Acid-base abnormalities are frequently present in sick calves. The mechanism for an acid-base disturbance can be characterized using the strong ion approach, which requires accurate values for the total concentration of plasma nonvolatile buffers (A tot ) and the effective dissociation constant for plasma weak acids (K a ). The aims of this study were to experimentally determine A tot , K a , and net protein charge values for calf plasma and to apply these values quantitatively to data from sick calves to determine underlying mechanisms for the observed acid-base disturbance. Plasma was harvested from 9 healthy Holstein-Friesian calves and concentrations of quantitatively important strong ions (Na ϩ , K ϩ , Ca 2ϩ , Mg 2ϩ , Cl Ϫ , L-lactate) and nonvolatile buffer ions (total protein, albumin, phosphate) were determined. Plasma was tonometered with CO 2 at 37ЊC, and plasma PCO 2 and pH measured over a range of 15-159 mm Hg and 6.93-7.79, respectively. Strong ion difference (SID) was calculated from the measured strong ion concentrations, and nonlinear regression was used to estimate values for A tot and K a from the measured pH and PCO 2 and calculated SID. The estimated A tot and K a values were then validated using data from 2 in vivo studies. Mean (Ϯ SD) values for calf plasma were A tot ϭ 0.343 mmol/g of total protein or 0.622 mmol/g of albumin; K a ϭ (0.84 Ϯ 0.41) ϫ 10 Ϫ7 ; pK a ϭ 7.08. The net protein charge of calf plasma was 10.5 mEq/L, equivalent to 0.19 mEq/g of total protein or 0.34 mEq/g of albumin. Application of the strong ion approach to acid-base disturbances in 231 sick calves with or without diarrhea indicated that acidemia was due predominantly to a strong ion acidosis in response to hyponatremia accompanied by normochloremia or hyperchloremia and the presence of unidentified strong anions. These results confirm current recommendations that treatment of acidemia in sick calves with or without diarrhea should focus on intravenous or PO administration of a fluid containing sodium and a high effective SID.Key words: Calf diarrhea; D-lactic acidosis; Hyponatremia; Metabolic acidosis.A cidemia and metabolic acidosis occur commonly in sick calves with or without diarrhea. Metabolic acidosis in diarrheic calves was originally attributed to fecal bonate loss as well as the presence of unidentified organic acids in plasma and a decrease in glomerular filtration rate in response to severe dehydration.1-4 These proposed mechanisms for development of metabolic acidosis were based, in part, on the presence of hyper-L-lactatemia in diarrheic calves, 1,2,5,6 hyper-L-lactatemia and extensive loss of bicarbonate in the watery stool of humans with cholera, 7 and from (personal communication) of a high fecal bicarbonate concentration (40 mEq/L) in 4 calves with experimentally induced enterotoxigenic Escherichia coli diarrhea.c However, metabolic acidosis in diarrheic calves is probably predominantly due to causes other than fecal bicarbonate loss because diarrheic calves have measured mean daily fecal losses of s...

Severely dehydrated calves that are unable to suckle need intravenous fluids for effective resuscitation. Intravenous fluid therapy is also indicated for sick calves without obvious dehydration, such as calves with strong ion acidosis, ruminal acidosis (rumen drinkers), severe pneumonia, septicemia, or hypothermia. This article presents an updated overview of intravenous fluid therapy for calves, recent insights into the development of metabolic acidosis in young calves resulting from accumulation of D-lactate, a simplified algorithm for intravenous fluid therapy, and a procedure for ear vein catheterization under field conditions.

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Acid-base abnormalities are frequently present in sick calves. The mechanism for an acid-base disturbance can be characterized using the strong ion approach, which requires accurate values for the total concentration of plasma nonvolatile buffers (A tot) and the effective dissociation constant for plasma weak acids (K a). The aims of this study were to experimentally determine A tot , K a , and net protein charge values for calf plasma and to apply these values quantitatively to data from sick calves to determine underlying mechanisms for the observed acid-base disturbance. Plasma was harvested from 9 healthy Holstein-Friesian calves and concentrations of quantitatively important strong ions (Na , K , Ca 2 , Mg 2 , Cl , L-lactate) and nonvolatile buffer ions (total protein, albumin, phosphate) were determined. Plasma was tonometered with CO 2 at 37C, and plasma PCO 2 and pH measured over a range of 15-159 mm Hg and 6.93-7.79, respectively. Strong ion difference (SID) was calculated from the measured strong ion concentrations, and nonlinear regression was used to estimate values for A tot and K a from the measured pH and PCO 2 and calculated SID. The estimated A tot and K a values were then validated using data from 2 in vivo studies. Mean (SD) values for calf plasma were A tot 0.343 mmol/g of total protein or 0.622 mmol/g of albumin; K a (0.84 0.41) 10 7 ; pK a 7.08. The net protein charge of calf plasma was 10.5 mEq/L, equivalent to 0.19 mEq/g of total protein or 0.34 mEq/g of albumin. Application of the strong ion approach to acid-base disturbances in 231 sick calves with or without diarrhea indicated that acidemia was due predominantly to a strong ion acidosis in response to hyponatremia accompanied by normochloremia or hyperchloremia and the presence of unidentified strong anions. These results confirm current recommendations that treatment of acidemia in sick calves with or without diarrhea should focus on intravenous or PO administration of a fluid containing sodium and a high effective SID. A cidemia and metabolic acidosis occur commonly in sick calves with or without diarrhea. Metabolic aci-dosis in diarrheic calves was originally attributed to fecal bonate loss as well as the presence of unidentified organic acids in plasma and a decrease in glomerular filtration rate in response to severe dehydration. 1-4 These proposed mechanisms for development of metabolic acidosis were based, in part, on the presence of hyper-L-lactatemia in diarrheic calves, 1,2,5,6 hyper-L-lactatemia and extensive loss of bicar-bonate in the watery stool of humans with cholera, 7 and from (personal communication) of a high fecal bicarbonate concentration (40 mEq/L) in 4 calves with experimentally induced enterotoxigenic Escherichia coli diarrhea. c However , metabolic acidosis in diarrheic calves is probably predominantly due to causes other than fecal bicarbonate loss because diarrheic calves have measured mean daily fecal losses of sodium (10.3 mEq/kg body weight), potassium (1.7 mEq/kg body weight), and chloride (7.9 mEq/kg bo...

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