Mixed acid-base disorders

Mixed acid-base disturbances are combinations of two or more primary acid-base disturbances. Mixed acid-base disturbances may be suspected on the basis of findings obtained from the medical history, physical examination, serum electrolytes and chemistries, and anion gap. The history, physical examination, and serum biochemical profile may reveal disease processes commonly associated with acid-base disturbances. Changes in serum total CO2, serum potassium and chloride concentrations, or increased anion gap may provide clues to the existence of acid-base disorders. Blood gas analysis is usually required to confirm mixed acid-base disorders. To identify mixed acid-base disorders, blood gas analysis is used to identify primary acid-base disturbance and determine if an appropriate compensatory response has developed. Inappropriate compensatory responses (inadequate or excessive) are evidence of a mixed respiratory and metabolic disorder. The anion gap is also of value in detecting mixed acid-base disturbances. In high anion gap metabolic acidosis, the change in the anion gap should approximate the change in serum bicarbonate. Absence of this relationship should prompt consideration of a mixed metabolic acid-base disorder. Finding an elevated anion gap, regardless of serum bicarbonate concentration, suggests metabolic acidosis. In some instances, elevated anion gap is the only evidence of metabolic acidosis. In patients with hyperchloremic metabolic acidosis, increases in the serum chloride concentration should approximate the reduction in the serum bicarbonate concentration. Significant alterations from this relationship also indicate that a mixed metabolic disorder may be present. In treatment of mixed acid-base disorders, careful consideration should be given to the potential impact of therapeutically altering one acid-base disorder without correcting others.     

Ventilatory and Metabolic Compensation in Dogs With Acid-Base Disturbances

Ventilatory and metabolic compensation to acid-base disturbances is reviewed. The mechanisms for compensation as well as the values obtained from several studies using normal dogs and dogs with experimentally induced diseases are provided. Compensation is not the same in dogs and human beings. Dogs have a better ability to adapt to most respiratory disorders, and human beings adapt better to metabolic acidosis. In metabolic alkalosis and chronic respiratory acidosis there is no difference in compensation between these species. Ventilatory compensation for metabolic disorders in dogs is the same whether they have metabolic acidosis or metabolic alkalosis, whereas metabolic compensation in respiratory disturbances is less effective in acidosis. Values for the expected changes in PCO₂ in dogs with metabolic acidosis and metabolic alkalosis, and for bicarbonate concentration (HCO₃-) in dogs with acute and chronic respiratory alkalosis and acidosis are presented.     

Changes in the acid-base index of blood in dairy cows in relation to the seasonal composition of feed rations and phases of the reproductive cycle

The changes in the acid-base indices of the blood of dairy cows in different stages of reproduction cycle were studied in relation to the composition of feed ration in the autumn, winter, spring and summer feeding seasons. The cows were in the following stages of their reproduction cycle: Group I the fourth to sixth month of gravidity, II eighth to ninth month of gravidity, III one to two months after calving. The seasonal composition of feed ration was demonstrated to exert a significant influence on the acid-base balance of the blood of cows in the studied stages of reproduction. A considerable occurrence of metabolic acidoses with different levels of compensation was observed when the cows were given the autumn and winter feed rations. Subclinical acid-base disorders of different directions (metabolic and respiratory alkaloses, acidoses) frequently occurred in the green feeding season. The frequency of acid-base disorders as a result of incorrect nutrition was found to be the highest in highly pregnant cows (group II) and in those one to two months after parturition (group III), i. e. in the periods with a significant influence on the reproduction process. On the whole, the best situation as to the acid-base balance was found in cows in the fourth to sixth month of their gravidity, irrespective of the seasonal effect of feed ration.     

