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Congestive Heart Failure
Inability of the heart to handle the
volume of blood returned to it
Congestive Heart Failure
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To learn the etiologic factors of congestive
heart failure
To learn the effects of heart failure
Types of Heart Disease
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Four categories of disease account for about 85 to
90% of all cardiac deaths:
(1) ischemic heart disease (responsible for the
great majority of the cardiac deaths)
(2) hypertensive heart disease and pulmonary
hypertensive heart disease (cor pulmonale);
(3) certain valvular diseases–calcific aortic valve
stenosis, mitral valve prolapse, infective
endocarditis, and rheumatic heart disease; and
(4) congenital heart disease.
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Any one of the causes mentioned above,
when sufficiently severe or advanced, may
ultimately impair cardiac function and render
the heart unable to maintain an output
sufficient for the metabolic requirements of
the tissues and organs of the body, producing
congestive heart failure (CHF).
Etiology
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Either the heart muscle cannot pump
because of intrinsic disease,
or the heart must pump against excessive
resistance,
or the heart must pump a preposterously
large amount of blood
Pathophysiology
In summary: CHF occurs
(1) either because of a decreased myocardial
capacity to contract
"forward failure" (i.e., inability to perfuse the
arteries) ,
(2) because of an inability to fill the cardiac
chambers with blood.
"backward failure" (i.e., congestion and its
problems).
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Difference
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"Cardiogenic shock" is a term reserved for
the acute situation (usually a myocardial
infarct),
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“Failure" can simply mean inability to handle
the ordinary venous return.
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Most instances of heart failure are the
consequence of progressive deterioration of
myocardial contractile function (systolic
dysfunction), as often occurs
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with ischemic injury,
pressure or volume overload,
or dilated cardiomyopathy.
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Sometimes, however, failure results from an
inability of the heart chambers to expand
sufficiently during diastole to accommodate an
adequate ventricular blood volume (diastolic
dysfunction), as can occur
- with massive left ventricular hypertrophy,
- myocardial fibrosis,
- deposition of amyloid, or
- constrictive pericarditis.
Cardiac Hypertrophy:
Pathophysiology and Progression to
Failure
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Cardiac hypertrophy is the compensatory response of
the myocardium to increased work.
Myocardial hyperfunction induces increased myocyte
size (cellular hypertrophy through addition of
sarcomeres, the contractile elements) that causes an
increase in the overall mass and size of the heart.
Because adult cardiac myocytes cannot divide,
augmentation of myocyte number (hyperplasia) cannot
occur in the adult heart.
The pattern of hypertrophy reflects the
stimulus.
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Concentric hypertrophy : Pressure-overloaded
ventricles (e.g., hypertension or aortic stenosis)
develop concentric hypertrophy, with an increased
ratio of wall thickness to cavity radius.
Eccentric hypertrophy : In contrast, volumeoverloaded ventricles (e.g., mitral regurgitation)
develop hypertrophy with dilatation (eccentric
hypertrophy), with proportionate increases in
ventricular radius and wall thickness.
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Geometry, structure, and composition (cells
and extracellular matrix) of the hypertrophied
heart are not normal.
It should not be surprising that cardiac
hypertrophy often evolves to cardiac failure.
Besides predisposing to CHF, left ventricular
hypertrophy is an independent risk factor for
cardiac mortality and morbidity, especially for
sudden death and ischemic heart disease.
Cardiac hypertrophy
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350 gm... Normal
upper limit of weight
for an adult
1.5 cm... Normal
upper limit of
thickness for an adult
left ventricle
0.5 cm... Normal
upper limit of
thickness for an adult
right ventricle
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Whatever the underlying basis for CHF, a variety of
compensatory mechanisms come into play when the
hypertrophied heart can no longer accommodate
the increased demand.
The heart begins to dilate, thereby stretching the
sarcomeres and increasing the force of contraction
and secondarily the stroke volume.
