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At least 433 records · Page 24Linked to original sources
PubMed2003

Re-evaluation of acid-base prediction rules in patients with chronic respiratory acidosis.

RATIONALE: The prediction rules for the evaluation of the acid-base status in patients with chronic respiratory acidosis, derived primarily from an experimental canine model, suggest that complete compensation should not occur. This appears to contradict frequent observations of normal or near-normal pH levels in patients with chronic hypercapnia. METHODS: Linear regression analysis was used to estimate the relationships between arterial pH, bicarbonate and partial pressure of carbon dioxide (PCO2) from 18 separate arterial blood gas measurements in 18 clinically stable outpatients with chronic hypercapnic respiratory failure from chronic obstructive lung disease, and without clinical conditions or medications likely to cause a primary metabolic alkalosis. RESULTS: The PCO2 ranged from 45 mmHg to 77 mmHg, and pH ranged from 7.37 to 7.44. In only three of the arterial blood gas measurements were the pH values lower than 7.38. From the regression equations derived from these measurements, the pH decreased by 0.014 for each 10 mmHg increase in the PCO2, and the bicarbonate level increased by 5.1 mmol/L. These values are quite different from a decrease in pH of 0.03 and an increase in bicarbonate of 3.5 mmol/L predicted using the rules derived from the canine model. CONCLUSIONS: In patients with chronic stable hypercapnia, acid-base compensatory mechanisms appear to be more effective than would be predicted using the classic rules.

Acid-Base Imbalance↗
PubMed1991

Delivery dependence of early proximal bicarbonate reabsorption in the rat in respiratory acidosis and alkalosis.

In the intact rat kidney, bicarbonate reabsorption in the early proximal tubule (EP) is strongly dependent on delivery. Independent of delivery, metabolic acidosis stimulates EP bicarbonate reabsorption. In this study, we investigated whether systemic pH changes induced by acute or chronic respiratory acid-base disorders also affect EP HCO3- reabsorption, independent of delivery (FLHCO3, filtered load of bicarbonate). Hypercapnia was induced in rats acutely (1-3 h) and chronically (4-5 d) by increasing inspired PCO2. Hypocapnia was induced acutely (1-3 h) by mechanical hyperventilation, and chronically (4-5 d) using hypoxemia to stimulate ventilation. When compared with normocapneic rats with similar FLHCO3, no stimulation of EP or overall proximal HCO3 reabsorption was found with either acute hypercapnia (PaCO2 = 74 mmHg, pH = 7.23) or chronic hypercapnia (PaCO2 = 84 mmHg, pH = 7.31). Acute hypocapnia (PaCO2 = 29 mmHg, pH = 7.56) did not suppress EP or overall HCO3 reabsorption. Chronic hypocapnia (PaCO2 = 26 mmHg, pH = 7.54) reduced proximal HCO3 reabsorption, but this effect was reversed when FLHCO3 was increased to levels comparable to euvolemic normocapneic rats. Thus, when delivery is accounted for, we could find no additional stimulation of proximal bicarbonate reabsorption in respiratory acidosis and, except at low delivery rates, no reduction in bicarbonate reabsorption in respiratory alkalosis.

Acidosis, Respiratory↗
PubMed1982

Fast bicarbonate-chloride exchange between brain cells and brain extracellular fluid in respiratory acidosis.

The extracellular pH, PCO2, and [Cl-] at the surface of the brain cortex, expiratory PCO2 and arterial blood pressure were continuously recorded in anaesthetized and artificially ventilated cats. The observations from such a preparation were: 1. In response to a nearly step increase in end-tidal PCO2, the brain ECF pH, PCO2, [Cl-] and calculated [HCO-3] changed in the form of a nearly mono-exponential time function after a delay of 5-7 s. 2. The time constants of the changes in the extracellular pH, PCO2, [Cl-] and [HCO-3] were in the range of 30-40 s. 3. The extracellular [HCO-3] increased markedly at an initial rate of 4.22 mmol.1(-1) . min-1 after 36 s. 4. This increase occurred almost simultaneously with a decrease in the extracellular [Cl-]. An [HCO-3]-[Cl-] exchange ratio was determined which very closely approached one. It is concluded that the brain extracellular bicarbonate concentration in respiratory acidosis increases because the H+ formed from the hydrated CO2 reacts with the intracellular buffers of brain cells, mainly glial cells, and HCO-3 inside the cell is formed and exchanged for Cl- outside the cell similar to the HCO-3/Cl- exchange which occurs between red cells and blood plasma during CO2 loading. The described time constants of the anion exchange represent the wash in or wash out time of CO2 in a tissue containing intracellular buffer.

