Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACIDOSIS, RESPIRATORY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 847 records · Page 47Linked to original sources
PubMed1986

Hepatic glutaminase flux regulation of glutamine homeostasis. Studies in vivo.

The role of hepatic glutaminase flux in regulating plasma glutamine homeostasis was studied in the intact rat. Interorgan glutamine flow during chronic metabolic acidosis was away from the splanchnic bed and to the kidneys. Hindquarter and hepatic glutamine release were the major sources of glutamine removed by the kidneys. Interorgan glutamate flow was from the liver to the hindquarters and kidneys. Chronic metabolic acidosis reduced arterial glutamine concentration 30%. Acute respiratory acidosis (pH 7.12 +/- 0.02) returned arterial glutamine concentration to normal values, increasing and decreasing hepatic glutamine and glutamate release respectively; renal and gut glutamine removal rates were not decreased. Hepatic unidirectional glutamine utilization measured isotopically was decreased 51% by acute acidosis; unidirectional glutamine production was unchanged. The results are consistent with the proposed role of ammonia-activated hepatic glutaminase in the regulation of glutamine homeostasis during acute acidosis.

Acid-Base Equilibrium↗
PubMedDate not supplied

[Acid-base equilibrium in cerebrospinal fluid following intracranial surgery].

In 48 patients the acid-base equilibrium in the CSF and blood was determined on the 2nd day after intracranial operation. In the postopertive period various disturbances of this equilibrium were found which were probably various stages of metabolic acidosis compensation in the CSF which was a reflection of metabolic (lactate) acidosis developing primarily in the damaged brain area. On the basis of determinations it was found that changes in the CSF of the type of metabolic acidosis (21 cases) corresponded most frequently to respiratory alkalosis in the blood (11 cases). Changes of the type of respiratory acidosis in the CSF(13 cases) corresponded usually to metabolic alkalosis in the blood (7 cases). The development of metabolic acidosis in patients in severe and moderately severe condition (19 cases) was associated with poor prognosis as to survival since the mortality in this group was 10 (about 53%). The favourable effect of dehydrating treatment may be due also to facilitation of passage of bicarbonates from the blood into the cerebral tissue and CSF since their level is increased in the blood during metabolic alkalosis (during a decrease in the extracellular space) resulting from dehydration.

Acid-Base Imbalance↗
PubMed2003

Metabolic alkalosis contributes to acute hypercapnic respiratory failure in adult cystic fibrosis.

BACKGROUND: and study objectives: Patients with end-stage cystic fibrosis (CF) develop respiratory failure and hypercapnia. In contrast to COPD patients, altered electrolyte transport and malnutrition in CF patients may predispose them to metabolic alkalosis and, therefore, may contribute to hypercapnia. The aim of this study was to determine the prevalence of metabolic alkalosis in adults with hypercapnic respiratory failure in the setting of acute exacerbations of CF compared with COPD. DESIGN: Levels of arterial blood gases, plasma electrolytes, and serum albumin from 14 consecutive hypercapnic CF patients who had been admitted to the hospital with a respiratory exacerbation were compared with 49 consecutive hypercapnic patients with exacerbations of COPD. Hypercapnia was defined as a PaCO(2) of > or = 45 mm Hg. RESULTS: Despite similar PaCO(2) values, patients in the CF group were significantly more alkalotic than were those in the COPD group (mean [+/- SD] pH, 7.43 +/- 0.03 vs 7.37 +/- 0.05, respectively; p < 0.01). A mixed respiratory acidosis and metabolic alkalosis was evident in 71% of CF patients and 22% of COPD patients (p < 0.01). The mean concentrations of plasma chloride (95.1 +/- 4.9 vs 99.8 +/- 5.2 mmol/L, respectively; p < 0.01) and sodium (136.5 +/- 2.8 vs 140.4 +/- 4.5 mmol/L, respectively; p < 0.01) were significantly lower in the CF group, and the levels of serum albumin were significantly reduced (27.4 +/- 5.8 vs 33.7 +/- 4.8 mmol/L, respectively; p < 0.01). CONCLUSION: Metabolic alkalosis contributes to hypercapnic respiratory failure in adults with acute exacerbations of CF. This acid-base disturbance occurs in conjunction with reduced total body salt levels and hypoalbuminemia.

