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.     

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.     

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.     

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.     

Pyometra in the dog--a pathophysiological investigation. VI: Acid-base status and serum electrolytes

Arterial pH, oxygen and carbon dioxide tensions, and standard bicarbonate, as well as serum electrolytes (Na, Cl, K, inorganic P, Ca and anion gap) have been investigated in bitches with pyometra. A respiratory alkalosis was a common finding in the patients, and a smaller group showed a metabolic acidosis of mixed origin superimposed on the respiratory alkalosis. In this group 4 out of 9 patients died. In addition, the patients showed moderate electrolyte disturbances indicating a "sick cell syndrome" and a mild to severe renal dysfunction.     

Contemporary approach to acid-base balance and its disorders in dogs and cats

The issue of the acid-base balance (ABB) parameters and their disorders in pets is rarely raised and analysed, though it affects almost 30% of veterinary clinics patients. Traditionally, ABB is described by the Henderson-Hasselbach equation, where blood pH is the resultant of HCO3- and pCO2 concentrations. Changes in blood pH caused by an original increase or decrease in pCO2 are called respiratory acidosis or alkalosis, respectively. Metabolic acidosis or alkalosis are characterized by an original increase or decrease in HCO3- concentration in the blood. When comparing concentration of main cations with this of main anions in the blood serum, the apparent absence of anions, i.e., anion gap (AG), is observed. The AG value is used in the diagnostics of metabolic acidosis. In 1980s Stewart noted, that the analysis of: pCO2, difference between concentrations of strong cations and anions in serum (SID) and total concentration of nonvolatile weak acids (Atot), provides a reliable insight into the body ABB. The Stewart model analyses relationships between pH change and movement of ions across membranes. Six basic types of ABB disorders are distinguished. Respiratory acidosis and alkalosis, strong ion acidosis, strong ion alkalosis, nonvolatile buffer ion acidosis and nonvolatile buffer ion alkalosis. The Stewart model provides the concept of strong ions gap (SIG), which is an apparent difference between concentrations of all strong cations and all strong anions. Its diagnostic value is greater than AG, because it includes concentration of albumin and phosphate. The therapy of ABB disorders consists, first of all, of diagnosis and treatment of the main disease. However, it is sometimes necessary to administer sodium bicarbonate (NaHCO3) or tromethamine (THAM).     

Acid-base status and electrolyte alterations associated with diarrhea in non-suckling horses

A retrospective search of medical records of 56 adult horses with diarrhea of variable duration disclosed a variety of blood gas and electrolyte abnormalities at the time of admission. The acid-base and electrolyte disturbances were analyzed and classified according to the duration of diarrhea. In horses with acute diarrhea (duration <6 days) the most common disorder was combined anion gap metabolic acidosis and metabolic alkalosis (72%)characterized by significant hyponatremia, hypochloridemia, and hyperkalemia. The most severe acidemia was found in horses with diarrheas of intermediate duration (1–2 weeks). In this group hyperchloremic metabolic acidosis was commonly found (43%). In horses with diarrhea of long duration (>4 weeks) blood gas and electrolyte values were usually within normal limits. Although the above findings suggest differing therapeutic approaches might be based on the duration of the diarrhea, many cases differed markedly from the mean with respect to their underlying disturbances and, therefore, optimal fluid therapy should be based on the patient's blood gas and electrolyte status.     

Further studies on the clinical features and clinicopathological findings of a syndrome of metabolic acidosis with minimal dehydration in neonatal calves.

A syndrome of metabolic acidosis of unknown etiology was diagnosed in twelve beef calves 7 to 31 days old. Principal clinical signs were unconsciousness or depression concomitant with weakness and ataxia. Other signs included weak or absent suckle and menace reflexes, succussable nontympanic fluid sounds in the anterior abdomen, and a slow, deep thoracic and abdominal pattern of respiration. The variation in clinical signs between calves was highly correlated (r = 0.87, P less than 0.001) with their acid-base (base deficit) status. Abnormal laboratory findings included reduced venous blood pH, pCO2 and bicarbonate ion concentration as well as hyperchloremia, elevated blood urea nitrogen, increased anion gap and neutrophilic leukocytosis with a left shift. Sodium bicarbonate solution administered intravenously effectively raised blood pH and improved demeanor, ambulation and appetite. All calves did well following a return to a normal acid-base status.     