Annual dynamics of acid-base equilibrium indices in dairy cows

Annual dynamics of the indices of acid-base homeostasis of blood was studied in dairy cows in two production regions, the corn production region and the potato-grain production region; venous blood was examined gasometrically by the Astrup apparatus. The examinations were performed eight times during the year and pH, pCO2, BE, PB, SB, AB and tCO2 were studied. In dairy cows from the corn production region lower values of the studied parameters were obtained than in dairy cows oriented to similar milk production in the potato-grain production region. In the corn production region besides the normal values also the lower values of the indices of acid-base balance were found, indicating the incidence of latent metabolic acidosis. A particularly critical situation occurred in the herd from the corn production region in September when the average value of blood pH was 7.35 logmolc and the following disorders were observed: clinical symptoms of metabolic acidosis, drop of milk yield, drop of milk fat content, hypomagnesemia and hypocalcemia as disorders of the mineral metabolism.     

Acid-base disorders in milk-fed calves with chronic indigestion.

Acid-base disorders were investigated in 50 calves with chronic indigestion and metabolic acidosis. In the calves that were unable to stand up, the acidosis was significantly more severe than in the calves that could stand up. The anion gap and four different components of the base excess were calculated by the method described by Fencl. The anion gap was high in more than half of the calves, and it was significantly associated with the base excess due to unidentified anions. However, in seven of the calves, the excess of unidentified anions would not have been detected without the calculations, which made it possible to measure the effect of sodium, chloride, plasma protein and unidentified anions on the acid-base balance. Twenty-four of the calves had a combination of hyperchloraemic and high anion gap metabolic acidosis. Changes in sodium and plasma protein concentrations had a minor impact on the calves' acid-base status.     

Simple acid-base disorders

The body regulates pH closely to maintain homeostasis. The pH of blood can be represented by the Henderson-Hasselbalch equation: pH = pK + log [HCO3-]/PCO2 Thus, pH is a function of the ratio between bicarbonate ion concentration [HCO3-] and carbon dioxide tension (PCO2). There are four simple acid base disorders: (1) Metabolic acidosis, (2) respiratory acidosis, (3) metabolic alkalosis, and (4) respiratory alkalosis. Metabolic acidosis is the most common disorder encountered in clinical practice. The respiratory contribution to a change in pH can be determined by measuring PCO2 and the metabolic component by measuring the base excess. Unless it is desirable to know the oxygenation status of a patient, venous blood samples will usually be sufficient. Metabolic acidosis can result from an increase of acid in the body or by excess loss of bicarbonate. Measurement of the "anion-gap" [(Na+ + K+) - (Cl- + HCO3-)], may help to diagnose the cause of the metabolic acidosis. Treatment of all acid-base disorders must be aimed at diagnosis and correction of the underlying disease process. Specific treatment may be required when changes in pH are severe (pH less than 7.2 or pH greater than 7.6). Treatment of severe metabolic acidosis requires the use of sodium bicarbonate, but blood pH and gases should be monitored closely to avoid an "overshoot" alkalosis. Changes in pH may be accompanied by alterations in plasma potassium concentrations, and it is recommended that plasma potassium be monitored closely during treatment of acid-base disturbances.     

Paradoxic aciduria in bovine metabolic alkalosis.

Cows with metabolic alkalosis secondary to abomasal displacement and other abomasal disorders were often found to excrete acidic urine. This paradoxic aciduria contradictsthe classical view that the pH of the urine may be used to estimate the acid-base status of the body. Data from bovine clinical patients with metabolic alkalosis, serum electrolyte changes, and paradoxic aciduria suggested that the balance of sodium potassium, and chloride in the body places limits on the kidneys' ability to regulate the acid-basebalance.     

