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

The influence of lactic acidosis and of extreme hypercapnia on free radical generation and lipid peroxidation in brain tissues was studied. Cortical homogenates were prepared from the rat brain in a bicarbonate buffer and incubated for 60 min. Lipid peroxidation was evaluated by measurements of thiobarbituric acid reactive (TBAR) material and alpha-tocopherol analysis. The pH during incubations were decreased to 6.10-6.20 by either lactic acid administration or equilibration with 60% CO2 gas in paired experiments. In homogenates treated with lactic acid there was a 20-fold increase in TBAR material and the alpha-tocopherol concentration decreased to approximately 60% of control. There was only a 10-fold increase in TBAR material and no change in alpha-tocopherol concentration if acidosis was induced by CO2. These differences between lactic acidosis and hypercapnic acidosis were statistically highly significant. The results indicate that lactic acidosis has a more pronounced effect in augmenting free radical generation in brain tissues than acidosis due to an increase in CO2 tension. It is suggested that this effect of lactic acid is mediated by increased dissociation of catalytic iron from proteins of the transferrin type.
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PMID:Enhancement of iron-catalyzed free radical formation by acidosis in brain homogenates: differences in effect by lactic acid and CO2. 249 27

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

To examine whether CPB influences pulmonary vascular sensitivity to CO2, we compared the effect of slight induced hypocarbia and hypercarbia on pulmonary circulation before and after CPB in ten mechanically ventilated patients undergoing CABG. Hypocarbia was produced by increasing tidal volume slightly and hypercarbia was then induced by adding CO2 to the inspired gas mixture. In another ten patients, hypercarbia was produced after CPB by decreasing ventilator rate and the cardiopulmonary responses to hypercarbia, produced by the two methods of CO2 elevation, were compared. Slight respiratory acidosis induced by CO2 inhalation did not change PVR before CPB but effected a 50 percent increase after CPB. Hypercarbia induced by alveolar hypoventilation after CPB increased PVR by 40 percent. During the increased CO2 production after hypothermic CPB, pulmonary vasoconstriction would be expected to occur and impair right ventricular performance. Therefore, tight control of PaCO2 with appropriate adjustment of ventilatory support is mandatory.
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PMID:Pulmonary vascular resistance before and after cardiopulmonary bypass. The effect of PaCO2. 249 21

This study was undertaken to search for an alternative experimental model in the evaluation of fentanyl-induced muscle rigidity. Unanesthetized, spontaneously ventilating Sprague-Dawley rats, and rats anesthetized with either ketamine or thiopental whose ventilation was mechanically controlled, were studied. Intravenous administration of fentanyl (25, 50, or 100 micrograms/kg) caused an increase in electromyographic (EMG) activity in both unanesthetized and ketamine-anesthetized, but not in thiopental-anesthetized, animals. Muscle rigidity was more prominently manifested in the gastrocnemius muscle, when compared with the rectus abdominis muscle. Hypoxemia was exhibited during the course of rigidity by both spontaneously ventilating and ketamine-anesthetized rats, but not by thiopental-anesthetized animals. In addition, unanesthetized, spontaneously ventilating rats developed hypercarbia and respiratory acidosis. The authors suggest that, in addition to using unanesthetized animals, EMG activity in the gastrocnemius muscle of rats anesthetized with ketamine in whom ventilation is controlled may provide an alternative approach in the evaluation of fentanyl-induced muscle rigidity.
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PMID:Fentanyl-induced muscle rigidity in unanesthetized and ketamine- or thiopental-anesthetized rats. 249 24

Rats subjected to ammonium chloride-induced metabolic acidosis or respiratory acidosis caused by hypercapnia were given alkalinization therapy with either sodium bicarbonate or Carbicarb. Ammonium chloride induced dose-dependent systemic acidosis but did not affect intracellular brain pH. Hypercapnia caused dose-dependent systemic acidosis as well as decreases in intracellular brain pH. Sodium bicarbonate treatment resulted in systemic alkalinization and increases in arterial PCO2 in both acidosis models, but it caused intracellular brain acidification in rats with ammonium chloride acidosis. Carbicarb therapy resulted in systemic alkalinization without major changes in arterial PCO2 and intracellular brain alkalinization in both acidosis models. These data demonstrate that bicarbonate therapy of systemic acidosis may be associated with "paradoxical" intracellular brain acidosis, whereas Carbicarb causes both systemic and intracellular alkalinization under conditions of fixed ventilation.
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PMID:Brain pH responses to sodium bicarbonate and Carbicarb during systemic acidosis. 254 32