Myocardial hypertrophy may become increasingly
detrimental because of the increased metabolic
requirements of the enlarged muscle mass.
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The downward slide of stroke volume and cardiac
output often ends in death.
Thus at autopsy, the heart of patients having CHF is
generally characterized by
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increased weight,
progressive wall thinning,
chamber dilatation, and
microscopic changes of hypertrophy.
Nevertheless, because the vascular
system is a closed circuit, failure of one
side cannot exist for long without
eventually producing excessive strain on
the other, terminating in total heart failure.
Congestive Heart Failure :
Left-Sided Heart Failure
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Left-sided heart failure is most often caused
by
(1) ischemic heart disease,
(2) hypertension,
(3) aortic and mitral valvular diseases
(particularly calcific aortic stenosis and
rheumatic heart disease), and
(4) myocardial diseases.
The common effects of left-sided failure
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Dyspnea (from pulmonary edema and total-body hypoxia)
 paroxysmal nocturnal dyspnea ("cardiac dyspnea"); on lying down for a
while, fluid redistributes itself in the body, resulting in pulmonary
edema. The lungs become heavier (i.e., congestion, edema) their
weight presses on the pulmonary veins which in turn makes them more
congested. Patients may throw the windows open at night, or learn to
sleep on various numbers of pillows; you the physician will hear rales;
the pathologist may see "brown induration" and hemosiderin-laden
"heart failure" macrophages.
Cough ("from the left atrium pushing on the bronchus"; this is common
in mitral valve disease even in the absence of failure)
Prerenal azotemia
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Hypoxic encephalopathy
Sodium overload and systemic dependent edema (from
hypoperfused kidneys; these patients may also have nocturia )
High-output failure is a special situation, in which the heart fails
because it must pump an excessive among of blood. The causes:
 Anemia
 Hyperthyroidism
 High fever
 Shunts between an artery and a vein
 Beriberi (arterioles open)
 Paget's disease of bone (abnormal bone vasculature)
 Iatrogenic (i.e., shunts in dialysis)
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Left ventricle is usually hypertrophied and
often dilated, sometimes quite massively.
Secondary enlargement of the left atrium is
frequently present.
Atrial fibrillation (i.e., uncoordinated, chaotic
contraction of the atrium) often results.
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A fibrillating left atrium carries an increased
risk of embolic stroke.
The distant effects of left-sided failure are
manifested most prominently in the lungs,
although the function of the kidneys and
brain may also be markedly impaired.
Lungs in Left-Sided Heart Failure
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With the progressive damming of blood within
the pulmonary circulation, pressure in the
pulmonary veins mounts and is ultimately
transmitted retrogradely to the capillaries.
The result is
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pulmonary congestion
Edema (heavy, wet lungs).
Lung : hyperemia&edema
Lung edema
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The lung changes include:
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(1) a perivascular and interstitial transudate, particularly in
the interlobular septa;
(2) progressive edematous widening of alveolar septa; and
(3) accumulation of edema fluid in the alveolar spaces.
(4) Transferrin in edema fluid and hemoglobin from
erythrocytes, which leak from congested capillaries, are
phagocytosed by macrophages and converted to
hemosiderin. Hemosiderin-containing macrophages in the
alveoli (called heart failure cells) denote previous
episodes of pulmonary edema.
Heart failure cells
Kidneys in Left-Sided Heart Failure
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With left-sided heart failure, the decreased cardiac
output causes a reduction in renal perfusion, which
activates the renin-angiotensin-aldosterone system,
inducing retention of salt and water with consequent
expansion of the interstitial fluid and blood volumes.
In kidneys already suffering from hypoperfusion, the
reduced cardiac output may lead to ischemic acute
tubular necrosis.
If the perfusion deficit of the kidney becomes
sufficiently severe, impaired excretion of nitrogenous
products may cause azotemia, known as prerenal
azotemia.
