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PubMed2000

Evaluation of models of acute and subacute acidosis on dry matter intake, ruminal fermentation, blood chemistry, and endocrine profiles of beef steers.

Crossbred steers (n = 20; 316 +/- 4 kg BW), each fitted with a ruminal cannula, were used to evaluate the effects of acute acidosis (AA) and subacute acidosis (SA) on DMI, ruminal fermentation, blood chemistry, and endocrine profiles. Animals were blocked by BW and assigned to treatments including 1) intraruminal (via cannula) steam-flaked corn (3% of BW; AA); 2) intraruminal dry-rolled wheat:dry-rolled corn (50:50; 1.5% of BW; SA); 3) offering forage-adapted steers ad libitum access to a 50% concentrate diet (AA control; AC); and 4) offering 50% concentrate diet-adapted steers ad libitum access to a 50% concentrate diet (SA control; SC). Samples of ruminal fluid and whole blood were collected on the day of the challenge (d 0) and 3, 7, 10, and 14 d after the challenge. Daily DMI responded quadratically (P < 0.01) through d 7 for AA and SA steers and increased linearly (P < 0.01) for AC steers. Dry matter intake by AA steers reached a nadir (< 3 kg/d) on d 3 and gradually increased to a level similar to other treatments (7 kg/d) by d 10, whereas DMI by SA steers increased through d 3. Blood pH, bicarbonate, base excess, and total CO2 were decreased (P < 0.03) for AA steers and increased (P < 0.03) for SC steers through d 7. Ruminal pH decreased quadratically (P < 0.01) in AA and AC steers and increased (P = 0.01) in SA steers through d 7. Ruminal total lactate concentration and osmolality responded quadratically (P < 0.01) for AA and AC steers. Ruminal total lactate peaked on d 3 for AA steers and on d 0 for AC and decreased to basal concentrations by d 7. Plasma NEFA concentration increased (P < 0.04) on d 3 and 7 for AA steers. Serum Na decreased (P < 0.05) on d 0 for AA and SA steers and on d 7 and 14 for AA steers. Serum P decreased (P = 0.01) for AA steers through d 7 and decreased quadratically (P = 0.01) for AC steers through d 7. Serum albumin and cholesterol decreased (P < 0.02) for AA and AC steers through d 7. Area under the GH curve decreased (P = 0.02) for AA and AC steers through d 7. Considerable variation was evident in the ability of an animal to cope with a carbohydrate challenge. Results of data modeling generally suggest that serum amylase activity, cholesterol and potassium concentrations, and plasma NEFA concentrations were useful in distinguishing between steers classified as experiencing subacute acidosis or not affected by a carbohydrate challenge.

Acidosis↗
PubMed2003

Interaction between bunk management and monensin concentration on finishing performance, feeding behavior, and ruminal metabolism during an acidosis challenge with feedlot cattle.

Two commercial feedlot experiments and a metabolism study were conducted to evaluate the effects of monensin concentrations and bunk management strategies on performance, feed intake, and ruminal metabolism. In the feedlot experiments, 1,793 and 1,615 steers were used in Exp. 1 and 2, respectively, in 18 pens for each experiment (six pens/treatment). Three treatments were evaluated: 1) ad libitum bunk management with 28.6 mg/kg monensin and clean bunk management strategies with either 2) 28.6 or 3) 36.3 mg/kg monensin. In both experiments, 54 to 59% of the clean bunk pens were clean at targeted clean time, or 2200, compared with 24 to 28% of the ad libitum pens. However, only 13% of the pens were clean by 2000 in Exp. 1 (summer), whereas 44% of the pens in Exp. 2 (winter) were clean by 2000. In Exp. 1, bunk management and monensin concentration did not affect carcass-adjusted performance. In Exp. 2, steers fed ad libitum had greater DMI (P < 0.01) and carcass-adjusted ADG (P < 0.01) but feed efficiency (P > 0.13) similar to that of clean bunk-fed steers. Monensin concentration had no effect on carcass-adjusted performance (P > 0.20) in either experiment. A metabolism experiment was conducted with eight fistulated steers in a replicated 4 x 4 Latin square acidosis challenge experiment. An acidosis challenge was imposed by feeding 125% of the previous day's DMI, 4 h later than normal. Treatments consisted of monensin concentrations (mg/kg) of 0, 36.7, 48.9, or 36.7 until challenged and switched to 48.9 on the challenge day and 4 d following. Each replicate of the Latin square was managed with separate bunk management strategies (clean bunk or ad libitum). Feeding any concentration of monensin increased number of meals and decreased DMI rate (%/h) (P < 0.12) for the 4 d following the acidosis challenge. Meal size, pH change, and pH variance were lower (P < 0.10) for steers fed monensin with clean bunk management. However, no monensin effect was observed for steers fed ad libitum. Bunk management strategy has the potential to decrease DMI and ADG when steers managed on a clean bunk program are restricted relative to traditional, ad libitum bunk programs. Monensin helps control intake patterns for individuals, but increasing concentration above currently approved levels in this study seemed to have little effect.

