Page 83 - Small Animal Internal Medicine, 6th Edition

CHAPTER 3
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Management of

Heart Failure

OVERVIEW OF HEART FAILURE and, in some cases, concentric patterns of hypertrophy. Ven-
tricular hypertrophy can increase chamber stiffness, impair
Heart failure entails abnormalities of cardiac systolic or dia- relaxation, and increase filling pressures. These abnormali-
stolic function, or both. These can occur without evidence ties of diastolic function also can have a negative effect on
of abnormal fluid accumulation (congestion), especially in systolic function. Ventricular remodeling also can promote
the initial stages of disease. Congestive heart failure (CHF) is the development of arrhythmias. The initiating stimulus
characterized by high cardiac filling pressure, which leads to underlying chronic cardiac remodeling might occur years
venous congestion and tissue fluid accumulation. It is con- before clinical evidence of heart failure appears.
sidered a clinical syndrome rather than a specific etiologic Acute increases in ventricular filling (preload) induce
diagnosis. The pathophysiology of heart failure is complex. greater contraction force and blood ejection. This response,
It involves structural and functional changes within the heart known as the Frank-Starling mechanism, allows beat-to-beat
and vasculature, as well as other organs. The process of pro- adjustments that balance the output of the two ventricles and
gressive cardiac remodeling inherent to heart failure can increase overall cardiac output in response to acute increases
develop secondary to cardiac injury or stress from valvular in hemodynamic load. In the short term, the Frank-Starling
disease, genetic mutations, acute inflammation, ischemia, effect helps normalize cardiac output under conditions of
increased systolic pressure load, and other causes. increased volume or pressure loading, but these conditions
also increase ventricular wall stress and oxygen consumption.
CARDIAC RESPONSES Ventricular wall stress is directly related to ventricular
Cardiac remodeling refers to the changes in myocardial pressure and internal dimensions, and inversely related to
size, shape, and stiffness that occur in response to various wall thickness (Laplace’s law). Increased wall stress induces
mechanical, biochemical, and molecular signals induced myocardial hypertrophy. The hypertrophy pattern that
by the underlying injury or stress. These changes include develops depends on underlying disease conditions. A
myocardial cell hypertrophy, cardiac cell drop-out or self- ventricular systolic pressure load induces concentric hyper-
destruction (apoptosis), excessive interstitial matrix forma- trophy; myocardial fibers and ventricular walls thicken as
tion, fibrosis, and destruction of normal collagen binding contractile units (sarcomeres) are added in parallel. With
between individual myocytes. The latter, resulting from severe hypertrophy, capillary density and myocardial per-
effects of myocardial collagenases or matrix metalloprotein- fusion may become inadequate, especially in subendo-
ases, can lead to cardiac chamber dilation or distortion from cardial areas. Chronic myocardial hypoxia and ischemia
myocyte slippage. Stimuli for remodeling include mechani- stimulate further fibrosis and dysfunction. Chronic volume
cal forces (for example, increased wall stress from volume loading increases diastolic wall stress and leads to eccen-
or pressure overload) and the effects of various neurohor- tric hypertrophy; myocardial fiber elongation and chamber
mones (such as angiotensin II, norepinephrine, endothelin, dilation occur as new sarcomeres are laid down in series.
and aldosterone) and proinflammatory cytokines (including Reductions in the extracellular collagen matrix and inter-
tumor necrosis factor [TNF]-α), as well as other cytokines cellular support structure have been documented in dogs
(such as osteopontin and cardiotrophin-1). Contributing with chronic volume overload from mitral insufficiency.
biochemical abnormalities, related to cellular energy produc- Compensatory hypertrophy lessens the importance of the
tion, calcium fluxes, protein synthesis, and catecholamine Frank-Starling mechanism in stable, chronic heart failure.
metabolism, have been variably identified in different models Although volume loads are better tolerated because myocar-
of heart failure and in clinical patients. Myocyte hypertrophy dial oxygen demand is not as severe, both abnormal pressure
and reactive fibrosis increase total cardiac mass by eccentric and volume loading impair cardiac performance over time.

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