Twenty-seven newborn Holstein bull calves were bottle-fed 2 litres of pooled colostrum which had been stored at -20 degrees C. Blood gas analysis before feeding showed a partially compensated respiratory acidosis in most of the calves, although they all appeared to be clinically normal. Mean venous blood pH was 7.346, carbon dioxide tension (PCO2) was 57.5 mmHg (7.6 kPa), bicarbonate was 30.6 mmol/l and base excess was 3.82 mmol/l. Mean serum IgG1 increased to 8.1 g/l after feeding colostrum. Several significant positive correlations were observed between post-absorptive serum protein, IgG1, IgM, gamma-glutamyltransferase (gamma GT) and D-xylose. Calves with either low serum albumin, high serum CK or low serum gamma GT before feeding tended to have less absorption of colostral protein. It was concluded that reduced absorption of IgG1 from colostrum is associated with hypercapnia in apparently healthy newborn calves.
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PMID:Relationships between acid-base balance, serum composition and colostrum absorption in newborn calves. 256 18

Hypoxia and hypercapnic acidosis have been shown to have a negative inotropic effect on diaphragmatic contractility. The effect of combined hypercapnia and hypoxia was studied in vitro using hamster diaphragm strips. A 12% CO2, 21% O2, and 67% N2 gas mixture was used to produce hypoxic, hypercapnic acidosis. Force-frequency curves were generated using twitches and maximal tetanic contractions produced by stimulating with 0.2-ms pulses at 10 to 120 Hz for 300 to 500 ms. Moderate fatigue was then induced by repeated submaximal contractions (25 Hz, 160 ms, at the rate of 1/s for 45 contractions). Muscle strips exposed to hypoxic, hypercapnic acidosis had a decreased force response at all frequencies. The decrease in force was not different from that seen with hypoxia alone but was significantly worse than with hypercapnia alone. In the combined hypercapnic, hypoxia solution, tension produced by stimulating at 25 Hz for 160 ms was decreased to 52 +/- 11% of control (p less than 0.001). For these submaximal contractions, hypercapnic acidosis had a greater negative inotropic effect than did hypoxia alone. With repeated contractions, tension declined at a faster rate than in control, hypoxia alone, or hypercapnia alone. In the combined hypoxic, hypercapnic solution, the time constant of relaxation (tau) was increased prior to the start of the fatigue run compared to the control (tau = 35 +/- 6 versus 45 +/- 5 ms; p less than 0.001), and the tau increased at a faster rate than in control. These studies suggest that hypoxic, hypercapnic acidosis has a greater detrimental effect on the muscle than either abnormality alone and makes the muscle more susceptible to fatigue.
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PMID:Hypoxic, hypercapnic acidosis decreases tension and increases fatigue in hamster diaphragm muscle in vitro. 265 1

