SEARCH · Search PubMed

Results for “ACIDOSIS”

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.

SourceResearch connectionFrom yearThrough year

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

At least 433 records · Page 24Linked to original sources

PubMed1999

Lactic acidosis caused by thiamine deficiency in a pregnant alcoholic patient.

BACKGROUND: Metabolic acidosis from accumulation of lactic acid is a relatively common condition, whereas its causation by thiamine deficiency is not. METHODS: We studied a pregnant alcoholic patient who presented with hyperemesis and a high anion gap acidosis. RESULTS: Lactic acidosis and thiamine deficiency were confirmed. The patient's symptoms and acidosis resolved with thiamine administration. CONCLUSIONS: Lactic acidosis caused by thiamine deficiency must be suspected when pregnant patients at risk for thiamine deficiency present with a high anion gap acidosis. A large dose of thiamine must be administered immediately.

Acidosis, Lactic↗

PubMed1997

The effects of bupivacaine and ropivacaine on baroreflex sensitivity with or without respiratory acidosis and alkalosis in rats.

Systemic toxicity of local anesthetics causes cardiac and central nervous system (CNS) depression that could be enhanced in the presence of respiratory acidosis. We examined a potential suppression of baroreflex function with bupivacaine and ropivacaine during hypercapnic acidosis or hypocapnic alkalosis. Baroreflex sensitivity (BRS) was randomly tested in rats with one of 13 conditions during intravenous administration of saline (control), bupivacaine 1, 2, or 3 mg/kg, or ropivacaine 2, 4, or 6 mg/kg. The effects of bupivacaine (3 mg/kg) or ropivacaine (6 mg/kg) on BRS were also examined during hypercapnic acidosis or hypocapnic alkalosis. The BRS was assessed using a value of delta heart rate/ delta mean arterial pressure after infusion of phenylephrine (3 micrograms/kg). Both bupivacaine and ropivacaine (at the largest dose) significantly suppressed BRS. Acute respiratory acidosis (pHa 7.24 +/- 0.04, Paco2 63 +/- 4 mm Hg) enhanced BRS. The BRS enhanced during acidosis was also suppressed with bupivacaine and ropivacaine, but less so than in the absence of acidosis. The presence of hypocapnic alkalosis (pHa 7.55 +/- 0.03, Paco2 25 +/- 2 mm Hg) did not affect BRS and reversed BRS suppression caused by both drugs. Thus, bupivacaine and ropivacaine affect neuronal control mechanisms for maintaining cardiovascular stability, and acute changes of respiration could significantly modify such suppression.

Acidosis, Respiratory↗

PubMed1994

Hyperventilation in the treatment of metabolic acidosis does not adversely affect pulmonary gas exchange.

BACKGROUND: Hyperventilation has been recommended to increase blood pH during metabolic acidosis. However, hypocapnia may adversely affect arterial blood oxygenation, especially in the presence of lung disease. We therefore studied the effects of metabolic acidosis, with and without normalization of pH by hyperventilation, on pulmonary gas exchange in dogs with permeability pulmonary edema. METHODS: Six pentobarbital-anesthetized dogs were administered 0.06 ml/kg of oleic acid at least 150 min before study. Ventilation was set with an inspired O2 fraction of 0.90 and a tidal volume of 18 ml/kg, and the respiratory rate was adjusted to alter the arterial CO2 tension (PaCO2) per the experimental protocol. The protocol in random order was (1) normal pH (7.36 +/- 0.01)/normal PaCO2 (39 +/- 1 mmHg); (2) low pH 7.20 +/- 0.01)/normal PaCO2 (40 +/- 1 mmHg); (3) low pH (7.18 +/- 0.01)/hyperventilation with inspired CO2 (PaCO2 = 40 +/- 1 mmHg); and (4) normal pH (7.35 +/- 0.01)/hyperventilation with low PaCO2 (24 +/- 1 mmHg). In phases 2-4, the pH was slowly reduced by intravenous infusion of 2 N hydrochloric acid. The pH was normalized in phase 1 where necessary by infusion of sodium bicarbonate. The pH in phase 4 was normalized by reducing the PaCO2 by increasing the respiratory rate. Gas exchange was assessed by the multiple inert-gas elimination technique. RESULTS: The hemodynamic measurements remained constant throughout the protocol. Arterial O2 tension increased from 244 +/- 55 to 293 +/- 49 mmHg in the presence of metabolic acidosis (P < 0.05). Hyperventilation to normalize the pH during metabolic acidosis (phase 4), increased arterial O2 tension (313 +/- 44 mmHg, P < 0.05), and reduced shunt (from 20 +/- 5% to 12 +/- 3%, P < 0.05) compared with normal acid-base conditions (phase 1). No change in shunt was observed with hyperventilation compared with metabolic acidosis alone (phase 2). The decrease in pulmonary shunt was not attributable to the direct effects of hyperventilation, because shunt was increased (20 +/- 5%) when PaCO2 was normalized during hyperventilation by inspiration of CO2 (phase 3). CONCLUSIONS: Hyperventilation to normalize blood pH during hydrochloric acid-induced metabolic acidosis did not adversely affect pulmonary gas exchange in dogs with permeability pulmonary edema.

