Download Heart Failure BY Dr.Arshad Fuad

‫بورد عراقي (دكتوراه) في الطب الباطني‬
‫بورد عربي (دكتوراه) في الطب الباطني‬
‫بورد عراقي (دكتوراه) تخصص دقيق في أمراض‬
‫وقسطرة القلب والشرايين‬
DEFINITION

Heart failure (HF) is a clinical syndrome that
occurs in patients who, because of an inherited
or acquired abnormality of cardiac structure
and/or function, develop a constellation of
clinical symptoms (dyspnea and fatigue) and
signs (edema and rales) that lead to frequent
hospitalizations, a poor quality of life, and a
shortened life expectancy.
EPIDEMIOLOGY
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The overall prevalence of HF in the adult population in developed countries
is 2%. rising with age, and affects 6–10% of people over age 65.
Although the relative incidence of HF is lower in women than in men, women
constitute at least one-half the cases of HF because of their longer life
expectancy.
The overall prevalence of HF is thought to be increasing, in part because
current therapies for cardiac disorders, such as myocardial infarction (MI),
valvular heart disease, and arrhythmias, are allowing patients to survive
longer.
Although HF once was thought to arise primarily in the setting of a
depressed left ventricular (LV) ejection fraction (EF), epidemiologic studies
have shown that approximately one-half of patients who develop HF have a
normal or preserved EF (EF >50%).
Accordingly, HF patients are now broadly categorized into one of two groups:
(1) HF with a depressed EF (commonly referred to as systolic failure) or (2)
HF with a preserved EF (commonly referred to as diastolic failure).
ETIOLOGY
Depressed Ejection Fraction (<40%)
Preserved Ejection Fraction (>50%)
Coronary artery disease
• Myocardial infarction
• Myocardial ischemia
Pathologic hypertrophy
• Primary (hypertrophic cardiomyopathies)
• Secondary (hypertension)
Chronic pressure overload
• Hypertension
• Obstructive valvular disease
Aging
Chronic volume overload
• Regurgitant valvular disease
• Intracardiac shunting (L to R)
• Extrracardiac shunting
Restrictive cardiomyopathy
• Infiltrative disorders (amyloidosis,
sarcoidosis)
• Storage diseases (hemochromatosis)
• Fibrosis
• Endomyocardial disorders
Nonischemic dilated cardiomyopathy
• Familial or genetic disorders
• Toxic or drug-induced damage
• Metabolic disorder
• Viral or other infectious agents
Disorders of rate and rhythm
• Chronic bradyarrhythmias
• Chronic tachyarrhythmias
Pulmonary Heart Disease
High-Output States
Cor pulmonale
Metabolic disorders
• Thyrotoxicosis
• Nutritional disorders (beriberi)
Pulmonary vascular disorders
Excessive blood-flow requirements
• Systemic arteriovenous shunting
• Chronic anemia
• In 20–30% of the cases of HF with a depressed EF, the exact etiologic basis is not
known. These patients are referred to as having nonischemic, dilated, or idiopathic
cardiomyopathy if the cause is unknown
PROGNOSIS
Despite many recent advances in the evaluation
and management of HF, the development of
symptomatic HF still carries a poor prognosis.
 Although it is difficult to predict prognosis in an
individual, patients with symptoms at rest [New
York Heart Association (NYHA) class IV] have a
30–70% annual mortality rate, whereas patients
with symptoms with moderate activity (NYHA class
II) have an annual mortality rate of 5–10%.
 Thus, functional status is an important predictor
of patient outcome

NEW YORK HEART ASSOCIATION
CLASSIFICATION
PATHOGENESIS
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HF may be viewed as a progressive disorder that is
initiated after an index event either damages the heart
muscle, with a resultant loss of functioning cardiac
myocytes, or, alternatively, disrupts the ability of the
myocardium to generate force, thereby preventing the
heart from contracting normally.
This index event may have an abrupt onset, as in the
case of a myocardial infarction (MI); it may have a
gradual or insidious onset, as in the case of
hemodynamic pressure or volume overloading; or it may
be hereditary, as in the case of many of the genetic
cardiomyopathies.
