Page 114 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

104 ELECTROLYTE DISORDERS

potential, and increases automaticity. The electrocar- vomiting and hypokalemia (2.0 mEq/L) developed poly-
diographic changes associated with hypokalemia in uria, polydipsia, and a urinary concentrating defect that
human patients (e.g., decreased amplitude T waves, ST persisted after correction of hypokalemia. 86 These
segment depression, and U waves) are not consistently abnormalities were attributed to medullary washout of
observed in dogs and cats, but supraventricular and ven- solute and were corrected by partial water restriction
tricular arrhythmias may occur. Prolongation of the and dietary supplementation with NaCl and KCl. In yet
QT–intervalandUwaveshave been reportedin adog with another study, dogs subjected to potassium depletion
severe hypokalemia (2.0 mEq/L) caused by chronic (serum potassium concentration, 2.9 mEq/L) experi-
vomiting and in dogs with experimentally induced potas- enced a doubling of urine volume (596 to 1202 mL
sium depletion (serum potassium concentration, per 24 hours) and a 40% reduction in maximum urine
2.2 mEq/L). 14,86,91 In another study, development of osmolality (2006 to 1187 mOsm/kg). 167
hypokalemia in dogs over a 5-day period was associated Potassium depletion increases renal ammoniagenesis
with STsegment deviations, decreased amplitude Twaves, and urinary net acid excretion, whereas potassium load-
and the appearance of U waves. 68 The appearance of T ing tends to have the opposite effect. 189 In the rat,
waves in normal dogs is variable (e.g., positive, negative, increased ammoniagenesis during potassium depletion
and biphasic), and interpretation of the effects of hypoka- occurs primarily via enhanced phosphate-dependent
lemia on ventricular repolarization is difficult unless a glutaminase activity and increased mitochondrial
baseline electrocardiogram has been obtained previously. ammoniagenesis in the proximal tubular cells of the renal
Hypokalemia potentiates the toxic effects of digitalis on cortex. The decrease in ammoniagenesis during potas-
cardiac conduction and may potentiate premature sium loading may occur in renal tubular cells from the
contractions. Hypokalemia also renders the myocardium outer medullary region. Many experimental studies on
refractory to the effects of class I antiarrhythmic agents potassium depletion and renal regulation of acid-base bal-
(e.g., lidocaine, quinidine, procainamide). Therefore, ance have been performed in rats. The renal response of
serum potassium concentration should be measured and the dog to acute acidosis is known to differ somewhat
hypokalemia should be corrected in dogs with ventricular from that of the rat, and care must be taken in
arrhythmias unresponsive to antiarrhythmic therapy. extrapolating data about the renal response to potassium
depletion in the rat to dogs. 190
Effects on the Kidneys Proximal renal tubular sodium reabsorption is
Potassium depletion produces functional and morpho- increased during potassium depletion, possibly as a result
þ
logic abnormalities in the kidneys, referred to as hypoka- of an increase in the activity of the proximal Na -H þ
lemic nephropathy. Renal vasoconstriction leads to antiporter. However, distal sodium reabsorption is
decreases in renal blood flow and glomerular filtration decreased during potassium depletion. This presumably
rate (GFR). Polyuria and polydipsia are observed in occurs as a result of decreased aldosterone secretion
potassium depletion and result from impaired and is a direct effect of decreased ECF potassium concen-
responsiveness of the kidneys to ADH. Defective tration on the zona glomerulosa of the adrenal glands.
þ
collecting duct responsiveness to ADH is associated with Decreased distal sodium reabsorption decreases K and
decreased medullary tonicity, increased medullary blood H ion secretion by decreasing luminal electronegativity.
þ
flow, and impaired cyclic adenosine monophosphate This decreases potassium loss in the urine but also tends
(cAMP) generation in response to ADH. The urinary to impair renal acid excretion. Thus, increased renal
concentrating defect in potassium depletion results from ammoniagenesis during potassium depletion may repre-
decreased expression of ADH-regulated aquaporin- sent a mechanism for enhancing urinary excretion of fixed
þ
þ
2 water channels in the luminal membranes of the renal acid (as NH 4 ) at a time when distal H ion secretion
epithelial cells of the cortical and medullary collecting is impaired. Consequently, derangements in acid-base
10,125
ducts. balance are minimized.
In one study, potassium depletion in dogs over an aver- The cytoplasmic and mitochondrial enzyme activity
age of 51 days led to a decrease in total exchangeable profile of renal tubular cells during potassium depletion
potassium from 47.1 to 35.3 mEq/kg and a decrease in is strikingly similar to that observed during chronic met-
serum potassium concentration from more than abolic acidosis. 189 This similarity suggests the possibility
1
4.0 mEq/L to approximately 2.5 mEq/L. These dogs of a common effector mechanism for stimulation of renal
experienced decreases in GFR, renal blood flow, and uri- ammoniagenesis. Intracellular pH would be a logical can-
þ
nary concentrating capacity (U Osm after 20 hours of water didate for such an effector. As K ions leave cells to main-
deprivation) of approximately 25%. In another study, tain ECF potassium concentration during potassium
potassium depletion (serum potassium concentration, depletion, H þ ions enter cells and presumably lower
2.1 mEq/L) in dogs had little effect on GFR but caused intracellular pH. Reduced intracellular pH may in turn
a 45% reduction in maximal U Osm (1902 to 1055 be the signal for increased renal ammoniagenesis from
mOsm/kg). 19 In a clinical report, a dog with chronic glutamine. Some studies have demonstrated reduced