Acidosis↗
PubMed2003

Effects of bacterial direct-fed microbials and yeast on site and extent of digestion, blood chemistry, and subclinical ruminal acidosis in feedlot cattle.

Two studies were conducted to determine whether a bacterial direct-fed microbial (DFM) alone or with yeast could minimize the risk of acidosis and improve feed utilization in feedlot cattle receiving high-concentrate diets. Eight ruminally cannulated steers, previously adapted to a high-concentrate diet, were used in crossover designs to study the effects of DFM on feed intake, ruminal pH, ruminal fermentation, blood characteristics, site and extent of digestion, and microbial protein synthesis. Steers were provided ad libitum access to a diet containing steam-rolled barley, barley silage, and a protein-mineral supplement (87, 8, and 5% on a DM basis, respectively). In Exp. 1, treatments were control vs. the lactic-acid producing bacterium Enterococcus faecium EF212 (EF; 6 x 10(9) cfu/d). In Exp. 2, treatments were control vs EF (6 x 10(9) cfu/d) and yeast (Saccharomyces cerevisiae; 6 x 10(9) cfu/d). Supplementing feedlot cattle diets with EF in Exp. 1 increased (P < 0.05) propionate and (P < 0.05) decreased butyrate concentrations, decreased the nadir of ruminal pH (P < 0.05), enhanced the flow of feed N (P < 0.10) to the duodenum but reduced that of microbial N (P < 0.10), reduced (P < 0.10) intestinal digestion of NDF, and increased (P < 0.10) fecal coliform numbers. Other than the increase in propionate concentrations that signify an increase in energy precursors for growth, the other metabolic changes were generally considered to be undesirable. In Exp. 2, providing EF together with yeast abolished most of these undesirable effects. Combining EF with yeast increased the DM digestion of corn grain incubated in sacco, but there were no effects on altering the site or extent of nutrient digestion. The diets used in this study were highly fermentable, and the incidence of subclinical ruminal acidosis, defined as steers with ruminal pH below 5.5 for prolonged periods of time, was high. Supplementing the diet with EF, with or without yeast, had limited effects on reducing ruminal acidosis. It seems that cattle adapted to high-grain diets are able to maintain relatively high feed intake and high fiber digestion despite low ruminal pH. The Enterococcus faecium bacterium and yeast used in this study were of limited value for feedlot cattle already adapted to high-grain diets.

Acidosis↗
PubMed1982

Effect of lasalocid, monensin or thiopeptin on lactic acidosis in cattle.

Lasalocid, monensin or thiopeptin was administered intraruminally each at .33, .65 or 1.3 mg/kg body weight and evaluated for its effectiveness in preventing experimentally induced lactic acidosis in cattle. Four rumen-fistulated cattle were used for each dosage level and the design was a 4 x 4 Latin square with each animal receiving lasalocid, monensin, thiopeptin or no antibiotic. Acidosis was induced by intraruminal administration of glucose (12.5 g/kg body weight). Control cattle exhibited the typical drop in rumen pH and concurrent increases in L(+) and D(-) lactate concentrations commonly observed in cases of lactic acidosis. Alkali reserves were depleted in the control cattle as evidenced by a decrease in blood bicarbonate and a negative shift in base excess. In all three trials, cattle given lasalocid had higher rumen pH and lower lactate concentrations than did control cattle or cattle given monensin or thiopeptin. Cattle given monensin had a significantly higher rumen pH and a lower lactate concentration than the controls only at the .65 and 1.3 mg/kg body weight dosages, whereas thiopeptin was effective only at the 1.3-mg dosage. Concentrations of total VFA in rumen fluid decreased in the controls but remained unchanged in cattle given antibiotics. A significant reduction in the molar proportion of acetate and an increase in the molar proportion of propionate were observed in the rumen fluid of the cattle given antibiotics. Colony counts of Streptococcus bovis and Lactobacillus were significantly reduced in rumen fluid of cattle given 1.3 mg antibiotic/kg body weight. Counts of lactate-utilizing bacteria increased in both control cattle and cattle given antibiotics. Cattle given antibiotics showed no evidence of lacticacidemia, hemoconcentration or change in acid-base balance.

