Page 381 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster
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results in concentric hypertrophy—the ventricular wall Heart Failure 367
thickness increases without an increase in the size of
the chamber. dilation can result in mitral insufficiency and left atrial enlarge-
In volume overload states (e.g., valvular regurgitation ment, which is associated with an increased incidence of atrial
or shunts), the new sarcomeres are added in series fibrillation. The microscopic changes in heart failure are
with existing sarcomeres, so that the muscle fiber nonspecific, consisting primarily of myocyte hypertrophy
length increases. Consequently, the ventricle tends with interstitial fibrosis of variable severity. Superimposed on
to dilate, and the resulting wall thickness can be this background may be other lesions that contribute to the
increased, normal, or decreased; thus, heart weight— development of heart failure (e.g., recent or old myocardial
rather than wall thickness—is the best measure of infarction).
hypertrophy in volume-overloaded hearts. Lungs. Rising pressure in the pulmonary veins is ultimately
Compensatory hypertrophy comes at a cost to the myocyte. transmitted back to the capillaries and arteries of the lungs,
The oxygen requirements of hypertrophic myocardium are resulting in congestion and edema as well as pleural effusion
amplified owing to increased myocardial cell mass. Because due to an increase in hydrostatic pressure in the venules of
the myocardial capillary bed does not expand in step with the visceral pleura. The lungs are heavy and boggy, and micro-
the increased myocardial oxygen demands, the myocar- scopically show perivascular and interstitial transudates,
dium becomes vulnerable to ischemic injury. Hypertrophy alveolar septal edema, and accumulation of edema fluid in
also typically is associated with altered patterns of gene the alveolar spaces. In addition, variable numbers of red cells
expression reminiscent of the fetal myocytes, such as extravasate from the leaky capillaries into alveolar spaces,
changes in the dominant form of myosin heavy chain pro- where they are phagocytosed by macrophages The subse-
duced. Altered gene expression may contribute to changes quent breakdown of red cells and hemoglobin leads to the
in myocyte function that lead to increases in heart rate and appearance of hemosiderin-laden alveolar macrophages—
force of contraction, both of which improve cardiac output, so-called heart failure cells—that reflect previous epi-
but which also lead to higher cardiac oxygen consumption. sodes of pulmonary edema.
In the face of ischemia and chronic increases in workload,
other untoward changes also eventually supervene, Clinical Features
including myocyte apoptosis, cytoskeletal alterations, and Dyspnea (shortness of breath) on exertion is usually the
increased extracellular matrix (ECM) deposition. earliest and most significant symptom of left-sided heart
Pathologic compensatory cardiac hypertrophy is corre- failure; cough also is common as a consequence of fluid
lated with increased mortality; indeed, cardiac hypertro- transudation into air spaces. As failure progresses, patients
phy is an independent risk factor for sudden cardiac death. experience dyspnea when recumbent (orthopnea); this
By contrast, the volume-loaded hypertrophy induced by occurs because the supine position increases venous return
regular aerobic exercise (physiologic hypertrophy) typically is from the lower extremities and also elevates the diaphragm.
accompanied by an increase in capillary density, with Orthopnea typically is relieved by sitting or standing, so
decreased resting heart rate and blood pressure. These patients usually sleep in a semiseated position. Paroxysmal
physiologic adaptations reduce overall cardiovascular nocturnal dyspnea is a particularly dramatic form of breath-
morbidity and mortality. In comparison, static exercise lessness, awakening patients from sleep with extreme
(e.g., weight lifting) is associated with pressure hypertro- dyspnea bordering on feelings of suffocation.
phy and may not have the same beneficial effects.
Other manifestations of left ventricular failure include
Left-Sided Heart Failure an enlarged heart (cardiomegaly), tachycardia, a third
heart sound (S3), and fine rales at the lung bases, caused by
Heart failure can affect predominantly the left or the right the opening of edematous pulmonary alveoli. With pro-
side of the heart or may involve both sides. The most gressive ventricular dilation, the papillary muscles are
common causes of left-sided cardiac failure are ischemic displaced outwards, causing mitral regurgitation and a
heart disease (IHD), systemic hypertension, mitral or aortic systolic murmur. Subsequent chronic dilation of the left
valve disease, and primary diseases of the myocardium atrium can cause atrial fibrillation, manifested by an “irregu-
(e.g., amyloidosis). The morphologic and clinical effects of larly irregular” heartbeat. Such uncoordinated, chaotic
left-sided CHF stem from diminished systemic perfusion atrial contractions reduce the ventricular stroke volume
and the elevated back-pressures within the pulmonary and also can cause stasis. The stagnant blood is prone to
circulation. form thrombi (particularly in the atrial appendage) that
can shed emboli and cause strokes and manifestations of
MORPHOLOGY infarction in other organs.
Heart. The gross cardiac findings depend on the underlying Systemically, diminished cardiac output leads to
disease process, for example, myocardial infarction or valvu- decreased renal perfusion that in turn triggers the renin-
lar deformities may be present. With the exception of failure angiotension-aldosterone axis, increasing intravascular
due to mitral valve stenosis or restrictive cardiomyopathies volume and pressures (Chapter 3). Unfortunately, these
(described later), the left ventricle usually is hypertrophied compensatory effects exacerbate the pulmonary edema.
and can be dilated, sometimes massively. Left ventricular With further reduction in renal perfusion, prerenal azotemia
may supervene, with impaired excretion of nitrogenous
wastes and increasing metabolic derangement. In severe
CHF, diminished cerebral perfusion can manifest as hypoxic
encephalopathy with irritability, diminished cognition, and
restlessness that can progress to stupor and coma.