Chloride Ion in Small Animal Practice: The Forgotten Ion

The Physiology of chioride ion and its relationship to clinical disorders in small animall practice is reviewed. Chioride is the major anion in the extracellular fluid and is important in the metabolic regulation of acid-base balance. A new clinical approach is used to assess chloride ion changes after accounting for changes in free water. Using this approach chloride disorders can be divided into corrected and artifactual. Changes in free water are solely responsible for the chioride ion changes in artifactual disorders, whereas in corrected chloride disorders, chloride ion itself changes. Corrected hypochioremia is associated with increases in the strong ion differece (SID) and metabolic alkalosis and is caused by administration of solution containing a high concentration of sodium relative to chioride (e.g., Sodium bicarbonate) or the excessive loss chioride relative to sodium (e.g., vomiting of stomach contents). Administration of chioride is correction of hypochioremic metabolic alkalosis. Corrected hyperchioremia is associated with a decreased SID and metabolic acidosis and is usually the result of excessive loss of sodium relative to chloride (e.g., diarrhea), chioride retention (e.g., renal tubular acidosis), or therapy with solutions containing a high concentration of chioride relative to sodium (e.g.,0.9% sodium chloride;3–24% hypertonic saline). Treatment with sodium bicarbonate should be attempted in patients with corrected hyperchioremia and a plasma pH beiow 7.2.     

A comparison of traditional and quantitative analysis of acid-base and electrolyte imbalances in horses with gastrointestinal disorders

The purpose of this study was to compare traditional and quantitative approaches in analysis of the acid-base and electrolyte imbalances in horses with acute gastrointestinal disorders. Venous blood samples were collected from 115 colic horses, and from 45 control animals. Horses with colic were grouped according to the clinical diagnosis into 4 categories: obstructive, ischemic, inflammatory, and diarrheic problems. Plasma electrolytes, total protein, albumin, pH, pCO2, tCO2, HCO3-, base excess, anion gap, measured strong ion difference (SIDm), nonvolatile weak buffers (A(tot)), and strong ion gap were determined in all samples. All colic horses revealed a mild but statistically significant decrease in iCa2+ concentration. Potassium levels were mildly but significantly decreased in horses with colic, except in those within the inflammatory group. Additionally, the diarrheic group revealed a mild but significant decrease in Na+, tCa, tMg, total protein, albumin, SIDm, and A(tot). Although pH was not severely altered in any colic group, 26% of the horses in the obstructive group, 74% in the ischemic group, 87% in the inflammatory group, and 22% in the diarrheic group had a metabolic imbalance. In contrast, when using the quantitative approach, 78% of the diarrheic horses revealed a metabolic imbalance consisting mainly of a strong ion acidosis and nonvolatile buffer ion alkalosis. In conclusion, mild acid-base and electrolyte disturbances were observed in horses with gastrointestinal disorders. However, the quantitative approach should be used in these animals, especially when strong ion imbalances and hypoproteinemia are detected, so that abnormalities in acid-base status are evident.     

Hyperkalemic Atrial Standstill in Neonatal Calf Diarrhea

Hyperkalemia has been associated with cardiac abnormalities and muscular disorders. Hyperkalemia is a common problem associated with the acid-base and electrolyte disturbances that occur in neonatal calves having acute diarrhea. Occasional calves with acute neonatal diarrhea, metabolic acidosis, and hyperkalemia have cardiac rate or rhythm abnormalities. Bradycardia observed in three such calves was found to represent atrial standstill and was attributed to hyperkalemia. (Journal of Veterinary Internal Medicine 1992; 6:294–297)     

Determination of the acid-base status in 50 horses admitted with colic between December 1998 and May 1999

The purpose of the present study was to investigate the acid-base status and the concentration of organic acids in horses with colic caused by various disorders. Blood samples were collected from 50 horses with colic and from 20 controls. No intravenous fluids had been given prior to sample collection. Identified causes of colic included gastric ulceration, small intestinal volvulus, cecal intussusception, cecal rupture, colonic impaction, left dorsal colon displacement, right dorsal colon displacement, colonic volvulus, colitis, peritonitis, and uterine torsion. Thirty-seven horses recovered from treatment of colic, 8 horses were euthanized, and 5 died. Most cases were not in severe metabolic acidosis. In previous studies, most horses presented for diagnosis and treatment of colic were in metabolic acidosis and in shock.     

