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

This study was designed to establish the relationship between urinary pCO2 and systemic blood pCO2 during acute hypercapnia and to investigate the significance of this relationship to collecting duct hydrogen ion (H+) secretion when the urine is acid and when it is highly alkaline. In rats excreting a highly alkaline urine, an acute increase in blood pCO2 (from 42 +/- 0.8 to 87 +/- 0.8 mmHg) resulted in a significant fall in urine minus blood (U-B) pCO2 (from 31 +/- 2.0 to 16 +/- 4.2 mmHg, P less than 0.005), a finding which could be interpreted to indicate inhibition of collecting duct H+ secretion by hypercapnia. The urinary pCO2 of rats with hypercapnia, unlike that of normocapnic controls, was significantly lower than that of blood when the urine was acid (58 +/- 6.3 and 86 +/- 1.7 mmHg, P less than 0.001) and when it was alkalinized in the face of accelerated carbonic acid dehydration by infusion of carbonic anhydrase (78 +/- 2.7 and 87 +/- 1.8 mmHg, P less than 0.02). The finding of a urinary pCO2 lower than systemic blood pCO2 during hypercapnia suggested that the urine pCO2 prevailing before bicarbonate loading should be known and the blood pCO2 kept constant to evaluate collecting duct H+ secretion using the urinary pCO2 technique. In experiments performed under these conditions, sodium bicarbonate infusion resulted in an increment in urinary pCO2 (i.e., a delta pCO2) which was comparable in hypercapnic and normocapnic rats (40 +/- 7.2 and 42 +/- 4.6 mmHg, respectively) that were alkalemic (blood pH 7.53 +/- 0.02 and 7.69 +/- 0.01, respectively). The U-B pCO2, however, was again lower in hypercapnic than in normocapnic rats (15 +/- 4.0 and 39 +/- 2.5 mmHg, respectively, P less than 0.001). In hypercapnic rats in which blood pH during bicarbonate infusion was not allowed to become alkalemic (7.38 +/- 0.01), the delta pCO2 was higher than that of normocapnic rats which were alkalemic (70 +/- 5.6 and 42 +/- 4.6 mmHg, respectively, P less than 0.005) while the U-B pCO2 was about the same (39 +/- 3.7 and 39 +/- 2.5 mmHg). We further examined urine pCO2 generation by measuring the difference between the urine pCO2 of a highly alkaline urine not containing carbonic anhydrase and that of an equally alkaline urine containing this enzyme. Carbonic anhydrase infusion to hypercapnic rats that were not alkalemic resulted in a fall in urine pCO(2) (from 122+/-5.7 to 77+/-2.2 mmHg) which was greater (P <0.02) than that seen in alkalemic normocapnic controls (from 73+/- 1.9 to 43+/-1.3 mmHg) with a comparable urine bicarbonate concentration and urine nonbicarbonate buffer capacity. CO(2) generation, therefore, from collecting dust H(+) secretion and titration of bicarbonate, was higher in hypercapnic rats that in normocapnic controls. We conclude that in rats with actue hypercapnia, the U-B p(CO(2)) achieved during bicarbonate loading greatly underestimates collecting duct H(+) secretion because it is artificially influenced by systemic blood pCO(2). the deltapCO(2) is a better qualitative index of collecting duct H+ secretion that the U-B pCO(2), because it is not artificially influenced by systemic blood pCO(2) and it takes into account the urine PCO(2) prevailing before bicarbonate loading.
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PMID:Relationship of urinary and blood carbon dioxide tension during hypercapnia in the rat. Its significance in the evaluation of collecting duct hydrogen ion secretion. 298 5

Acetazolamide, an inhibitor of carbonic anhydrase, which catalyzes hydration/dehydration of carbon dioxide, has been used for correction of metabolic alkalosis in patients with chronic obstructive pulmonary disease (COPD). Animal experiments have shown that the gradient between tissue and the alveolar CO2 tension increases after inhibition of carbonic anhydrase, suggesting retention of CO2. In order to determine the true degree of carbon dioxide retention after total inhibition of carbonic anhydrase, 10 patients with COPD and pronounced metabolic alkalosis (base excess above 6) under controlled mechanical ventilation were studied. The study showed that there was a statistically significant increase in tissue PCO2 and a temporary decrease in pulmonary carbon dioxide excretion. Furthermore, it was found that PaO2 and PVO2 increased significantly after inhibition of carbonic anhydrase, which could, at least partly, explain the improvement seen in patients with COPD and metabolic alkalosis after treatment with acetazolamide.
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PMID:Carbon dioxide elimination after acetazolamide in patients with chronic obstructive pulmonary disease and metabolic alkalosis. 641 Jun 68

