PaO2/PAO2 increased from 59 +/- 17 to 66 +/- 17% (p less than .001). The effects of HCl were still present 12 h after the end of the infusion. No complications related to the acid infusion were noted. These results indicate that, even in the absence of alkalemia, active correction of metabolic alkalosis by HCl infusion can improve CO2 and oxygen exchange in critically ill patients with mixed respiratory acidosis and metabolic alkalosis.
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PMID:Hydrochloric acid infusion for treatment of metabolic alkalosis associated with respiratory acidosis. 249 54

Arterialized blood gases were analyzed in 143 patients with Duchenne muscular dystrophy (DMD) to assess the relationship between forced vital capacity (FVC) and hypercapnia. The majority of patients studied had PaCO2 values in the low or normal range. Only six older patients had hypercapnia (PaCO2 greater than or equal to 45 mm Hg), and all these patients had FVC values less than or equal to 40% predicted. We conclude that hypercapnic respiratory failure occurs as a late preterminal event in DMD.
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PMID:Hypercapnia in relation to pulmonary function in Duchenne muscular dystrophy. 249 32

The ventilatory response to hypoxia and the ventilatory and mouth occlusion pressure response to hypercapnia was measured in 13 subjects who had previously developed respiratory failure or respiratory arrest during an acute asthma attack. In 11 of 12 subjects tested there was a normal response to hypercapnia. Six of the 13 subjects had an impaired response to hypoxia. Impaired hypoxic responsiveness may contribute to the early onset of hypercapnic respiratory failure during acute severe asthma.
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PMID:Ventilatory responses to hypoxia and hypercapnia in asthmatics with previous respiratory failure. 259 90

The effects of chronic respiratory failure (hypoxia and hypercapnia) on the contractile properties of cardiac muscle are not established. A study was performed of the isometric contractile properties of isolated papillary muscle removed from rats exposed in a normobaric environmental chamber to 28 days of hypoxia (fractional inspired oxygen (FIO2) 10%, fractional inspired carbon dioxide (FICO2) less than 1%), hypercapnia (FIO2 21%, FICO2 5%), and hypoxia with hypercapnia (FIO2 10%, FICO2 5%). Rats exposed to both hypoxia and hypoxia with hypercapnia developed selective right ventricular hypertrophy. Exposure to hypercapnia alone did not alter right ventricular weight. No change in right ventricular papillary muscle contractility per unit muscle mass was observed as measured by maximum active tension, maximum rate of rise or fall of tension, or time to peak tension. Rat cardiac muscle adapts successfully to the altered acid-base environment and increased work load associated with prolonged exposure to hypoxia and mild hypercapnia.
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PMID:Contractility of papillary muscle from rats exposed to 28 days of hypoxia, hypercapnia, and hypoxia with hypercapnia. 259 23

A female case of Japanese summer-type hypersensitivity pneumonitis who was a smoker developed in chronic respiratory failure several years later. Biopsy specimen on first admission showed findings of granulomatous bronchioloalveolitis distributed in the center of secondary lobules. Pulmonary function studies demonstrated restrictive disease with high RV% and low airway conductance. In spite of steroid therapy, dyspnea persisted and the same symptoms were found on next summer. Six years later symptoms of chronic respiratory failure and cor pulmonale developed. Chest X-Ray showed dilated pulmonary artery, cardiomegaly and overinflation without apparent fibrosis. Hypoxemia and hypercapnia were also seen on blood gas analysis. Pulmonary function was unchanged compared to the findings on first admission. Since then long term oxygen therapy was started. It was thought that irreversible small airway disease caused by hypersensitivity pneumonitis was attributable to cor pulmonale and chronic respiratory failure because of her smoking habit and long period of exposure to antigen. As a patient with summer type hypersensitivity pneumonitis always has a possibility of chronic disease developing after long term exposure to antigen, such as a farmer's lung, the cessation of exposure to antigen by complete cleaning up of the patient's environment or moving out were considered to be important.
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PMID:[A case of summer type hypersensitivity pneumonitis resulting in chronic respiratory failure and cor pulmonale]. 262 12

In 75 COPD patients with (group I) or without (group II) cor Pulmonale, we measured plasma renin activity (PRA), angiotensin I and II (ATI and ATII), and aldosterone (Ald) by RIA. We found that the levels of PRA, ATI, ATII, Ald in group I are all higher than those in 25 healthy subjects and in group II (P less than 0.05, P less than 0.001), The PRA, ATI, ATII, Ald also increased in patients with respiratory failure, especially accompanied by hypercapnia, and in patients with hyponatrium. In addition, the strong correlation was found between PaO2, PaCO2 and RAAS activation. These findings suggest that the activation of RAAS increased significantly in COPD patients with cor pulmonale or with respiratory failure, and the changes may involve in the pathophysiologic process in COPD patients.
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PMID:[The renin-angiotensin-aldosterone system changes in chronic obstructive pulmonary disease]. 263 30

Renal function was assessed in 89 patients with advanced chronic obstructive pulmonary disease and chronic cor pulmonale, 62 of them had respiratory failure, 18 health aged served as control. The results showed that the creatinine clearance and the free water clearance were decreased in 82.3% and 69.5% of patients with respiratory failure respectively. The renal function was impaired in case of hypoxia, PaO2 less than or equal to 6.0 kPa (45 mmHg), mean 5.33 kPa (40 mmHg). Hypercapnia was one of the most important factors that effected the renal function. There was a clinical threshold which effected the renal function, i.e. PaCO2 equals more than 8.67 kPa (65 mmHg). Renal function was greatly impaired if hypercapnia and hypoxia exist at the same time. The impairment of renal function was further marked when right heart failure and acidosis developed. The causes and effects of the abnormality of renal function were preliminarily discussed.
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PMID:[Influence of acute respiratory failure on renal function in advanced chronic obstructive pulmonary disease and chronic cor pulmonale]. 263 31

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

Plasma ADH, PA and PRA in patients with respiratory failure (RF) were studied. RF patients were divided into 4 groups, i.e. acute RF (ARF) and chronic RF (CRF), with or without hypercapnia. The levels of these hormones were significantly higher in RF than those in control subjects, moreover, they were markedly elevated in ARF than those in CRF. In multiple regression analysis, ADH correlated with PaO2, pH and PRA in RF patients, but correlated with serum osmolality in control subjects. It was considered that ADH in RF was affected by the direct effect of blood gases and circulatory disorder. The mechanism of elevated PA and PRA in RF probably was mediated through restriction of intake of water and Na, reduction of renal blood flow and decreased ACE often occurred in RF. Abnormally elevated hormones are more often recognized in edematous patients than in nonedematous patients. It was suggested that many patients with RF develop heart failure or edema due to hormonal abnormalities.
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PMID:[ADH (anti-diuretic hormone), aldosterone (PA) and renin activity (PRA) in patients with respiratory failure]. 269 88

A female neonate who had been diagnosed as having congenital diaphragmatic hernia by ultrasonography was delivered by cesarean section. After the hernia was repaired, she developed hypoxemia and hypercapnia, probably due to persistent fetal circulation (PFC). Neither conventional mechanical ventilation (CMV) nor manual ventilation improved the respiratory status. High-frequency oscillation (HFO) successfully improved pulmonary gas exchange, but we failed to wean the patient from HFO by using intermittent HFO. The patient was again placed on CMV for weaning and was extubated on the 12th ICU day. We conclude that HFO can be an alternative respiratory modality in patients with respiratory failure due to PFC after the repair of congenital diaphragmatic hernia.
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PMID:High-frequency oscillation for persistent fetal circulation after repair of congenital diaphragmatic hernia. 270 45


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