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CHAPTER 3 Management of Heart Failure 59
insults also can lead to myocardial failure (see Chapters 7
and 8). Diseases that impose a volume or flow overload on TABLE 3.1
VetBooks.ir the heart usually involve a primary “plumbing” problem Common Causes of Congestive Heart Failure (CHF)
(e.g., a leaky valve or abnormal systemic-to-pulmonary con-
nection). Cardiac pump function often is maintained at a
MANIFESTATION*
near-normal level for a prolonged time, although myocar- MAJOR PATHOPHYSIOLOGY TYPICAL CHF
dial contractility does eventually deteriorate (see Chapters
5 and 6). Pressure overload results when the ventricle must Myocardial Failure
generate higher-than-normal systolic pressure to eject blood. Idiopathic dilated cardiomyopathy Either L- or R-CHF
The concentric hypertrophy that develops as a compensatory Infective myocarditis Either L- or R-CHF
mechanism increases ventricular wall thickness and stiff- Drug toxicities (e.g., doxorubicin) L-CHF
ness, and can predispose to myocardial ischemia. Excessive Myocardial ischemia/infarction L-CHF
pressure loads also eventually lead to declining myocardial (rare)
contractility. Myocardial pressure overload is caused by
ventricular outflow obstructions (congenital or acquired) Volume-Flow Overload
and systemic or pulmonary hypertension (see Chapters 5, Mitral valve regurgitation L-CHF
10, and 11). Diseases that restrict ventricular filling impair (degenerative, congenital,
diastolic function. These include hypertrophic and restric- infective)
tive cardiomyopathies and pericardial diseases (see Chap- Aortic regurgitation (infective L-CHF
ters 8 and 9). Contractile ability usually is well maintained endocarditis, congenital)
initially; however, elevated ventricular filling pressure Ventricular septal defect L-CHF
leads to congestion behind the affected ventricle(s) and Patent ductus arteriosus L-CHF
may diminish cardiac output. Other, less common causes
of impaired filling include intracardiac mass lesions, con- Tricuspid valve regurgitation R-CHF
(degenerative, congenital,
genital atrioventricular (AV) valve stenosis, and cor tria- infective)
triatum. Table 3.1 lists common diseases according to their
major initiating pathophysiology and typical clinical CHF Tricuspid endocarditis (rare) R-CHF
manifestations. Chronic anemia Either L- or R-CHF
Thyrotoxicosis Either L- or R-CHF
APPROACH TO TREATING
HEART FAILURE Pressure Overload
Current perspectives on CHF management are based not (Sub)aortic stenosis L-CHF
only on mitigating the results of excessive NH activation Systemic hypertension L-CHF (rare)
(especially sodium and water retention) but also on modify- Pulmonic stenosis R-CHF
ing or blocking the activation process itself, with the aim of Heartworm disease R-CHF
minimizing the progression of myocardial remodeling and Pulmonary hypertension R-CHF
dysfunction. Diuretics, dietary salt restriction, and some
vasodilators help control signs of congestion. ACEIs, aldos- Impaired Ventricular Filling
terone, and sympathetic antagonists help modulate NH Hypertrophic cardiomyopathy L-(±R-) CHF
responses. Treatment strategies center on controlling edema Restrictive cardiomyopathy L-(±R-) CHF
and effusions, improving cardiac output, reducing cardiac Cardiac tamponade R-CHF
workload, supporting myocardial function, and managing
concurrent arrhythmias. The approach to these goals varies Constrictive pericardial disease R-CHF
somewhat with different diseases, most notably those causing *L-CHF, Left-sided congestive heart failure signs (pulmonary edema
restriction to ventricular filling. as main congestive sign); R-CHF, right-sided congestive heart failure
signs (pleural effusion and/or ascites as main congestive signs).
Classification of Severity Weakness and other low-output signs can occur with any of these
Guidelines for clinical staging of heart failure (based on the diseases, especially those associated with arrhythmias.
American Heart Association and American College of Car-
diology [AHA/ACC] system) also are applied to veterinary
patients (Table 3.2). These describe disease progression effusions are not necessarily present all the time during the
through four stages over time. This system emphasizes the later stages (i.e., when CHF is “compensated” through appro-
importance of patient screening and early diagnosis. It is priate medical therapy). Nevertheless, attention to the
recommended as a guide in coordinating appropriate (and patient’s fluid status is highly important.
ideally, evidence-based) treatment to the severity of the clini- The clinical severity of heart failure also is sometimes
cal signs at each stage of disease. It also deemphasizes the described according to the modified New York Heart Asso-
term “congestive” in CHF because clinical signs of edema or ciation (NYHA) classification scheme or the International