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.
Epidemiology
 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,
Etiology
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
Underlying causes Underlying causes of
Specific underlying factors systolic heart failure
cause various forms of include the following:
heart failure, such as Coronary artery disease
systolic heart failure (most Diabetes mellitus
commonly, left ventricular Hypertension
systolic dysfunction), heart
Valvular heart disease
failure with preserved LVEF,
(stenosis or regurgitant
acute heart failure, high-
lesions)
output heart failure, and
right heart 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 Underlying causes of high-
diastolic heart failure include output heart failure
the following: include the following:
Coronary artery disease Anemia
Diabetes mellitus Systemic arteriovenous
Hypertension fistulas
Valvular heart disease (aortic Hyperthyroidism
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 Pregnancy
following: Glomerulonephritis
Acute valvular (mitral or aortic) Polycythemia vera
regurgitation Carcinoid syndrome
Myocardial infarction
Myocarditis
Arrhythmia
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
Pathophysiology
 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
dyspnea at rest pulsation of eyes
Orthopnea Distention of neck veins
Acute pulmonary edema Weak, rapid, and thready pulse
Rales, wheezing
Chest pain/pressure and
palpitations S3 gallop and/or pulsus
alternans
Tachycardia
Increased intensity of P2 heart
Fatigue and weakness
sound
Nocturia and oliguria Hepatojugular reflux
Anorexia, weight loss, Ascites, hepatomegaly, and/or
nausea anasarca
Central or peripheral cyanosis,
pallor
Diagnosis
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 Minor criteria are as

following: follows:
Paroxysmal nocturnal dyspnea Nocturnal cough
Weight loss of 4.5 kg in 5 days
Dyspnea on ordinary
in response to treatment
exertion
Neck vein distention
Rales
A decrease in vital capacity
Acute pulmonary edema by one third the maximal
value recorded
Hepatojugular reflux
S 3 gallop
Pleural effusion
Central venous pressure Tachycardia (rate of 120
greater than 16 cm water bpm)
Circulation time of 25 seconds Bilateral ankle edema
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
Management
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].