Clinical signs, diagnosis, and treatment of alkalemia in dogs: 20 cases (1982-1984)

Alkalemia (pH greater than 7.50) was measured in 20 dogs admitted over a 3-year period for various clinical disorders. Alkalemia was detected in only 2.08% of all dogs in which blood pH and blood-gas estimations were made. Thirteen dogs had metabolic alkalosis (HCO3- greater than 24 mEq/L, PCO2 greater than 30 mm of Hg), of which 8 had uncompensated metabolic alkalosis, and of which 5 had partially compensated metabolic alkalosis. Seven dogs had respiratory alkalosis (PCO2 less than 30 mm of Hg, HCO3- less than 24 mEq/L); 4 of these had uncompensated respiratory alkalosis and 3 had partially compensated respiratory alkalosis. Ten dogs had double or triple acid-base abnormalities. Dogs with metabolic alkalosis had a preponderance of clinical signs associated with gastrointestinal disorders (10 dogs). Overzealous administration of sodium bicarbonate or diuretics, in addition to anorexia, polyuria, or hyperbilirubinemia may have contributed to metabolic alkalosis in 8 of the dogs. Most of the dogs in this group had low serum K+ and Cl- values. Two dogs with metabolic alkalosis had PCO2 values greater than 60 mm of Hg, and 1 of these had arterial hypoxemia (PaO2 less than 80 mm of Hg). Treatments included replacement of fluid and electrolytes (Na+, K+, and Cl-), and surgery as indicated (8 dogs). Six dogs with respiratory alkalosis had a variety of airway, pulmonary, or cardiac disorders, and 3 of these had arterial hypoxemia. Two other dogs were excessively ventilated during surgery, and 1 dog had apparent postoperative pain that may have contributed to the respiratory alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Chronic metabolic acidosis in dairy cows]

Complex clinical and clinico-biochemical examination of the blood, urine and rumen liquor in a herd of dairy cows revealed chronical metabolic acidosis accompanied by rumen dysfunction and by a reduced butterfat content of milk. During the first examination of the acid-base state of the blood was almost at a standard level. An increased level of urea in blood plasma and a higher GOT transaminase activity testified to an excessive load on the liver. Urine pH was considerably deviated towards the acidic side and inorganic phosphorus was present in urine in a greater concentration. The pH of rumen liquor was slightly shifted towards alkalinity owing to the release of NH3 from urea in the food ration. The diagnosis--suspect chronical metabolic acidosis--was determined on the basis of the first examination. Chronical metabolic acidosis was definitely proved by the second examination when urea had been excluded from the feed ration. Repeated examinations revealed chronical metabolic acidosis which had originally been accompanied by a higher rumen liquor pH. On the basis of case histories and mechanisms of chronical acidosis, measures were proposed, resulting in an increase of the butterfat content of milk. Chronical metabolic disorders often follow a long-lasting latent pattern, manifesting themselves as a reduced milk yield and lower resistance; the clinical form of disease appears only at a later stage. The system of preventive diagnostics provides information on the changes in the composition of internal medium and of the faeces before a drop occurs in milk and fat production. These measures prevent metabolic disorders and high losses of produce which otherwise remain hidden for a long time.     

Acid-base and electrolyte abnormalities in dogs with gastrointestinal foreign bodies

