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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanisms of oedema in cor pulmonale remain unexplained. On the basis of a small number of studies, cor pulmonale is not caused by cardiac muscle failure, at least in early oedematous phases. Progressive and persistent elevation of pulmonary vascular resistance may exceed the pumping capacity of the right ventricle in later stages. Alternative explanations for the sharp fall in renal blood flow as oedema appears should be sought. The renin-angiotensin-aldosterone system seems causally related to oedema. The curious position of hypercapnia remains an enigma. Surprisingly few studies of hypercapnia, renal blood flow and renal hormones are reported. Redistribution of body water from intracellular to the extracellular space may be in part due to the need to buffer extracellular respiratory acidosis caused by hypercapnia. It provides an explanation for one form of hypercapnic oedema. Cyclical loss and gain of tissue mass seems more evident in cor pulmonale than ischaemic or valvular heart failure.
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PMID:Oedema in cor pulmonale. 703 67

It is well known that the alternations on humoral homeostasis such as a decrease of pH, an elevation of PaCO2 and changes of electrolytes have been detected during respiratory acidosis. The author is of the opinion that the renin-angiotensin-aldosterone system might be related to these changes during respiratory acidosis. Recently, Fujii and Morita have reported that an increase in plasma renin activity appeared during acute respiratory acidosis. These reports prompted me to question whether the renin-angiotensin-aldosterone system was related to the pathophysiological evidence concerning the respiratory acidosis. It is generally accepted that plasma aldosterone concentration is controlled by (1) the renin-angiotensin system, (2) ACTH and (3) serum potassium. Therefore, the purpose of this experiment was to investigate the roles of the renin-angiotensin system and electrolyte metabolism on plasma aldosterone concentration during acute respiratory acidosis. I initiated acute respiratory acidosis with 10% CO2 inhalation in healthy mongrel dogs, and then plasma aldosterone concentration, plasma renin activity, electrolytes and cardiorenal hemodynamics were measured. The results were as follows: 1. The increase of plasma aldosterone concentration was delayed and blurred, in contrast with a significant increase of plasma renin activity, during the acute respiratory acidosis, due to delayed time course of angiotensin II stimulation and also the expected changes in the concentration of angiotensin II receptors on the zona glomerulosa in the adrenal cortex. 2. There was a possibility that the increase in the reabsorption of sodium and water in the proximal tubules, and the increase of ADH secretion during the acute respiratory acidosis, could be related to a decrease in excreted sodium and potassium as well as urine volume. These results suggest that the changes of plasma aldosterone concentration may be affected partially by renin-angiotensin system but not by serum potassium, and plasma aldosterone should be a minimal determinant on the electrolyte metabolism during respiratory acidosis with 10% CO2 inhalation.
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PMID:[The changes on plasma aldosterone concentration during acute respiratory acidosis in dogs. The relationship to renin-angiotensin system and electrolyte metabolism (author's transl)]. 706 60

Effects of acute-base disturbances on fractional delivery of potassium to the juxtamedullary end-descending limb were examined by micropuncture in the rat to test the hypothesis that potassium is reabsorbed from the collecting duct and is secreted in juxtamedullary pars recta or descending limb in the renal medulla. In metabolic acidosis, fractional potassium delivery was only slightly reduced compared with control values and was a function of potassium excretion, as the hypothesis predicts. Fractional potassium delivery was sharply reduced both in respiratory acidosis and metabolic alkalosis and was no longer a function of potassium excretion. Although seemingly inconsistent with the recycling hypothesis, the latter finding may be reconciled by the following observations. In respiratory acidosis, vasa recta blood flow nearly doubled, which would lead to vascular washout of interstitial potassium. In metabolic alkalosis, flow rate in the pars recta or descending limb was reduced by 28%, which would limit transepithelial potassium addition. The results indicate complex effects of acid-base disturbances on fractional potassium delivery to the end-descending limb, which can be unified by postulated changes in transepithelial potassium concentration differences across the juxtamedullary pars recta or descending limb. An unexpected observation emerged--fractional delivery of water to the end-descending limb declined as a function of plasma bicarbonate concentration when all groups were combined.
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PMID:Effects of acute acid-base disturbances on K+ delivery to the juxtamedullary end-descending limb. 711 18

