Page 287 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

278 ACID-BASE DISORDERS

Dog Z – 14.4 kg Control Period I Period II Period III
Gastric
drainage NaCl-72 mm/day
K (Phosphate) – 38 mEq/day
Na (Phosphate) – 18 mEq/day Na (Phos.) – 58 mEq/day
Plasma
30 30
HCO 3
mEq/L 25 25
20 20
110 110
Cl
mEq/L 100 100
90 90
0 0
K –100 100–
(corr. for N) –200 200–
Cumulative balance (mEq) Cl +100 0 100+

0
–100
100–
Na +100 0 100+
0
–100 100–
2 4 6 8 10 12 14 16 18 20 22 24
Days
Figure 10-12 Plasma composition and electrolyte balance in a representative study of selective HCl
depletion. (From Needle MA, Kaloyanides GJ, Schwartz WB. The effects of selective depletion of
hydrochloric acid on acid-base and electrolyte equilibrium. J Clin Invest 1964;43:1839, with copyright
permission of the American Society for Clinical Investigation.)

Posthypercapnia occur in small animal practice. However, chloride-resis-
issuddenlyreduced tant metabolic alkalosis is rare in dogs and cats.
BloodpHincreases rapidly whenP CO 2
in patients with chronic hypercapnia. This has been called
posthypercapnic metabolic alkalosis. In such patients, Primary Hyperaldosteronism

plasma HCO 3 concentration has previously been In primary hyperaldosteronism, increased secretion of

increased by adaptive changes in renal HCO 3 reabsorp- aldosterone, usually by an adrenocortical tumor, results
,ittakesseveralhours in sodium retention, volume expansion, hypernatremia,
tion.InresponsetotheloweredP CO 2
for thekidneystodecreaseNa -H exchange andbeginto mild to moderate hypertension, potassium deficiency,
þ
þ

excretethepreviouslyretainedHCO 3 .Itmaytakeseveral hypokalemia, and metabolic alkalosis resistant to chloride

days for the kidneys to excrete all of the excess HCO 3 , administration. Plasma renin activity is low, but plasma
and sufficient chloride must be available during this time aldosterone concentration is high. Affected human
for reabsorption with sodium. Chloride deficiency during patients are in salt balance at an expanded ECFV and
recovery from chronic hypercapnia plays a role in excrete ingested NaCl in the urine. Stimulation of distal
þ
þ
sustaining posthypercapnic metabolic alkalosis. Provision nephron Na -H þ and Na -K þ exchange by excess
of chloride allows the alkalosis to be corrected. 209 mineralocorticoids is probably the most important path-
Posthypercapnic metabolic alkalosis occurs most com- ophysiologic feature of primary hyperaldosteronism.
monly in human patients with chronic pulmonary disease Several dogs and cats with primary hyperaldosteronism
who are treated by mechanical ventilation. It is important caused by aldosterone-producing adenomas or
is decreased slowly and that adequate chloride adenocarcinomas of the adrenal gland have been reported
that P CO 2
intake is provided to prevent this complication. in the veterinary literature. Clinical features in affected
animals included polyuria, polydipsia, weakness, hyper-
Chloride-Resistant Metabolic Alkalosis tension, hypokalemia, hypernatremia, mild metabolic
Several disorders in human medicine may cause chloride- alkalosis, dilute urine, and extremely high serum aldoste-
resistant metabolic alkalosis. Of these, primary rone concentrations (for additional information and
hyperaldosteronism and hyperadrenocorticism may references see Chapter 5).