Comparison of the measurement of total carbon dioxide and strong ion difference for the evaluation of metabolic acidosis in diarrhoeic calves

Eighty-four calves with diarrhoea were treated with fluids and 13 apparently healthy calves of similar ages were sampled as controls. Their total blood carbon dioxide (TCO2) was measured with a Harleco apparatus and 31 of the calves were treated with oral fluids and 53 with parenteral fluids. The oral fluid contained 118 mmol/litre Na+, 25 mmol/litre K+, 110 mmol/litre glucose, 108 mmol/litre bicarbonate (HCO3- as citrate), 43 mmol/litre Cl-, 4 mmol/litre Ca++, 4 mmol/litre Mg++ and 20 mmol/litre glycine, and the parenteral fluid contained 144 mmol/litre Na+, 4 mmol/litre K+, 35 mmol/litre HCO3- and 113 mmol/litre Cl-. Both treatments resulted in significant improvements in acid-base status as demonstrated by an increase in TCO2, and the treatment was successful in 27 of the 31 calves receiving oral fluids and in 45 of the 53 calves receiving parenteral fluids. Thirty-seven of the calves treated parenterally were very severely acidotic (TCO2 <8 mmol/litre) initially and they received an additional 400 mmol HCO3- added to the first 5 litres of infusion. Treatment was successful in 33 of these calves. The decision to administer additional bicarbonate was made on the basis of their acid-base status as measured with a Harleco apparatus. The strong ion difference (Na++K+-Cl-) (SID) of the calves was calculated retrospectively. There was a significant correlation between the SID and TCO2 of the calves treated with oral fluids but not among the control calves or the calves treated parenterally. Furthermore, measurements of the change in SID during therapy gave little indication of the change in acid-base status as measured by the Harleco apparatus, with the SID decreasing (suggesting a worsening of acid-base status) in 16 calves in which the TCO2 increased (suggesting an improvement in acid-base status). There was a significant correlation between the change in SID and the change in TCO2 during treatment in the calves receiving oral fluids but not in the calves treated parenterally.     

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.     

Evaluation of the Total Carbon Dioxide Apparatus and pH Meter for the Determination of Acid-Base Status in Diarrheic and Healthy Calves

Three simple tests of acid-base status were evaluated for field use. Blood samples were collected from 20 diarrheic and 24 healthy calves less than six weeks of age. One sample was collected anaerobically and immediately analyzed on a blood gas analyzer. The other samples were used for measurement of blood and serum pH using a pH meter and pH paper, and for serum total carbon dioxide (TCO₂) using a TCO₂ apparatus. The TCO₂ apparatus gave the best results and would be useful in the field. TCO₂ apparatus measurements had a high correlation, r=0.91, with blood gas analyzer blood bicarbonate values. Healthy calves have a serum TCO₂ content of 30 mmol/L and bicarbonate requirements for correcting metabolic acidosis in diarrheic calves can be calculated:

Bicarbonate required (mmol) = (30-TCO₂) × Body Weight × 0.6 This can be converted to grams of sodium bicarbonate by dividing by 12.

     

Comparison of sodium bicarbonate and carbicarb for the treatment of metabolic acidosis in newborn calves

Carbicarb (an equimolar mixture of sodium bicarbonate and sodium carbonate) was compared with sodium bicarbonate alone for the treatment of acidosis in newborn calves: 25 of 49 calves with a blood pH at birth of less than 7-2 and a base deficit of less than -3 mmol/litre were treated intravenously with sodium bicarbonate and 24 were treated with carbicarb. The doses were calculated on the basis of the base deficit in a blood sample taken 10 minutes after birth, and further blood samples were taken immediately after the treatment and 30 and 60 minutes after the treatment for the determination of acid-base status, blood gases and haematological and biochemical variables. Both treatments resulted in a significant increase in blood pH, but there was no difference between them. The mean (sd) blood pH before treatment was 7.09 (0.02) and after treatment it was 7.28 (0.01). There was no increase in the partial pressure of carbon dioxide after treatment with either sodium bicarbonate or carbicarb. Both treatments were associated with an increase in sodium concentration and decreases in the total erythrocyte count, haematocrit and haemoglobin concentration.     

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.     

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.     