Shifts of Na+, K+, Cl- and HCO3- between the cells and extracellular fluid of nephrectomized mammals in acute response to hypercapnia and to HCl or KCl infusion are simulated in steady state models involving just intracellular buffering and a simply defined interdependence of ionic gradients. Such models integrate diverse kinds of data and suggest new interpretations. In respiratory acidosis K+, HCO3- and water leave some cells and move both to where chemical buffering is least (ECF and other cells) and to cells that regulate pH particularly well by active transport. Buffering by erythrocytes is important, but the effects of distinguishing erythrocytes from other cells in a model is mainly just to emphasize Cl- movements. Effects of departures from the mammalian norm of body composition are explored.
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PMID:The role of intracellular buffers in acid-base disturbances: mathematical modelling. 736 Oct 19

Phosphorus plays an essential role in cellular metabolism, especially in the oxidative phosphorylation process and in the synthesis of 2-3 DPG and membrane phospholipids. Moreover phosphorus is necessary as a buffer, mainly when the organism's principal buffer, the H2CO3/HCO3- system, is working at maximal rate. The authors describe a case of severe hypophosphatemia in a ICU patient with a mixed disorder of the acid-base balance. C.P., a woman, aged 71, obese (IBW 145%), at admission in ICU showed increasing dyspnea, hypoxemia and acidosis. Besides alkaline drugs a Venturi mask with FiO2 = 0.3 alternated to CPAP cycles (7 cm H2O) with facial mask applied. Bading on CVP, MAP and ABG results, a pharmacologic therapy with enoximone, furosemide, bronchodilators, mucolytics, antacids, antibiotics and inotropics was performed. TPN with only essential amino acids was performed, in order to activate lipolysis and ketogenesis; but the ABG showed over again mixed disorder of acid-base balance (metabolic and chronic respiratory acidosis), only partially leading to ketogenesis. The reduction of the hematic HCO3-, without changes of PaCO2, was justified by the blood lactic acid of 6.2 mmol/L. And what about blood lactic acid increase? During patient hospitalization, the hematic phosphorus had decreased to, 0.8 mg/dl. Diuretic therapy together with acidosis tamponage, and reduced phosphorus feed had been responsible of severe hypo-phosphatemia. Therapy adjustments brought the phosphatemia to normal values and to a substantial improvement of clinical conditions.
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PMID:[Severe hypophosphatemia in intensive care]. 761 39

Retrospective analysis of all patients with acute bronchial asthma who required intubation and mechanical ventilation was performed in 1987-1993. Our study group comprised 29 patients with a total of 31 episodes of mechanical ventilation. Indications for intubation and ventilation were cardio-respiratory arrest in 9 episodes, and deterioration of clinical status despite aggressive therapy in 22 episodes. Mechanical ventilation strategy was to avoid high air-way pressures of more than 50 cm H2O even if respiratory acidosis persisted. The risk of barotrauma was thus eliminated; other complications were few and reversible, and all patients survived. We conclude that intubation and mechanical ventilation in severe asthma is beneficial and safe, and the prognosis very good.
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PMID:[Endotracheal intubation and mechanical ventilation in severe asthma]. 775 1

Previous studies have shown that chronic acidosis induced by NH4Cl is associated with disturbances in enamel mineralization that resemble severe fluorosis and increased fluoride concentrations in both soft and hard tissues. It has not been shown whether these effects are due to acidosis per se or exposure to high levels of NH+4. This 42-day study with rats fed a low-fluoride diet was done to identify the etiological factor. Two control groups received deionized water or water containing NaCl. Two groups received NH+4-containing compounds that did not produce acidosis (NH4HCO3 or HN4 acetate). Two other groups were rendered acidotic by exposure to NH4Cl in the drinking water (metabolic acidosis) or to an atmosphere containing 10% CO2 (respiratory acidosis). The femur epiphysial fluoride concentrations were elevated in the NH4Cl and NH4 acetate groups, and the magnesium concentrations were elevated in the groups exposed to NH+4 compounds and in the 10% CO2 group. Microradiographic analysis revealed severe disturbances in the mineralization pattern of incisor enamel in both acidotic groups, but normal enamel in the other groups. Enamel fluoride and magnesium concentrations were highest in the acidotic groups. The enamel fluoride concentrations were low (8-14 ppm) and not regarded as the cause of the defective mineralization. It was concluded that the effects on structure and composition of enamel were due to acidosis and not to exposure to high levels of NH+4.
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PMID:Fluorosis-like effects of acidosis, but not NH+4, on rat incisor enamel. 786 46

