Page 380 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster

366 C H A P T E R 10 Heart virtually every other organ is eventually affected by some
condition that carries an extremely poor prognosis. In the combination of forward and backward failure.
United States alone, nearly 5 million persons are affected,
resulting in more than 1 million hospitalizations and The cardiovascular system attempts to compensate for
300,000 deaths each year, with a financial burden in excess reduced myocardial contractility or increased hemody-
of $18 billion. Most cases of heart failure are due to systolic namic burden through several homeostatic mechanisms:
dysfunction—inadequate myocardial contractile function,
characteristically a consequence of ischemic heart disease • The Frank-Starling mechanism. Increased end-diastolic
or hypertension. Alternatively, CHF also can result from filling volumes dilate the heart and cause increased
diastolic dysfunction—inability of the heart to adequately cardiac myofiber stretching; these lengthened fibers con-
relax and fill, such as in massive left ventricular hypertro- tract more forcibly, thereby increasing cardiac output. If
phy, myocardial fibrosis, amyloid deposition, or constric- the dilated ventricle is able to maintain cardiac output
tive pericarditis. Indeed, heart failure in elderly persons, by this means, the patient is said to be in compensated
diabetic patients, and women may be more commonly heart failure. However, ventricular dilation comes at the
attributable to diastolic dysfunction. Various studies expense of increased wall tension and amplifies the
suggest that 40–60% of cases of CHF may be due to dia- oxygen requirements of an already-compromised myo-
stolic dysfunction. Finally, heart failure also can be caused cardium. With time, the failing muscle is no longer able
by valve dysfunction (e.g., due to endocarditis) or can to propel sufficient blood to meet the needs of the body,
occur in normal hearts suddenly burdened with an abnor- and the patient develops decompensated heart failure.
mal load (e.g., with fluid or pressure overload).
CHF occurs when the heart cannot generate sufficient • Activation of neurohumoral systems:
output to meet the metabolic demands of the tissues—or  Release of the neurotransmitter norepinephrine by
can only do so at higher-than-normal filling pressures; in the autonomic nervous system increases heart rate
a minority of cases, heart failure can be a consequence of and augments myocardial contractility and vascular
greatly increased tissue demands, as in hyperthyroidism, resistance.
or poor oxygen carrying capacity as in anemia (high-output  Activation of the renin-angiotensin-aldosterone
failure). CHF onset can be abrupt, as in the setting of a large system spurs water and salt retention (augmenting
myocardial infarct or acute valve dysfunction. In many circulatory volume) and increases vascular tone.
cases, however, CHF develops gradually and insidiously  Release of atrial natriuretic peptide acts to balance the
owing to the cumulative effects of chronic work overload renin-angiotensin-aldosterone system through diure-
or progressive loss of myocardium. sis and vascular smooth muscle relaxation.
In CHF, the failing heart can no longer efficiently pump
the blood delivered to it by the venous circulation. The • Myocardial structural changes, including augmented muscle
result is an increased end-diastolic ventricular volume, mass. Cardiac myocytes cannot proliferate, yet can
leading to increased end-diastolic pressures and, finally, adapt to increased workloads by assembling increased
elevated venous pressures. Thus, inadequate cardiac numbers of sarcomeres, a change that is accompanied
output—called forward failure—is almost always accompa- by myocyte enlargement (hypertrophy) (Fig. 10–1).
nied by increased congestion of the venous circulation—  In pressure overload states (e.g., hypertension or valvu-
that is, backward failure. As a consequence, although the root lar stenosis), new sarcomeres tend to be added paral-
problem in CHF typically is deficient cardiac function, lel to the long axis of the myocytes, adjacent to existing
sarcomeres. The growing muscle fiber diameter thus

Figure 10–1 Left ventricular hypertrophy, with and without dilation, viewed in transverse sections. Compared with a normal heart (center), the
pressure-overloaded heart (left) has an increased mass, a thick wall, and a smaller lumen. The volume-overloaded heart (right) has an increased mass,
larger lumen, and enlarged size, but a normal wall thickness.

(Reproduced by permission from Edwards WD: Cardiac anatomy and examination of cardiac specimens. In Emmanouilides GC, Allen HD, Riemenschneider TA, Gutgesell HP [eds]: Moss and Adams’
Heart Disease in Infants, Children, and Adolescents: Including the Fetus and Young Adults, 5th ed. Philadelphia, Williams & Wilkins, 1995, p 86.)