Acidosis and clinical condition in asphyctic calves

In depressed calves (modified APGAR score 4-6) there is at birth an evident combined respiratory-metabolic acidosis (pH = 7.082 +/- 0.175; pCO2 = 73.3 +/- 26.8 mm Hg; BE = -10.6 +/- 7.2 mmol/l). The metabolic adaptation is completed after 6 hours, the respiratory acidosis is present up to 24 hours after delivery. In comparison to normal calves there are significant deviations in pH-values, base excess standard bicarbonate and actual bicarbonate during the whole investigation time. The carbon dioxide tensions of the depressed calves are at birth similar to those of normal calves, but in the following hours they are significantly higher. A definite relationship can be demonstrated between the 1 minute APGAR score and pH-value, base excess, standard bicarbonate and actual bicarbonate. Oxygen tension, oxygen saturation and carbon dioxide do not correlate with the clinical condition.     

A retrospective study of the relationship between clinical signs and severity of acidosis in diarrheic calves

A retrospective study of 123 calves under two months of age with signs of diarrhea was performed to investigate the relationships among the calf's demeanor, dehydration, rectal temperature, and base deficit. The severity of dehydration, hypothermia, and metabolic acidosis were associated with level of depression. Clinical signs and age of calf could be used to predict the severity of acidosis. Acidosis was more severe in calves over eight days of age and also increased in severity with the degree of depression. The most severe metabolic acidosis was seen in calves over eight days of age presented in sternal or lateral recumbency; the base deficit in these groups was 16.3 ± 8.3 (means ± 1SD) and 20.3 ± 10.1 mmol/L respectively, and on average these calves require 2.4 and 3.0 L respectively of 1.3% sodium bicarbonate solution to correct the acidosis.     

Experimentally induced lactic acidosis in the goat

Lactic acidosis was produced experimentally twice in each of 4 adult, female goats, by giving sucrose orally at the rate of 18 g/kg bodyweight. Changes in pH, osmolality, lactic acid concentration, and other constituents in ruminal fluid, plasma and blood were monitored over a period of 48 h. Also changes in urinary pH and sediment were examined. To ameliorate the metabolic disturbance, calcium hydroxide and bicarbonate treatment was employed after the 24 h samples had been collected and their acid-base status determined. A feature of the disturbance in the goats was that a metabolic alkalosis preceded the onset of lactic acidosis.     

A Comparison of Simultaneously Collected Arterial, Mixed Venous, Jugular Venous and Cephalic Venous Blood Samples in the Assessment of Blood-Gas and Acid-Base Status in the Dog

Blood samples were collected simultaneously from the pulmonary artery, jugular vein, cephalic vein, and carotid artery in awake dogs. Blood-gas and acid-base values were measured from these blood samples in normal dogs and in dogs after production of metabolic acidosis and metabolic alkalosis. The values obtained from each of the venous sites were compared with those obtained from arterial blood to determine if venous blood from various sites accurately reflected acid-base balance and could therefore be used in the clinical patient. The results of this study demonstrated significant differences between the blood from various venous sites and the arterial site for PCO2 and pH in all acid-base states. Significant differences for standard bicarbonate (SHCO3) were found only when jugular and cephalic venous blood were compared with arterial blood in dogs with a metabolic acidosis. No significant differences were found for BE when blood from the venous sites was compared with arterial blood. The values for pH, HCO3, TCO2, BE, and SHCO3 measured on blood collected at the various venous sites were found to correlate well with those obtained from arterial blood, with a correlation coefficient of 0.99 for HCO3, TCO2, BE, and SHCO3. These correlation coefficients, together with similar values in BE at all collection sites, indicate that, in the dog with normal circulatory status, blood from any venous site will accurately reflect the acid-base status of the patient.     

Acid-base and electrolyte alterations associated with salivary loss in the pony

Esophageal fistulas were made in 6 ponies to evaluate whole blood acid-base values and serum and salivary electrolyte alterations associated with salivary depletion. Acid-base and electrolyte values remained within normal ranges for 15 days in 3 control ponies fed a pelleted diet through nasogastric tubes. In 6 ponies with esophageal fistulas that were fed the same diet through esophagostomy tubes, hypochloremia and hyponatremia developed during the same period. Serum K concentrations were only marginally depleted, probably because of dietary replacement. Salivary depletion resulted in transient metabolic acidosis from bicarbonate lost in saliva followed by progressive metabolic alkalosis. The alkalosis probably resulted from renal compensation of electrolyte imbalances. Salivary electrolytes were in high concentrations, probably because of increased salivary flow rates. Initial saliva was rich in Na, Cl, and K, but progressive reduction in salivary Na and Cl concentrations occurred during the 5-day collection period. These electrolyte savings could be explained by dietary influences and hormonal control of electrolyte transport in salivary ducts. Therapy for correction of acid-base and electrolyte alterations was also discussed.     