Acidosis↗
PubMedDate not supplied

Severe lactic acidosis and renal involvement in a patient with relapsed Burkitt's lymphoma.

We describe an 8-year-old patient with relapsed Burkitt's lymphoma who developed complex metabolic problems, including renal diabetes insipidus and severe lactic acidosis. The lactic acidosis responded temporarily to chemo- and radiotherapy but not to bicarbonate or thiamine administration. These metabolic changes were most likely due to the lymphomatous infiltration of the kidneys. Severe lactic acidosis, without evidence of thiamine deficiency, seems to be a very rare event in children with cancer.

Acidosis, Lactic↗
PubMed1977

Effect of hypercapnic acidosis on induction of arrhythmias by catecholamines in cat papillary muscles.

The effect of changes in PCO2 upon induction of arrhythmias in cat papillary muscles was studied. The average norepinephrine (NE) dose necessary to produce spontaneous contractions in muscles stimulated at rates of 10/min was higher at high PCO2. Whereas 2 100 +/- 295 X 10(-8) mol/litre of NE was necessary during acidosis, only 824 +/- 295 X 10(-8) mol/litre was necessary to produce spontaneous contractions in alkalosis. In quiescent muscles, the necessary doses in acidosis and alkalosis were 2 209 +/- 531 X 10(-8) and 518 +/- 159 X 10(-8) mol/litre respectively. With isoproterenol 458 +/- 84 X 10(-8) mol/litre was necessary to reach the end point at high PCO2, whereas only 131 +/- 52 X 10(-8) mol/litre was required at low PCO2. The lower sensitivity to catecholamine-induced arrhythmias with hypercapnic acidosis does not appear to be related to the re-uptake of the neurotransmitter by the nerve ending since it is also present with isoproterenol.

Acid-Base Equilibrium↗
PubMed1981

Unexpected metabolic acidosis in severe lye poisoning.

Prolonged metabolic acidosis developed in a 38-year-old patient suffering from severe peroral liquid lye poisoning without shock syndrome. Metabolic acidosis was caused by lactic acid. The combination of increased lactic acid production in the marginal regions of the necrotic intestinal areas and impaired lactate removal by the liver were most probably responsible for this lactic acidosis.

Acidosis↗
PubMed1998

[Renal tubular acidosis type II secondary to gamma-light chain excretion in an elderly patient with multiple myeloma].

A 73-year-old woman was admitted to the geriatric ward of the University of Tokyo Hospital with anemia, osteepeina, and renal dysfunction. Although symptoms typical of multiple myeloma such as punched-out lesions and hyperproteinemia were not found, protein electrophoresis revealed that lambda type Bence-Jones protein was excreted in urine. Multiple myeloma was diagnosed. Furthermore, renal dysfunction was accompanied renal tubular acidosis type II (proximal type). Renal dysfunction in patient with multiple myeloma in usually caused by so-called myeloma casts in the distal tubules, but renal tubular acidosis type II is rarely observed. It is possible that injury of the proximal renal tubular eithelium by Bence-Jones protein resulted in renal tubular acidosis type II in this patient.

Acidosis, Renal Tubular↗
PubMed2007

Severity of ruminal acidosis in primiparous holstein cows during the periparturient period.