Brain in Left-Sided Heart Failure
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In far-advanced CHF, cerebral hypoxia may
give rise to hypoxic encephalopathy
(ischemia, and infarction ), with
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irritability,
loss of attention span,
and restlessness, which may even progress to
stupor and coma.
Hypoxic encephalopathy
Congestive Heart Failure :
Right-Sided Heart Failure
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Right-sided heart failure occurs in pure form in
only a few diseases.
Usually it is a consequence of left-sided failure
because any increase in pressure in pulmonary
circulation incident to left-sided failure
inevitably produces an increased burden on the
right side of the heart.
Pure right-sided failure most often occurs with
cor pulmonale, i.e., right ventricular pressure
overload induced by intrinsic disease of the
lungs or pulmonary vasculature.
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In these cases, the right ventricle is
burdened by increased resistance within the
pulmonary circulation; dilatation is generally
confined to the right ventricle and atrium.
This can be acute with right-sided dilatation
and thinning in massive pulmonary
embolism.
In chronic right-sided overload (e.g., owing
to chronic obstructive pulmonary disease),
right ventricular and atrial hypertrophy is
usually present.
Dilatation
Dilatation
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The major morphologic and clinical effects of
pure right-sided failure differ from those of
left-sided failure in that pulmonary congestion
is minimal, whereas engorgement of the
systemic and portal venous systems is
pronounced.
The major organs affected by right-sided
heart failure are the liver, spleen, kidneys,
subcutaneous tissues, and brain as well as
the entire portal area of venous drainage.
Liver in Right-Sided Heart Failure
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The liver is usually slightly increased in size and weight;
a cut section displays the prominent “nutmeg” pattern of
chronic passive congestion of the liver.
When left-sided failure is also present, the severe
central hypoxia produces centrilobular necrosis along
with the sinusoidal congestion.
If the right-sided failure is severe and rapidly
developing, rupture of sinusoids produces central
hemorrhagic necrosis.
With long-standing severe right-sided cardiac failure,
the central areas in time can become fibrotic, creating
the so-called cardiac sclerosis.
“Nutmeg” pattern of chronic passive
congestion of the liver
Chronic passive congestion of the liver
Cardiac sclerosis (cirrhosis)
Kidneys in Right-Sided Heart Failure
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Congestion of the kidneys is more marked
with right-sided heart failure than with leftsided failure, leading to
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greater fluid retention,
peripheral edema, and
more pronounced azotemia.
Portal System of Drainage in
Right-Sided Heart Failure
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Right-sided heart failure leads to elevated pressure in the
portal vein and its tributaries.
Splenic congestion produces a tense, enlarged spleen.
Microscopically there may be marked sinusoidal dilatation,
accompanied by areas of recent hemorrhage.
With long-standing congestion, the enlarged spleen may
achieve a weight of 500 to 600 gm (normal, approximately
150 gm), and the long-standing edema may produce
fibrous thickening of the sinusoidal walls, to create the firm
organ characteristic of congestive splenomegaly.
In addition, abnormal accumulations of transudate in the
peritoneal cavity may give rise to ascites.
Splenomegaly
Subcutaneous Tissues in Right-Sided Heart Failure
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Peripheral edema of dependent portions of
the body, especially ankle edema, is a
hallmark of right-sided failure.
In severe or long-standing cases, edema may
be quite massive and generalized, a
condition termed anasarca.
Edema
Pleural and Pericardial Spaces in
Right-Sided Heart Failure
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Effusions may appear, particularly in the right
thoracic cavity.
Brain in Right-Sided Heart Failure
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Symptoms essentially identical to those
described in left-sided failure may occur,
representing venous congestion and hypoxia
of the central nervous system.
Brain: venous congestion
In summary
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The effects of pure left-sided heart failure are
largely due to pulmonary congestion and edema.
Right-sided heart failure induces essentially a
systemic (and secondary portal) venous
congestive syndrome, with hepatic and splenic
enlargement, peripheral edema, pleural and
pericardial effusions, and ascites.
Congestive Heart failure
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