Acidosis, Respiratory↗
PubMed1984

Distribution of cardiac output in fetal and neonatal lambs with acute respiratory acidosis.

The effects of changes in PaCO2 on the circulation are complex, involving local vasodilation, vasodilation mediated by the pulmonary inflation reflex, and vasoconstriction due to effects on central vasomotor centers and peripheral chemoreceptors. One might anticipate that some or all of these might differ between the fetus in utero and the newborn. Distribution of cardiac output was measured in unanesthetized fetal (n = 6) and newborn (n = 7) sheep, using the radioactive microsphere technique. PaCO2 rose from 44 to 70 (fetus) and 38 to 60 torr (newborn) with the addition of CO2 to room air. In the fetus, there were significant increases in central nervous system (CNS), diaphragm, and lung blood flows. No organ showed a significant decrease in flow. Local vasodilation by CO2 was the likely cause of the increased flow to CNS. The large increase in pulmonary blood flow was most likely due to the associated rise in fetal PaO2 (23 to 28 torr) that accompanied respiratory acidosis and the presence of fetal breathing movements. The rise in diaphragmatic blood flow was likely the result of fetal breathing. In the newborn, CNS and diaphragm flows rose, but unlike the fetus, spleen and stomach flows decreased. These decreased flows in the hypercapnic newborn may have been due to stimulation of either central vasomotor centers or peripheral chemoreceptors.

Acidosis, Respiratory↗
PubMed2003

CO2 induced acute respiratory acidosis and brain tissue intracellular pH: a 31P NMR study in swine.

High concentration carbon dioxide (CO(2)) is used to promote pre-slaughter anaesthesia in swine and poultry, as well as short-lasting surgical anaesthesia and euthanasia in laboratory animals. Questions related to animal welfare have been raised, as CO(2) anaesthesia does not set in momentarily. Carbon dioxide promotes anaesthesia by lowering the intracellular pH in the brain cells, but the dynamics of the changes in response to a high concentration of CO(2) is not known. Based on (31)P NMR spectroscopy, we describe CO(2)-induced changes in intracellular pH in the brains of five pigs inhaling 90% CO(2) in ambient air for a period of 60 s, and compare the results to changes in arterial blood pH, P(CO2), O(2) saturation and HCO(3)(-) concentration. The intracellular pH paralleled the arterial pH and P(CO2) during inhalation of CO(2); and it is suggested that the acute reaction to CO(2) inhalation mainly reflects respiratory acidosis, and not metabolic regulation as for example transmembrane fluxes of H(+)/HCO(3)(-). The intracellular pH decreased to approximately 6.7 within the 60 s inhalation period, and the situation was metabolically reversible after the end of CO(2) inhalation. The fast decrease in intracellular pH supports the conclusion that high concentration CO(2) leads to anaesthesia soon after the start of inhalation.

Acidosis, Respiratory↗
PubMed1996

Effect of acute respiratory acidosis on the limits of oxygen extraction during hemorrhage.

