[Significance of respiratory compensation in acidosis in calves].

The respiratory component PvCO2 of acid-base-status was observed in n = 36 calves (age: x +/- s = 8.7 +/- 5.0 d) with neonatal diarrhea and an acidosis (venous blood-pH: < 7.30; x +/- s = 7.08 +/- 0.15). In n = 10 (28%) calves with a severe metabolic acidosis (pH: x +/- s = 7.03 +/- 0.12; BE: x +/- s = -22.1 +/- 5.3 mmol/l) the PvCO2 was decreased < 5.3 kPa (x +/- s = 4.5 +/- 0.5 kPa) and showed a distinct respiratory compensation. A PvCO2 between 5.3-6.7 kPa (x +/- s = 6.0 +/- 0.4 kPa) was observed in n = 16 (44%) acidotic calves (pH: x +/- s = 7.11 +/- 0.13; BE: x +/- s = -15.2 +/- 7.4 mmol/l). These n = 26 (72%) calves showed a simple metabolic acidosis which is well known for calves with neonatal diarrhea. The remaining n = 10 (28%) calves showed an increase of the PvCO2 > 6.7 kPa (x +/- s = 8.0 +/- 1.5 kPa). These animals had a mixed respiratory-metabolic acidosis (pH: x +/- s = 7.08 +/- 0.20; BE: x +/- s = -13.9 +/- 10.3 mmol/l), as the decrease of the pH could not be determined by the decreased metabolic component HCO3- of acid-base-status alone. Calves which died during hospitalization and calves with a PvCO2 > 6.7 kPa tended to be younger and showed partially significant lower values for the parameters of oxygen-supply PvO2 and SvO2. Lactate was significantly higher in dying calves but not in calves with a mixed acidosis which on the other hand were more dehydrated. The functional capacity of respiratory compensation of acidotic disorders in the calves studied promised to be almost the same as in dog and man. One reason for the failure of respiratory compensation in some calves could be a more severe hypovolemia. With the use of "venous hypoxemia" (decrease PvO2 and decrease SvO2) the detection of tissue hypoxia was easier than with lactate concentration.