Acidosis↗

PubMed1989

Tall T waves during metabolic acidosis without hyperkalemia: a prospective study.

The specific ECG characteristics of metabolic acidosis have not been satisfactorily defined in man. We addressed this question by prospectively studying 14 consecutive patients admitted with metabolic acidosis and without hyperkalemia. Arterial blood gas analysis and serum potassium determinations were performed during acidosis and after its correction. ECGs were recorded at the same times. Mean pHa increased from 7.11 +/- 0.05 to 7.40 +/- 0.01 (p less than .001) in response to an increase in total CO2 content from 6.8 +/- 1.4 to 21.2 +/- 0.7 mmol/L (p less than .001). Serum potassium concentration decreased only slightly after correction of the acidosis from 4.2 +/- 0.1 to 3.9 +/- 0.14 mmol/L (p less than .05). T waves were taller during acidosis than after correction (0.68 +/- 0.1 vs. 0.28 +/- 0.04 mV, p less than .001 and 0.64 +/- 0.08 vs. 0.38 +/- 0.04, p less than .005, in precordial leads V2 and V3, respectively). Moreover, the amplitude of T waves in V2 was correlated positively with the arterial concentration of H+ (r = .786, p less than .001) and negatively with the arterial total CO2 content (r = -.71, p less than .005). In addition to their augmented amplitude, T waves were peaked and symmetrical with a narrow base ("tent-shaped"). Thus, metabolic acidosis may be accompanied by an increase in the amplitude of T waves, even in the absence of hyperkalemia.

Acid-Base Equilibrium↗

PubMed1992

Lactic acidosis in critical illness.

PURPOSE: This article reviews the current body of knowledge regarding lactic acidosis in critically ill patients. The classification of disordered lactate metabolism and its pathogenesis are examined. The utility of lactate as a metabolic monitor of shock is examined and current therapeutic strategies in the treatment of patients suffering from lactic acidosis are extensively reviewed. The paper is designed to integrate basic concepts with a current approach to lactate in critical illness that the clinician can use at the bedside. DATA SOURCES: Comprehensive review of the available, basic science, medical, surgical, and critical care literature. CONCLUSIONS: The severity of lactic acidosis in critically ill patients correlates with overall oxygen debt and survival. Lactate determinations may be useful as an ongoing monitor of perfusion as resuscitation proceeds. Therapy of critically ill patients with lactic acidosis is designed to maximize oxygen delivery in order to reduce tissue hypoxia by increasing cardiac index, while maintaining hemoglobin concentration. Buffering agents have not been shown to materially affect outcome from lactic acidosis caused by shock. The benefits of other specific therapies designed to reduce the severity of lactic acidosis remain unproven.

Acidosis, Lactic↗

PubMed1997

Epinephrine-induced lactic acidosis following cardiopulmonary bypass.

