Page 538 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

526 FLUID THERAPY

filtration pressure. They may be especially hazardous Consequently, ACE inhibitors must be used very carefully
when used in combination with furosemide and ACE in such patients. However, such treatment often is effec-
inhibitors. Practically speaking, the use of cyclooxygenase tive in improving CHF and, despite a reduction in serum
(COX) inhibitors can be tolerated in heart failure, but it is aldosterone concentration, increasing serum sodium
prudent to start at one third to one half of the normal concentration (see Therapy of Fluid and Electrolyte
dose and increase the dose while monitoring renal func- Imbalances section). Another reason for profound
tion (and for signs of gastrointestinal ulceration). Other hyponatremia is concurrent use of several diuretics creat-
drugs, including ß-adrenergic blockers, human BNP, ing sequential nephron blockade from furosemide, a thia-
neutral endopeptidase inhibitors, and direct vasodilators, zide, and spironolactone. Although thiazides can
also may affect renal function. Some of the major reduce fluid retention in CHF of dogs and cats, when
effects of these drugs are summarized in Table 21-1. added to furosemide, azotemia, hyponatremia, hypokale-
The effects of BNP on renal hemodynamics are still under mia, and hypochloremia can develop (sometimes in a
investigation, and these effects may differ in normal matter of 1 or 2 days). Thiazides are more commonly
subjects from those in patients with CHF or systemic associated with hyponatremia than are loop diuretics
hypertension. 73,172 because they induce loss of effective solutes (sodium
and potassium) in excess of water and do not interfere
140
SERUM BIOCHEMICAL with the renal effects of ADH.
ABNORMALITIES IN POTASSIUM
CONGESTIVE HEART FAILURE Serum potassium concentration may be normal,
increased, or decreased in patients with heart failure. Mild
The majority of serum biochemical abnormalities in heart hyperkalemia may be observed in acute low output heart
failure can be attributed to alterations in renal function, failure because of an abrupt reduction in the GFR. Over-
changes in dietary intake of water and electrolytes, zealous administration of potassium salts and potassium
diuretic and other drug therapy, and drug toxicosis. Most supplementation in the presence of potassium-sparing
alterations are mild, and two surveys of serum biochemi- diuretics, b-blockers, orACEinhibitorsare causes ofiatro-
cal concentrations of patients at our hospitals have failed genic hyperkalemia. 143 Profound hyperkalemia can occur
to demonstrate severe changes in the majority of cardiac in cats with CHF and concurrent aortic thromboembo-
patients. 10,12 Nevertheless, some animals with CHF lism. This probably is related to multiple factors, such as
develop substantial disorders of fluid and electrolyte bal- muscle necrosis, reperfusion of infarcted tissues, 126 meta-
ance that may require fluid therapy and adjustment of car- bolic acidosis, and renal failure with inadequate urinary
diac medications. excretion of potassium. Management of life-threatening
hyperkalemia may be required as discussed in Chapter 5.
SODIUM Hypokalemia is particularly injurious because it
Serum sodium concentration usually is normal in heart predisposes to premature complexes, digitalis intoxica-
failure, but total body sodium and total body water are tion, and muscular weakness along with rhabdomyolysis
likely to be increased. Severe right-sided or biventricular (with elevated serum creatine kinase concentration) in
CHF can be associated with hyponatremia. Salt wasting cats. Hypokalemia in the cat has been linked to abnormal
secondary to concurrent diuretic use may contribute to taurine metabolism and taurine deficiency-associated
hyponatremia, but it is uncommon for low serum sodium myocardial failure. 33 Numerous factors predispose to
concentration in an edematous patient to be caused solely hypokalemia in the cardiac patient. 141 Anorexia resulting
by salt depletion. Multiple factors are probably from chronic disease or drug intoxication can lead to
35,43,52,99,120
involved. One likely cause of hyponatremia inadequate potassium intake. Cardiac cachexia and tissue
in CHF is dilution resulting from markedly reduced renal wasting also lead to increased potassium loss. Activation
free-water clearance (see Chapter 3). This effect probably of the RAAS may be important because potassium excre-
is mediated by the nonosmotic release of arginine vaso- tion is enhanced by aldosterone. Fortunately, aldosterone
pressin (ADH) and indicates insufficient cardiac output. concentrations are readily reduced by administration of
Continued release of ADH and polydipsia are important an ACE inhibitor. Reduced renal perfusion may influence
factors to be considered in the pathogenesis of potassium handling because inadequate delivery of
hyponatremia in the patient with CHF. In one study of sodium to the distal tubule causes potassium to be
dogs with CHF, dogs with severe heart failure caused secreted with organic acids. 75,142 Kaliuresis of variable
by dilated cardiomyopathy were more likely to develop magnitude occurs with diuretic therapy unless a potas-
hyponatremia. 178 Activation of the RAAS is predictable sium-sparing diuretic, such as spironolactone or
in the setting of severe CHF, and glomerular filtration triamterene, or an ACE inhibitor is prescribed. We have
pressure may depend largely on efferent arteriolar con- observed hypokalemia even when potassium-sparing
striction mediated in part by angiotensin II. 116,138 diuretics have been administered. Cats seem particularly