Page 96 - Basic Monitoring in Canine and Feline Emergency Patients

Table 5.3. Common differentials for metabolic alkalosis.

VetBooks.ir Gastric losses of chloride
Furosemide/diuretic therapy
Rebound post hypercapnia
Primary hyperaldosteronism
Hyperadrenocorticism
Administration of exogenous bicarbonate or products broken down into bicarbonate (lactate, acetate, gluconate,
citrate, ketones)
Phosphorus binders
Severe hypokalemia or hypomagnesemia causing persistent hypochloremia
Free water deficit (aka “contraction alkalosis”)
High dose penicillin administration

Adapted from Dibartola, S.P. (ed.), Fluid, Electrolyte and Acid–Base Disorders in Small Animal Practice, 4th edn. Elsevier, St. Louis,
Missouri, USA.
Table 5.4. Expected compensation for primary acid–base abnormalities.
Primary acid–base disorder Expected compensation a

−
Metabolic acidosis  PCO of 0.7 mmHg per each 1 mEq/L  in HCO (±3)
3
2
Metabolic alkalosis  PCO of 0.7 mmHg per each 1 mEq/L  in HCO (±3)
−
2
3
−
Respiratory acidosis (acute, <24 hours)  HCO of 0.15 mEq/L per each 1 mmHg  in PCO (±2)
3
2
−
Respiratory acidosis (chronic, >2–5 days)  HCO of 0.35 mEq/L per each 1 mmHg  in PCO (±2)
2
3
−
Respiratory alkalosis (acute, <24 hours)  HCO of 0.25 mEq/L per each 1 mmHg  in PCO (±2)
3
2
−
Respiratory alkalosis (chronic, >2–5 days)  HCO of 0.55 mEq/L per each 1 mmHg  in PCO (±2)
2
3
a These values are derived in healthy laboratory dogs and have not been validated in cats or ill dogs.
Adapted from In: Silverstein, D.C., Hopper, K. (eds), Small Animal Critical Care Medicine, 2nd edn. Elsevier, St. Louis, Missouri, USA.
Therefore, a patient with no acid–base abnormali- Due to the laws of electroneutrality, there must
ties should have a BE of zero. While the reader always be an equilibrium between cations and ani-
should always use the normal values provided by ons. This can be shown visually in a representation
their analyzer, a BE of 0 ± 3 would generally be called a Gamblegram (Fig. 5.1). The anions and
considered normal. Since BE corrects for abnormal cations not included in the AG equation are often
PCO levels, it is considered to be a more ‘pure’ called ‘unmeasured’ despite the fact that many can
2
representation of the metabolic side of acid–base be measured with modern analyzers. The unmeas-
assessment in the presence of concurrent respira- ured anions (UA) include molecules such as albu-
tory abnormalities. min and phosphate, whereas the unmeasured
cations (UC) include molecules such as calcium and
anion gap Another modification to traditional magnesium. Because the UA slightly exceed the UC
analysis is the AG. The equation shown in Box 5.3 in health, there is a normal AG range of 12–24 in
the difference between the major cations (positively the dog and 13–27 in the cat. An increasing AG
charged molecules) and anions (negatively charged almost always results from an increase in UA. This
molecules) in the blood. is often due to the presence of a ‘new’ anion such
as lactate or ketones. Various toxins (ethylene gly-
col) and drugs (aspirin) will also act as anions and
create an increased AG. Common differentials for
high AG metabolic acidosis are shown in Table 5.2.
Box 5.3. Anion gap calculation.
+
+
−
−
−

AG =(Na +K )(HCO+ Cl ) non–traditional acid–base interpretation A
3
common complaint of traditional acid–base analy-
−
Cl, chloride; HCO , bicarbonate; K, potassium; sis is that, while it helps define the acid–base abnor-
3
Na, sodium. mality, it does not necessarily help the clinician
determine the underlying cause. This limitation led
88 A.C. Brooks