Page 539 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Fluid and Diuretic Therapy in Heart Failure 527

prone to diuretic-induced hypokalemia. The potent loop encountered acid-base disorders in acute heart failure.
diuretics, such as furosemide, also promote kaliuresis by Mild metabolic alkalosis is not uncommon in patients
accelerating delivery of sodium to the distal nephron, receiving chronic diuretic therapy.
leading to an overall increase in the rate of sodium-potas- Metabolic acidosis may be caused by a stagnant circu-
sium exchange. 20,75,142 Combination diuretic therapy lation with hypoxia and lactic acidemia, 53 by prerenal azo-
with furosemide-hydrochlorothiazide is especially likely temia, or by tissue ischemia as may occur with aortic
to lead to hypokalemia, even in the presence of thromboembolism. In uncomplicated cases, the venous
ACE inhibitors or spironolactone. Lastly, metabolic pH and bicarbonate concentrations are mildly decreased
alkalosis is a frequent complication of volume contrac- and arteriovenous oxygen difference is increased.
tion, vomiting, or diuretic-induced chloriuresis. 141,142 In severe CHF or cardiogenic shock, with avid vasocon-
Alkalosis increases the concentration of potassium in striction, mixed venous PO 2 often is less than 30 mm Hg.
the renal tubular cell and promotes its secretion into Respiratory acidosis is a less common but more serious
the tubular fluid. complication and indicates the presence of respiratory
failure, pulmonary edema, compression atelectasis (from
OTHER ELECTROLYTES pleural effusion), or respiratory muscle fatigue. Respira-
tory acidosis is characterized by the development of arte-
Serum chloride concentration usually is normal in heart
rial hypoxemia and hypercapnia and a decrease in blood
failure. However, it is common for an animal to develop
pH unless a mixed disorder is present (see Chapter 12).
mild hypochloremia after diuretic therapy. Mild
Metabolic alkalosis, with increased bicarbonate
hypochloremia is the most commonly observed
concentration and blood pH, is common and often is a
diuretic-induced electrolyte disturbance in our practice.
complication of diuretic therapy with resultant volume
This observation probably is the result of the inhibitory
effect of furosemide and other loop diuretics on chloride contraction (contraction alkalosis) and renal loss of chlo-
75,142
transport and may be associated with a small but com- ride and potassium. Vomiting, a complication of
mensurate increase in serum bicarbonate concentration drug intoxication, also leads to chloride loss and meta-
as estimated by the total CO 2 . Serum calcium and phos- bolic alkalosis. Respiratory alkalosis with a low PCO 2
may be detected in some patients because animals with
phorus concentrations are normal in CHF unless renal
moderate pulmonary edema tend to hyperventilate as a
failure or another unrelated disorder is present.
result of stimulation of stretch and nociceptive receptors
Hypomagnesemia has received little attention in vet- 141
in the lungs. Patients with low cardiac output without
erinary medicine, but it is common in human patients
undergoing diuresis induced by loop diuretics. 28,146,162 pulmonary edema have increased muscle fatigability
that may be manifested as dyspnea and subsequent
In one veterinary hospital survey, cardiovascular disease
hypocapnia. Apparent dyspnea in this subset of patients
was a prominent risk factor for development of hypomag-
nesemia. 79 The potential importance of magnesium is may be related to skeletal muscle changes that occur
during CHF. Abnormal muscle function during CHF
emphasized by the association of hypomagnesemia with
has been linked to the decrease in muscle bulk, increased
cardiac arrhythmias and the use of magnesium infusions
reliance on anaerobic metabolism, decreased muscle
to treat digitalis-induced cardiac arrhythmias in human 19
blood flow, and metaboreceptor activation.
patients. Serum magnesium concentration in dogs with
CHF did not decrease significantly after furosemide ther-
apy in one study of dogs 40 but was 20% lower than that of SERUM PROTEINS
a control population in another canine study. 20 As with Serum protein concentration frequently is decreased in
potassium, serum magnesium poorly reflects intracellular severe heart failure, especially in dogs with right-sided
stores. 70 Digitalis also has been shown to increase urinary or biventricular failure. In a survey of dogs with CHF
magnesium excretion. and atrial fibrillation, about one fourth had low serum
protein concentrations. 12 Concurrent disorders (e.g.,
ACID-BASE DISTURBANCES liver disease, renal disease, gastrointestinal disease) also
Blood pH in heart failure is the product of competing may influence serum protein concentration.
factors that alter acid-base balance. Complex acid-base The mechanisms responsible for decreased serum pro-
disorders are common because of disturbances in tissue tein concentration in CHF are undetermined. Possible
oxygenation and in pulmonary and renal function. As a explanations include lymphatic loss of protein through
result, simple determination of total CO 2 without direct a congested intestine, decreased hepatic synthesis, cardiac
measurement of blood pH and calculation of bicarbonate cachexia, and enhanced endothelial permeability caused
may lead to erroneous conclusions (see Chapters 9 by increased capillary pressure and hypoxia. Ascitic fluid
through 13). In our experience, respiratory alkalosis is higher in protein concentration than is a transudate
and metabolic acidosis are the most commonly collecting in the pleural space because the hepatic