OBJECTIVE: To determine if lactic acidosis occurring after cardiopulmonary bypass could be attributed to the metabolic or other effects of epinephrine administration. DESIGN: Prospective, randomized study. SETTING: Postsurgical cardiothoracic intensive therapy unit. PATIENTS: Thirty-six adult patients, without acidosis, requiring vasoconstrictors for the management of hypotension after cardiopulmonary bypass. INTERVENTIONS: Randomized administration of either epinephrine or norepinephrine by infusion. MEASUREMENTS AND MAIN RESULTS: Hemodynamic and metabolic data were collected before commencement of vasoconstrictor therapy (time 0) and then 1 hr (time 1), 6 to 10 hrs (time 2), and 22 to 30 hrs (time 3) later. Six of the 19 patients who received epinephrine developed lactic acidosis. None of the 17 patients receiving norepinephrine developed lactic acidosis. In the epinephrine group, but not in the norepinephrine group, lactate concentration increased significantly at times 1 and 2 (p = .01), while pH and base excess decreased (p < or = .01). Blood glucose concentration was higher in the epinephrine group at time 2 (p = .02), while the cardiac index (p < .03) and the mixed venous Po2 (p = .04) were higher at time 1. compared with the norepinephrine group, the patients receiving epinephrine had higher femoral venous lactate concentrations (p = .03), increased lower limb blood flow (p = .05), and increased femoral venous oxygen saturations (p = .04). CONCLUSIONS: The use of epinephrine after cardiopulmonary bypass precipitates the development of lactic acidosis in some patients. This phenomenon is presumably a beta-mediated effect, and is associated with an increase in whole-body and lower limb blood flow and a decrease in whole-body and transfemoral oxygen extraction. The phenomenon does not appear to be related to reduced tissue perfusion and does not have the poor outlook of lactic acidosis associated with shock.

Acidosis, Lactic↗

PubMed2004

Defining acidosis in postoperative cardiac patients using Stewart's method of strong ion difference.

OBJECTIVE: To define the true incidence and nature of acidosis in pediatric patients postcardiac surgery, using Stewart's direct method of measuring strong ion difference. We also wished to compare the ability of standard indirect methods (base deficit, lactate, anion gap, and corrected anion gap) to accurately predict tissue acidosis. DESIGN: A single-center prospective observational study. SETTING: A pediatric intensive care unit in a tertiary referral center. PATIENTS: Pediatric patients who had undergone cardiac surgery were studied in the immediate postoperative period. Patients who had undergone both open and closed cardiac surgery were included. INTERVENTIONS: Routine arterial blood gas analysis and laboratory electrolyte measurements were made in patients immediately on admission to the pediatric intensive care unit (PICU) after cardiac surgery and each morning until discharge from the PICU. MEASUREMENTS AND MAIN RESULTS: Figge's equations were used to calculate strong ion difference and total tissue acids (unmeasured acids and lactate). These direct methods then were compared to indirect measurements: base deficit, lactate anion gap, and anion gap corrected for albumin. We collected 150 samples from 44 patients. Tissue acidosis occurred overall in 60 of 150 samples. This was due to raised unmeasured acids alone in 44 of 60 (73.3%), raised lactate alone in six of 60 (10%), and a combination of the two in ten of 60 (16.6%). Hyperchloremia occurred in 19 of 150 samples overall and 12 of 25 (48%) samples immediately after cardiopulmonary bypass. Measured base deficit showed a poor correlation with true tissue acidosis (r = -.48, p <.001) and the worst discriminatory ability (area under the curve, 0.72; 0.62-0.82). Anion gap corrected for albumin had the best correlation (r =.95, p <.001) and highest area under the curve (0.90; 0.85-0.95). CONCLUSIONS: Metabolic acidosis occurs frequently postcardiac surgery and is largely due to raised unmeasured acids and less commonly raised lactate. Hyperchloremia is common, particularly after cardiopulmonary bypass. Base deficit correlates poorly with true tissue acidosis, and corrected anion gap offers the most accurate bedside alternative to Stewart's method of tissue acid calculation.

Acid-Base Equilibrium↗

PubMed2006

Acidosis in models of cardiac ventricular myocytes.

The effects of acidosis on cardiac electrophysiology and excitation-contraction coupling have been studied extensively. Acidosis decreases the strength of contraction and leads to altered calcium transients as a net result of complex interactions between protons and a variety of intracellular processes. The relative contributions of each of the changes under acidosis are difficult to establish experimentally, however, and significant uncertainties remain about the key mechanisms of impaired cardiac function. In this paper, we review the experimental findings concerning the effects of acidosis on the action potential and calcium handling in the cardiac ventricular myocyte, and we present a modelling study that establishes the contribution of the different effects to altered Ca2+ transients during acidosis. These interactions are incorporated into a dynamical model of pH regulation in the myocyte to simulate respiratory acidosis in the heart.