Recent studies and reviews continue to report a high mortality associated with the acute respiratory distress syndrome (ARDS), which involves a severe inflammatory reaction within the whole lung that is frequently associated with multiple-organ failure. Important factors contributing to the poor results in severe ARDS are the aggressive procedures required to maintain sufficient arterial oxygenation, such as mechanical ventilation with high inspiratory pressures and high inspired oxygen concentrations (FiO2) which themselves contribute to the progression of the disease. As no specific therapy that reduces or prevents the general inflammatory reaction is known, current therapy is limited to procedures that minimize peak inspiratory pressures and FiO2. Therefore, pressure- and volume-limited ventilation modes with positive end-expiratory pressure, controlled hypercapnia, differential lung ventilation when appropriate, positioning (particularly prone), and aggressive dehydration are used. Should these procedures fail to improve arterial gas exchange, the patients may be additionally treated by veno-venous extracorporeal gas exchange. To reduce the risk of severe haemorrhagic complications due to high levels of systemic heparinization, systems internally coated with covalently bound heparin, which allow a lower level of systemic anticoagulation, should be used. From April 1989 to August 1993, 89 patients were transferred to our intensive care unit for treatment of severe ARDS; 52 were treated by combining the described conventional methods without artificial gas exchange (survival rate 88%) and 37 additionally underwent artificial gas exchange (survival rate 57%). The overall survival rate was 75%. On the basis of these experiences, we conclude that this step-by-step approach may improve survival in patients with severe ARDS.
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PMID:[Therapy of ARDS. 1. Current therapeutic strategy including extracorporeal gas exchange]. 804 58

Conventional treatment of the adult respiratory distress syndrome (ARDS) includes pressure-limited ventilation, permissive hypercapnia, posture changes, aggressive dehydration, selective lung ventilation, and extracorporeal gas exchange. New strategies such as nitric oxide inhalation, the implantation of an intravenous membrane oxygenator (IVOX), and surfactant replacement are currently under evaluation. Nitric oxide (NO) is an important endothelium-derived relaxing factor that is rapidly inactivated by binding to haemoglobin. Inhaling this substance has been shown to induce selective vasodilatation of ventilated lung regions. Thus, inhaled NO reduces pulmonary hypertension, increases right heart ejection fraction, and improves arterial oxygenation by redistributing blood flow away from areas with intrapulmonary shunts to areas with a normal ventilation/perfusion ratio. Dose-response analysis has revealed that effective doses for improvement of oxygenation are lower than for reduction of mean pulmonary artery pressure. The use of a miniaturised membrane lung, IVOX, for intracaval oxygen and carbon dioxide exchange is a new approach to augment gas exchange. The IVOX is inserted via an introducer into the femoral vein and is designed for placement in the full length of the vena cava. Initial experiences with this device show that the currently used prototype provides a maximum of one-third of basal gas exchange. Therefore, a more efficient device will be needed to significantly reduce high inspired oxygen concentrations and airway pressures. Moreover, there exists evidence that IVOX causes caval obstruction. Lung surfactant recovered in BAL from patients with ARDS demonstrates that fractional contents of phosphatidylcholine and phosphatidylglycerol are reduced, and that the total concentration of apoproteins is decreased. Furthermore, the surfactant surface tension-lowering activity is abnormal. Thus, administration of exogenous surfactant may have therapeutic benefits. However, the optimal surfactant preparation, the optimal amount required to restore lung surfactant activity, and the optimal method to deliver it to patients with ARDS are unknown and currently under evaluation.
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PMID:[Therapy of ARDS. 2. New management methods--first clinical experiences]. 804 71