Acidosis, Respiratory↗
PubMed1981

Evidence of active regulation of cerebrospinal fluid acid-base balance.

To test the passive transport hypothesis of cerebrospinal fluid (CSF) [H+] regulation, we altered the relationship between plasma [H+] and the electrical potential difference between CSF and blood (PD) by elevating plasma [K+] during 6-h systemic acid-base disturbances. In five groups of pentobarbital-anesthetized dogs, we increased plasma [K+] from 3.5 to an average of 7.8 meq/l. Hyperkalemia produced an increase in the PD of 6.3 mV by 6 h with normal plasma acid-base status (pHa 7.4), of 8.3 mV with isocapnic metabolic acidosis (pHa 7.2), of 5.3 mV with isocapnic metabolic alkalosis (pHa 7.6), of 9.2 mV with isobicarbonate respiratory acidosis (PaCO2 61 Torr) and of 5.7 mV with isobicarbonate respiratory alkalosis (PaCO2 25 Torr). The change in CSF [H+] at 6 h in each group was the same as that observed in normokalemic animals (Am. J. Physiol. 228: 1134-1154, 1975). This result is not consistent with the passive transport hypothesis. The CSF-blood PD is therefore not an important determinant of CSF [H+] CSF [H+] homeostasis must result from some form of active transport control.

Acid-Base Equilibrium↗
PubMed1995

Permissive hypercapnia as a ventilatory strategy in burned children: effect on barotrauma, pneumonia, and mortality.

OBJECTIVE: To document the incidence of barotrauma, pneumonia, and respiratory death associated with a mechanical ventilation protocol based on permissive hypercapnia in pediatric burn patients. DESIGN: Retrospective review. MATERIALS AND METHODS: Patients were managed using a mechanical ventilation protocol based on permissive hypercapnia, tolerating moderate (pH > 7.20) respiratory acidosis to keep inflating pressures below 40 cm H2O. MAIN RESULTS: Over a 2.5-year interval, 54 burned children (11% of 495 acute admissions) with an average age of 6.5 years (range 5 weeks to 17 years), average burn size of 44% (range 0 to 98%), and median burn size of 46% required mechanical ventilatory support for an average of 12.5 days (range 1 to 56 days). Inhalation injury was diagnosed in 34 (63%) of the children and 72% percent were admitted within 24 hours of injury. Overt barotrauma occurred in 5.6% of the patients, pneumonia in 32%, and respiratory death in 0%. CONCLUSIONS: A conventional ventilation protocol based on permissive hypercapnia is associated with acceptable rates of barotrauma and pneumonia. The low incidence of respiratory death associated with this strategy suggests that it also minimizes ventilator-induced lung injury.

Acidosis, Respiratory↗
PubMed1980

Renal and systemic acid-base effects of chronic dichloroacetate administration in dogs.

Dichloroacetate (DCA) increases metabolic disposal of lactic acid secondary to activation of pyruvate dehydrogenase and consequent acceleration of pyruvate oxidation. DCA has thus been proposed as a therapeutic agent for clinical states of lactic acidosis. Yet, DCA has a potential metabolic acidosis-producing effect by virtue of reported effects of (A) increasing blood ketoacid concentration, (B) decreasing tubular reabsorption of filtered ketoacid anions, and (C) decreasing renal NH3 production. In the present study chronic administration of DCA, 50 mg/kg p.o. daily for 6-8 days, resulted in a cumulative increase in renal net acid excretion (NAE) (sigma delta NAE, +61 meq, p < 0.05). The increase in NAE was accounted for entirely by increased NH4+ excretion. Production of ammonia by the kidney appeared to be increased since the increased excretion of NH4+ was accompanied by an increase in urine pH (delta UpH, +0.18 +/- 0.07, p < 0.05). The increase in NAE was accompanied by a nearly identical increase in urinary anion gap (UAG) (UAG = [NH4+ + Na+ + K+] - [Cl- + HCO3- + HPO4(2-) + H2PO4-]). The increase in UAG was caused by increased urinary total organic anions, accounted for at least in part by a significant increase in urinary acetoacetate. No significant increase in urinary potassium or sodium excretion occurred. A change in plasma acid-base composition occurred that was consistent with a mild respiratory acidosis without associated primary metabolic acidosis or alkalosis. These findings indicate that chronic DCA administration results in (1) increased steady state endogenous noncarbonic organic acid production, and (2) retention of carbonic acid. Further investigation of the potential metabolic and respiratory acidosis-producing effects of DCA is required to determine its clinical efficacy in the treatment of clinical lactic acidosis.

