Page 262 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

CHAPTER • 10

Metabolic Acid-Base Disorders

Stephen P. DiBartola

Metabolic disturbances of acid-base balance are BODY BUFFER RESPONSE TO AN
associated with many disease states, and identification ACUTE ACID LOAD
of the acid-base disturbance may facilitate diagnosis of When HCl was infused acutely into nephrectomized
the underlying disease process. For example, observation dogs, approximately 40% of the acid was buffered by
of hypochloremic metabolic alkalosis on a serum bio- extracellular HCO 3 , 10% by red cell buffers (primarily

chemical profile of a vomiting dog may lead to recogni- hemoglobin), and 50% by intracellular buffers of soft
tion of gastrointestinal obstruction as the cause. The tissues and bone (primarily proteins and phosphates). 223
regulation of normal acid-base balance is considered in In nonnephrectomized unanesthetized dogs infused
detail in Chapter 9. intermittently with HCl, intracellular buffers contributed
approximately 50% of the buffer response, regardless of
METABOLIC ACIDOSIS the magnitude of the H load. 210 Within a few minutes
þ
þ
of an acute fixed acid load, administered H is buffered
Metabolic acidosis is characterized by a primary decrease by HCO 3 in plasma water. Plasma proteins and
þ
in plasma HCO 3 concentration, increased [H ], phosphates play a minor role in this acute response. Some
decreased pH, and a secondary, or adaptive, decrease in of the administered acid enters red cells and is buffered by
. In one study, metabolic acidosis was the most hemoglobin. The CO 2 produced by the combination of
P CO 2
common acid-base disturbance in dogs and cats. 61 the H with HCO 3 ions is rapidly removed from the

þ

MetabolicacidosiscanbecausedbylossofHCO 3 -rich body by alveolar ventilation. Within 30 minutes, the acid
fluidfromthebody,addition of fixedacidtothebodyorits load has been distributed to the interstitial fluid, where
production by metabolism within the body, or failure of HCO 3 again plays the dominant role in the acute buffer

renal excretion of fixed acid. Loss of HCO 3 - rich fluid response. After several hours, H þ enters intracellular

usually occurs via the gastrointestinal tract (e.g., small water in exchange for sodium and potassium ions. These
bowel diarrhea), but it also may occur via the kidneys hydrogen ions are buffered within cells by proteins and
(e.g., carbonic anhydrase inhibitors, proximal renal tubu- phosphates. In early studies, 210,223 serum potassium con-
lar acidosis). The HCO 3 concentration of diarrheal fluid centration increased, but serum sodium concentration

exceeds that of plasma, whereas its Cl concentration is decreased after infusion of HCl. The relative roles of these
lower. The loss of such fluid results in a hyperchloremic buffers are depicted in Figure 10-1.
metabolic acidosis. Examples of the addition of fixed acid
to the body includetoxins (e.g.,ethyleneglycol, salicylate) RESPIRATORY RESPONSE TO AN
and compounds used therapeutically (e.g., ammonium ACUTE ACID LOAD
chloride, cationic amino acids). Examples of metabolic A fixed acid load increases [H ] and thereby stimulates
þ
production of fixed acid within the body include lactic aci- peripheral and central chemoreceptors to increase alveolar
dosis and diabetic ketoacidosis. Renal failure, hypoadre- ventilation.Thiseffectbeginswithinhoursandiscomplete
nocorticism, and distal renal tubular acidosis are within 12 to 24 hours. In humans, there is an approxi-
examples of impaired urinary excretion of fixed acid. Small mately 1.2-mm Hg reduction in P CO 2 for each 1-mEq/L
bowel diarrhea, renal failure, hypoadrenocorticism, dia- decrementinplasmaHCO 3 concentrationtoaminimum

betic ketoacidosis, and lactic acidosis during cardiovascu- P CO 2 of approximately 10 mm Hg. 99,195 In dogs with
lar collapse are the most common causes of metabolic uncomplicated metabolic acidosis induced by chronic
acidosis in small animal practice. feeding of HCl, the observed compensatory respiratory

253