The objectives of this study were: 1) to determine the effect of providing additional prepartum concentrate on the occurrence and severity of ruminal acidosis (RA) and lactational performance during the periparturient period in primiparous cows; and 2) to characterize the occurrence and severity of RA during the periparturient period. We hypothesized that providing additional concentrate prepartum would reduce postpartum RA. Fourteen ruminally cannulated Holstein heifers were paired by expected calving date and body condition score. The heifers were assigned to 1 of 2 prepartum feeding regimens: 1) a control treatment consisting of a far-off diet (forage:concentrate, F:C = 80:20) fed from d -60 to d -25 and a close-up diet (F:C = 54:46) fed from d -24 until parturition; or 2) a high-concentrate (HC) feeding program consisting of 4 prepartum diets, HC-1 (F:C = 68:32) fed from d -60 to d -43, HC-2 (F:C = 60:40) fed from d -42 to d -25, HC-3 (F:C = 52:48) fed from d -24 to d -13, and HC-4 (F:C = 46:54) fed from d -12 until parturition. All cows received the same lactation diet postpartum. Ruminal pH was measured continuously from d -5 to d +5, and for 3 consecutive days starting on d +17 +/- 1.2, d +37 +/- 1.4, and d +58 +/- 1.5 relative to parturition using an indwelling ruminal pH system. Ruminal acidosis was considered to occur when ruminal pH was <5.8 (total RA). Ruminal acidosis was further partitioned into: 1) mild RA (5.8 > ruminal pH > 5.5), 2) moderate RA (5.5 > ruminal pH > 5.2), and 3) acute RA (ruminal pH < 5.2). Feeding additional concentrate prepartum did not reduce postpartum RA. In fact, cows fed the HC treatment had more daily episodes of acute RA than cows fed the control treatment. Day relative to parturition affected the occurrence and severity of RA; RA increased following parturition and was sustained thereafter. The DM intake during the last 5 d of gestation was lower for cows fed the HC treatment compared with cows fed the control treatment, but lactational performance was not affected. We conclude that, under the conditions imposed, feeding additional concentrate prepartum does not reduce postpartum RA. Furthermore, the incidence and severity of RA increases immediately postpartum, emphasizing the need to develop and implement feeding strategies that reduce this risk.

Acidosis↗
PubMed1984

Experimental brain injury: successful therapy with the weak base, tromethamine. With an overview of CNS acidosis.

The presence of lactic acidosis in the cerebrospinal fluid of patients suffering brain injury as the result of trauma, subarachnoid hemorrhage, neoplasia, or ischemia has been well documented. The authors theorized that this acidosis becomes harmful in itself, and that treatment with an alkalinizing agent (tris(hydroxymethyl)aminomethane: tromethamine) capable of penetrating the blood-brain barrier would be efficacious. Fifteen pairs of mongrel cats were subjected to a 2.85-atmosphere fluid-percussion injury (LD80), and were supported by respirators for up to 72 hours prior to being placed in cages for an additional 4 days of observation. Experimental cats underwent continuous infusion of tromethamine (begun 10 minutes after injury); control animals were infused with an equal volume of lactated Ringer's solution. Twenty percent of the control group survived until sacrificed on Day 7 post-injury. Survival in the tromethamine group was 60% (p less than 0.05), and morbidity also appeared to be reduced in the treated cats. Intracranial pressure (ICP) in treated cats was 60% (p less than 0.05) of that in the control cats after respirator support for 3 days. Tromethamine infusion was associated with improved survival, decreased morbidity, and decreased ICP when compared with results in control animals. The literature with regard to central nervous system acidosis has been reviewed in an attempt to clarify and define this problem.

Acidosis↗
PubMed1986

CSF brain creatine kinase levels and lactic acidosis in severe head injury.

The posttraumatic creatine kinase-BB isoenzyme (CKBB) activity and lactate concentration in ventricular cerebrospinal fluid (CSF) have been studied in 29 patients with severe head injuries. The CKBB activity reaches its maximum a few hours after trauma, and has a monoexponential drop with a half-time of approximately 10 hours. Ventricular CSF lactate concentration continues to rise in patients with a poor outcome, and decreases only slowly and inconsistently in most of the other patients. Thus, increase of lactate in the ventricular CSF is not, like CKBB, a direct one-stage consequence of the trauma but is due to continuous production from a derangement of metabolism caused by the trauma. Since even higher ventricular CSF lactate levels can be survived when not caused by head injury, and since no significant pH changes were related to the ventricular CSF lactic acidosis in these artificially ventilated patients, it is concluded that ventricular CSF lactic acidosis is indicative of a severe, although not necessarily intractable, disturbance of brain function associated with intracellular lactate production and acidosis.

Acidosis, Lactic↗
PubMed1994

Early reversal of acidosis and metabolic recovery following ischemia.

