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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several hypotheses have been put forward to explain postdialysis hypocapnia. Three were tested in this study: impairment of tissue oxygenation by dialysis (D)-induced alkalosis (Bohr effect), the D disequilibrium syndrome, and the loss of carbon dioxide (CO2) in D fluid. In 17 patients pre-DPCO2 was significantly correlated with plasma bicarbonate concentration (HCO3) and no disproportionate reduction of PCO2 was discernible. In 10 patients using a bath acetate concentration of 38 mEq/1 PCO2 was unchanged after D (35.4 versus 35.9 mm Hg before D), and was low relative to HCO3 whic increased from 21.2 to 28.0 mEq/1. After a dialysis using an acetate concentration of 25 mEq/1 HCO3 remained constant (20.4 versus 21.1 mEq/1 pre-D), whereas PCO2 fell from 35.3 to 30.8 mm Hg (P less than 0.001). Consequently PCO2 was again low relative to HCO3. Removal of CO2 by D fluid was excluded as a cause for low blood PCO2: addition of gaseous CO2 to the bath had no influence on arterial blood gases. Since post-D hypocapnia was not prevented when HCO3 was kept constant, it was concluded that post-D alkalosis cannot be the main reason for post-D hyperventilation, and that other factors related to the process of D are responsible.
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PMID:Mechanism of post dialysis hyperventilation in patients with chronic renal insufficiency. 0 52

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

Arterial pH, pO2 and pCO2 were analysed with Astup's micromethod on one hundred and three acute myocardial infarctions (A.M.I.) without metabolic, pulmonary and renal diseases. Following the clinical picute, the patients were divided into five groups and results were clinically and statistically evaluated (mean, standard deviation, Student's test "t", correlation coefficient "r" between pO2 and pulmonary arterial diastolic pressure): --Ist group (A.M.I. without complications): only mild hypoxemia; --IInd group (A.M.I. with slight left ventricular failure): more remarkable hypoxemia and hypocapnia, often with respiratory alkalosis; --IIIrd group (A.M.I. complicated by acute pulmonary oedema): mixed acidosis and severe hypoxemia; --IVth group (A.M.I. complicated by shock): prevailing metabolic acidosis and severe hypoxemia. Acidosis shows good correlations with the clinical picture; --Vth group (A.M.I. with serious arrhythmias): mixed and profound acidosis and important hypoxemia during ventricular fibrillation and cardiac arrest. In twenty patients hypoxemia and arterial pulmonary diastolic pressure showed a significant correlation.
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PMID:[Blood gas analysis and acid-base balance in acute myocardial infarction. Personal observations (author's transl)]. 1 Feb 18

Awake domestic pigeons, either maintained at 22 degrees C (series I) or acutely exposed at 2 degrees C (series II), were studied in a hypobaric chamber at 140 m and at various stages during a 4-week exposure to 4000 m. Steady-state pulmonary ventilation (Vg) and breathing pattern (VT, fr), oxygen consumption (MO2), O2 concentrations and pressures in the arterial (a) and mixed venous blood (v), hematocrit (Ht) and acid-base status in arterial blood, systolic blood pressure and heart frequency (fH) were measured. From these data cardiac output (Vb) and stroke volume (Vs), ventilatory and circulatory requirements (Vg/MO2, Vb/MO2), extraction of O2 from inspired air (EgO2) and blood EbO2), and capacitance coefficient of blood for oxygen (betabo2) were calculated. At 140 m, by comparison with predicted values for mammals of same body weight, pigeons at 22 degrees C extracted more O2 from the inspired gas, with lower fR, larger VT, similar Vg; they extracted O2 from the blood like mammals, with lower fH, larger VS, greater Vb, similar betabO2=70 mumol-L-1-torr-1. Acute exposure to 2 degrees C provoked a two-fold increase in MO2 which was achieved by doubling Vg and increasing O2 extraction from the blood. At 4000 m, in both series, pigeons hyperventilated within the first 30 min, with a resultant hypocapnic alkalosis comparable to that in mammals. Further hyperventilation with consequent greater hypocapnia and increase of arterial PO2 was complete beyond 3 hr. After a few weeks, the pH remained 0.07 above control normoxic value, Ht increased from 45 to 52%, betabO2 reached about 172 mumol-L-1-torr-1. At 2 degrees C, Vb also increased, mainly due to tachycardia.
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PMID:Ventilatory and circulatory O2 convection at 4000 m in pigeon at neutral or cold temperature. 1 65

This study examines the possibility that changes of cerebral extracellular pH (PH e) or adenosine concentration may provide coupling mechanisms of a general nautre, adjusting cerebral blood flow (CBF) to metabolic demands. Although there is considerable indirect evidence that CBF varies inversely with pHe, results obtained during the last few years indicate that large increases in flow may occur in the absence of a fall in pHe. Thus, induction of hypoxia or epileptic seizures leads to maximal increase in CBF before pHe falls or even when there is initial alkalosis due to concomitant hypocapnia. Furthermore, CBF increases in hypoglycaemia and after administration of amphetamine, two conditions unassociated with tissue acidosis. The possibility that adenosine may be a coupling factor was examined in hypoxia and during epileptic seizures in rats. In both conditions a four- to fivefold increase in CBF occurs in spite of the fact that tissue adenosine concentrations remain at or below 1 mumolkg-u. It is concluded that adenosine accumulates first when there is a perturbation of cerebral energy state with a rise in AMP concentration. It seems unlikely that adenosine, formed by breakdown of AMP, acts as a general coupling factor.
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PMID:Coupling of cerebral metabolism and blood flow in epileptic seizures, hypoxia and hypoglycaemia. 2 37