Regardless of the nature of the inciting event, the
feature that is common to each of these index events is
that they all in some manner produce a decline in the
pumping capacity of the heart.
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Although the precise reasons why patients with LV dysfunction may remain
asymptomatic is not certain, one potential explanation is that a number of
compensatory mechanisms become activated in the presence of cardiac
injury and/or LV dysfunction allowing patients to sustain and modulate LV
function for a period of months to years.
The list of compensatory mechanisms that have been described thus far
include:
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(1) activation of the renin-angiotensin-aldosterone (RAA) and adrenergic nervous
systems, which are responsible for maintaining cardiac output through
increased retention of salt and water
and (2) increased myocardial contractility.
In addition, there is activation of a family of countervailing vasodilatory
molecules, including the atrial and brain natriuretic peptides (ANP and
BNP), prostaglandins (PGE2 and PGI2), and nitric oxide (NO), that offsets
the excessive peripheral vascular vasoconstriction.
Thus, patients may remain asymptomatic or
minimally symptomatic for a period of years;
however, at some point patients become overtly
symptomatic, with a resultant striking increase in
morbidity and mortality rates.
 the transition to symptomatic HF is accompanied
by increasing activation of neurohormonal,
adrenergic, and cytokine systems that lead to a
series of adaptive changes within the myocardium
collectively referred to as LV remodeling.
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PATHOPHYSIOLOGICAL CHANGES IN
HEART FAILURE
Ventricular dilatation
 Myocyte hypertrophy
 Increased collagen synthesis
 Altered myosin gene expression
 Altered sarcoplasmic Ca2+-ATPase density
 Increased ANP secretion
 Salt and water retention
 Sympathetic stimulation
 Peripheral vasoconstriction
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TYPES OF HEART FAILURE
Left, right and biventricular heart failure
Left-sided heart failure. There is a reduction in the
left ventricular output and an increase in the left
atrial or pulmonary venous pressure.
 Right-sided heart failure. There is a reduction in
right ventricular output for any given right atrial
pressure.
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Causes of isolated right heart failure include chronic
lung disease (cor pulmonale), multiple pulmonary
emboli and pulmonary valvular stenosis.
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Biventricular heart failure. Failure of the left
and right heart may develop because
the disease process, such as dilated
cardiomyopathy or ischaemic heart disease, affects
both ventricles
 or because disease of the left heart leads to
chronic elevation of the left atrial pressure,
pulmonary hypertension and right heart failure.

Diastolic and systolic dysfunction
Heart failure may develop as a result of
 impaired myocardial contraction (systolic
dysfunction)
 but can also be due to poor ventricular filling and
high filling pressures caused by abnormal
ventricular relaxation (diastolic dysfunction).
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The latter is caused by a stiff non-compliant ventricle
and is commonly found in patients with left ventricular
hypertrophy.
NB: Systolic and diastolic dysfunction often coexist,
particularly in patients with coronary artery disease.
Heart failure may develop suddenly, as in MI, or
gradually, as in progressive valvular heart
disease.
 When there is gradual impairment of cardiac
function, a variety of compensatory changes
may take place.
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High-output failure
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Conditions such as large arteriovenous shunt,
beri-beri , severe anaemia or thyrotoxicosis can
occasionally cause heart failure due to an
excessively high cardiac output.
Stages of HF
Stage A: patients at high risk for developing heart
failure but without structural disorders of the heart
 Stage B: patients with a structural disorder of the
heart but no symptoms of heart failure
 Stage C: patients with past or current symptoms of
heart failure associated with underlying structural
heart disease
 Stage D: patients with end-stage disease who
require specialized treatment strategies such as
mechanical circulatory support, continuous
inotropic infusions, cardiac transplantation, or
hospice care
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Heart Failure Clinical Stages
NORMAL
No symptoms
Normal exercise
Normal LV fxn
Asymptomatic
LV Dysfunction
No symptoms
Normal exercise
Abnormal LV fxn
Compensated
No symptoms
Exercise
Abnormal LV fxn
Decompensated
Symptoms
Exercise
Abnormal LV fxn
Refractory
ATA-01-SK-0416-0418-NE
Symptoms not
controlled
with treatment
Clinical Manifestations
Symptoms
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The cardinal symptoms of HF are fatigue and
shortness of breath.
