Page 853 - Cote clinical veterinary advisor dogs and cats 4th

410 Heart Failure, Chronic

Epidemiology distention, syncope, lethargy, and weight Initial Database
SPECIES, AGE, SEX loss may persist. Patients with chronic HF • Thoracic radiography
VetBooks.ir cally any cardiac disease; signalment reflects decompensated HF. ible, left atrial enlargement with pulmo-
○ When other clinical findings are compat-
are subject to additional episodes of acute/
HF is a syndrome that can result from practi-
nary opacities is diagnostic for left-sided
predispositions for the causative disorder:
HF.
• Geriatric small-breed dogs: chronic mitral
• Patients with HF due to mitral/tricuspid
and tricuspid regurgitation due to myxo- PHYSICAL EXAM FINDINGS ○ With diuretic treatment of decompensated
matous valve disease myxomatous valve disease have a cardiac HF, clinical improvement is usually rapid
• Adult large- and giant-breed dogs: dilated murmur; usually the murmur is loud, and its (minutes to hours), but radiographic
cardiomyopathy (DCM) intensity is generally not affected by treatment. resolution of pulmonary infiltrates may
• Cats: hypertrophic cardiomyopathy (HCM; • An audible third or fourth heart sound—a take 24 hours or more.
males > females), restrictive/unclassified gallop—reflects high atrial pressures and ○ Cats commonly develop pleural effusion
cardiomyopathy reduced ventricular compliance. In dogs, it in association with left-sided cardiac
is a relatively specific marker of HF. disease.
GENETICS, BREED PREDISPOSITION • Electrocardiography (ECG) is indicated when
• DCM: canine DCM is generally familial. Etiology and Pathophysiology arrhythmias complicate the presentation.
Doberman pinschers, Great Danes, Irish • Congestive signs result when high venous Atrial fibrillation is commonly associated with
wolfhounds, and other large- and giant-breed pressures cause the development of edema HF in large-breed dogs, but tachyarrhythmia
dogs. A genetic mutation associated with or cavitary effusions. of virtually any type may complicate the
the development of DCM in Doberman • In dogs, HF that results primarily from presentation of HF (pp. 94 and 1033).
pinschers has been identified. systolic dysfunction (impaired ventricular • Noninvasive estimation of systemic blood
• Mitral and tricuspid regurgitation due to emptying) is most common. pressure using Doppler or the oscillometric
myxomatous valve disease: geriatric small- • HF in cats usually results from diseases that method should be considered. The finding of
breed dogs, including Cavalier King Charles impair ventricular filling; diastolic ventricular systemic hypertension (SH) provides evidence
spaniels, dachshunds, and many others (filling) pressures are abnormally high when of concurrent disease; SH may complicate
• HCM: inherited in Maine coon cats and ventricular volume is normal or small. HF, but it is not a result of HF. However,
Ragdoll cats. It is possible that feline HCM • A high filling pressure is reflected upstream documented SH should be treated because
in other breeds, and in mix-breeds, has a to the venous circulation, resulting in edema untreated SH may accelerate the progression
genetic basis. or pleural effusion. of the primary cardiac disorder.
• HF is associated with neuroendocrine • Serum biochemistry profiles provide useful
RISK FACTORS activation: specifically, impaired cardiac ancillary information and are important in
• Electrocardiographic and echocardiographic performance leads to increased activity of the monitoring the effects of therapy (especially
variables that predict the development of renin-angiotensin-aldosterone system (RAAS) renal and electrolyte effects).
stage C HF in Doberman pinschers have and the adrenergic nervous system (ANS).
been described. Elevated serum B-type • Angiotensin II (ATII) is the biologically active Advanced or Confirmatory Testing
natriuretic peptide (BNP) concentration product of a biochemical cascade for which • BNP is released by cardiomyocytes in
identifies Doberman pinschers at risk for the final step is catalyzed by angiotensin- response to increases in ventricular filling
HF with high specificity but relatively low converting enzyme (ACE). pressures; elevated circulating BNP is a
sensitivity. • ATII is a vasoconstrictor, but it also stimulates marker of the HF state.
• In Irish wolfhounds and other giant-breed the release of aldosterone, augments activity • Echocardiography generally provides the
dogs, atrial fibrillation sometimes precedes of the ANS, and acts as a cardiomyotrophic diagnosis of the underlying cardiac disorder.
the development of HF. factor. Echocardiography is complementary to
• In small-breed dogs, a murmur caused by • Activation of the RAAS and ANS serves to physical exam and thoracic radiography
myxomatous mitral degeneration is a risk temporarily maintain perfusion pressure and but does not replace them.
factor for development of HF, but there is cardiac output.
great interindividual variability in the rate • Vasoconstriction increases vascular resistance TREATMENT
at which valvular disease progresses. so that blood pressure is maintained when
• Supraphysiologic BNP concentration and cardiac output is subnormal. In patients with Treatment Overview
left atrial enlargement independently predict mitral/tricuspid myxomatous valve disease or • Increase in quality and duration of life is
the onset of stage C HF in dogs with DCM, vascular resistance is high, causing a the goal.
myxomatous valve disease. detrimental increase in afterload; this partly • Although individual patient characteristics
• In cats, echocardiographically evident left explains the beneficial effect of vasodilators. must be taken into account, polytherapy
atrial enlargement is associated with the consisting of furosemide, an ACE inhibi-
development of HF. DIAGNOSIS tor, and pimobendan has become standard
Clinical Presentation Diagnostic Overview treatment for management of stage C HF
in dogs.
DISEASE FORMS/SUBTYPES Chronic HF occurs when acute/decompensated • There is uncertainty regarding optimal
• Left-sided HF results in pulmonary edema. HF is treated successfully, but the underlying therapy for cats with HF resulting from
• Right-sided HF causes ascites and sometimes cause cannot be cured. Clinical features of diastolic dysfunction; furosemide and an
concurrent pleural effusion. chronic HF can include a history of acute/ ACE inhibitor are widely used.
• In cats, pleural effusion results from left- decompensated HF, with partial or complete
sided, right-sided, or biventricular HF; ascites resolution of signs with treatment but persis- Chronic Treatment
is uncommon. tence of the underlying cardiac disease. • Diuretics: furosemide is the most effective
agent for management of congestive signs.
HISTORY, CHIEF COMPLAINT Differential Diagnosis ○ In dogs, a dose of 1-2 mg/kg PO q 12h
Clinical signs such as respiratory distress Other causes of respiratory distress, cough, is often initially adequate when given
generally improve or resolve with initial treat- abdominal distention, lethargy, inappetence, concurrently with ancillary agents such
ment, but signs such as progressive abdominal and weight loss (cardiac cachexia) as ACE inhibitors and pimobendan. Cats

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