Separate and combined effects of acute metabolic acidosis and hypocapnia were determined in skeletal and cardiac muscles of intact rats. Normocapnic metabolic acidosis, imposed by intraperitoneal injection of hydrochloric acid (6 mEq/kg), did not change skeletal muscle intracellular acid--base parameters. Hypocapnia, induced by mechanical hyperventilation, resulted in intracellular alkalosis within skeletal muscle during both respiratory alkalosis and compensated metabolic acidosis; changes of skeletal muscle intracellular bicarbonate concentration per unit change in carbon dioxide tension were identical during these two experimental procedures. These data suggest that processes other than physicochemical buffering neutralize protons taken into skeletal muscle cells during acute metabolic acidosis. The acid--base state of the heart was quite stable during these experimental manipulations; thus, it appears that cardiac muscle has an extraordinary buffering ability. Moreover, our data suggest that processes other than physicochemical buffering maintain cardiac intracellular pH normal during hypocapnia.
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PMID:Effect of hypocapnia on intracellular pH during metabolic acidosis. 4 59

Two groups of anesthetized, splenectomized, and paralyzed dogs were hyperventilated (Vt 40 ml/kg). Normocapnia was maintained in one group (mean Paco2 37.6 mm"h'g, mean p"h '7.41) and respiratory alkalosis (mean Paco2 8 mmHg, mean pH 7.75) in the other. Splanchnic hemodynamic responses were similar in both groups. Average hepatic venous pressure increased from 3.2 to 6.4 mmHg in the normocapnic group and from 3.8 to 7.7 mmHg in the hypocapnic group. Average portal venous pressure increased from 10.7 to 12.0 mmHg and 10.8 to 12.7 mmHg in the normocapnic and hypocapnic groups, respectively. Mesenteric vascular resistance increased in 93 per cent of dogs. A decrease in functional intestinal capillary surface area during hyperventilation was indicated by a significant reduction in mesenteric Vo2 (from 15 to 11 ml/min, average 30 per cent), and a concomitant reduction in mesenteric O2 extraction ratio. Changes in mesenteric Vo2 were reflected in calculated splanchinic Vo2. Hepatic O2 uptake was essentially unchanged by tidal hyperventilation with or without hypocapnia.
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PMID:Splanchnic hemodynamic response to passive hyperventilation. 23 21

Three patients with paralytic poliomyelitis have been ventilated via tracheostomy with uncuffed silver cannula for 21 years, with high tidal volumes of atmospheric air (8.3, 7.2, and 5.4 ml/kg b.wt.), at a frequency of 20, passive expiration, and without periodic hyperinflation. No pulmonary complications were seen during the whole of this period. The total compliance was significantly decreased. The pulmonary physiological shunt relative to the total pulmonary blood flow (Qs/Qt) was slightly increased. PaO2 was nevertheless normal, probably due to a high alveolar PO2 caused by the hyperventilation. The physiological dead space realtive to the tidal volume (VD/VT) was within the noraml range, but VD was high in one case. Two of the patients disclosed an extremely low CO2 production and a PaCO2 averaging 12 mmHg, with small fluctuations during a 24-hour study. This profound respiratory alkalosis was only partly compensated in the arterial blood (pH: 7.54 and 7.50), suggesting a new state of acid-base equilibrium. The cerebrospinal fluid lactate was significantly increased to about 4 mmol/l, but the patients revealed no signs of impaired cerebral function. A reduction of the degree of hypocapnia by the use of a mechanical dead space is recommended.
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PMID:Artificial hyperventilation during 21 years in three cases of complete respiratory paralysis. 81 38

The influence of hypoxemia on the brain content of several organic acids and NH+4, AND ITS RELATIONship to the accompanying hypocapnia was studied in unanesthetized rats subjected to hypoxemia for periods ranging between 2 hours and 7 days. Under acute conditions, 'mild' hypoxemia (FO2 = 6--7%), these increases were greater and accompanied by increased gamma-aminobutyric acid (GABA) and decreased glutamic and aspartic acid levels; glutamine and NH+4 remained normal. When hypocapnia was prevented, 'severe' hypoxemia induced only a rise in GABA and slight elevations in lactic and alpha-ketoglutaric acid. During prolonged severe hypoxemia, the effects on the brain amino acids were maintained throughout, indicating that they are independent from the intracerebral pH which should progressively normalize. The effect on lactic acid gradually disappeared. The results show that during hypocapnic hypoxemia the rise in brain GABA is hypoxemia dependent, the decrease in glutamic and aspartic acid is hypocapnia dependent and the increase in lactic acid is in a large way alkalosis dependent.
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PMID:Brain amino acids in conscious rats in chronic normocapnic and hypocapnic hypoxemia. 92

Cardiovascular effects of hypocapnia and hypocapnic alkalosis with and without a fluid load were studied in four groups of dogs (group I: fluid load control; group II: fluid load-isolated hypocapnia; group III: fluid load-hypocapnic alkalosis; group IV: no fluid load-hypocapnic alkalosis). Hypocapnic alkalosis was induced by mechanical hyperventilation, and isolated hypocapnia by the simultaneous administration of 0.1 N HCl. Respiratory alkalosis was also studied during administration of a saline fluid load. Cardiac output and stroke volume increased in all groups receiving a fluid load (including isolated hypocapnia and hypocapnic alkalosis groups), but both fell significantly during hypocapnic alkalosis without fluid load. Pulmonary artery wedge pressure rose in groups with hypocapnic alkalosis with fluid load and isolated hypocapnia with fluid load, but did not change significantly with hypocapnic alkalosis without fluid load or in the normocapnic group with fluid load. It is concluded that cardiac output and stroke volume fall in response to hypocapnic alkalosis but both are maintained with a fluid load at the expense of an increased left ventricular preload.
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PMID:Effects of hypocapnia and hypocapnic alkalosis on cardiovascular function. 93 46


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