Assessment of acid-base status of cats with naturally occurring chronic renal failure

Metabolic acidosis is reported to be a common complication of feline chronic renal failure (CRF) but acid-base status of feline patients with this disease is rarely assessed by general practitioners. A cross-sectional study involving 59 cases of naturally occurring feline CRF was conducted to determine the prevalence of acid-base disturbances. Cases were categorised on the basis of their plasma creatinine concentrations as mild, moderate or severe. A group of 27 clinically healthy, age-matched cats was assessed for comparison. A low venous blood pH (<7.270) was found in 10 of the 19 severe cases (52.6 per cent), three of the 20 moderate cases (15 per cent) and none of the 20 mild cases. Acidaemia was associated with an increased anion gap contributed to by both low plasma bicarbonate and low chloride ion concentrations. Biochemical analysis of urine samples showed urine pH to decrease with increasing severity of renal failure. Urinary loss of bicarbonate was not associated with the occurrence of acidaemia and there was a tendency for urinary ammonium ion excretion to decrease as the severity of renal failure increased. Cats with naturally occurring CRF do not show plasma biochemical evidence of acid-base disturbances until the disease is advanced.     

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.     

Clinical Applications of Quantitative Acid-Base Chemistry

Stewart used physicochemical principles of aqueous solutions to develop an understanding of variables that control hydrogen ion concentration (H+) in body fluids. He proposed that H+ concentration in body fluids was determined by PCO₂, strong ion difference (SID = sum of strong positive ion concentrations minus the sum of the strong anion concentrations) and the total concentration of nonvolatile weak acid (A_tot) under normal circumstances. Albumin is the major weak acid in plasma and represents the majority of A_tot. These 3 variables were defined as independent variables, which determined the values of all other relevant variables (dependent) in plasma, including H+. The major strong ions in plasma are sodium and chloride. The difference between Na+ and Cl^- may be used as an estimation of SID. A decrease in SID below normal results in acidosis (increase in H+) and an increase in SID above normal results in alkalosis (decrease in H+). Unidentified strong anions such as lactate will decrease the SID, if present. Equations developed by Fencl allow Stewart's work to be easily applied clinically for evaluating the metabolic (nonrespiratory) contribution to acid-base balance. This approach separates the net metabolic abnormality into components, and allows one to easily detect mixed metabolic acid-base abnormalities. The Fencl approach provides insight into the nature and severity of the disturbances that exist in the patient. Sodium, chloride, protein, and unidentified anion derangements may contribute to the observed metabolic acid-base imbalance.     

Determination of serum organic acids in puppies with naturally acquired parvoviral enteritis

The purpose of the present study was to investigate the acid-base status and the serum concentration of organic acids in puppies with naturally occurring canine parvoviral enteritis. Between July 1999 and July 2000, 25 client-owned puppies admitted to the St. Louis Animal Emergency Clinic South for treatment of enteritis caused by parvovirus infection were used in our study. Control blood samples were collected from 22 healthy puppies less than 9 months of age. Serum organic acid concentrations were quantitatively determined by HPLC. Puppies infected with parvovirus had significantly lower plasma concentrations of sodium, potassium, chloride, and bicarbonate than controls. Although serum L-lactate tended to increase in some puppies with canine parvoviral enteritis, our study demonstrated that most affected puppies developed only mild compensated metabolic acidosis. None of the affected puppies had an elevated serum D-lactate concentration at admission.     

Relationship between urine ammonium ion excretion and urine anion gap in dogs.