Acetates↗
PubMed1982

[Tissue chemoreceptors].

Intraarterial administration of acids or perfusion with solutions inducing acidosis in the small intestine tissue, increase the afferent impulsation in the splanchnic nerves as well as the arterial pressure in anesthetized cats. Threshold concentrations of lactic and carbonic acids don't exceed, at that, their normal contents in the blood and tissues. Similar data were obtained in perfusion of the small intestine with blood of a donor animal whose acid--alkaline balance (AAB) was altered. The tissue receptors were found to be more sensitive to the metabolic rather than respiratory acidosis, due to different alteration of of the intratissue pH. Sensitivity of the skeletal muscles' chemoreceptors proved somewhat lower as compared with the small intestine receptors. Nevertheless, the threshold shifts of the AAB parameters in the m. gastrocnemius perfusion developed within the normal range. The changes of minute volume of ventilation revealed the possibility of tissue receptors participation in the reflex control of respiration as well. The data on adequate sensitivity of the tissue receptors to terminal products of aerobic and anaerobic metabolism: carbonic and lactic acids, once more corroborate V. N. Tchernigosky's ideas of the tissue chemoreceptors as a special class of receptor structures providing the c.n.s. with necessary information on intensity of the tissue metabolism.

Acid-Base Imbalance↗
PubMed1983

Influence of steady-state alterations in acid-base equilibrium on the fate of administered bicarbonate in the dog.

Previous workers have shown that metabolic acidosis increases the apparent space through which administered bicarbonate is distributed. This finding has been ascribed to the accompanying acidemia and to the consequent availability of a large quantity of hydrogen ion that accumulates on nonbicarbonate tissue buffers during the development of acidosis. To test this hypothesis, bicarbonate space was measured in dogs with a broad range of steady-state plasma [HCO-3] in association with alkalemia as well as with acidemia. Appropriate combinations of pH and plasma [HCO-3] were achieved by pretreating the animals to produce graded degrees of each of the four cardinal, chronic acid-base disorders. Metabolic acidosis (n = 15) was produced by prolonged HCl-feeding; metabolic alkalosis (n = 17) by diuretics and a chloride-free diet; and respiratory acidosis (n = 9) and alkalosis (n = 8) by means of an environmental chamber. Animals with normal acid-base status (n = 4) were also studied. Sodium bicarbonate (5 mmol/kg) was infused over 10 min to the unanesthetized animals; observations were carried out over 90 min. The results obtained from animals with metabolic acid-base disturbances demonstrated an inverse relationship between bicarbonate space and initial plasma pH, confirming the previous findings of others. By contrast, the results obtained in animals with respiratory acid-base disturbances demonstrated a direct relationship between bicarbonate space and initial plasma pH. The pooled data revealed that bicarbonate space is, in fact, quite independent of the initial pH but is highly correlated with the initial level of extracellular [HCO-3]; dogs with low extracellular [HCO-3] (congruent to 10 meq/liter) whether acidemic or alkalemic, have a bicarbonate space that is 25% larger than normal and some 50% larger than in dogs with high extracellular [HCO-3] (congruent to 50 meq/liter). We conclude from these results that the increased bicarbonate space in metabolic acidosis (and respiratory alkalosis) does not reflect the availability of more hydrogen ions for release during bicarbonate administration, but merely evidences the wider range of titration (delta pH) of nonbicarbonate buffers that occurs during alkali loading whenever plasma [HCO-3] is low.

