CHF

Congestive Heart Failure

 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
Specific underlying factors cause
various forms of heart failure,
such as systolic heart failure
(most commonly, left ventricular
systolic dysfunction), heart failure
with preserved LVEF, acute heart
failure, high-output heart failure,
and right heart failure.
Underlying causes of systolic heart
failure include the following:
Coronary artery disease
Diabetes mellitus
Hypertension
Valvular heart disease (stenosis
or regurgitant lesions)
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 effects, such as doxorubicin)
Idiopathic cardiomyopathy
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 Beriberi heart disease
stenosis)
Paget disease of bone
Hypertrophic cardiomyopathy
Albright syndrome (fibrous
Restrictive cardiomyopathy
dysplasia)
(amyloidosis, sarcoidosis)
Constrictive pericarditis Multiple myeloma
Underlying causes of acute heart Pregnancy
failure include the following: Glomerulonephritis
Acute valvular (mitral or aortic) Polycythemia vera
regurgitation Carcinoid syndrome
Myocardial infarction
Myocarditis
Arrhythmia
Sepsis
Underlying causes of right heart
failure include the following:
Left ventricular failure
Coronary artery disease
(ischemia)
Pulmonary hypertension
Pulmonary valve stenosis
Pulmonary embolism
Chronic pulmonary disease
Neuromuscular disease
 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
dyspnea at rest
Orthopnea
Acute pulmonary edema
Chest pain/pressure and
palpitations
Tachycardia
Fatigue and weakness
Nocturia and oliguria
Anorexia, weight loss, nausea
Exophthalmos and/or visible
pulsation of eyes
Distention of neck veins
Weak, rapid, and thready pulse
Rales, wheezing
S3 gallop and/or pulsus alternans
Increased intensity of P2 heart
sound
Hepatojugular reflux
Ascites, hepatomegaly, and/or
anasarca
Central or peripheral cyanosis,
pallor
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
Neck vein distention
one third the maximal value
Rales
recorded
Acute pulmonary edema
Pleural effusion
Hepatojugular reflux
S 3 gallop
Tachycardia (rate of 120 bpm)
Central venous pressure greater than Bilateral ankle edema
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/Cla
sses-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].