Despite more than 25 years of extensive research, the mortality of ARDS patients remains high. The inflammatory process within the lung and the associated gas exchange disturbances require an aggressive ventilatory regimen, which itself may harm the lung. Therapeutic measures which are used to reduce iatrogenic damage to the lung are pressure controlled mechanical ventilation in combination with PEEP and permissive hypercapnia, dehydration and extracorporeal gas exchange. At present, new strategies such as intratracheal instillation of surfactant, partial liquid ventilation and inhalation of nitric oxide (NO) are being evaluated. Surfactant reduces the surface tension, forming a monomolecular layer at the air/tissue interface. It thereby decreases the forces necessary to expand the alveoli and prevents alveoli with small diameter from collapsing. In ARDS, a disturbance of surfactant synthesis, function and re-uptake is the rationale for treatment with exogenous surfactant. Initial clinical results suggest a limited positive effect independently of the surfactant preparation used, the dose and the application mode. Experience with partial liquid ventilation with perfluorocarbons in ARDS has also been reported. Perfluorocarbons are liquids with a high binding capacity for oxygen and carbon dioxide. During normal mechanical ventilation with gas, repetitive doses of perfluorocarbons are instilled into the lungs up to a volume equal to the functional residual capacity. The liquid is pushed into collapsed alveoli and keeps them open by reducing the surface tension. First clinical studies have demonstrated the possible improvement in pulmonary gas exchange. In ARDS, inhalation of NO may cause a predominantly selective vasodilation in blood vessels of ventilated lung regions, resulting in an increase in PaO2 and a decrease in pulmonary artery pressure. The effect of NO on the pulmonary vasculature also induces a reduction in right ventricular afterload and also in pulmonary capillary pressure, which may lead to a faster resolution of pulmonary edema. However, in spite of the promising results of these new strategies, further studies are needed to evaluate their influence on morbidity and mortality.
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PMID:[Perspectives in mechanical ventilation in ARDS]. 928 30

The electrometric [Delta]pH method and an in vitro radioisotopic HCO3- dehydration assay were used to demonstrate the presence of true extracellular carbonic anhydrase (CA) activity in the blood of the Pacific spiny dogfish Squalus acanthias. An extracorporeal circulation and stopflow technique were then used to characterise the acidbase disequilibrium in the arterial (postbranchial) blood. During the stopflow period, arterial pH (pHa) decreased by 0.028±0.003 units (mean ± s.e.m., N=27), in contrast to the increase in pHa of 0.029±0.006 units (mean ± s.e.m., N=6) observed in seawater-acclimated rainbow trout Oncorhynchus mykiss under similar conditions. The negative disequilibrium in dogfish blood was abolished by the addition of bovine CA to the circulation, while inhibition by benzolamide of extracellular and gill membrane-bound CA activities reversed the direction of the acidbase disequilibrium such that pHa increased by 0.059±0.016 units (mean ± s.e.m., N=6) during the stopflow period. When the CA activity of red blood cells (rbcs) was additionally inhibited using acetazolamide, the magnitude of the negative disequilibrium was increased significantly to -0.045±0.007 units (mean ± s.e.m., N=6). Blockage of the rbc Cl-/HCO3- exchanger using 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS) also increased the magnitude of the negative disequilibrium, in this case to -0.089±0.008 units (mean ± s.e.m., N=6). Exposure of dogfish to hypercapnia had no effect on the disequilibrium, whereas the disequilibrium was significantly larger under hypoxic conditions, at -0.049±0.008 units (mean ± s.e.m., N=6). The results are interpreted within a framework in which the absence of a positive CO2 excretion disequilibrium in the arterial blood of the spiny dogfish is attributed to the membrane-bound and extracellular CA activities. The negative disequilibrium may arise from the continuation of Cl-/HCO3- exchange in the postbranchial blood and/or the hydration of CO2 added to the plasma postbranchially. Two possible sources of this CO2 are discussed; rbc CO2 production or the admixture of blood having 'low' and 'high' CO2 tensions, i.e. the mixing of postbranchial blood with blood which has bypassed the respiratory exchange surface.
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PMID:Extracellular carbonic anhydrase and an acid-base disequilibrium in the blood of the dogfish Squalus acanthias 931 77

Metabolic complications from overfeeding critically ill patients are serious and sometimes fatal. Nutrition care is best provided through repeated evaluation of patients' responses to feeding. Nutrition support may need to be modified over time to maintain metabolic stability and promote recovery. This article describes the etiology of 10 metabolic complications of overfeeding. Guidelines for recommending macronutrients are discussed, as are factors that could increase the risk of overfeeding. Patients who are very small, very large, or very old are particularly vulnerable to overfeeding. Overfeeding protein has led to azotemia, hypertonic dehydration, and metabolic acidosis. Excessive carbohydrate infusion has resulted in hyperglycemia, hypertriglyceridemia, and hepatic steatosis. High-fat infusions have caused hypertriglyceridemia and fat-overload syndrome. Hypercapnia and refeeding syndrome have also been caused by aggressive overfeeding. Dietitians can prevent or curtail the metabolic complications of overfeeding by identifying patients at risk, providing adequate assessment, coordinating interdisciplinary care plans, and delivering timely and appropriate monitoring and intervention. Dietitians need to document complications, interventions, and the outcomes of their clinical care to evaluate the appropriateness of existing nutrition guidelines.
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PMID:Overfeeding macronutrients to critically ill adults: metabolic complications. 966 22

