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Heart Failure
DEFINITION
Heart Failure is defined as the inability of the heart to pump blood forward at a sufficient rate to meet the
metabolic demands of the body (forward failure), or the ability to do so only if the cardiac filling pressures are
abnormally high (backward failure), or both.
Heart failure may be the final and most severe manifestation of nearly every form of cardiac disease, including
Coronary Atherosclerosis, Myocardial Infarction, Valvular Diseases, Hypertension, Congenital Heart Disease, and
the Cardiomyopathies.
Heart failure may be caused by myocardial failure (impaired left ventricular function) but may also occur in the
presence of near-normal cardiac function under conditions of high demand. Heart failure always causes circulatory
failure, but the converse is not necessarily the case because various Noncardiac conditions (eg, Hypovolemic
shock, Septic shock) can produce circulatory failure in the presence of normal, modestly impaired, or even
supranormal cardiac function
PHYSIOLOGY
First, it begins with reviewing the physiology of normal myocardial contraction and relaxation.
DETERMINANTS OF CONTRACTILE FUNCTION IN THE INTACT HEART
In a healthy person, Cardiac Output is matched to the bodys total metabolic need. Cardiac Output (CO) is equal
to the product of stroke
volume (SV, the volume of blood ejected with each contraction) and the heart rate (HR):
CO (mL/min) = SV (mL/beat) X HR (beat/min)
The three major determinants of stroke volume are:
Preload:
Contraction increases their force of contraction. Preload can be
compared to the stretching of a rubber band. The more the
rubber band is stretched, the more forcefully it will snap back.
Within limits, the more the heart fills with blood during Diastole,
the greater the force of contraction during Systole. This
relationship is known as the FrankStarling law of the heart:
The preload is proportional to the end-diastolic volume (EDV)
(the volume of blood that fills the ventricles at the end of
diastole). Normally, the greater the EDV, the more forceful the
next contraction.
Two key factors determine EDV:
(1) The duration of ventricular diastole
When heart rate
increases, the
duration of diastole
is shorter. Less filling
time means a
smaller EDV, and the
ventricles may
contract before they
are adequately filled.
By contrast, when
venous return
increases, a greater
volume of blood
flows into the
ventricles, and the
Contractility (Inotropic State):
The second factor that influences stroke volume is myocardial contractility, the strength of contraction at any
given preload. Substances that increase contractility are Positive Inotropic Agents; those that decrease
contractility are Negative Inotropic Agents. Thus, for a constant preload,
PATHOPHYSIOLOGY
Chronic Heart failure may result from a wide variety of cardiovascular insults. The etiologies can be grouped
into:
Heart failure that results from an abnormality of ventricular
emptying (due to impaired contractility or greatly excessive
afterload) is termed Systolic
Dysfunction, whereas heart failure caused by abnormalities of
diastolic relaxation or ventricular filling is termed Diastolic
Dysfunction.
However, it is now common to categorize heart failure
patients into two general categories, based on the Left
Ventricular Ejection Fraction (EF), a measure of cardiac
performance
Heart Failure with Reduced EF
In states of systolic dysfunction, the affected ventricle has a
diminished capacity to eject blood because of impaired
myocardial contractility or pressure overload (i.e., excessive
afterload). Loss of contractility may result from destruction of
myocytes, abnormal myocyte function, or fibrosis. Pressure
overload impairs ventricular ejection by signifi cantly
increasing resistance to flow
Heart Failure with Preserved EF
Patients who exhibit heart failure with preserved EF frequently
demonstrate abnormalities of ventricular diastolic function:
either impaired early diastolic relaxation (an active, energydependent process), increased stiffness of the ventricular wall
(a passive property), or both. Acute myocardial ischemia is
an example of a condition that transiently inhibits energy
delivery and diastolic relaxation. Conversely, left ventricular
PRECIPITATING FACTORS
Many patients with heart failure remain asymptomatic for extended periods either because the impairment is mild
or because cardiac dysfunction is balanced by the compensatory mechanisms described earlier. Often clinical
CLINICAL MANIFESTATION
The clinical manifestations of heart failure result from impaired forward cardiac output and/or elevated venous
pressures, and relate to the ventricle that has failed
The symptoms of heart failure are commonly graded according to the New York Heart Association (NYHA)
classification, and patients may shift from one class to another, in either direction, over time:
A newer system classifies patients according to their stage in the temporal course of heart failure. In this system,
progression is in only one direction, from Stage A to Stage D, reflecting the typical sequence of heart failure
manifestations in clinical practice
TREATMENT
Diuretics
Vasodilator
Inotropic drugs
-blockers
Aldosterone Antagonist Therapy
Cardiac Resynchronization Therapy
Cardiac Replacement Therapy
DIFFERENTIAL DIAGNOSIS
Differential diagnosis for Heart Failure
Cirrhosis
Emphysema
Goodpasture syndrome
Myocardial Infarction
Nephrotic syndrome
Respiratory failure
Venous Insufficiency
References:
Leonard S. Lilly, Pathophysiology of Heart Disease 5 th Edition
G.J. Tortora, Principles of Anatomy and Physiology 13 th Edition
Braunwalds Heart Disease: A Textbook of Cardiovascular Medicine
9th Edition
Endocarditis is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart
valves (native or prosthetic valves). Other structures that may be involved include the interventricular septum,
the chordae tendineae, the mural endocardium, or even the surfaces of intracardiac devices. Endocarditis is
characterized by a prototypic lesion, the vegetation, which is a mass of platelets, fibrin, microcolonies of
microorganisms, and scant inflammatory cells.
There are multiple ways to classify Endocarditis. The simplest classification is based on etiology:
either infective or non-infective, depending on whether a microorganism is the source of the inflammation or not
DD for Infective Endocarditis:
DD for Non-Bacterial (Non-infective)
Atrial Myxoma
Infective endocarditis with septic emboli and a
Endocarditis
Lyme Disease
Polymyalgia Rheumatica
Reactive Arthritis
References:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1079236/
http://emedicine.medscape.com/article/216650-differential