Page 546 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

534 FLUID THERAPY

animals, higher dosages of potassium chloride are used up in cats unless prevented by an ACE inhibitor,
to a rate not to exceed 0.5 mEq/ kg/hr intravenously. spironolactone, or potassium supplementation.
Oliguria, hyperkalemia, and concurrent administration Hypokalemia can be prevented in the hospital setting
of potassium-sparing diuretics, b-blockers, or ACE by encouraging food intake and supplementing paren-
inhibitors are relative contraindications for parenteral teral fluids with KCl. Constant-rate infusion of furose-
potassium therapy, unless serum potassium concentration mide also may be associated with less severe urinary
is known to be low. When providing the patient with oral potassium loss. Routine oral potassium supplementation
potassium chloride supplementation, the clinician should is not needed in chronic CHF, 143 but a KCl “salt substi-
consider that there is 1 mEq of potassium in each 89 mg tute” or solution (such as Renacare) can be administered
of potassium chloride salt (or in 234 mg of potassium if indicated by serum biochemical monitoring. In prac-
gluconate). tice, mild hyperkalemia is not uncommon in patients
receiving both an ACE inhibitor and spironolactone,
Blood Products but it usually is ignored. Use of oral potassium
Moderate to severe anemia increases the demand for car- supplements and the hospital management of severe
diac output and can precipitate CHF. In most cases, the hypokalemia are described in detail in Chapter 5.
packed cell volume must decrease to less than 22% or it Serum sodium concentration generally is normal in
must decrease rapidly for cardiac complications to occur. cardiac patients, and the finding of hyponatremia is a seri-
Although anemia alone can cause high output heart fail- ous sign. Low serum sodium concentration in the setting
ure, the development of pulmonary edema or pleural of excess extracellular fluid volume suggests decreased
effusion is even more common in the setting of a effective arterial blood volume with impaired renal water
preexisting heart disease, such as cardiomyopathy or excretion related to persistent release of ADH. Diuretics
chronic valvular heart disease. Anemic patients often also may contribute to hyponatremia (and
receive fluid therapy to maintain blood pressure and hypochloremia) by causing hypokalemia, inducing
organ perfusion, and this poses another risk for the dog plasma volume depletion and release of ADH, and
or cat with underlying cardiac dysfunction. Similarly, impairing function in the diluting segments of the neph-
the hemoglobin solution Oxyglobin (Biopure Corp., ron. 43,52,75 Thiazide diuretics are especially likely to cause
Cambridge, Mass.) expands plasma volume and can cause hyponatremia because they favor excretion of relatively
CHF in susceptible patients (this product is at times concentrated urine. These abnormalities are exacerbated
unavailable). Management of these animals involves med- by increased water intake associated with polydipsia,
ical therapy of CHF, treatment of the underlying cause of which can be prominent in dogs with CHF, or by infusion
anemia, and often a slow infusion of packed cells to of a sodium-poor crystalloid. The general causes of and
reduce the demand for cardiac output. approach to hyponatremia are described in Chapter 3.
Therapy for hyponatremia in CHF is difficult. Mild
MANAGING ELECTROLYTE hyponatremia (130 to 145 mEq/L in dogs) simply is
DISORDERS IN CHF an indication to adjust cardiac therapy. Moderate

Electrolyte disturbances, notably hypokalemia, hyponatremia (<130 mEq/L), especially when
hypochloremia, and metabolic alkalosis, are common associated with prerenal azotemia, is an indication for
complications of diuretic therapy. Digitalis intoxication cage rest, mild water restriction, frequent determination
with anorexia and vomiting can have similar effects. Mild of body weight and serum biochemistry, and vigorous
reductions in serum chloride concentration are of limited therapy for CHF. Furosemide is continued because stud-
concern, but hypokalemia should be avoided in cardiac ies in human patients suggest that furosemide may pro-
patients because it predisposes them to cardiac mote the formation of more dilute urine, thereby
arrhythmias, digitalis intoxication, muscle weakness increasing free-water clearance, whereas thiazides do
142
(and necrosis), and renal fibrosis and may decrease serum not. Thiazide diuretics should be discontinued. If
taurine concentration in cats. 33 Fortunately, most dogs the patient is receiving fluids, either lactated Ringer’s
develop only mild hypokalemia during the initial hospital solution or 0.9% NaCl, supplemented with KCl, should
therapy of CHF. 11 With the widespread use of ACE be used initially at conservative infusion rates (e.g., 20
inhibitors and spironolactone (which spare potassium to 30 mL/kg per 24 hours). Infusion for 48 to 72 hours
loss), hypokalemia also is relatively uncommon during of a catecholamine (dobutamine or dopamine) should
chronic management of CHF, except in the settings of be considered to increase cardiac output and the
digitalis intoxication, vomiting, or prolonged anorexia pimobendan dose in dogs may be administered
or when combination diuretic therapy is prescribed. Cats (extralabel) at 0.2 mg/kg every 8 hours. Gradually
are more prone to hypokalemia. Even a 1-day course of increasing the dosage of the ACE inhibitor up to the max-
parenteral furosemide can decrease the serum potassium imal dosage tolerated (at least 0.5 mg/kg of enalapril or
concentration significantly in cats. Hypokalemia is also benazepril every 12 hours) is important to antagonize the
more common with chronic furosemide administration RAAS. 35,120 Despite the theoretical concern that an ACE