Acidosis↗

PubMed2006

Investigations on the association of D-lactate blood concentrations with the outcome of therapy of acidosis, and with posture and demeanour in young calves with diarrhoea.

The objective of this prospective study was to elucidate whether amounts of bicarbonate needed for correction of acidosis and normalization of clinical signs are influenced by blood D-lactate concentrations in calves with diarrhoea. In 73 calves up to 3 weeks old with acute diarrhoea and base excess values below -10 mmol/l correction of acidosis was carried out within 3.5-h by intravenous administration of an amount of sodium bicarbonate which was calculated using the formula: HCO (mmol) = body mass (kg) x base deficit (mmol/l) x 0.6 (l/kg). Clinical signs, venous base excess, and plasma D-lactate concentrations were monitored immediately following admission, following correction of acidosis at 4 h and 24 h after admission. The base excess and plasma D-lactate concentrations throughout the study were -17.8 +/- 4.0, -0.4 +/- 0.4, -3.0 +/- 5.5 mmol/l (base excess), and 10.0 +/- 4.9, 9.8 +/- 4.8, 5.4 +/- 3.4 mmol/l (D-lactate) for the three times of examination. Metabolic acidosis was not corrected in more than half of the calves (n = 43) by the calculated amount of bicarbonate, whereas the risk of failure to correct acidosis increases with D-lactate concentrations. The study shows that calves with elevated D-lactate concentrations do not need additional specific therapy, as D-lactate concentrations regularly fall following correction of acidosis and restitution of body fluid volume, for reasons that remain unclear. However, calves with distinct changes in posture and demeanour need higher doses of bicarbonate than calculated with the factor of 0.6 in the formula mentioned above probably because of D-hyperlactataemia.

Acid-Base Equilibrium↗

PubMed1997

Mechanism of oxidative stress-induced intracellular acidosis in rat cerebellar astrocytes and C6 glioma cells.

1. Following ischaemic reperfusion, large amounts of superoxide anion (.O2-), hydroxyl radical (.OH) and H2O2 are produced, resulting in brain oedema and changes in cerebral vascular permeability. We have found that H2O2 (100 microM) induces a significant intracellular acidosis in both cultured rat cerebellar astrocytes (0.37 +/- 0.04 pH units) and C6 glioma cells (0.33 +/- 0.07 pH units). 2. Two membrane-crossing ferrous iron chelators, phenanthroline and deferoxamine, almost completely inhibited H2O2-induced intracellular acidosis, while the non-membrane-crossing iron chelator apo-transferrin had no effect. Furthermore, the acidosis was completely inhibited by two potent membrane-crossing .OH scavengers, N-(2-mercaptopropionyl)-glycine (N-MPG) and dimethyl thiourea (DMTU). Since .OH can be produced during iron-catalysed H2O2 breakdown (Fenton reaction), we have shown that a large reduction in pH1 in glial cells can result from the production of intracellular .OH via H2O2 oxidation. 3. We have ruled out the possible involvement of: (i) an increase in intracellular Ca2+ levels; and (ii) inhibition of oxidative phosphorylation. 4. Our results suggest that .OH inhibits glycolysis, leading to ATP hydrolysis and intracellular acidosis. This conclusion is based on the following observations: (i) in glucose-free medium, or in the presence of iodoacetate or 2-deoxy-D-glucose, H2O2-induced acidosis is completely suppressed; (ii) H2O2 and iodoacetate both produce an increase in levels of intracellular free Mg2+, an indicator of ATP breakdown; and (iii) direct measurement of intracellular ATP levels and lactate production show 50 and 55% reductions in ATP content and lactate production, respectively, following treatment with 100 microM H2O2. 5. Inhibition of the pH1 regulators (i.e. the Na(+)-H+ exchange and possibly the Na(+)-HCO3(-)-dependent pH1 transporters) resulting from H2O2-induced intracellular ATP reduction may also be involved in the H2O2-evoked intracellular acidosis in glial cells.