Tissue acidosis is believed to be a key element in ischemic injury of neural tissue. The goal of this study was to determine whether persisting postischemic acidosis or the extent of acidosis would affect metabolic recovery following an ischemic event. Intracellular pH (pHi), adenosine triphosphate, phosphocreatine, and lactate levels were measured in the cerebral cortex during the early stages of reperfusion, following either 5 or 10 minutes of global ischemia in both normo- and hyperglycemic gerbils. A total of 130 gerbils were injected with a solution containing 1.5 ml Neutral Red (1%) (+/- 2.5 gm/kg glucose); 30 minutes later, the gerbils were placed under halothane anesthesia, and the carotid arteries were occluded for either 5 or 10 minutes. The brains were frozen in liquid nitrogen at 0, 15, 30, 60, and 120 seconds after reperfusion; they were sectioned and the block face was photographed to determine the pHi by using Neutral Red histophotometry. At the conclusion of the ischemia, the pHi in all groups had decreased significantly from a control value of 7.05 +/- 0.03) (mean +/- standard error of the mean). In normoglycemic brains, the pHi values fell to 6.71 +/- 0.04 and 6.68 +/- 0.11 after 5 and 10 minutes of ischemia, respectively. Hyperglycemic brains were more acidotic; values fell to 6.57 +/- 0.10 and 6.52 +/- 0.24 after 5 and 10 minutes of ischemia, respectively. Lactate levels were approximately fivefold greater than those of control tissue in normoglycemic brains, while lactate levels in hyperglycemic brains were increased eightfold. The adenosine triphosphate and phosphocreatine levels were depleted at the end of ischemia in all groups. After 2 minutes of reflow activity, the pHi levels in both normo- and hyperglycemic brains were restored to those of control values in the '5-minute ischemic group, while the pHi levels remained significantly depressed in the 10-minute ischemic group. Restoration of high-energy phosphates was similar in normoglycemic brains regardless of ischemic duration, recovering to only 20% of the restoration obtained in control tissue at 2 minutes. In hyperglycemic brains, however, there was complete recovery of high-energy phosphates by 2 minutes of reflow activity following 5 minutes of ischemia. Extending the ischemic period to 10 minutes in hyperglycemic brains slowed the rate of metabolic recovery to that observed in normoglycemic brains. The results indicate that the reflow period permits the rapid restoration of pHi levels substantially before the normalization of primary energetic compounds.(ABSTRACT TRUNCATED AT 400 WORDS)

Acidosis↗
PubMed1990

Adaptation to respiratory acidosis in the turtle bladder.

The effect of in vivo respiratory acidosis for 4 and 48 hr was examined in the turtle bladder by placing turtles in hypercapnic chambers. Blood pH was significantly lowered and pCO2 was significantly elevated over control values both 4 and 48 hr, while blood bicarbonate was only increased after 48 hr. In vitro rates for H+ secretion determined by the reverse short-circuit current were significantly greater in bladders from 48 hr of respiratory acidosis than those of controls (27.3 +/- 2.7 vs 20.6 +/- 1.7 microA, P less than 0.05). In vitro rates for HCO3- secretion determined by pH stat were not altered. Fluorescence microscopy was used to study cell morphology. The number of carbonic anhydrase cells (corrected for the total number of cells) as determined by four different fluorescence stains (6-carboxyfluorescein, rhodamine 123, acridine orange, and 3,3'-diethyloxacarbocyaninine iodide) was increased both after 4 and 48 hr of respiratory acidosis. However, the number of HCO3(-)-secreting (beta subtype) carbonic anhydrase cells, determined by a probe for the anion exchanger, NBD-taurine, was not increased. In vitro 1% CO2 for 4 hr also resulted in an increase in H+ secretion and in the number of 6-carboxyfluorescein-positive cells, both of which could be blocked with SITS pretreatment. We conclude that CO2 changes the mucosal cells more toward the carbonic anhydrase phenotype, and that if NBD-taurine accurately identifies the beta cells, that the adaptation produces or recruits more alpha-carbonic anhydrase cells.

Acidosis, Respiratory↗
PubMed2000

A stepwise approach to acid-base disorders. Practical patient evaluation for metabolic acidosis and other conditions.

Acid-base disorders can usually be approached by following the steps outlined in the text and doing the calculations shown in the box on page 257. Clues about the underlying disorder can be obtained from history taking and physical examination. Assessment of pH, PaCO2, and HCO3- allows determination of whether a primary metabolic or respiratory disorder is present. Calculation of the predicted compensatory response for simple acid-base disorders might suggest the presence of an additional disease process if compensation is not appropriate. Calculation of the various gaps can be helpful in differential diagnosis (i.e., anion gap for diagnosis of metabolic acidosis, delta anion gap for diagnosis of high-anion-gap metabolic acidosis, and urine anion gap for diagnosis of a non-anion gap metabolic acidosis). Most acid-base problems can be solved with use of the stepwise approach described.

Acid-Base Equilibrium↗
PubMed2004

A case of lactic acidosis caused by stavudine in an AIDS patient.

