DEFINITION

Congestive heart failure (CHF) is a clinical syndrome in which the heart fails to pump
blood at the rate required by the metabolizing tissues or in which the heart can
do so only with an elevation in filling pressure.
According to the American Heart Association, heart failure affects nearly
5.7 million Americans of all ages

Heart failure statistics for the United States are as follows:

Heart failure is the fastest-growing clinical cardiac disease entity in the
United States, affecting 2% of the population
Heart failure accounts for 34% of cardiovascular-related deaths
Approximately 670,000 new cases of heart failure are diagnosed each year
About 277,000 deaths are caused by heart failure each year
Heart failure is the most frequent cause of hospitalization in patients older
than 65 years, with an annual incidence of 10 per 1,000
The prevalence of heart failure increases with age. The prevalence is 1-2%
of the population younger than 55 years and increases to a rate of 10%
for persons older than 75 years. Nonetheless, heart failure can occur at
any age, depending on the cause.
From a clinical standpoint, classifying the causes of heart failure into the
following 4 broad categories is useful:
Underlying causes: Underlying causes of heart failure include structural
abnormalities (congenital or acquired) that affect the peripheral and
coronary arterial circulation, pericardium, myocardium, or cardiac valves,
thus leading to increased hemodynamic burden or myocardial or coronary
insufficiency
Fundamental causes: Fundamental causes include the biochemical and
physiologic mechanisms, through which either an increased hemodynamic
burden or a reduction in oxygen delivery to the myocardium results in
impairment of myocardial contraction
Precipitating causes: Overt heart failure may be precipitated by progression of
the underlying heart disease (eg, further narrowing of a stenotic aortic
valve or mitral valve) or various conditions (fever, anemia, infection) or
medications (chemotherapy, NSAIDs) that alter the homeostasis of heart
failure patients
Genetics of cardiomyopathy: Dilated, arrhythmic right ventricular and
restrictive cardiomyopathies are known genetic causes of heart failure.
Underlying causes Underlying causes of systolic heart
Specific underlying factors cause failure include the following:
various forms of heart failure, Coronary artery disease
such as systolic heart failure Diabetes mellitus
(most commonly, left ventricular
systolic dysfunction), heart Hypertension
failure with preserved LVEF, Valvular heart disease (stenosis or
acute heart failure, high-output regurgitant lesions)
heart failure, and right heart Arrhythmia (supraventricular or
failure. ventricular)
Infections and inflammation
(myocarditis)
Peripartum cardiomyopathy
Congenital heart disease
Drugs (either recreational, such as
alcohol and cocaine, or
therapeutic drugs with cardiac
side effects, such as
doxorubicin)
Underlying causes of diastolic heart Underlying causes of high-output
failure include the following: heart failure include the following:
Coronary artery disease Anemia
Diabetes mellitus Systemic arteriovenous fistulas
Hypertension Hyperthyroidism
Valvular heart disease (aortic stenosis) Beriberi heart disease
Hypertrophic cardiomyopathy Paget disease of bone
Restrictive cardiomyopathy Albright syndrome (fibrous
(amyloidosis, sarcoidosis)
dysplasia)
Constrictive pericarditis
Multiple myeloma
Underlying causes of acute heart failure
include the following:
Pregnancy

Acute valvular (mitral or aortic) Glomerulonephritis

regurgitation Polycythemia vera
Myocardial infarction Carcinoid syndrome
Myocarditis
Arrhythmia
Sepsis
The Frank-Starling mechanism, in which an increased preload helps to sustain
cardiac performance
Alterations in myocyte regeneration and death
Myocardial hypertrophy with or without cardiac chamber dilatation, in which the
mass of contractile tissue is augmented
Activation of neurohumoral systems
The release of norepinephrine by adrenergic cardiac nerves augments
myocardial contractility and includes activation of the renin-angiotensin-
aldosterone system [RAAS], the sympathetic nervous system [SNS], and
other neurohumoral adjustments that act to maintain arterial pressure and
perfusion of vital organs.
In acute heart failure the finite adaptive mechanisms that may be adequate
to maintain the overall contractile performance of the heart at relatively
normal levels become maladaptive when trying to sustain adequate cardiac
performance.
The primary myocardial response to chronic increased wall stress is
myocyte hypertrophy, death/apoptosis, and regeneration eventually
leads to remodeling, usually the eccentric type Eccentric remodeling
further worsens the loading conditions on the remaining myocytes and
perpetuates the deleterious cycle. The idea of lowering wall stress to
slow the process of remodeling has long been exploited in treating
heart failure patients.
The reduction of cardiac output following myocardial injury sets into motion
a cascade of hemodynamic and neurohormonal derangements that
provoke activation of neuroendocrine systems, most notably the above-
mentioned adrenergic systems and RAAS.
The release of epinephrine and norepinephrine, along with the vasoactive
substances endothelin-1 (ET-1) and vasopressin, causes vasoconstriction,
which increases calcium afterload and, via an increase in cyclic adenosine
monophosphate (cAMP), causes an increase in cytosolic calcium entry
The increased calcium entry into the myocytes augments myocardial
contractility and impairs myocardial relaxation (lusitropy).
The calcium overload may induce arrhythmias and lead to sudden death. The
increase in afterload and myocardial contractility (known as inotropy) and
the impairment in myocardial lusitropy lead to an increase in myocardial
energy expenditure and a further decrease in cardiac output. The increase
in myocardial energy expenditure leads to myocardial cell death/apoptosis,
which results in heart failure and further reduction in cardiac output,
perpetuating a cycle of further increased neurohumoral stimulation and
further adverse hemodynamic and myocardial responses.
CLINICAL
PRESENTATION
Exertional dyspnea and/or Exophthalmos and/or visible
pulsation of eyes
dyspnea at rest
Distention of neck veins
Orthopnea Weak, rapid, and thready pulse
Acute pulmonary edema Rales, wheezing
Chest pain/pressure and S3 gallop and/or pulsus
alternans
palpitations
Increased intensity of P2 heart
Tachycardia sound
Hepatojugular reflux
Fatigue and weakness
Ascites, hepatomegaly, and/or
Nocturia and oliguria anasarca
Anorexia, weight loss, Central or peripheral cyanosis,
pallor
nausea
 THE FRAMINGHAM CRITERIA FOR THE DIAGNOSIS OF
HEART FAILURE CONSISTS OF THE CONCURRENT
PRESENCE OF EITHER 2 MAJOR CRITERIA OR 1 MAJOR
AND 2 MINOR CRITERIA.