Gastrointestinal foreign bodies occur commonly in dogs. The objective of the study was to describe the acid-base and electrolyte abnormalities identified in dogs with gastrointestinal foreign bodies and determine if these abnormalities are related to the site or type of foreign body present. Medical records of 138 dogs were reviewed, and information on signalment, initial venous electrolyte and acid-base values, surgical findings, relevant historical information, imaging modalities used, cost of hospital visit, intra- or postoperative complications, and survival was obtained. The site of the foreign body was recorded in 94.9% of cases and the most common site was the stomach (50%), followed by the jejunum (27.5%). The foreign bodies were linear in 36.2% of cases. The most common electrolyte and acid-base abnormalities regardless of the site or type of foreign body were hypochloremia (51.2%), metabolic alkalosis (45.2%), hypokalemia (25%), and hyponatremia (20.5%). No significant association was found between electrolyte or acid-base abnormalities and the site of foreign body. Linear, as opposed to discrete, foreign bodies were more likely to be associated with a low serum sodium concentration (odds ratio, 0.85; 95% confidence interval, 0.75-0.95). Hyperlactatemia (> 2.4 mmol/L) was seen in 40.5% of dogs. A wide variety of electrolyte and acid-base derangements are found in dogs with gastrointestinal foreign bodies. Hypochloremia and metabolic alkalosis are common in these dogs. Hypochloremic, hypokalemic metabolic alkalosis is seen with both proximal and distal gastrointestinal foreign bodies.     

Metabolic reactions of calves to the feeding with Laktosan or unpasteurized whole milk]

The acid-base and other metabolic reactions to nutrition with Laktosan produced by two feed plants and with unpasteurized whole milk after transport to a dairy plant were studied in calves up to the ninth week of age. Laktosan feeding reduces the metabolic component of the acid-base balance; the use of a lower-quality Laktosan mixture, containing drum-dried milk, gives a picture of metabolic acidosis lasting about 11 days. The changes are cuased by an increased intensity of dissimilation, by the release of metabolic H+, and, in part, by the loss of bases during diarrhoea. With the use of low-quality Laktosan, the utilization of the nutrients of the feed ration is much lower than the utilization of the nutrients of unpasteurized milk or high-quality Laktosan. The use of high-quality Laktosan causes much lower acid-base changes, far from reaching pathological values. At the same time, the utilization of nutrients is higher than with the use of unpasteurized milk. This milk which cannot be considered microbially or chemically undamaged offers no advantages from the health-condition and economic point of view. The facts, revealed by the study, emphasize the high health and economic importance of the production of calf feed mixtures. At the same time the results show that enither milk nor Laktosan feeding provides enough magnesium for the calves to grow. Other metabolic aspects of different calf nutrition are discussed.     

A review of the role of acid-base balance in amino acid nutrition

Acid-base balance and amino acid metabolism are intimately related. Changes in acid-base balance influence the metabolic fate of many amino acids. Also, acid-base homeostasis is achieved in part by alteration of amino acid metabolism, not only in the kidney, but also in liver, muscle and splanchnic tissue. Glutamine is the primary amino acid involved in renal ammonia-genesis, a process intimately related to acid excretion. The metabolism of other amino acids, such a serine, glycine and the branched-chain amino acids, also appears to be influenced by acid-base balance. Conversely, the metabolic fate of various amino acids will influence the daily acid load experienced by the animal. Oxidation of amino acids contributes to the total acid and base load imposed on the pig. The basic (cationic) amino acids (lysine, arginine and histidine) yield neutral end-products plus a proton; sulfur (methionine and cysteine) amino acids are also acidogenic because they generate sulfuric acid when oxidized. The dicarboxylic (anionic) amino acids (aspartate and glutamate, but not asparagine and glutamine) consume acid when oxidized and thus reduce the acid load of the diet. Acid-base balance and related phenomena are discussed in the context of practical and metabolic aspects of amino acid nutrition.     

Blood gas and acid-base changes in the neonatal foal

This article reviews what are considered the basic concepts of gas transport, blood gases, and acid-base physiology is most mammalian species. Techniques for the appropriate collection of blood samples for blood gas and acid-base determinations in the newborn foal are described. Guidelines for interpretation of these values in the normal foal and those animals undergoing respiratory and metabolic derangements are provided.     

Respiratory acid-base disorders.

Respiratory acid-base disorders, although infrequently diagnosed in veterinary medicine, can cause or contribute to adverse clinical outcomes. Recognition of the mechanisms and causes of respiratory acidosis and alkalosis can prompt clinical detection of the acid-base derangement, allowing for appropriate intervention.