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Although fatigue traditionally has been ascribed to the
low cardiac output in HF, it is likely that skeletal-muscle
abnormalities and other noncardiac comorbidities (e.g.,
anemia) also contribute to this symptom.
Orthopnea, which is defined as dyspnea occurring
in the recumbent position, is usually a later
manifestation of HF than is exertional dyspnea.
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It results from redistribution of fluid from the
splanchnic circulation and lower extremities into the
central circulation during recumbency, with a resultant
increase in pulmonary capillary pressure.
Paroxysmal Nocturnal Dyspnea (PND): This term
refers to acute episodes of severe shortness of
breath and coughing that generally occur at night
and awaken the patient from sleep, usually 1–3
hours after the patient retires. PND may be
manifest by coughing or wheezing, possibly
because of increased pressure in the bronchial
arteries leading to airway compression, along with
interstitial pulmonary edema that leads to
increased airway resistance
 Cheyne-Stokes Respiration( 40%)
 Acute Pulmonary Edema
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OTHER SYMPTOMS
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Gastrointestinal symptoms. Anorexia, nausea, and early
satiety associated with abdominal pain and fullness are
common complaints and may be related to edema of
the bowel wall and/or a congested liver.
Cerebral symptoms such as confusion, disorientation,
and sleep and mood disturbances may be observed in
patients with severe HF, particularly elderly patients with
cerebral arteriosclerosis and reduced cerebral
perfusion.
Nocturia is common in HF and may contribute to
insomnia.
Physical Examination
General Appearance and Vital Signs
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In mild or moderately severe HF, the patient appears to be in no
distress at rest except for feeling uncomfortable when lying flat for
more than a few minutes.
In more severe HF, the patient must sit upright, may have labored
breathing, and may not be able to finish a sentence because of
shortness of breath.
Systolic blood pressure may be normal or high in early HF, but
generally is reduced in advanced HF because of severe LV
dysfunction.
The pulse pressure may be diminished, reflecting a reduction in
stroke volume.
Sinus tachycardia is a nonspecific sign caused by increased
adrenergic activity.
Peripheral vasoconstriction leading to cool peripheral extremities and
cyanosis of the lips and nail beds is also caused by excessive
adrenergic activity.
JUGULAR VEINS
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Elevated
PULMONARY EXAMINATION
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Pulmonary crackles (rales or crepitations)
result from the transudation of fluid from the
intravascular space into the alveoli.
 In
patients with pulmonary edema, rales may be
heard widely over both lung fields and may be
accompanied by expiratory wheezing (cardiac
asthma).
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Pleural effusions(unilateral on the right or
bilateral)
CARDIAC EXAMINATION
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Cardiomegaly , the point of maximal impulse (PMI)
usually is displaced below the fifth intercostal space
and/or lateral to the midclavicular line, and the impulse
is palpable over two interspaces.
In some patients, a third heart sound (S3) is audible and
palpable at the apex.
Patients with enlarged or hypertrophied right ventricles
may have a sustained and prolonged left parasternal
impulse extending throughout systole.
A fourth heart sound (S4) is not a specific indicator of HF
but is usually present in patients with diastolic
dysfunction.
The murmurs of mitral and tricuspid regurgitation are
frequently present in patients with advanced HF.
ABDOMEN AND EXTREMITIES
Hepatomegaly is an important sign in patients with
HF. When it is present, the enlarged liver is
frequently tender and may pulsate during systole if
tricuspid regurgitation is present.
 Ascites, a late sign, occurs as a consequence of
increased pressure in the hepatic veins and the
veins draining the peritoneum.
 Jaundice, also a late finding in HF, results from
impairment of hepatic function secondary to
hepatic congestion and hepatocellular hypoxemia
and is associated with elevations of both direct
and indirect bilirubin.
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Peripheral edema is a cardinal manifestation of
HF, but it is nonspecific and usually is absent in
patients who have been treated adequately
with diuretics.
 Long-standing
edema may be associated with
indurated and pigmented skin.
