Page 531 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Fluid and Diuretic Therapy in Heart Failure 519

can be explained by the dual venous drainage of the pleu- indicate biventricular CHF. Although pleural effusion
ral surfaces (i.e., parietal drainage is systemic, whereas vis- does occur in some dogs and cats with predominantly
ceral drainage is pulmonary). Although veterinary right-sided cardiac disease (e.g., pulmonic stenosis, tri-
textbooks usually attribute pleural effusion to isolated cuspid malformation), ascites is more common in dogs.
right-sided CHF, this is not common in human patients. Clinically significant pleural effusions are rare in animals
Pleural effusion correlates better with pulmonary capil- with isolated right ventricular failure caused by heart-
lary wedge pressure than with right atrial pressure. 183 worm-induced pulmonary hypertension. 15,169 Con-
Similarly, pleural effusions in small animals most often versely, pleural effusions are common when end-stage
CHF develops in dogs with severe mitral regurgitation,
pulmonary hypertension, and secondary right ventricular
BOX 21-5 Hemodynamic dysfunction or in cats with any form of severe cardiomy-
Consequences of opathy. Pleural effusion may become chylous in nature in
Congestive Heart those with advanced CHF.
The relative contribution of renal sodium retention in
Failure CHF probably depends on the type and acuteness of heart
failure. The development of ascites, pleural effusion, or
Reduced cardiac output subcutaneous edema in right-sided or biventricular car-
Increased systemic vascular resistance and diac failure is accompanied by avid renal sodium retention
arterial impedance
(see Renal Function in Heart Failure section). Dramatic
Increased pulmonary vascular resistance
weight loss, sometimes exceeding 5 kg in giant-breed
Increased plasma volume
dogs, may be observed after successful diuresis. This
Increased ventricular end-diastolic pressure
Increased venous pressure degree of weight loss after diuretic therapy is uncommon
Systemic (central) venous pressure in isolated left-sided failure. Thus successful therapy of
Pulmonary venous pressure right-sided CHF depends in the short term on initiation
Increased capillary hydrostatic pressure ofabriskdiuresisorparacentesis.Long-termmanagement
Edema hinges on improving cardiac function, reducing
Serous cavity effusion neurohormonal activation, and overcoming the potent
sodium-retaining effects of forward cardiac failure.

Cardiac output Heart Cardiac failure

"Forward failure" – Atrial natriuretic peptide
Effective plasma ADH "Backward failure"
volume/pressure
Kidney-adrenal gland Sympathetic
activity
Venous
pressure
Sodium and H O
2
Filtration fraction retention
Edema
+
Renin-angiotensin effusions
Thirst
Aldosterone
Figure 21-3 Prominent mechanisms responsible for fluid accumulation in heart failure. The combined
effects of abnormally high venous pressure and renal retention of sodium and water can explain the
development of pulmonary edema, subcutaneous edema, or the transudative effusions in body cavities.
Ventricular systolic or diastolic failure increases venous pressure behind the failing ventricle (“backward”
failure). This may be the predominant mechanism of edema formation in acute left-sided heart failure.
In contrast, chronic heart failure, especially when right-sided or biventricular in nature, is characterized
by avid sodium retention. Although atrial distention causes the release of atrial natriuretic peptide (ANP),
the effects of sympathetic activity, angiotensin II, aldosterone, vasopressin (ADH), and local vasoconstrictor
factors dominate, leading to vasoconstriction in systemic vessels and increased sodium and water
reabsorption in the renal tubules. This is a simplified view because other local and systemic factors can be
involved. (Modified from Bonagura JD. Fluid management of the cardiac patient. Vet Clin North Am Small
Anim Pract 1982;12:503.)