Acidosis↗

PubMed2006

Determinants of metabolic acidosis among hemodialysis patients.

Metabolic acidosis is frequently present, poorly controlled, and associated with adverse effects among hemodialysis patients. Potential determinants of metabolic acidosis include endogenous acid production, administration of alkali, neutralization of acid by buffers, dilution of serum bicarbonate by interdialytic fluid gain, and loss of bicarbonate in stool. Understanding the relative importance of these determinants may help guide efforts to manage metabolic acidosis. We used chart abstraction, patient interviews, and laboratory testing to assess variables related to acid production (protein breakdown), alkali administration (dialysis dose, missed treatments, dialysate bicarbonate concentration, oral bicarbonate supplements), acid buffering (phosphorus binders), dilution of bicarbonate (interdialytic weight gain), and loss of bicarbonate in stool (diarrhea) for 190 randomly selected patients from 44 hemodialysis facilities. We used multivariate analyses to determine which potential determinants were independently associated with predialysis serum bicarbonate levels. Of all patients, 30% had metabolic acidosis (serum bicarbonate level <22 mEq/L). On multivariate analysis, metabolic acidosis was more likely with increased protein nitrogen appearance (odds ratio [OR] 1.60 per 0.2 g/kg/day, p=0.001) and less likely with increased Kt/V (OR 0.61 per 0.20 increase in Kt/V, p<0.001) and with increased calcium carbonate use (OR 0.38 per 2 g/day, p=0.003). Key determinants of metabolic acidosis among hemodialysis patients are protein breakdown, dialysis dose, and specific phosphorus binders. Further work is needed to develop interventions to address these determinants.

Acidosis↗

PubMed2006

Optic nerve pH and PO2: the effects of carbonic anhydrase inhibition, and metabolic and respiratory acidosis.

PURPOSE: Earlier studies have demonstrated that carbonic anhydrase inhibitors (CAIs) increase optic nerve oxygen tension (ONPO(2)) in pigs. We hypothesized that the mechanism of this effect was either a CO(2) increase or a pH decrease in tissue and blood. To test this hypothesis we investigated and compared how optic nerve pH (ONpH) and ONPO(2) are affected by: (1) carbonic anhydrase inhibition; (2) respiratory acidosis, and (3) metabolic acidosis. We measured ONpH with a glass pH electrode and ONPO(2) with a polarographic oxygen electrode. One of the electrodes was placed in the vitreous cavity 0.5 mm over the optic nerve in the eyes of domestic pigs. METHODS: We measured ONpH during carbonic anhydrase inhibition and ONpH or ONPO(2) during NH(4)Cl-induced metabolic acidosis and during CO(2) breathing (respiratory acidosis). RESULTS: Baseline ONpH was 0.12 +/- 0.06 lower than arterial pH (mean +/- SD, n = 10, p < 0.001). Optic nerve pH decreased with arterial pH during carbonic anhydrase inhibition, metabolic and respiratory acidosis. Optic nerve oxygen tension was not affected by metabolic acidosis but increased during CO(2) breathing, as it has been shown to do during carbonic anhydrase inhibition. CONCLUSIONS: There is a close correlation between arterial blood pH and intraocular pH. Isolated ONpH changes do not affect ONPO(2), thus the ONPO(2) increase seen with carbonic anhydrase inhibition is probably not only due to pH changes in the blood and optic nerve. Accumulation of CO(2), either alone or in combination with a pH change, is likely to cause the ONPO(2) increase, but a direct vascular effect should also be considered.

Acidosis, Respiratory↗

PubMed1976

Inhibition by acidosis of adenosine 3',5'-cyclic monophosphate accumulation and lipolysis in isolated rat fat cells.

