Page 279 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

270 ACID-BASE DISORDERS

metabolic acidosis may be all that is necessary (e.g., fluids where V d is the volume of distribution for HCO 3 . How-
and insulin in diabetic ketoacidosis). In some instances, ever, the volume of distribution of HCO 3 varies
however, the underlying disease cannot be corrected inversely with the initial HCO 3 concentration and

(e.g., chronic renal failure), and alkali therapy must be changes for at least 90 minutes after HCO 3 administra-
3
considered. tion to dogs. In this study, dogs with chronic metabolic

In general, administration of NaHCO 3 should be acidosis and initial plasma HCO 3 concentrations of 10
reserved for clinical settings in which the patient’s blood mEq/L were given 5 mEq/kg NaHCO 3 and had average
pH is less than 7.1 to 7.2, and NaHCO 3 should be V d values of 60% at 30 minutes and 76% at 90 minutes.
administered only in amounts necessary to increase the This increase in V d represents distribution of

pH to 7.2. Therapy with sodium bicarbonate is less likely administered HCO 3 from extracellular to intracellular
to be harmful in animals with simple hyperchloremic met- sites. Bicarbonate distributes to ECF within 15 minutes
abolic acidosis (normal anion gap) because of the absence and to intracellular and bone buffers within 2 to 4
of unmeasured organic anions. In patients with hours. 198 Thus, it is impossible to assign a single value
normochloremic metabolic acidosis (increased anion for the V d of NaHCO 3 administered to dogs with meta-
gap), unmeasured organic anions (e.g., ketoacids, lactate) bolic acidosis. Any dosage recommendations must be

are present and can be metabolized to HCO 3 during considered only rough guidelines to treatment.
3
recovery. Administration of NaHCO 3 in such a setting The dogs in this study had ECFVs equal to approxi-
may result in late development of metabolic alkalosis. mately 24.5% of body weight as measured by radiosulfate
This complication should not be serious if renal function space. If we arbitrarily choose 0.5, a value approximately
is normal because the kidneys can excrete the excess twice ECFV:

HCO 3 .

Severe acidosis may lead to life-threatening cardiovas- HCO 3 ðmEqÞ¼ 0:5 10 ð9:5 6Þ¼ 17:5 mEq
cular complications (e.g., impaired cardiac contractility,
impaired pressor response to catecholamines, sensitiza- or
tion to ventricular arrhythmias). 161 Thus, if blood pH
HCO 3 ðmEqÞ¼ 0:5 10 ð10:7 6Þ¼ 23:5 mEq

is less than 7.1 to 7.2, judicious treatment with NaHCO 3
is justified. The aim of therapy should be to increase the
patient’s pH to 7.2 ([H ] ¼ 63 nEq/L), at which point Thus, the desired amount of NaHCO 3 is between 17.5
þ
the risk of life-threatening hemodynamic complications is and 23.5 mEq. The NaHCO 3 should be administered
reduced. over the first few hours of therapy and blood gases
For example, consider a 10-kg dog with a pH of 7.000, reevaluated before making a decision about additional
þ
¼ alkali administration. This amount of
[H ] ¼ 100 nEq/L, [HCO 3 ] ¼ 6 mEq/L, and P CO 2 NaHCO 3
25 mm Hg. We assume that normal values are a pH of represents a dose of 1.7 to 2.3 mEq/kg, and an empirical
þ

7.387, [H ] ¼ 41 nEq/L, [HCO 3 ] ¼ 21 mEq/L, dose of 2 mEq/kg could safely have been used.
¼ 36 mm Hg and that the normal compensa- In patients with severe acidosis, any additional small
and P CO 2

tory respiratory response to metabolic acidosis is a 0.7- reduction in plasma HCO 3 concentration represents a
per 1.0 mEq/L decrement large percentage change and can markedly increase
mm Hg decrement in P CO 2 199
þ

in [HCO 3 ]. How much NaHCO 3 must be administered [H ] (and reduce pH). For example, consider a nor-
þ
þ
to increase the dog’s pH to 7.200 ([H ] ¼ 63 nEq/L)? mal dog with a pH of 7.387, [H ] ¼ 41 nEq/L, P CO 2

This may be determined using the Henderson equation: ¼ 36 mm Hg, and [HCO 3 ] ¼ 21 mEq/L that sustains
a peracute reduction in [HCO 3 ] of 2 mEq/L (new

[HCO 3 ] ¼ 19 mEq/L) before respiratory compensa-

24PCO 2
þ
½ H Š ¼ þ
HCO 3 tion can develop. The new [H ] can be calculated from
the Henderson equation as 24(36)/19 ¼ 45 nEq/L

Thus, the desired [HCO 3 ] would be 24(25)/63 or 9.5 (p. 7.347). This represents a 0.04-U change in pH
þ
will not change. How- and a 4-nEq/L change in [H ]. Now consider a dog with
mEq/L if we assume that the P CO 2
ever, alveolar hyperventilation is likely to subside some- a pH of 7.102, [H ] ¼ 79 nEq/L, P CO 2 ¼ 23 mm Hg,
þ

what as the acidemia is partially corrected. If we assume and [HCO 3 ] ¼ 7 mEq/L that sustains a peracute reduc-

will increase to 28 mm Hg, the required tion in [HCO 3 ] of 2 mEq/L (new [HCO 3 ] ¼
that the P CO 2
[HCO 3 ] is 24(28)/63 or 10.7 mEq/L. Thus, we want 5 mEq/L) before respiratory compensation can develop.

to increase the dog’s [HCO 3 ] to 9.5 to 10.7 mEq/L. The dog’s new [H ] is 24(23)/5 ¼ 110 nEq/L

þ
We still must determine how much NaHCO 3 to (p. 6.959). This represents a 0.14-U change in pH and
þ
administer. This can be calculated using the formula: a 31-nEq/L change in [H ]. This change in [H ]
þ
is almost eight times greater than that observed in the

mEq HCO ¼ V d weight ðkgÞ HCO 3 deficit=L previous example. Thus, a small change in [HCO 3 ]
3