[Pathogenesis and diagnosis of systemic acidosis in animals with conclusions for effective forms of therapy]

Intermediary metabolism produces daily approximately 285 mmol hydrogen ions per kilogramm metabolic body weight (BWkg 0.75). If the lung fails to eliminate the volatile acid H2CO3 sufficiently and/or if the kidneys do not eliminate the also produced nonvolatile acids a retention of acids in the organism results. This way, as well as increased acid production through metabolic processes, leads to a systemic acidosis. Systemic acidosis develops after a primary dysfunction of an organ. If there is only one cause of an acid-base-disturbance, e.g. metabolic acidosis, the organism will respond with compensation by the correspondent organ, e.g. the lung, which reduces the drop in the pH. If metabolic and respiratory acidosis occur simultaneously normal compensation is impaired and the fall in the pH is greater by additive effects. This can lead to a severe, life-threatening decline in the blood-pH (< 7.00). If the pH falls from normal value of 7.40 below 7.20, buffer therapy is necessary. Most alkalinizing agents in veterinary medicine, such as bicarbonate, lactate or acetate are only effective after increased pulmonary elimination of CO2 produced in buffer reactions. These substances are not suitable and are even contraindicated in therapy of primary respiratory or mixed respiratory-metabolic acidosis. New buffer agents, e.g. an equimolar mixture of NaHCO3 and Na2CO3 (= Carbicarb) open new promising possibilities in the treatment of acidotic disorders in animals. However clinical trials to determine the efficacy of Carbicarb in animals are still to be conducted.