BACKGROUND: Hypercapnia can impair cells' capacity to maintain energy status anerobically and enhances the risk of hypoxic injury when oxygen availability is reduced. The ability to maintain tissue oxygenation is determined by both bulk blood flow and the efficiency of oxygen extraction. Bulk blood flow is maintained during hypercapnia through increased sympathetic activity. The effect of hypercapnia on oxygen extraction, however, is unknown. This study evaluates the effect of hypercapnia on cells' capacity to adapt to reductions in oxygen availability by increasing oxygen extraction. METHODS: In three groups of paralyzed, mechanically ventilated dogs that were anesthetized with alpha-chloralose, the concentration of carbon dioxide in the inhaled gas mixture was adjusted to achieve normocapnia, moderate hypercapnia (Paco2 = 72 +/- 3 [SE] mmHg) or severe hypercapnia (Paco2 = 118 +/- 4 [SE] mmHg). Stepwise hemorrhage was induced until each dog's blood pressure was destabilized. At each stage in the hemorrhage protocol, the oxygen delivery, oxygen consumption, and oxygen extraction ratios (ratio of arteriovenous oxygen content difference to arterial oxygen content) were determined. RESULTS: At the point of onset of delivery dependence of oxygen consumption, the oxygen delivery rate (critical oxygen delivery) was 7.8 +/- 1.5 (SE) ml.kg-1.min-1 and the oxygen extraction ratio (critical oxygen extraction ratio) was 0.72 +/- 0.04 (SE) in the normocapnic dogs. Moderate hypercapnia had no effect on these parameters. In the severely hypercapnic dogs, the critical values for oxygen delivery and extraction ratios were 12.5 +/- 1.8 (SE) ml.kg-1.min-1 and 0.54 +/- 0.035 (SE), respectively (P < 0.05 for differences from the normocapnic dogs). CONCLUSIONS: The results identify a previously unrecognized threat to tissue oxygenation and emphasize the importance of ensuring adequate oxygen delivery when adopting mechanical ventilatory strategies that permit respiratory acidosis to develop.

Acidosis, Respiratory↗
PubMed1984

Renal handling of phosphate during acute respiratory acidosis and alkalosis in the rat.

Clearance experiments were performed in acutely thyroparathyroidectomized rats to evaluate the renal handling of phosphate during respiratory acidosis (R ACID) and alkalosis (R ALK) in rats fed either a normal (0.7%) or low (0.07%) phosphate diet for 4 days. Different acid-base states were achieved by varying the mixture of carbon dioxide in the inspired air. Each group received graded infusions of phosphate to control for differences in plasma phosphate (PPi) and to determine the maximum transport capacity of phosphate reabsorption (TmPi/GFR). In rats fed a normal phosphate diet, PPi and the fractional excretion of phosphate (FEPi) were significantly greater in R ACID than in R ALK. However, there were no differences between R ACID and R ALK when FEPi was evaluated as a function of the PPi, and values for TmPi/GFR during R ACID were not different from those during R ALK. In rats fed low phosphate diet, PPi during R ACID was significantly greater than during R ALK, yet FEPi was less than 1% in all groups due to an adaptive increase in TmPi/GFR. Further, the TmPi/GFR was similar irrespective of the acid-base state. We conclude that acute respiratory acid-base changes do not alter the intrinsic capacity of the kidney to reabsorb phosphate.

Acidosis, Respiratory↗
PubMed1977

Respiratory acidosis and alkalosis.

The physiology of respiratory control of acid-base balance is reviewed. The pathophysiological mechanisms during hypercapnia and hypocapnia are discussed in the light of the causes and clinical manifestations of these disturbances. In addition to the role of the kidney in the compensatory processes of these disturbances, renal functional changes during acute and chronic pulmonary acid-base derangement is discussed. Some of the difficulties encountered in the patient with chronic renal disease in whom respiratory abnormalities may be present are also discussed.

Acidosis, Respiratory↗
PubMed2003

Carbon dioxide added late in inspiration reduces ventilation-perfusion heterogeneity without causing respiratory acidosis.

We have shown previously that inspired CO2 (3-5%) improves ventilation-perfusion (Va/Q) matching but with the consequence of mild arterial hypercapnia and respiratory acidosis. We hypothesized that adding CO2 only late in inspiration to limit its effects to the conducting airways would enhance Va/Q matching and improve oxygenation without arterial hypercapnia. CO2 was added in the latter half of inspiration in a volume aimed to reach a concentration of 5% in the conducting airways throughout the respiratory cycle. Ten mixed-breed dogs were anesthetized and, in a randomized order, ventilated with room air, 5% CO2 throughout inspiration, and CO2 added only to the latter half of inspiration. The multiple inert-gas elimination technique was used to assess Va/Q heterogeneity. Late-inspired CO2 produced only very small changes in arterial pH (7.38 vs. 7.40) and arterial CO2 (40.6 vs. 39.4 Torr). Compared with baseline, late-inspired CO2 significantly improved arterial oxygenation (97.5 vs. 94.2 Torr), decreased the alveolar-arterial Po2 difference (10.4 vs. 15.7 Torr) and decreased the multiple inert-gas elimination technique-derived arterial-alveolar inert gas area difference, a global measurement of Va/Q heterogeneity (0.36 vs. 0.22). These changes were equal to those with 5% CO2 throughout inspiration (arterial Po2, 102.5 Torr; alveolar-arterial Po2 difference, 10.1 Torr; and arterial-alveolar inert gas area difference, 0.21). In conclusion, we have established that the majority of the improvement in gas exchange efficiency with inspired CO2 can be achieved by limiting its application to the conducting airways and does not require systemic acidosis.

