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Heart (or cardiac) failure: pathophysiological state in which the heart is unable to pump blood at a rate commensurate with the requirements of the metabolizing tissues or can do so only from an elevated filling pressure

Congestive heart failure (CHF): complex clinical syndrome characterized by abnormalities of left ventricular function and neurohormonal regulation, which are accompanied by effort intolerance, fluid retention, and reduced longevity

It is a common end point for many diseases of cardiovascular system It can be caused by : -Inappropriate work load (volume or pressure overload) -Restricted filling -Myocyte loss

Causes of left ventricular failure

Volume over load: Regurgitate valve High output status Systemic hypertension Outflow obstruction Post MI, Chronic ischemia Connective tissue diseases Infection, Poisons (alcohol, cobalt) Pericardial diseases, Restrictive cardiomyopathy, tachyarrhythmia

Pressure overload:

Loss of muscles:

Restricted Filling:

According to AHA, CHF is a clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood

Heart failure (HF) may be acute or chronic

i) acute HF ii) chronic HF (CHF)


CHF develops in following states:

i) myocardial ischaemia from atherosclerotic coronary artery disease

ii) multivalvular heart disease iii) systemic arterial hypertension

iv) chronic lung disease resulting in hypoxia, pulmonary arterial hypertension

v) progression of acute into chronic failure

In chronic heart failure, compensatory mechanisms like tachycardia, cardiac dilatation and cardiac hypertrophy try to make adjustments so as to maintain adequate cardiac output

Clinical manifestations of heart failure result from the accumulation of excess fluid to the left or right cardiac chamber, whichever is initially affected

Stages in the Evolution of Heart Failure

Hypertension Diabetes, Hypercholesterolemia

Heart disease (any)

Asymptomatic LV dysfunction Systolic / Diastolic

Dyspnea, Fatigue Reduced exercise tolerance

Marked symptoms at rest despite max. therapy

AHA guidelines 2001

Left-sided Heart Failure

Initiated by stress to the left heart The major causes are: i) systemic hypertension ii) mitral or aortic valve disease (stenosis) iii) Ischaemic heart disease iv) Myocardial diseases e.g. cardiomyopathies, myocarditis v) Restrictive pericarditis

Result from accumulation of fluid in the lungs and

from decreased left ventricular output

Major pathological changes are: i) pulmonary congestion and oedema, causing dyspnoea and
orthopenia ii) decreased left ventricular output causing hypoperfusion and diminished oxygenation of tissues

Right-sided Heart Failure

consequence of left side heart failure The major causes are: i) as a consequence of left ventricular failure ii) intrinsic lung diseases iii) pulmonary or tricuspid valvular disease iv) pulmonary hypertension
v) myocardial diseases affecting right side of heart

Forward failure cardiac output

Left heart failure

IHD, Myocarditis, Valvular heart diseases Backward failure Residual blood in left ventricle

Tissue anoxia

Left atrial pressure and volume

renal perfusion

Pressure in pulmonary venous circulation

Pulmonary arterial hypertension Activation of RAAS

Right heart failure

Right side valvular disease Rt side myocardial disease Pulmonary hypertension

Right ventricular pressure

Na+, H2O retention



Lt. VENTRICULAR FAILURE IHD, Myocardits,Valvular heart


Rt. VENTRICULAR FAILURE Pulmonary HT, Valvular heart


Activation of NA, ANP Activation of RAAS mechanism Tachycardia Na+ Further stress on myocardium and water retention Cell stretching

Myocardial contractility
cardiac workload



Hemodynamic changes Neurohormonal changes Cellular changes

Hemodynamic changes

HF can be secondary to systolic dysfunction or diastolic dysfunction

Neurohormonal changes
N/H changes
Sympathetic activity

Favorable effect
HR , contractility, vasoconst. V return, filling Salt & water retention VR

Unfavorable effect
Arteriolar constriction After load workload O2 consumption Vasoconstriction after load

Renin-Angiotensin Aldosterone

interleukins &TNF- Endothelin

Same effect

Same effect

May have roles in myocyte hypertrophy Vasoconstriction VR

Apoptosis After load

Cellular changes
Changes in Ca+2 handling

Changes in adrenergic receptors:

Slight in 1 receptors 1 receptors desensitization followed by down regulation

Changes in contractile proteins Program cell death (Apoptosis) Increase amount of fibrous tissue

Orthopnea, paroxysmal nocturnal dyspnea Low cardiac output symptoms Abdominal symptoms: Anorexia,nausea, Abdominal fullness, Rt hypochondrial pain

Pale cold sweaty skin

Swelling of the ankles, legs, and hands

Orthopnea, or the shortness of breath when lying flat

Shortness of breath during exertion

Symptoms (involving circulation)

Cyanosis, or a bluish color that is seen in the lips and fingernails from a lack of oxygen Fatigue or weakness Rapid or irregular heart beat Changes of behavior such as restlessness, confusion, and decreased attention span

Symptoms (involving congestion)

Unexplained or unintentional weight gain
Chronic cough Increased urination Loss of appetite or indigestion

Congestive heart failure is a syndrome that can be caused by multiple underlying diseases such as:
Congenital heart disease Atherosclerosis Rheumatic fever Cardiomyopathy Valve disorders Ventricular failure Left or right-sided failure Hypertension Prolonged alcohol or drug addiction Previous heart attack Diabetes Chronic rapid heartbeats