CHF

Congestive Heart Failure

Definition
Congestiveheart 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
Specific underlying factors heart failure include the
cause various forms of heart following:
failure, such as systolic heart Coronary artery disease
failure (most commonly, left Diabetes mellitus
ventricular systolic Hypertension
dysfunction), heart failure
Valvular heart disease
with preserved LVEF, acute
heart failure, high-output (stenosis or regurgitant
heart failure, and right heart lesions)
failure. Arrhythmia (supraventricular
or ventricular)
Infections and inflammation
(myocarditis)
Peripartum cardiomyopathy
Congenital heart disease
Drugs (either recreational,
such as alcohol and
cocaine, or therapeutic
drugs with cardiac side
Underlying causes of diastolic Underlying causes of high-
heart failure include the following: output heart failure include the
Coronary artery disease following:
Diabetes mellitus Anemia
Hypertension Systemic arteriovenous
Valvular heart disease (aortic fistulas
stenosis) Hyperthyroidism
Hypertrophic cardiomyopathy Beriberi heart disease
Restrictive cardiomyopathy Paget disease of bone
(amyloidosis, sarcoidosis)
Albright syndrome (fibrous
Constrictive pericarditis
dysplasia)
Underlying causes of acute
Multiple myeloma
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
Exophthalmos and/or visible
Exertional dyspnea
pulsation of eyes
and/or dyspnea at rest Distention of neck veins
Weak, rapid, and thready
Orthopnea pulse
Acute pulmonary Rales, wheezing
S3 gallop and/or pulsus
edema alternans
Increased intensity of P2 heart
Chest pain/pressure
sound
and palpitations Hepatojugular reflux
Ascites, hepatomegaly, and/or
Tachycardia anasarca
Central or peripheral cyanosis,
Fatigue and weakness
pallor
Nocturia and oliguria
Anorexia, weight loss,
nausea
 The Framingham criteria for the diagnosis of heart failure
Majorconsists of the concurrent
criteria include the presence of either 2 major criteria
Minor criteria are as follows:
or 1
following: major and 2 minor criteria.
Nocturnal cough
Paroxysmal nocturnal dyspnea
Dyspnea on ordinary
Weight loss of 4.5 kg in 5 days in
exertion
response to treatment
A decrease in vital capacity
Neck vein distention
by one third the maximal
Rales
value recorded
Acute pulmonary edema
Pleural effusion
Hepatojugular reflux
S 3 gallop Tachycardia (rate of 120

Central venous pressure

bpm)
greater than 16 cm water Bilateral ankle edema
Circulation time of 25 seconds
Radiographic cardiomegaly
Pulmonary edema, visceral
congestion, or cardiomegaly at
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].