Acidemia stimulates renal ammonia production and excretion. This adaptive response allows increased H+ secretion and generation of new bicarbonate. To determine whether a relationship existed between urine ammonium (NH4+) concentration and excretion and urine anion gap (Na+ + K(+)- Cl-), ammonium chloride (NH4Cl) was administered per OS for 5 days to induce systemic acidemia in 12 healthy Beagles. During NH4Cl administration, a strong, statistically significant (P less than 0.0001) relationship was apparent between urine NH4+ concentration measured in millimoles per liter and urine anion gap. Regression equation: urine [NH4+] = 8.2 - 0.416 x urine anion gap; r = -0.897. A statistically significant (P = 0.0001) relationship existed between urine NH4+ excretion measured in millimoles per kilogram of body weight per day and urine anion gap. Regression equation: urine NH4+ excretion = 0.74 - 0.38 x urine anion gap; r = -0.768. As urine NH4+ concentration or excretion increased, urine anion gap became more negative. Before NH4Cl administration (no systemic acidemia), a weak, but statistically significant (P = 0.015) relationship was observed between urine NH4+ concentration and urine anion gap. Regression equation: urine [NH4+] = 65.2 - 0.141 x urine anion gap; r = -0.41. However, a relationship was not evident between urine NH4+ excretion and urine anion gap before NH4Cl administration. Hence, urine anion gap is a reliable index of urine NH4+ concentration and excretion only in dogs with metabolic acidosis. In human beings with distal renal tubular acidosis, NH4+ excretion is inappropriately low and results in a positive urine anion gap.(ABSTRACT TRUNCATED AT 250 WORDS)     

Poisoning induced by administration of a phosphate-containing urinary acidifier in a cat

Signs of depression, hyperphosphatemia, azotemia, high anion gap metabolic acidosis, and renal failure developed in an adult cat following administration of an excessive dose of a phosphate-containing urinary acidifier. After extracellular fluid volume expansion, diuresis, and administration of a phosphate binder, serum phosphorus concentration returned to normal in 12 hours; the cat recovered fully. The urinary acidifier had been given as part of treatment for a urinary tract infection. Findings suggest that phosphate-containing urinary acidifiers should be administered cautiously because, like other sources of phosphate, they are capable of causing life-threatening metabolic disturbances.     

The acid-base equilibrium and carbohydrate metabolism during infection with Eperythrozoon suis

Following on from clinical observations which point to severe metabolic disturbances in association with acute Eperythrozoon (E.) suis infection, the parameters of acid-base balance (pO2, pCO2, pH, actual bicarbonate, standard bicarbonate, base excess) as well as the glucose-, lactate- and pyruvate levels, were measured in venous blood during the course of eperythrozoonotic infection. Glucose consumption was investigated in in vitro experiments with differing numbers of pathogens. Acute E. suis infection is accompanied by a severe acidosis and hypoglycaemia. In vitro experiments showed that a rapid breakdown of glucose follows in E. suis infected blood. No significant reduction in glucose concentration was established in control blood in a comparable time period. The results give rise to the assumption that E. suis is capable of independent glucose breakdown. Both the increase in lactate concentration (metabolic component) and a disturbance of pulmonary gaseous exchange (respiratory component) are regarded as the cause of the acidosis.     

Effects of acid-base disturbances caused by differences in dietary fixed ion balance on kinetics of calcium metabolism in ruminants with high calcium demand

