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Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

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538<br />

Chapter | 17 Fluid, Electrolyte, and Acid-Base Balance<br />

and decreased p CO 2 may be associated with compensated<br />

respiratory alkalosis as well as compensated metabolic<br />

acidosis. Compensating responses for chronic respiratory<br />

alkalosis lasting several weeks may actually be sufficient to<br />

return pH to normal. In dogs, anticipated renal compensation<br />

for a chronic respiratory alkalosis results in a decrease<br />

<strong>of</strong> bicarbonate <strong>of</strong> 0.55 mEq/l for each mmHg decrease in<br />

p CO 2 ( de Morais, 1992a, 1992b ).<br />

E . Mixed Acid-Base Imbalances<br />

Mixed acid-base disorders occur when several primary acidbase<br />

imbalances coexist ( de Morais, 1992a ). Metabolic acidosis<br />

and alkalosis can coexist and either or sometimes both <strong>of</strong><br />

these metabolic abnormalities may occur with either respiratory<br />

acidosis or alkalosis ( Nairns and Emmett, 1980 ; Wilson<br />

and Green, 1985 ). Evaluation <strong>of</strong> mixed acid-base abnormalities<br />

requires an understanding <strong>of</strong> the anion gap, the relationship<br />

between the change in serum sodium and chloride<br />

concentration, and the limits <strong>of</strong> compensation for the primary<br />

acid-base imbalances ( Saxton and Seldin, 1986 ; Wilson and<br />

Green, 1985 ). <strong>Clinical</strong> findings and history are also necessary<br />

to define the factors that may contribute to the development <strong>of</strong><br />

mixed acid-base disorders. The following are important considerations<br />

in evaluating possible mixed acid-base disorders:<br />

1. Compensating responses to primary acid-base<br />

disturbances do not result in overcompensation.<br />

2. With the possible exception <strong>of</strong> chronic respiratory<br />

acidosis, compensating responses for primary acid-base<br />

disturbances rarely correct pH to normal. In patients<br />

with acid-base imbalances, a normal pH indicates a<br />

mixed acid-base disturbance.<br />

3. A change in pH in the opposite direction to that<br />

predicted for a known primary disorder indicates a<br />

mixed disturbance.<br />

4. With primary acid-base disturbances, bicarbonate and<br />

p CO 2 always deviate in the same direction. If these<br />

parameters deviate in opposite directions, a mixed<br />

abnormality exists.<br />

Although mixed acid-base abnormalities undoubtedly<br />

occur in animals and have been documented in the veterinary<br />

literature, they are <strong>of</strong>ten overlooked ( Wilson and Green,<br />

1985 ). An appreciation <strong>of</strong> the potential for the development<br />

<strong>of</strong> mixed abnormalities is essential for the correct interpretation<br />

<strong>of</strong> clinical and clinicopathological data, which would<br />

otherwise be quite confusing. Care should be taken when<br />

evaluating suspected mixed acid-base abnormalities that<br />

sufficient time has elapsed so that anticipated compensating<br />

responses could have occurred ( de Morais, 1992a ).<br />

F . Anion Gap<br />

The anion gap can be calculated as the difference between the<br />

major cation (sodium) and the measured anions (chloride <br />

TABLE 17-3 Causes <strong>of</strong> Alterations in Anion Gap<br />

Decreased anion gap:<br />

Increased cationic protein<br />

Polyclonal gammopathy (IgG)<br />

Hypoalbuminemia<br />

Hyperchloremic acidosis<br />

Altered protein anionic equivalents<br />

Laboratory error<br />

Increased anion gap:<br />

Metabolic acidosis<br />

Organic acids (lactic, keto acids)<br />

Hypovolemic shock<br />

Anaerobic exercise<br />

Diabetes<br />

Grain overload<br />

Ketosis<br />

Nonmetabolizable acids<br />

Inorganic acids (sulfate, phosphate)<br />

Uremic acidosis<br />

Intoxication or poisoning<br />

Salicylate<br />

Paraldehyde<br />

Metaldehyde<br />

Methanol<br />

Ethylene glycol<br />

Laboratory error<br />

bicarbonate) ( Emmett and Narins, 1977 ). Some investigators<br />

prefer to use the following formula:<br />

anion gap (sodium potassium)<br />

(chloride<br />

bicarbonate) (17-11)<br />

The addition <strong>of</strong> potassium to the equation, however, adds<br />

little to the diagnostic utility <strong>of</strong> this calculation ( Emmett<br />

and Narins, 1977 ; Epstein, 1984 ; Oh and Carroll, 1977 );<br />

the anion gap calculated with the inclusion <strong>of</strong> potassium<br />

concentration will be about 4 mEq/l higher. Because most<br />

<strong>of</strong> the published data on the anion gap in animal species<br />

are the result <strong>of</strong> calculations using the second equation (Eq.<br />

17-11), this form will be used in Table 17-3 . Provided the<br />

component determinations are valid, the calculated anion<br />

gap provides an approximation <strong>of</strong> the so-called “ unmeasured<br />

anions. ” Normally, these unmeasured anions consist<br />

primarily <strong>of</strong> negatively charged plasma proteins because<br />

the charges <strong>of</strong> the unmeasured cations (potassium, calcium,<br />

and magnesium) tend to balance out the charges <strong>of</strong> the<br />

unmeasured anions (phosphate, sulfate, and organic ions).<br />

The anion gap is most useful in situations where the concentrations<br />

<strong>of</strong> phosphate and plasma proteins, particularly<br />

albumin, are within the normal range (see Section V.I). The<br />

anion gap for most species <strong>of</strong> domestic animals appears to<br />

be similar to that defined for human subjects (i.e., approximately<br />

10 to 20 mEq/l) (10 to 20 mmol/l). However, there

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