Acidosis, Respiratory↗
PubMed1996

Hypercapnic respiratory acidosis precipitated by hypercaloric carbohydrate infusion in resolving septic acute respiratory distress syndrome: a case report.

Complications may occur when nutritional support is administered either parenterally or enterally. Inappropriate nutritional formulas with high carbohydrate loads can precipitate respiratory failure in patients with compromised lung function, induce respiratory distress which manifests as dyspnea and tachypnea in an originally normal lung condition, produce hypercapnic acidosis in mechanically ventilated patients with chronic obstructive pulmonary disease (COPD) as well as patients recovering from acute respiratory distress syndrome (ARDS) without chronic lung disease, or result in difficult weaning. Hypercaloric mixed substrates administered either parenterally or enterally can also have profound impacts on gas exchange and energy expenditure. This report describes a patient who experienced exacerbation of respiratory distress and hypercapnic acidosis during recovery from septic ARDS as the result of a nutritionally-related increase in CO2 production. As carbohydrate calories were decreased, CO2 production diminished and the hypercapnia was resolved. The importance of indirect calorimetry cannot be overemphasized during tailoring of nutritional support for the critically ill patients.

Acidosis, Respiratory↗
PubMed1979

Body temperature and ventilatory responses to CO2 during chronic respiratory acidosis.

During acute hypercapnia (5% carbon dioxide) in resting conscious dogs, ventilation (Ve) attained a new level above control within 5 min, but rectal temperature decreased gradually to reach a steady state lower than control after 40-60 min. At 2 days of breathing 5% carbon dioxide, Ve remained elevated, as in acute hypercapnia, but Paco2 increased and the threshold of the ventilatory response shifted to a higher Paco2. By 2 days of hypercapnia, rectal temperature (Tr) had returned to normal, reflecting an alteration of hypothalamic temperature control that might be expected to result in enhanced respiratory drive. Surprisingly, despite blood acid-base compensation between 2 and 14 days of hypercapnia, Ve did not decrease, whereas Paco2 decreased to the level observed during acute hypercapnia, and the threshold of the ventilatory response returned to normal. Therefore, at 14 days of respiratory acidosis, acid-based compensation resulting from increase in bicarbonate was not associated with reduced respiratory drive. This result could not be accounted for on the basis of a temperature mechanism because temperature adaptation occurred earlier.

Acidosis, Respiratory↗
PubMed2000

Mechanisms involved in coronary artery dilatation during respiratory acidosis in the isolated perfused rat heart.

A rat Langendorff heart preparation, perfused at constant pressure, was used to evaluate the role of K(ATP) channels in respiratory acidosis-induced coronary hyperemia. Prior administration of glibenclamide, an inhibitor of K(ATP) channels, reduced basal flow rates and eliminated the hyperemia associated with hypercapnia. These results implicate K(ATP) channels as a functional link in the respiratory acidosis-induced increase in coronary flow.

Acidosis, Respiratory↗
PubMed1998

Respiratory acidosis in carbonic anhydrase II-deficient mice.

