Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In respiratory alkalosis the fall in CSF bicarbonate is in part due to increased CSF lactate. The rest of CSF HCO3 fall may be actively regulated or as more recent evidence suggests is dependent on plasma HCO3 fall. Therefore, the relationship between plasma and CSF HCO3 changes was studied during 4 hours of respiratory alkalosis (PaCO2=20 mm Hg) in anesthetized dogs when plasma HCO3: (1) fell normally, (2) kept 'normal' by NaHCO3 infusion, (3) increased by infusing more NaHCO3, and (4) reduced by infusing HCl. In respiratory alkalosis plasma and CSF HCO3 fell 4.6 and 3.8 mEQ/L, respectively. In hypocapnia and 'normal' plasma HCO3 CSF HCO3 fell 2 mEq/L and lactate increased 1.33 mEq/L. In hypocapnia and metabolic alkalosis plasma HCO3 increased 6.5 mEq/L and CSF HCO3 remained unchanged and lactate increased 2.12 mEq/L. In combined hypocapnia and metabolic acidosis plasma HCO3 fall 10.5 mEq/L but CSF HCO3 fell 3.1 mEq/L and CSF pH returned to normal at 4 hours. Therefore CSF HCO3 fall in hypocapnia is primarily and critically dependent on the simultaneous fall in plasma HCO3 content, with a minimal contribution from CNS lactate increase. When CSF PH has returned to normal, however, CSF HCO3 fall is stopped despite further falls in plasma HCO3.
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PMID:Importance of changes in plasma HCO-3 on regulation of CSF HCO-3 in respiratory alkalosis. 0 12

A hypoxia test for placental sufficiency was performed on 24 healthy pregnant women nearing term and 23 high-risk pregnant women in advanced stages of gestation. Hypoxia was induced by inhalation of a breathing mixture containing 7% oxygen through a semi-open system which permitted partial rebreathing, thus preventing hypocapnia. The changes in fetal heart rate (FHR) resulting from maternal hypoxia were recorded continuously by external or internal monitoring. The changes observed in FHR were more marked in high-risk cases. Maternal blood gases were tested before and after 10 min of hypoxia in 10 normal and 10 high-risk patients. In no case was maternal acidosis observed. All pregnant patients regarded as high-risk because of hypertensive disorders or chronic renal disease manifested metabolic alkalosis. This finding cannot be explained. It is regarded as being responsible for the more severe FHR changes through a negative Bohr effect, which reduces the dynamic exchange of oxygen in the placenta. Metabolic alkalosis does not appear in high-risk pregnant women exposed to milder hypoxia by breathing 12% oxygen. The changes in FHR observed during severe maternal hypoxia, i.e., 7% oxygen, are probably due more to maternal metabolic alkalosis than to placental insufficiency. Consequently, the "severe hypoxia test" cannot be used as a test for placental insufficiency.
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PMID:Metabolic aspects of a hypoxia test for placental sufficiency. 95 67

The time course of changes in hemolymph pH, PCO2 and bicarbonate concentration were followed in euryhaline Chinese crabs, Eriocheir sinensis, after transfer from seawater (SW) to freshwater (FW) and vice versa. In order to correlate these changes with the animal's ionic status, hemolymph osmolarity and Na+ and Cl- concentrations as well as net exchanges of acid-base equivalents with the external water were also measured. Transfer from SW to FW induced a metabolic alkalosis which peaked after 3 days and declined thereafter but remained significant by 29 days. Hemolymph PCO2 was markedly elevated in FW, thus moderating the increase in hemolymph pH. Osmolarity and Na+ and Cl- concentrations reached a new steady state at lowered values by 24-48 h and a significant outflux of acidic equivalents was measured only during the first 2 days. Transfer from FW to SW conversely induced a metabolic acidosis which was almost fully compensated by a marked hypocapnia. It is concluded that external acid-base exchanges coupled to ionic readjustments following a salinity transition cannot solely explain the associated acid-base disturbances, the metabolic component of which must also rely on tissular processes probably linked to cell volume regulation.
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PMID:Acid-base changes on transfer between sea- and freshwater in the Chinese crab, Eriocheir sinensis. 160 63

The cardiorespiratory responses to exercise and forced hyperventilation were measured in 17 unselected patients with syndrome X (angina, positive exercise test, normal coronary arteriogram, no other cardiovascular disease) and compared with those in 15 healthy subjects. Forced hyperventilation produced hypocapnia and metabolic alkalosis but no chest pain or electrocardiographic change. Patients with syndrome X showed reduced maximum oxygen consumption with an increased respiratory exchange ratio at peak exercise, confirming that exercise was limited by skeletal muscle perfusion--and thus that the increase in cardiac output with exercise is limited in syndrome X as in heart failure. Arterial carbon dioxide tension (PCO2) homoeostasis during exercise was normal but the ventilatory cost of carbon dioxide excretion was increased in syndrome X (as in heart failure). End tidal PCO2 measurements correlated only poorly with arterial PCO2 in individual patients with syndrome X, providing a possible explanation for previous reports, based on end tidal PCO2 of inappropriate hyperventilation. Patients with syndrome X did not show inappropriate hyperventilation but they did show hyperventilation that was appropriate to maintain normal arterial PCO2 in the face of reduced cardiac reserve.
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PMID:Syndrome X and hyperventilation. 193 59