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Cardiac Cachexia
Diagnosis
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The diagnosis of heart failure should not be
based on history and clinical findings; it
requires evidence of cardiac dysfunction with
appropriate investigation using objective
measures of left ventricular structure and
function (usually echocardiography).
INVESTIGATIONS IN HEART FAILURE
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Blood tests: complete blood count, a panel of
electrolytes, blood urea nitrogen, serum
creatinine, hepatic enzymes, and a urinalysis.
 Selected
patients should have assessment for
diabetes mellitus (fasting serum glucose or oral
glucose tolerance test), dyslipidemia (fasting lipid
panel), and thyroid abnormalities (thyroidstimulating hormone level).
BIOMARKERS
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Circulating levels of natriuretic peptides are useful
adjunctive tools in the diagnosis of patients with HF.
Both B-type natriuretic peptide (BNP) and N-terminal
pro-BNP, which are released from the failing heart, are
relatively sensitive markers for the presence of HF with
depressed EF;
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they also are elevated in HF patients with a preserved EF,
albeit to a lesser degree.
However, it is important to recognize that natriuretic
peptide levels increase with age and renal impairment,
are more elevated in women, and can be elevated in
right HF from any cause.
Levels can be falsely low in obese patients and may
normalize in some patients after appropriate treatment.
Chest X-ray. Look for cardiomegaly, pulmonary
congestion with upper lobe diversion, fluid in
fissures, Kerley B lines, and pulmonary oedema.
 Electrocardiogram for ischaemia, chamber
enlargement or arrhythmia.
 Echocardiography. Cardiac chamber dimension,
systolic and diastolic function, regional wall motion
abnormalities, valvular heart disease,
cardiomyopathies.
 Stress echocardiography. Assessment of viability
in dysfunctional myocardium
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Nuclear cardiology. Radionucleotide angiography
(RNA) can quantify ventricular ejection fraction,
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single photon-emission computed tomography (SPECT)
or positron emission tomography (PET) can
demonstrate myocardial ischaemia and viability in
dysfunctional myocardium.
CMR (cardiac MRI). Assessment of viability in
dysfunctional myocardium with the use of
dobutamine for contractile reserve or with
gadolinium for delayed enhancement (‘infarct
imaging’).
 Cardiac catheterization. Diagnosis of ischaemic
heart failure (and suitability for revascularization),
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Cardiac biopsy.
Diagnosis of cardiomyopathies, e.g. amyloid,
 follow-up of transplanted patients to assess rejection.
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Cardiopulmonary exercise testing. Peak oxygen
consumption (VO2) is predictive of hospital
admission and death in heart failure.
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A 6-minute exercise walk is an alternative.
Ambulatory ECG monitoring (Holter). In patients
with suspected arrhythmia.
Complications
In advanced heart failure, the following may occur:
 Renal failure is caused by poor renal perfusion
due to a low cardiac output and may be
exacerbated by diuretic therapy, angiotensinconverting enzyme (ACE) inhibitors and
angiotensin receptor blockers.
 Hypokalaemia may be the result of treatment with
potassium-losing diuretics or hyperaldosteronism
caused by activation of the renin–angiotensin
system and impaired aldosterone metabolism due
to hepatic congestion.
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Hyperkalaemia may be due to the effects of drug
treatment, particularly the combination of ACE inhibitors
and spironolactone (which both promote potassium
retention), and renal dysfunction.
Hyponatraemia is a feature of severe heart failure and
is a poor prognostic sign.
Impaired liver function is caused by hepatic venous
congestion and poor arterial perfusion, which frequently
cause mild jaundice and abnormal liver function tests;
reduced synthesis of clotting factors can make
anticoagulant control difficult.
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Thromboembolism.
Deep vein thrombosis and pulmonary embolism may
occur due to the effects of a low cardiac output and
enforced immobility,
 whereas systemic emboli may be related to
arrhythmias, atrial flutter or fibrillation, or intracardiac
thrombus complicating conditions such as mitral
stenosis, MI or left ventricular aneurysm.
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Atrial and ventricular arrhythmias are very
common and may be related to
electrolyte changes (e.g. hypokalaemia,
hypomagnesaemia),
 the underlying structural heart disease,
 and the pro-arrhythmic effects of increased circulating
catecholamines or drugs.
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