Acid-Base Equilibrium↗
PubMed1984

Synergistic effect of acidosis and succinylcholine-induced hyperkalemia in spinal cord transected rats.

The effects of spinal cord transection and acidosis on succinylcholine (SCC)-induced hyperkalemia were studied in Sprague-Dawley rats. The effectiveness of pretreatment with subparalyzing doses ("self-taming") of SCC or with the cholinesterase inhibitor hexafluorenium bromide in preventing hyperkalemia was also studied. The increase in plasma potassium after administration of SCC (1 mg/kg) was found to be significantly increased 10 days after spinal cord transection. This potassium increase could not be prevented by pretreatment with either hexafluorenium (0.3 mg/kg) or subparalyzing doses (0.15 mg/kg) of SCC. Respiratory acidosis caused an increase in plasma K+ in both normal and in spinal cord transected rats. Acidosis had a synergistic effect on succinylcholine-induced hyperkalemia. These findings support the clinical practice of not using succinylcholine in patients at risk of having a pathological sensitivity to SCC. Furthermore, SCC may be especially dangerous when administered to patients who are acidotic.

Acidosis, Respiratory↗
PubMed1990

Rational treatment of acid-base disorders.

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.

Acid-Base Imbalance↗
PubMed1979

P pulmonale in status asthmaticus.

We studied 129 patients during acute, severe asthmatic attacks. Electrocardiograms showed P pulmonale in 49% of patients who had an arterial carbon dioxide tension (PaCo2) greater than or equal to 45 mm Hg and an arterial pH less than or equal to 7.37, whereas P pulmonale was present in only 2.5% of asthmatics who had a PaCO2 less than or equal to 44 mm Hg and a pH greater than or equal to 7.38 (p less than 0.001). P wave and QRS axes were 79 +/- 8 degrees and 80 +/- 20 degrees, respectively, in the presence of P pulmonale. When P pulmonale disappeared, the P wave and QRS axes shifted significantly to the left (p less than 0.001). Electrocardiographic P pulmonale persisted 12 to 60 hr after correction of hypoxemia, hypercapnia, and acidosis. In 7 patients with P pulmonale and respiratory acidosis, cardiac catheterization demonstrated normal artery pressures (PAPs) measured relative to atmospheric pressure. In 12 of these peak inspiratory pulmonary artery transmural pressures (PATPs) were increased. Since increased right heart transumural pressures could result in chamber distention, these data are consistent with the hypothesis that reversible P pulmonale in status asthmaticus is explainable on the basis of markedly negative tidal pleural pressures and increased right heart transmural pressures.

Adolescent↗
PubMed1983

Ammonia and acid-base homeostasis.

The metabolic pathways involved in renal ammonia production have been considered and potential sites of regulatory control have been delineated. New information that acute acidosis stimulates renal ammonia production and that chronic respiratory acidosis does not result in an adaptive increase in the renal capacity to produce ammonia has been emphasized. The effect of potassium on renal ammonia production and the physiologic and pathophysiologic implication of this relationship have been detailed. Finally, the mechanism of urinary ammonium excretion and the impact of altered ammoniagenesis on urinary acidification, and the interpretation of clinical acidification tests have been discussed.

Acid-Base Equilibrium↗
PubMed1982

Evaluation of bicarbonate transport in rat distal tubule: effects of acid-base status.

Previous micropuncture studies utilizing indirect methods to estimate bicarbonate transport in the rat superficial distal tubule have indicated that the distal bicarbonate reabsorptive process normally operates well below the saturation level. Recent studies from our laboratory failed to demonstrate a spontaneous acid disequilibrium pH in this segment, implying that the bicarbonate reabsorptive rate was less than previously estimated. The purpose of the present experiments were 1) to measure the rate of absolute bicarbonate reabsorption by the rat superficial distal tubule while controlling bicarbonate delivery, and 2) to examine the effects of alterations in acid-base status on the rate of bicarbonate reabsorption. Five groups of rats in different states of acid-base balance were studied. No significant bicarbonate reabsorption was detected in the control hydropenic, combined respiratory acidosis-metabolic alkalosis, acute respiratory acidosis, or acute metabolic acidosis groups. In contrast, metabolic acidosis of 3 days duration resulted in a significant bicarbonate reabsorptive rate of 52.6 +/- 13.9 pmol . mm-1 . min-1. The observation of significant bicarbonate reabsorption in the distal tubule only during chronic metabolic acidosis of 3 days duration is compatible with adaptation of this normally low-capacity segment to chronic changes in systemic acid-base states.