The severity of the alkalemia produced by a reduction in arterial carbon dioxide tension (PaCO2) in normal humans and animals is ameliorated by buffer and renal responses that diminish the levels of plasma bicarbonate concentration ([HCO3-]p). These adjustments have even greater potential importance in preventing extreme degrees of alkalemia when hypocapnia occurs in the presence of an initially elevated [HCO3-]p (mixed respiratory and metabolic alkalosis). The aim of the present study was to characterize the acute (approximately 3 h) and chronic (5 days) acid-base effects of respiratory alkalosis when superimposed on chronic metabolic alkalosis. Ten dogs were made alkalotic by the repeated administration of ethacrynic acid and the provision of a chloride-restricted diet. Hypocapnia (delta PaCO2 = 10 mmHg) was then superimposed by exposing the animals to 11% O2 in an environmental chamber. A large fall in [HCO3-]p occurred in the acute hypocapnic phase that was further augmented in the chronic phase; the corresponding delta [HCO3-]p/delta PaCO2 slopes were 0.43 and 0.71 meq.l-1.mmHg-1, respectively, values substantially larger than those previously reported for hypocapnia in normals as well as in animals with preexisting HCl acidosis. Hyperlactatemia was responsible, on average, for 43% of the decrement in [HCO3-]p during acute hypocapnia but for only 20% of the delta [HCO3-]p during the chronic phase of the study. The striking decrement in [HCO3-]p observed in response to the chronic reduction in PaCO2 was sufficient not only to prevent the development of extreme alkalemia but also to offset entirely the effect of hypocapnia on plasma [H+].
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PMID:Influence of acute and chronic respiratory alkalosis on preexisting chronic metabolic alkalosis. 210 57

Acid-base derangements are encountered frequently in clinical practice and many have life-threatening implications. Treatment is dependent on correctly identifying the acid-base disorder and, whenever possible, repairing the underlying causal process. Bicarbonate is the agent of choice for the treatment of acute metabolic acidosis. Controversy surrounds the use of alkali therapy in lactic acidosis and diabetic ketoacidosis, but bicarbonate should clearly be administered for severe acidosis. In most patients with mild to moderate chloride-responsive metabolic alkalosis, providing an adequate amount of a chloride salt will restore acid-base balance to normal over a matter of days. In contrast, therapy of the chloride-resistant metabolic alkalosis is best directed at the underlying disease. When alkalemia is severe, administering hydrochloric acid or a hydrochloric acid precursor may be necessary. Treatment of respiratory acidosis should be targeted at restoring ventilation; alkali should be administered only for superimposed metabolic acidosis. The therapy of respiratory alkalosis is centred on reversal of the root cause; short of this goal, there is no effective treatment of primary hypocapnia. The coexistence of more than one acid-base disorder (i.e. a mixed disorder) is not uncommon. When plasma bicarbonate concentration and arterial carbon dioxide tension (paCO2) are altered in opposite directions, extreme shifts in pH may occur. In such cases, it is imperative that the nature of the disturbance is identified early and therapy directed at both disorders.
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PMID:Rational treatment of acid-base disorders. 219 65

Mechanically induced hyperventilation is used in the treatment of newborn infants with persistent pulmonary hypertension syndrome to induce respiratory alkalosis, which may attenuate their pulmonary vasoconstriction. Whether this treatment is effective because of the increase in arterial pH or the decrease in Paco2 was investigated in nine sedated, mechanically ventilated newborn lambs with hypoxia-induced pulmonary vasoconstriction. We found that respiratory alkalosis and metabolic alkalosis were equally effective in attenuating hypoxia-induced pulmonary vasoconstriction, but that hypocapnia (low Paco2 with a normal arterial pH) was ineffective. These results indicate that increased arterial pH, not decreased Paco2, attenuates hypoxia-induced pulmonary vasoconstriction in newborn lambs and possibly the pulmonary vasoconstriction in newborn infants with persistent pulmonary hypertension syndrome.
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PMID:Increased arterial pH, not decreased PaCO2, attenuates hypoxia-induced pulmonary vasoconstriction in newborn lambs. 308 Jul 25