Lipolysis and cyclic AMP accumulation were studied in isolated rat fat cells at normal (7.4) and decreased (7.0, 6.6) pH. Acidosis inhibited lipolysis and cyclic AMP accumulation due to NA non-competetively. Maximal lipolysis (3 muM NA) was inhibited by 25% at pH 7.0 and by 61% at pH 6.6 Cyclic AMP accumulation 5 min after 3 muM NA was inhibited by 57% at pH 7.0 and by 83% at pH 6.6. Between 10 and 60 minutes of incubation NA-stimulated lipolysis was linear at pH 7.4, whereas a progressively increasing inhibition was seen at lower pH. The FFA production was inhibited to the same degree as glycerol production by acidosis. The fraction of FFA associated with the cells was the same at all pHs. Thus, we have no evidence that acidosis inhibits lipolysis via accumulation of FFA intracellularly. NA-induced accumulation of 3H-cAMP from 3H-ATP, endogenously formed by prelabelling the cells with 3H-adenine, was inhibited by acidosis both in the presence and absence of theophylline in the incubation medium (by 48 and 44% respectively at pH 7.0 and by 74 and 68% at pH 6.6). Cyclic nucleotide phosphodiesterase in homogenates of fat cells was inhibited by decreasing the pH, whether measured at high or low substrate concentrations. Basal adenylyl cyclase activity in a cell membrane fraction from fat cells was affected to a minor degree, while NA-stimulated activity was inhibited by decreased pH. The response to 3 muM NA at pH 6.6 was inhibited by 43% relative to control. The results show that acidosis inhibits NA-induced cyclic AMP accumulation by interfering with the formation, rather than the inactivation of the nucleotide. Since NA-induced lipolysis is a cyclic AMP-mediated process it is suggested that at least part of the antilipolytic effect of acidosis is due to inhibition of cyclic AMP formation.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed2001

The effect of acidosis on the ECG of the rat heart.

We have investigated the effect of acidosis on the ECG in isolated rat heart to determine whether acidosis has marked effects on the ECG, and have used pharmacological agents to investigate possible mechanisms whereby acidosis alters the ECG. Acidosis produced a marked decrease in heart rate and an increase in P-R interval with little apparent effect on the duration of the QRS complex. The effects of acidosis did not appear to be due to acidosis-induced changes in transmitter release from severed autonomic nerve terminals within the heart. Experimental Physiology (2001) 86.1, 27-31.

4-Aminopyridine↗

PubMed1995

The effect of mechanical loading on the response of rat ventricular myocytes to acidosis.

The effect of mechanical loading on the negative inotropic effect of acidosis in isolated rat ventricular myocytes was investigated. The mechanical loading of the myocytes was changed by attaching carbon fibres to the ends of the cell. To monitor intracellular Ca2+ and Na+ concentrations, cells were loaded with fluorescent dyes (fura-2 for Ca2+ and SBFI for Na+) using the acetoxymethyl (AM) esters. Mechanical loading reduced cell shortening by 73.0 +/- 3.5% (mean +/- S.E.M., n = 16) and abbreviated the time course of contraction. CO2-induced acidosis caused a rapid decrease in contraction followed by a slow partial recovery. The percentage changes in contraction were not significantly different in mechanically loaded and unloaded conditions. Mechanical loading had little effect on the time course of contraction during acidosis. Changes in intracellular Ca2+ and Na+ concentrations during acidosis were unaffected by mechanical loading. The mechanical loading conditions of a region of the heart can be modified by ischaemia and the subsequent acidosis. Our results suggest that the response of cardiac muscle to acidosis is not markedly modified by such changes in mechanical loading.

Acidosis↗

PubMed1993

Metabolic acidosis and breathlessness during exercise and hypercapnia in man.