Abdominal distension in collapsed diarrhoeic calves: biochemical findings and treatment.

Thirty-seven of 53 diarrhoeic calves hospitalised for intravenous fluid therapy were classified as very severely acidotic (total carbon dioxide less than 8 mmol/litre) by using a Harleco apparatus. All the calves were given intravenously 10 to 20 litres of electrolyte solution which contained 144 mmol/litre sodium, 4 mmol/litre potassium, 113 mmol/litre chloride and 35 mmol/litre bicarbonate, and in addition the 37 very severely acidotic calves received 400 ml of 1M sodium bicarbonate in the first 5 litres of fluid administered. Sixteen of the 37 very severely acidotic calves had a distended right flank, suggesting the presence of a dilated fluid-filled viscus. Neither their history nor other clinical signs were useful predictors of the distension. The distended calves had significantly higher plasma concentrations of sodium and chloride, and significantly lower plasma creatinine concentrations than the calves which were not distended. Treatment was successful in all the 21 non-distended calves but four of the distended calves died despite treatment. The resolution of the distension in the successfully treated calves, coincided with a significant increase in plasma bicarbonate concentration and the passage of large amounts of malodorous mucoid faeces.     

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.     

Relationship between depression score and acid-base status in Japanese Black calves with diarrhea

We evaluated the relationship between depression score and acid-base status in 84 purebred and crossbred Japanese Black calves. The bicarbonate (p<0.001) and base excess concentrations (p<0.001) were significantly and negatively correlated with the depression scores of the calves. The proposed diagnostic cutoff point for a depression score that indicates severe metabolic acidosis (BE < -10 mM) is 6.5 based on analysis of the ROC curve. The sensitivity and specificity were 88.4% and 81.2%, respectively. The depression scoring system is a useful tool for evaluation of the acid-base status of purebred and crossbred Japanese Black calves. In addition, a depression score of 6.5 suggests severe metabolic acidosis and that intravenous infusion of sodium bicarbonate solution is necessary.     

Decreased colostral immunoglobulin absorption in calves with postnatal respiratory acidosis

The effect of postnatal acid-base status on the absorption of colostral immunoglobulins by calves was examined in 2 field studies. In study 1, blood pH at 2 and 4 hours after birth was related to serum IgG1 concentration 12 hours after colostrum feeding (P less than 0.05). Decreased IgG1 absorption from colostrum was associated with respiratory, rather than metabolic, acidosis, because blood PCO2 at 2 and 4 hours after birth was negatively related to IgG1 absorption (P less than 0.05), whereas serum bicarbonate concentration was not significantly related to IgG1 absorption. Acidosis was frequently observed in the 30 calves of study 1. At birth, all calves had venous PCO2 value greater than or equal to 60 mm of Hg, 20 of the calves had blood pH less than 7.20, and 8 of the calves had blood bicarbonate concentration less than 24 mEq/L. Blood pH values were considerably improved by 4 hours after birth; only 7 calves had blood pH values less than 7.20. Calves lacking risk factors for acidosis were examined in study 2, and blood pH values at 4 hours after birth ranged from 7.25 to 7.39. Blood pH was unrelated to IgG1 absorption in the calves of study 2. However, blood PCO2 was again found to be negatively related to colostral IgG1 absorption (P less than 0.005). Results indicate that postnatal respiratory acidosis in calves can adversely affect colostral immunoglobulin absorption, despite adequate colostrum intake early in the absorptive period.     

Severity and nature of acidosis in diarrheic calves over and under one week of age

A prospective study of the severity of dehydration and acidosis was carried out in 42 calves under 35 days of age presented for treatment of neonatal diarrhea. Clinically the mean level of dehydration was 8 to 10%. The plasma volume was 65% of that in the hydrated calf but the calves only gained 6.5% in weight during therapy.

Calves under eight days of age often had a lactic acidosis. Blood pH was 7.118±0.026 (mean ± 1 standard error), bicarbonate concentration 18.8±1.3 mmol/L, base deficit 11.4±1.7 mmol/L and lactate of 3.6± 0.06 mmol/L. Calves over eight days usually had a nonlactic acidosis. Blood pH was 7.042±0.021, bicarbonate 10.8±1.0 mmol/L, base deficit 19.5±1.2 mmol/L and lactate 1.2±0.3 mmol/L. These values were all significantly different from those in younger calves.