Nucleoside reverse transcriptase inhibitors (NRTIs), which are used for the treatment of human immunodeficiency virus (HIV) infection have been associated with a wide spectrum of clinical manifestations, including hepatic steatosis, lipodystrophy, myopathy, and lactic acidosis. Such adverse effects are postulated to result from the inhibition of mitochondrial DNA gamma polymerase, which causes the depletion of mitochondrial DNA and eventual the disruption of oxidative phosphorylation. Although cases of severe decompensated lactic acidosis are rare, this syndrome is associated with a high mortality rate. We report upon the first Korean case, of severe lactic acidosis in an acquired immunodeficiency syndrome (AIDS) patient receiving stavudine, an anti-HIV drug.

Acidosis, Lactic↗
PubMed2003

Recurrent severe anion gap metabolic acidosis secondary to episodic ethylene glycol intoxication.

Acute ethylene glycol toxicity and its attendant metabolic derangement is a well described clinical entity. Recurrent severe anion gap metabolic acidosis consequent to episodic ingestion of ethylene glycol has not been previously reported. We present a patient who developed severe anion gap metabolic acidosis with no osmolar gap and hypokalemia, consequent to episodic ethylene glycol ingestion. Modest artifactual elevation of the serum lactic acid level and rapid response to intravenous bicarbonate infusion may serve as diagnostic clues. Consideration of these aberrant features should be included in the clinical assessment of severe anion gap metabolic acidosis.

Acid-Base Equilibrium↗
PubMed2004

Secondary erythrocytosis associated with distal renal tubular acidosis.

AIMS: Diagnosis and classification of renal tubular acidosis (RTA) have traditionally been made on the basis of functional studies. Despite recent expanding knowledge about the molecular abnormalities involved in renal bicarbonate (HCO3-) and H+ transport, the pathophysiology of secondary erythrocytosis in association with distal RTA remains obscure. CASE HISTORY: A 2-month-old boy with severe hyperchloremic metabolic acidosis with positive urine anion gap was diagnosed with distal RTA. Replacement therapy with sodium bicarbonate and potassium citrate succeeded in improving his metabolic acidosis and growth. His renal function remained normal. He had persistent erythrocytosis. CONCLUSION: Secondary erythrocytosis is a rarely reported association of distal RTA. It may increase the risk of thromboembolism.

Acidosis, Renal Tubular↗
PubMed1990

Bicarbonate does not improve hemodynamics in critically ill patients who have lactic acidosis. A prospective, controlled clinical study.

STUDY OBJECTIVE: To determine whether correction of acidemia using bicarbonate improves hemodynamics in patients who have lactic acidosis. DESIGN: Prospective, randomized, blinded, crossover study. Each patient sequentially received sodium bicarbonate and equimolar sodium chloride. The order of the infusions was randomized. SETTING: Intensive care unit of a tertiary care hospital. PATIENTS: Fourteen patients who had metabolic acidosis (bicarbonate less than 17 mmol/L and base excess less than -10) and increased arterial lactate (mean, 7.8 mmol/L). All had pulmonary artery catheters and 13 were receiving catecholamines. MEASUREMENTS AND MAIN RESULTS: Sodium bicarbonate (2 mmol/kg body weight over 15 minutes) increased arterial pH (7.22 to 7.36, P less than 0.001), serum bicarbonate (12 to 18 mmol/L, P less than 0.001), and partial pressure of CO2 in arterial blood (PaCO2) (35 to 40 mm Hg, P less than 0.001) and decreased plasma ionized calcium (0.95 to 0.87 mmol/L, P less than 0.001). Sodium bicarbonate and sodium chloride both transiently increased pulmonary capillary wedge pressure (15 to 17 mm Hg, and 14 to 17 mm Hg, P less than 0.001) and cardiac output (18% and 16%, P less than 0.01). The mean arterial pressure was unchanged. Hemodynamic responses to sodium bicarbonate and sodium chloride were the same. These data have more than 90% power of detecting a 0.5 L/min (7%) change in mean cardiac output after administration of sodium bicarbonate compared with that after sodium chloride. Even the 7 most acidemic patients (mean pH, 7.13; range, 6.90 to 7.20) had no significant hemodynamic changes after either infusion. CONCLUSIONS: Correction of acidemia using sodium bicarbonate does not improve hemodynamics in critically ill patients who have metabolic acidosis and increased blood lactate or the cardiovascular response to infused catecholamines in these patients. Sodium bicarbonate decreases plasma ionized calcium and increases PaCO2.

Acidosis, Lactic↗