Changes in metabolism and acid-base status were compared during dormancy in the pulmonate land snail Helix aspersa and a prosobranch amphibious snail Pomacea bridgesi. The typical condition of higher blood PCO2 and bicarbonate levels for air-breathing versus water-breathing vertebrates was shown for the two snail species. When exposed to dry air for 24 hr, both species depressed oxygen uptake by about 65%. In Pomacea, hypercapnia (increase in hemolymph PCO2 from 5.5 to 18 torr) resulting from dormancy produced no significant change in pH due to large increases in bicarbonate (over 17 mmol/l). In Helix, on the other hand, hypercapnia (increase in hemolymph PCO2 from 13 to 18 torr) resulting from dormancy produced a significant decrease in pH and a less than 7 mmol/l increase in bicarbonate. Pre-existing high levels of bicarbonate in Helix may prevent compensation of hypercapnia resulting from dormancy, similar to the case described for air-breathing vertebrates. Complete compensation of respiratory acidosis during the first 24 hr of dormancy in Pomacea suggests that metabolic rate suppression is independent of pH.
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PMID:Acid-base status of a pulmonate land snail (Helix aspersa) and a prosobranch amphibious snail (Pomacea bridgesi) during dormancy. 819 45

We investigated the effect of prolonged hypercapnia on human thermoregulation during immersion of seven male subjects in a 15 degrees C water bath until their esophageal temperature dropped to 35 degrees C or until 1 h had elapsed. In the control trial, subjects inspired room air, whereas in the other trial the inhaled gas mixture was a 4% CO2:20% O2:76% N2 gas mixture. Oxygen uptake (VO2, liter.min-1), inspired minute ventilation (VI, liter.min-1), esophageal temperature (Tes, degree C), mean unweighted skin temperature (Tsk, degree C), mean heat flux (Q, W.m-2), and electromyographic (EMG, mV) activity of the trapezius muscle were recorded. VO2 and integrated EMG (IEMG) activity were used as the primary indicators of shivering thermogenesis. There was a tendency for elevated VO2, albeit not significant, in the CO2 trial compared to the air trial. We observed no significant differences in the IEMG between the air and CO2 trials. These results suggest that prolonged inhalation of a gas mixture containing 4% CO2 does not have a significant inhibitory effect on shivering thermogenesis and does not enhance the cooling rate of the body core. The absence of any shivering attenuation is most likely due to the small blood PCO2 increase incurred by inhalation of 4% CO2, compensation of hypercapnic-induced respiratory acidosis, and a strong thermal drive from core and peripheral regions. It is unlikely that elevated PICO2 levels contribute significantly to the etiology of hypothermia in divers.
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PMID:Effects of prolonged CO2 inhalation on shivering thermogenesis during cold-water immersion. 840 Nov 51

The relative effects of respiratory and metabolic acidosis on diaphragm function are not known. To determine these effects, we compared the effects of respiratory and lactic acidosis on the contractile properties of the diaphragm. We estimated diaphragmatic performance from the change in transdiaphragmatic pressure after supramaximal stimulation of the phrenic nerves in an open-chested, casted-abdomen dog. Similarly, we stimulated the gastrocnemius motor nerve and examined force production and relaxation rate to determine if there was a difference in the response of this skeletal muscle. There was a fall in diaphragm performance with respiratory acidosis (77.1 +/- 16.9 cm H2O versus 93.8 +/- 15.0 cm H2O baseline), but not with lactic acidosis (96.7 +/- 15.7 cm H2O versus 93.8 +/- 15.0 cm H2O baseline); and the gastrocnemius was unaffected by either acidosis. The changes with respiratory acidosis were similar to those seen with diaphragmatic fatigue and had similar relaxation rate changes, suggesting that intracellular pH may play a mechanistic role in respiratory muscle fatigue. In addition, the absence of a respiratory acidosis effect on a non-diaphragmatic skeletal muscle's function represents another physiologic difference between the diaphragm and other skeletal muscles.
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PMID:The effect of respiratory and lactic acidosis on diaphragm function. 844 95


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