Despite more than 25 years of extensive research the mortality of ARDS patients remains high. Besides the often deleterious course of the underlying disease, another reason for this high mortality lies in the aggressive ventilatory regimen which is required to maintain arterial blood gases in a more or less normal range. Therapeutic methods which are used to reduce iatrogenic damage to the lungs are pressure controlled ventilation with permissive hypercapnia, differential lung ventilation, positioning therapy, dehydration, and extracorporeal gas exchange with membrane lungs. Nevertheless, many of these patients still die following hypoxaemia or multiple organ failure. Therefore, the need remains to develop new therapeutic strategies and to investigate their influence on the morbidity and mortality of this life-threatening disease. First experiences with nitric oxide (NO) inhalation, intravenous application of antioxidants, intratracheal instillation of surfactant, tracheal gas insufflation and combined fluid/gas ventilation with perfluorocarbon are presented. All these new methods have proved their efficacy, at least in animal studies, however, they should still be regarded as experimental.
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PMID:Recent advances in the treatment of ARDS. 1015 Aug 1

Although midazolam has been proposed for the treatment of a variety of conditions such as anxiety, dyspnoea, hiccups and status epilepticus, terminal agitation is the only condition where its use is based on a reasonably large number of published clinical studies. A causal approach is generally recommended. Whenever possible, the aetiological condition (pain, fever, constipation, etc.) should be corrected. Such general measures as ensuring a peaceful, familiar environment, and the use of a night light, fluid therapy to counteract dehydration, and antipyretics for fever are beneficial. When symptomatic treatment is needed, drugs with little anticholinergic effect are to be recommended. The use of benzodiazepines as single drug treatment may exacerbate the condition. Haloperidol or risperidone (which has fewer side effects) are recommended. If the agitation is marked, a common strategy is to add lorazepam. Chlormethiazole is an alternative. Subcutaneous midazolam should be reserved for refractory cases. Attention should be paid to dosage, reduced doses being given to the elderly, patients on opioid medication, and patients with impaired liver or renal function. Overdosage may induce deep sedation, and result in carbon dioxide retention and subsequently heart failure and pulmonary oedema which may be fatal.
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PMID:[Midazolam (Dormicum) in terminal anxiety and agitation. The last choice alternative in palliative care]. 1035 70

Red crabs, Gecarcoidea natalis, exhibit seasonal activity patterns: low activity during the dry season when they shelter in burrows to avoid dehydration, and high activity during the wet season. Red crabs were examined in situ in the rainforest of Christmas Island to determine if there were underlying seasonal differences in the capacity for exercise and associated metabolism. During both seasons, free-ranging (FR) crabs engaged in their normal activities and, together with crabs induced to exercise for 5 min, were sampled for haemolymph and muscle tissue. Respiratory gases in the haemolymph and key metabolites were measured to assess differences in metabolic status of FR and exercised crabs. Actively foraging FR crabs during the wet season exhibited a relative haemolymph hypoxia (2.9 kPa) and accumulated an extra 3 mmol. litre(-1) of CO(2) compared to the relatively inactive FR crabs during the dry season. Wet-season crabs appeared to be in a state of relative respiratory acidosis compared to dry-season animals. This hypercapnia may arise as a consequence of a relative hypoventilation in animals with a relatively higher metabolic rate during the wet season. Oxygenation of pulmonary and arterial haemolymph was similar and remained high after 5 min of exercise, indicating that the gills and lungs functioned similarly in gas exchange in both FR and exercised crabs. During exercise, venous O(2) reserves decreased and red crabs experienced a mixed respiratory/metabolic acidosis. Similar changes, after 5 min of enforced exercise, in metabolite concentrations, pH and respiratory gas status in the haemolymph during both sampling seasons suggest that the crabs maintain similar capacity to increase exercise during the wet and the dry seasons, despite the differences in underlying physiological status. This is important since after prolonged inactivity during the dry season, with the arrival of moonsoonal rains, red crabs must engage in their annual breeding migration.
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PMID:Respiratory gas transport, metabolic status, and locomotor capacity of the Christmas Island red crab Gecarcoidea natalis assessed in the field with respect to dichotomous seasonal activity levels. 1076 64

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