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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
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