Acid-Base Equilibrium↗
PubMed1995

Fluorosis-like effects of acidosis, but not NH+4, on rat incisor enamel.

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.

Acidosis↗
PubMed1997

Comparative physiologic effects of noninvasive assist-control and pressure support ventilation in acute hypercapnic respiratory failure.

STUDY OBJECTIVE: To compare the effects of noninvasive assist-control ventilation (ACV) and pressure support ventilation (PSV) by nasal mask on respiratory physiologic parameters and comfort in acute hypercapnic respiratory failure (AHRF). DESIGN: A prospective randomized study. SETTING: A medical ICU. PATIENTS AND INTERVENTIONS: Fifteen patients with COPD and AHRF were consecutively and randomly assigned to two noninvasive ventilation (NIV) sequences with ACV and PSV mode, spontaneous breathing (SB) via nasal mask being used as control. ACV and PSV settings were always subsequently adjusted according to patient's tolerance and air leaks. Fraction of inspired oxygen did not change between the sequences. MEASUREMENTS AND RESULTS: ACV and PSV mode strongly decreased the inspiratory effort in comparison with SB. The total inspiratory work of breathing (WOBinsp) expressed as WOBinsp/tidal volume (VT) and WOBinsp/respiratory rate (RR), the pressure time product (PTP), and esophageal pressure variations (deltaPes) were the most discriminant parameters (p<0.001). ACV most reduced WOBinsp/VT (p<0.05), deltaPes (p<0.05), and PTP (0.01) compared with PSV mode. The surface diaphragmatic electromyogram activity was also decreased >32% as compared with control values (p<0.01), with no difference between the two modes. Simultaneously, NIV significantly improved breathing pattern (p<0.01) with no difference between ACV and PSV for VT, RR, minute ventilation, and total cycle duration. As compared to SB, respiratory acidosis was similarly improved by both modes. The respiratory comfort assessed by visual analog scale was less with ACV (57.23+/-30.12 mm) than with SB (75.15+/-18.25 mm) (p<0.05) and PSV mode (81.62+/-25.2 mm) (p<0.01) in our patients. CONCLUSIONS: During NIV for AHRF using settings adapted to patient's clinical tolerance and mask air leaks, both ACV and PSV mode provide respiratory muscle rest and similarly improve breathing pattern and gas exchange. However, these physiologic effects are achieved with a lower inspiratory workload but at the expense of a higher respiratory discomfort with ACV than with PSV mode.

Acute Disease↗
PubMed2004

Remifentanil for foetal immobilisation and maternal sedation during endoscopic treatment of twin-to-twin transfusion syndrome : a preliminary dose-finding study.

Twin to twin transfusion syndrome (TTTS) affects 10 to 15% of monochorionic twin pregnancies. Untreated, perinatal loss exceeds 80%, of which survivors have a great risk for long-term neurological disorders as psychomotor retardation or cerebral palsy. TTTS can be treated using foetoscopy and selective ablation of the twin-to-twin blood vessels under local or regional anaesthesia. However, local or regional anaesthesia does not always result in excellent maternal comfort, nor does it provide foetal immobilisation, necessary for optimal surgical conditions. Using a continuous infusion rate of remifentanil 0.1 microg/kg/min, perfect foetal immobilisation and excellent maternal sedation was achieved. Only mild respiratory acidosis was observed as a result of mild respiratory depression. In no mother apnoe occurred. All haemodynamic parameters, both foetal and maternal, remained stable during the procedure. Maternal sedation, respiratory depression and foetal immobilisation were quickly reversible following cessation of the remifentanil infusion.

Adult↗