Major criteria include the following: Minor criteria are as follows:

Paroxysmal nocturnal dyspnea Nocturnal cough
Weight loss of 4.5 kg in 5 days in Dyspnea on ordinary exertion
response to treatment
A decrease in vital capacity by one
Neck vein distention
third the maximal value
Rales recorded
Acute pulmonary edema Pleural effusion
Hepatojugular reflux
Tachycardia (rate of 120 bpm)
S 3 gallop
Bilateral ankle edema
Central venous pressure greater than
16 cm water
Circulation time of 25 seconds
Radiographic cardiomegaly
Pulmonary edema, visceral congestion,
or cardiomegaly at autopsy
The New York Heart Association (NYHA) classification system categorizes heart failure on a scale of I
to IV, [as follows:
Class I: No limitation of physical activity
Class II: Slight limitation of physical activity
Class III: Marked limitation of physical activity
Class IV: Symptoms occur even at rest; discomfort with any physical activity
The American College of Cardiology/American Heart Association (ACC/AHA) staging system is defined by
the following 4 stages :
Stage A: High risk of heart failure but no structural heart disease or symptoms of heart failure
Stage B: Structural heart disease but no symptoms of heart failure
Stage C: Structural heart disease and symptoms of heart failure
Stage D: Refractory heart failure requiring specialized interventions
Treatment includes the following:
Nonpharmacologic therapy: Oxygen and noninvasive positive pressure ventilation, dietary sodium and fluid restriction, physical activity
as appropriate, and attention to weight gain
Pharmacotherapy: Diuretics, vasodilators, inotropic agents, anticoagulants, beta blockers, and digoxin
Surgical options
Electrophysiologic intervention
Revascularization procedures
Valve replacement/repair
Ventricular restoration
Extracorporeal membrane oxygenation
Ventricular assist devices
Heart transplantation
Total artificial heart
PROGNOSIS
In general, the mortality following hospitalization for patients with heart failure is 10.4% at 30 days, 22% at 1 year,
and 42.3% at 5 years, despite marked improvement in medical and device therapy.
Each rehospitalization increases mortality by about 20-22%.
Mortality is greater than 50% for patients with NYHA class IV, ACC/AHA stage D heart failure.
Heart failure associated with acute MI has an inpatient mortality of 20-40%; mortality approaches 80% in patients
who are also hypotensive (eg, cardiogenic shock).
Heart failure related to systolic dysfunction has an associated mortality of 50% after 5 years.
REFERENCES
Framingham Classification: Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol. 1993 Oct.
22(4 Suppl A):6A-13A. [Medline].
American Heart Association. Classes of heart failure. Available at
http://www.heart.org/HEARTORG/Conditions/HeartFailure/AboutHeartFailure/Classes-of-Heart-Failure_UCM_306328_Article.jsp. Accessed:
September 6, 2011.
[Guideline] Hunt SA, Abraham WT, Chin MH, et al, and the American College of Cardiology Foundation; American Heart Association. 2009 Focused
update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults: a report of the American
College of Cardiology Foundation/American Heart Association Task Force on practice guidelines developed in collaboration with the International
Society for Heart and Lung Transplantation. J Am Coll Cardiol. 2009 Apr 14. 53(15):e1-e90. [Medline].
[Guideline] Hunt SA, for the Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management
of Heart Failure). ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the
American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2005 Sep 20. 46(6):e1-82.
[Medline].