To investigate the role of carbonic anhydrase (CA) II on pulmonary CO2 exchange, we analyzed arterial blood gases from CA II-deficient and normal control mice. CA II-deficient mice had a low arterial blood pH (7.18 +/- 0.06) and HCO3- concentration ([HCO3-]; 17.5 +/- 1.9 meq/l) and a high Pco2 (47.4 +/- 5.3 mmHg), consistent with mixed respiratory and metabolic acidosis. To eliminate the influence of metabolic acidosis on arterial blood gases, NaHCO3 (4 mmol/kg body weight) was given intraperitoneally, and arterial blood gases were analyzed 4 h later. Normal mice had a small increase in pH and were able to maintain Pco2 and [HCO3-]. The metabolic acidosis in CA II-deficient mice was corrected ([HCO3-], 22.9 +/- 2.4 meq/l), and respiratory acidosis became more profound (Pco2, 50.4 +/- 2.4 mmHg). These results indicate that CA II-deficient mice have a partial respiratory compensation for metabolic acidosis. We conclude that CA II-deficient mice have a mixed respiratory and metabolic acidosis. It is most likely that CO2 retention in these animals is due to CA II deficiency in both red blood cells and type II pneumocytes.

Acidosis, Respiratory↗
PubMed1993

Effect of respiratory acidosis and alkalosis on plasma catecholamine concentrations in anaesthetized man.

1. Plasma concentrations of noradrenaline and adrenaline were measured in 11 anaesthetized patients during normocapnia, hypocapnia and hypercapnia. Hypocapnia was produced by deliberate hyperventilation and hypercapnia by adding carbon dioxide to the inspired gas mixture. 2. With a median (range) arterial partial pressure of carbon dioxide of 4.7 (4.2-5.2) kPa, the median (range) plasma concentration of noradrenaline was 0.41 (0.12-0.94) nmol/l and of adrenaline was 0.15 (0.05-0.31) nmol/l. 3. With an arterial partial pressure of carbon dioxide of 2.6 (2.2-3.3) kPa, there was no change in the plasma concentration of noradrenaline [0.37 (0.12-0.86) nmol/l] or that of adrenaline [0.16 (0.05-0.32) nmol/l]. 4. However, with an arterial partial pressure of carbon dioxide of 10.4 (7.6-13.2) kPa, there were significant increases in the plasma concentrations of both noradrenaline [1.13 (0.79-2.05) nmol/l, P < 0.01] and adrenaline [0.67 (0.20-2.92) nmol/l, P < 0.05]. 5. This is the first demonstration in man that respiratory acidosis causes an increase in plasma concentrations of catecholamines.

Adult↗
PubMed1990

Decreased colostral immunoglobulin absorption in calves with postnatal respiratory acidosis.

The effect of postnatal acid-base status on the absorption of colostral immunoglobulins by calves was examined in 2 field studies. In study 1, blood pH at 2 and 4 hours after birth was related to serum IgG1 concentration 12 hours after colostrum feeding (P less than 0.05). Decreased IgG1 absorption from colostrum was associated with respiratory, rather than metabolic, acidosis, because blood PCO2 at 2 and 4 hours after birth was negatively related to IgG1 absorption (P less than 0.05), whereas serum bicarbonate concentration was not significantly related to IgG1 absorption. Acidosis was frequently observed in the 30 calves of study 1. At birth, all calves had venous PCO2 value greater than or equal to 60 mm of Hg, 20 of the calves had blood pH less than 7.20, and 8 of the calves had blood bicarbonate concentration less than 24 mEq/L. Blood pH values were considerably improved by 4 hours after birth; only 7 calves had blood pH values less than 7.20. Calves lacking risk factors for acidosis were examined in study 2, and blood pH values at 4 hours after birth ranged from 7.25 to 7.39. Blood pH was unrelated to IgG1 absorption in the calves of study 2. However, blood PCO2 was again found to be negatively related to colostral IgG1 absorption (P less than 0.005). Results indicate that postnatal respiratory acidosis in calves can adversely affect colostral immunoglobulin absorption, despite adequate colostrum intake early in the absorptive period.

Absorption↗
PubMed2004

Death during polysomnography of a patient with cheyne-stokes respiration, respiratory acidosis, and chronic heart failure.

A patient with chronic heart failure and chronic respiratory failure (CRF) underwent ambulatory polysomnography at home. She was found dead on the morning after the recording. The tracings confirmed severe sleep apnea syndrome. After 8 h of incessant Cheyne-Stokes respiration during sleep, respiratory arrest occurred, followed 7 min later by asystole. This report illustrates a case of respiratory drive failure during sleep as the mode of death in a patient with heart failure, sleep apnea syndrome, and CRF.

Acidosis, Respiratory↗