Over all calves there was a poor correlation between the severity of acidosis and dehydration(r=0.05). The severity of lactic acidosis was related to the severity of dehydration. Mean bicarbonate requirements to correct acidosis were calculated to be 200 mmol(17 g of sodium bicarbonate)and 450 mmol(37 g of sodium bicarbonate)in calves under and over eight days of age respectively. Both groups of calves required a mean volume of 4L of fluid to correct dehydration.

     

Effects of intravenous hyperosmotic sodium bicarbonate on arterial and cerebrospinal fluid acid-base status and cardiovascular function in calves with experimentally induced respiratory and strong ion acidosis

The objectives of this study were to determine the effects of hyperosmotic sodium bicarbonate (HSB) administration on arterial and cerebrospinal fluid (CSF) acid-base balance and cardiovascular function in calves with experimentally induced respiratory and strong ion (metabolic) acidosis. Ten healthy male Holstein calves (30-47 kg body weight) were instrumented under halothane anesthesia to permit cardiovascular monitoring and collection of blood samples and CSE Respiratory acidosis was induced by allowing the calves to spontaneously ventilate, and strong ion acidosis was subsequently induced by i.v. administration of L-lactic acid. Calves were then randomly assigned to receive either HSB (8.4% NaHCO3; 5 ml/kg over 5 minutes, i.v.; n=5) or no treatment (controls, n=5) and monitored for 1 hour. Mixed respiratory and strong ion acidosis was accompanied by increased heart rate, cardiac index, mean arterial pressure, cardiac contractility (maximal rate of change of left ventricular pressure), and mean pulmonary artery pressure. Rapid administration of HSB immediately corrected the strong ion acidosis, transiently increased arterial partial pressure of carbon dioxide (P(CO2)), and expanded the plasma volume. The transient increase in arterial P(CO2) did not alter CSF P(CO2) or induce paradoxical CSF acidosis. Compared to untreated control calves, HSB-treated calves had higher cardiac index and contractility and a faster rate of left ventricular relaxation for 1 hour after treatment, indicating that HSB administration improved myocardial systolic function. We conclude that rapid i.v. administration of HSB provided an effective and safe method for treating strong ion acidosis in normovolemic halothane-anesthetized calves with experimentally induced respiratory and strong ion acidosis. Fear of inducing paradoxical CSF acidosis is not a valid reason for withholding HSB administration in calves with mixed respiratory and strong ion acidosis.     

Effect of intravenous infusion of isotonic sodium bicarbonate solution on acidemic calves with diarrhea

The effect of 1.35% isotonic sodium bicarbonate solution (ISB) administered intravenously on acid-base equilibrium was examined in 18 acidemic Japanese black beef calves with spontaneous diarrhea. The infusion volumes of ISB were decided based on the first half volumes of base needed. In 72.2% (13/18) of calves, improvement of acidemia was detected. There was good correlation (r=0.693, p<0.01) between infused volume of ISB and changes in base excess (y=1.097x + 4.762). Infusion volumes of ISB were 7.5, 10.2, 12.9 and 15.7 ml/kg, respectively, enough to correcting the first half of 5, 10, 15 and 20 mEq/l of base deficit in acidemic calves. Our finding suggested that ISB could be used to correct metabolic acidosis without altering electrolyte concentrations in calves.     

Experimentally induced systemic hyperchloremic acidosis in calves

Background: Among the various metabolic disturbances occurring in calves affected by neonatal diarrhea or ruminal acidosis, acidemia constitutes an important condition requiring specific therapy. Although various attempts have been made to estimate the degree of metabolic acidosis on the basis of clinical signs alone, some doubts have been raised regarding the accuracy and predictive value of the clinical variables suggested. HYPOTHESIS: The induction of metabolic acidosis in healthy calves via the infusion of hydrochloric acid (HCl) will lead to a clinical picture similar to that seen in neonatal calves with diarrhea or ruminal acidosis. ANIMALS: The study was carried out on 15 Holstein male calves between 5 and 19 days of age. METHODS: Hyperchloremic metabolic acidosis was induced over a period of 80 minutes by an IV infusion of 4,000 mL of 0.9% NaCl solution containing 400 mM HCl. RESULTS: Acidemia occurred rapidly and increased constantly up to a maximum value, which was reached in all calves by the end of the administration and amounted to a 22.4 mM/L mean base deficit (range from 17.0 to 33.1 mM/L). Despite the relatively severe acute acid-base imbalance during the entire observation period, no calves showed any clinical signs or depressed appetite. CONCLUSIONS AND CLINICAL IMPORTANCE: Factors other than a disturbance of the acid-base balance should be considered to be primarily responsible for the clinical picture in calves affected by diarrhea or ruminal acidosis.