1. A previous study showed that when combined with exercise in normal subjects, hypercapnic and hypoxic ventilatory stimuli did not have a specific effect on the intensity of the sensation of breathlessness in addition to their stimulation of ventilation. The aim of the present study was to assess the significance of another reflex ventilatory stimulus, metabolic acidosis, in the genesis of this sensation. 2. Six subjects performed progressive exercise tests (mean workload, 103 W; range, 88-125 W) with normal acid-base status. Following NH4Cl-induced metabolic acidosis (mean change in base excess, -3.6 mmol l-1; range, -0.3 to -6.8 mmol l-1) exercise was repeated (mean workload, 91 W; range, 53-116 W) such that the combined ventilatory stimulation resulted in levels of ventilation (mean maximum, 65 l min-1) 'matched' to those resulting from exercise alone. A third, 'matched ventilation', exercise test was performed during metabolic acidosis but with end-tidal PCO2 controlled to a normal level (mean workload, 56 W; range, 17-103 W). Breathlessness was assessed using a visual analogue scale (VAS). 3. Progressive hypercapnic ventilatory stimulation was given before (mean maximum end-tidal PCO2 (PET,CO2), 61 mmHg) and during metabolic acidosis (mean maximum PET,CO2, 57 mmHg) to achieve the same peak level of ventilation (mean maximum, 59 l min-1). Breathlessness was assessed with the VAS. 4. As ventilation increased during a test, there were no statistically significant differences in the increasing breathlessness scores with metabolic acidosis compared to control, for either exercise (mean VAS, 22 mm vs. 24 mm) or progressive hypercapnia (mean peak VAS, 31 mm vs. 32 mm). 5. These results do not support the idea that metabolic acidosis is associated with a change in the relationship between the intensity of breathlessness and ventilation; this is similar to results found with other reflex ventilatory stimuli. 6. These findings are consistent with the hypothesis that the degree of reflex ventilatory activation is an important determinant of the intensity of the sensation of breathlessness in healthy humans, irrespective of the exact nature of ventilatory stimulus.

Acidosis↗

PubMed2006

The anion gap does not accurately screen for lactic acidosis in emergency department patients.

INTRODUCTION: Lactic acidosis portends a poor prognosis in trauma, sepsis, and other shock states and is useful for triaging and resuscitating emergency department (ED) patients. The authors sought to determine whether the AG is a reliable screen for lactic acidosis when applied specifically in the ED setting. METHODS: The authors performed a retrospective cohort study over a seven month period. Subjects were all ED patients that had a serum lactate obtained. Sensitivity analyses of the AG for detecting presence of lactic acidosis were calculated for the traditional AG normal value (AG <12) and for the lower AG normal value when using newer ion selective electrode assays (AG <6). RESULTS: Serum lactate levels were ordered in the ED on 440 occasions. 137 samples were excluded by protocol. Using an AG cutoff of 12, the sensitivity for detecting lactic acidosis was 58.2%, specificity was 81.0%, and the negative predictive value was 89.7%. Using the AG cutoff of 6, the sensitivity was 93.2%, the specificity was 17.3%, and the negative predictive value was 91.8%. CONCLUSIONS: The traditional definition of AG >12 was insensitive for the presence of lactic acidosis. Using the revised AG of >6 is more sensitive but non-specific for lactic acidosis. The authors conclude that employing the AG as a screen for LA may be inappropriate in ED patients. Instead, they recommend ordering a serum lactate immediately upon suspicion of a shock state. A prospective study to confirm these findings is needed.

Acidosis, Lactic↗

PubMed1986

Renal metabolism during four types of lactic acidosis in the dog including anoxia.

The present study was undertaken to evaluate the metabolic response of the kidney to lactic acidosis. Four types of lactic acidosis were induced in the dog: infusion of lactic acid, infusion of lactic acid with phenformin, administration of phenformin alone, and hypoxia by breathing 95% nitrogen. In all groups of animals, the same degree of acidosis was observed with plasma bicarbonate ranging from 12.8 to 14.9 mM. Plasma lactate concentration ranged from 3.0 to 8.1 mumol/mL. Renal ammoniagenesis failed to be influenced by lactic acidosis. As a matter of fact, it fell during anoxia. The extraction of glutamine by the kidney rose except during anoxia where it fell. The renal production of alanine rose during the infusion of lactic acid with and without phenformin. This coincided with the extraction of glutamine. The renal extraction of lactate rose in all forms of acidosis as well as the production of pyruvate. In the renal cortical tissue, the concentration of malate, pyruvate, and lactate rose. Alanine also rose except during anoxia. An important fall in cytosolic redox potential (NAD+/NADH lactate dehydrogenase) was observed, as well as a fall in mitochondrial redox (NAD+/NADH beta-hydroxybutyrate dehydrogenase). Lactate also accumulated in the liver and in the muscle. We propose that the kidney is unable to respond to lactic acidosis in terms of ammonia production and that this phenomenon is explained by transamination of pyruvate and glutamate into alanine and also by the observed fall in cytosolic redox potential. It is likely that renal gluconeogenesis is also inhibited and this is reflected by the rise in the concentration of malate in the kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