Effects of subclinical metabolic acid-base disturbances, caused by dietary fixed ion imbalances on kinetics of calcium (Ca) metabolism were examined in eucalcemic caprine does (period 1) and does during simulated lactational Ca loss (period 2). In both experiments, Ca balance data and serial blood, fecal and urine samples were collected after an iv injection of 45Ca. In period 2, lactational Ca loss was simulated by continuous infusion of ethylene glycol-bis (beta-amino ethyl ether)N,N,N'N'-tetraacetic acid (EGTA) to standardize the loss of Ca among goats. The data were fit to a four-compartment model of Ca metabolism. In period 1, fixed anion excess, [sodium + potassium - chloride] = -2 meq/100 g diet dry matter (ANEX) increased urinary Ca excretion relative to fixed cation excess, [sodium + potassium - chloride] = 71 meq/100 g diet dry matter (CATEX). Consequently, rates of Ca absorption and resorption were elevated in goats made acidotic by dietary fixed anion excess. During period 2 (EGTA infusion), urinary Ca loss was elevated to similar levels in goats fed ANEX and CATEX, but Ca absorption remained higher in goats fed ANEX. Consequently, size of the exchangeable Ca pool, accretion rate and balance across bone were higher in these goats. Fixed anion excesses (found in corn silage and grains) cause subclinical metabolic acidosis, which elevates rates of Ca absorption but does not affect size of the exchangeable Ca pool. Fixed cation excesses (associated with diets containing alfalfa and buffers) cause subclinical metabolic alkalosis, which diminishes Ca absorption and urinary Ca excretion. Acidosis-induced hypercalciuria is the metabolic cost of maintaining high prepartum Ca absorption rates and high flux of Ca through the exchangeable Ca pool that may aid in adjustment to sudden Ca losses at parturition.     

Renal tubular acidosis in horses (1980-1999)

Renal tubular acidosis (RTA) is characterized by altered renal tubular function resulting in hyperchloremic metabolic acidosis. The purpose of the study was to describe RTA in 16 horses. No breed or sex predilection was found. The mean age at onset of the disease was 7 years of age. The type of diet had no apparent effect on development of RTA. The most common clinical signs were depression, poor performance, weight loss, and anorexia. Initial blood work revealed a marked hyperchloremic metabolic acidosis in all horses and a compensatory respiratory response in most horses. Sixty-three percent (10/16) of the horses had some evidence of renal damage or disease. Initial treatment consisted of large amounts of sodium bicarbonate given intravenously and orally for the prompt correction of the acidosis. Response to treatment was largely dependent on the rate of sodium bicarbonate administration. Long-term oral supplementation with NaHCO3 was required for the maintenance of normal acid-base status in individual horses. Recurrence of RTA was noted in 56% (9/16) of the horses. Horses with evidence of renal disease had multiple relapses. RTA should be considered as a differential diagnosis in horses with vague signs of depression, weight loss, and anorexia. The pathogenesis of RTA in horses remains uncertain, but prompt recognition and early aggressive intravenous sodium bicarbonate therapy followed by long-term oral supplementation seem to be important to successful management.     

Right displacement of the abomasum and abomasal volvulus in dairy cows: 458 cases (1980-1987)

Clinical and surgical findings in 458 dairy cows with right displacement of the abomasum or abomasal volvulus (AV) were analyzed to determine the association between these variables and the outcome (productive, salvaged, or terminal) of the affected cow. Heart rate at initial examination was higher in the salvaged and terminal groups of cows (P less than 0.0001) than in the productive group. The plasma Na+ concentration was lower in the salvaged and terminal groups of cows (P less than 0.0001) than in the productive group. The plasma C1- concentration was lower in the salvaged group of cows than in cows with either productive or terminal outcomes (P less than 0.0001). Anion gap was significantly higher (P less than 0.0001) in the salvaged and terminal groups than in cows classified as productive. On the basis of surgical findings, cattle with right displacement of the abomasum were more likely to survive than cows with AV. Cows that required fluid decompression of the abomasum via abomasotomy were less likely to survive than those in which gaseous decompression was performed. Cows with evidence of vascular compromise of the abomasal wall were less likely to survive than those with normal abomasal serosa. Preoperative heart rate and anion gap had positive correlations with the presence of abomasal necrosis, whereas temperature, venous blood pH, plasma bicarbonate, and base excess concentrations had negative correlations. Cows in terminal stages of AV were likely to have a mixed primary acid-base disturbance, consisting of metabolic alkalosis with superimposed metabolic acidosis. These findings were highly correlated with abomasal necrosis.