Hypoproteinemia by itself produces a metabolic alkalosis. It is not clear whether a respiratory compensation (hypercapnia) develops with this alkalosis; patients with liver cirrhosis, most of them with hypoproteinemia, are known to hyperventilate. We studied 23 clinically stable patients with hypoproteinemia, with very low albumin-to-globulin ratios (range 0.4 to 1.1), who had either liver cirrhosis (n = 12) or other medical conditions (n = 11). In both groups, there was marked hypocapnia, accompanied by alkalemia (PaCO2 values (mean +/- SD) 31 +/- 2 and 32 +/- 3 torr; pH (mean +/- SD) 7.45 +/- 0.03 and 7.47 +/- 0.03, for the patients with cirrhosis and those without, respectively). Hypoxemia was not the stimulus provoking hyperventilation. The lowering of PaCO2 was proportional to the reduction of serum albumin and total protein concentrations; no detectable difference was seen between the patients with cirrhosis and those without cirrhosis in this apparent dependence of PaCO2 on the concentration of serum proteins. Many of these clinically stable patients with hypoproteinemia, with or without liver cirrhosis, had appreciable concentrations of unidentified anions in plasma (inappropriately high anion gap). Whatever the nonrespiratory acid-base status of the patients with hypoproteinemia, their pulmonary ventilation (hypocapnia) appeared excessive when compared with subjects (presumably) without proteinemia who had similar nonrespiratory acid-base states. The mechanism responsible for the hyperventilation in hypoproteinemia and the nature of the unidentified anions in this condition are obscure.
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PMID:Hyperventilation with hypoproteinemia. 318 88

The purpose of this work was determination of the effect of physical exercise on maximal gastric output. The study was carried out in 21 men aged 20-56 years with chronic duodenal ulcer. The control group comprised 17 healthy men aged 20-28 years. During three successive hours the maximal acid output was determined at rest, during one-hour exercise on a cycle ergometer and during one-hour restitution. Gastric secretion was stimulated with pentagastrin administered subcutaneously in a dose of 6 mcg/kg at the beginning of each hour of the study. Besides that the parameters of acid-base equilibrium were determined before the beginning of resting MAO measurement, immediately after its completion, and then after one hour of exercise and one hour of restitution. Physical exercise caused in the group of patients a significant increase of MAO (p less than 0.001), which was due to increased volume of gastric juice (p less than 0.001) and the concentration of acid in it (p less than 0.02). During the restitution the value of MAO was significantly below that obtained at rest. On the other hand, in healthy subjects exercise caused a significant reduction of MAO value (p less than 0.005) as a result of decreased volume of gastric juice (p less than 0.005). During MAO determination at rest a rise was observed in the pH of blood, increased concentration of bicarbonates and base excess (p less than 0.05). During the exercise with further aspiration of gastric juice a further significant increase of pH and pO2 and reduction of pCO2 (p less than 0.05) was observed. Exercise caused in patients an increase of gastric secretion in contrast to healthy subjects. Changes in acid-base balance showed a tendency for metabolic alkalosis with hypocapnia, and were similar in both groups.
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PMID:[Maximal gastric secretion during physical exertion and restitution in patients with chronic duodenal ulcer]. 327 64

Altogether 228 patients with hereditary microspherocytic anemia (HMA), autoimmune hemolytic anemia (AIHA) and hypoplastic anemia (HA) were examined over time for the acid-base state of the arterial blood with the use of the pCO2-buffer bases coordinate system (BE/pCO2 and pCO2/BE diagrams). Prior to surgery the respiratory alkalosis was diagnosed in 60% of HMA patients (of these, 41.7% of patients had a decompensated alkalosis), in 61.7% of AIHA patients (73%), and in 69.7% of HA patients (82.1%). It is shown that the development in the patients of chronic respiratory alkalosis should be regarded as a compensatory mechanisms associated with hemic hypoxia complicated by arterial hypoxemia. During splenectomy, there was an increase in the incidence of decompensated respiratory alkalosis. Mixed respiratory and metabolic alkalosis occurred in 8.3% of AIHA patients and in 19.6% of HA patients because of artificial ventilation of the lungs. Two hours after operation compensated metabolic acytosis was identified in 72% of HMA patients, in 33.3% of AIHA patients, and in 33.9% of HA patients. Twenty-four hours following operation the patients of all the groups had arterial hypoxemia and hypocapnia. In view of this fact the blood acid-base state was determined by the presence of respiratory alkalosis: in 47.5% of patients with HMA, in 60% of patients with AIHA, and in 54% of patients with HA. Analysis of the BE/pCO2 diagram demonstrated that in 2/3 of the patients with HMA and AIHA and in all the patients with HA, respiratory alkalosis was decompensated. It was established that electrolyte imbalance detected in the patients interfered with metabolic compensation for chronic respiratory alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mechanisms of compensation of disorders of acid-base status of the blood in patients with chronic anemia]. 404 71


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