Respiratory insufficiency of any cause has significant effects on the nervous system. Headache, mental status changes, papilledema, and numerous motor abnormalities including asterixis are commonly seen. Abnormalities in ventilation and gas exchange result in hypoxia, hypercapnia, and respiratory acidosis, and these, in turn, interfere with cerebral metabolism, increase CBF, and may raise intracranial pressure. Chronic respiratory insufficiency can persist for many months with minimal neurologic symptoms, as numerous compensatory mechanisms, particularly renal, may take effect. Treatment includes restoring adequate ventilation and improving gas exchange and may require tracheal intubation and assisted ventilation. Supplemental oxygen therapy should be carefully monitored, as high rates of flow may suppress the hypoxic drive for respiration and lead to significant carbon dioxide retention. The sleep apnea syndromes are a group of disorders in which abnormal respiratory patterns during sleep result in hypercapnia and hypoxemia. Intermittent obstruction of the upper airway and abnormalities of brainstem respiratory centers cause frequent nocturnal awakenings and apneas in these patients. Treatments vary and include weight loss in obese subjects, respiratory stimulants, tracheostomy, and diaphragmatic pacing. Rapid ascent to high altitudes may result in headache, changes in mental status, papilledema, and other neurologic symptoms in certain individuals: a syndrome known as high-altitude sickness. Hypoxia leading to cerebral edema, nocturnal periodic breathing, and hypobaria produces neurologic symptoms in these individuals. Acetazolamide and dexamethasone may be effective in minimizing symptoms of this disorder. Sustained hyperventilation produces acral and circumoral paresthesias and lightheadedness in anxious individuals and can be maintained by relatively normal ventilatory patterns once established. These symptoms are due to hypophosphatemia and respiratory alkalosis, the latter reducing CBF and causing localized tissue hypoxia. Rebreathing into a paper bag at the first awareness of symptoms is the most effective form of treatment.
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PMID:Neurologic manifestations of pulmonary disease. 267 37

A case is reported of acute respiratory failure occurring during upper abdominal surgery in a patient not previously known to have chronic respiratory failure. Preoperatively, this 68 year old patient presented with mild obesity, slight effort dyspnoea and paralysis of the right hemidiaphragm, a sequela of polytrauma she suffered the year before. Respiratory tests were not considered useful with regard to the results of clinical examination. Moreover, she had already several previous general anaesthetics without any problems. A thoracic epidural anaesthesia was performed with a mixture of 150 mg lidocaine, 37.5 mg bupivacaine with adrenaline and 100 micrograms fentanyl, injected in the T8-T9 epidural space via a catheter. Ten minutes after the starting of surgery, the patient became agitated and complained of difficulty in breathing. Blood gas analysis showed hypercapnia, with respiratory acidosis (Pao2: 28.19 kPa; Paco2: 9.2 kPa; pH 7.273). Clinical examination revealed a bilateral Horner syndrome (T1-T4 sympathetic blockade). The patient was intubated and ventilated after adequate sedation. She was extubated 3 h 30 min after the initial epidural injection. Epidural analgesia was maintained during 72 h, with 0.1% bupivacaine, with no recurrence of respiratory failure.
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PMID:[Transient acute respiratory failure and thoracic epidural anesthesia]. 273 73

The involvement of catecholamines in regulating arterial oxygen content (CaO2) during hypercapnic acidosis in rainbow trout (Salmo gairdneri) was investigated by comparing physiological responses during acute normoxic hypercapnia (a condition in which plasma epinephrine is elevated) and acute hyperoxic hypercapnia (a condition in which plasma epinephrine is not elevated). Red blood cell pH (rbc pH) was maintained significantly higher in the normoxic hypercapnic fish despite similar reductions in whole blood pH (pHe) in both groups. Elevation of rbc pH in the normoxic hypercapnic fish was abolished by pre-treatment with the beta-adrenoceptor antagonist, propranolol, whereas injection of epinephrine into hyperoxic hypercapnic fish significantly raised rbc pH. Arterial blood oxygen carrying capacity increased only in the normoxic hypercapnic fish due to significant increases in blood haemoglobin (Hb) levels. The ability of trout to elevate blood Hb was abolished by pre-treatment with the alpha-adrenoceptor antagonist, phentolamine. Injections of epinephrine into normocapnic fish caused increases in blood Hb and concomitant decreases in spleen wet weight and Hb content. Adrenergic elevation of blood Hb was not observed in splenectomized fish. CaO2, although depressed during normoxic hypercapnia, was indeed regulated when compared to CaO2 values predicted from the in vitro Root effect. Pre-treatment with phentolamine, but not propranolol, abolished the ability of trout to regulate CaO2.
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PMID:The role of catecholamines in regulating arterial oxygen content during acute hypercapnic acidosis in rainbow trout (Salmo gairdneri). 278 Nov 71


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