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Alya Putri Khairani / 130110110220 / B2

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,

Alya Putri Khairani / 130110110220 / B2


the stroke volume increases when a positive inotropic substance is present. Positive inotropic agents often promote
Ca2+ inflow during cardiac action potentials, which strengthens the force of the next contraction. Stimulation of the
sympathetic division of the autonomic nervous system (ANS), hormones such as epinephrine and norepinephrine,
increased Ca2+ level in the interstitial fluid, and the drug digitalis all have positive inotropic effects. In contrast,
inhibition of the sympathetic division of the ANS, anoxia, acidosis, some anesthetics, and increased K_ level in the
interstitial fluid have negative inotropic effects. Calcium channel blockers are drugs that can have a negative
inotropic effect by reducing Ca2_ inflow, thereby decreasing the strength of the heartbeat.
Afterload
Ejection of blood from the heart begins when pressure in the right ventricle exceeds the pressure in the pulmonary
trunk (about 20 mmHg), and when the pressure in the left ventricle exceeds the pressure in the aorta (about 80
mmHg). At that point, the higher pressure in the ventricles causes blood to push the semilunar valves open. The
pressure that must be overcome before a semilunar valve can open is termed the afterload. An increase in
afterload causes stroke volume to decrease, so that more blood remains in the ventricles at the end of systole.
Conditions that can increase afterload include hypertension (elevated blood pressure) and narrowing of arteries by
atherosclerosis

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

Right-Sided Heart Failure


Compared with the left ventricle, the right ventricle (RV) is a thin-walled, highly compliant chamber that accepts its
blood volume at low
pressures and ejects against a low pulmonary vascular resistance. As a result of its high compliance, the RV has
little difficulty accepting a wide range of filling volumes without significant changes in its filling pressures.
Conversely, the RV is quite susceptible to failure in situations that present a sudden increase in afterload, such as
acute pulmonary embolism. The most common cause of right-sided heart failure is actually the presence of Leftsided Heart Failure. In this situation, excessive afterload confronts the right ventricle because of the elevated
pulmonary vascular pressures that result from LV dysfunction.

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

Alya Putri Khairani / 130110110220 / B2


manifestations are precipitated by circumstances that increase the cardiac workload and tip the balanced state
into one of decompensation
Common precipitating factors are:

Increased metabolic demands


Fever, Infection, Anemia, Tachycardia, Hyperthyroidism, Pregnancy

Increased circulating volume (increased preload)


Excessive sodium content in diet, Excessive fluid administration, Renal failure

Conditions that increase afterload


Uncontrolled hypertension, Pulmonary embolism (increased right ventricular afterload)

Conditions that impair contractility


Negative inotropic medications, Myocardial ischemia or infarction, Excessive ethanol ingestion

Failure to take prescribed heart failure medications

Excessively slow heart rate

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

Alya Putri Khairani / 130110110220 / B2

For Heart Failure with Reduced EF

Diuretics
Vasodilator
Inotropic drugs
-blockers
Aldosterone Antagonist Therapy
Cardiac Resynchronization Therapy
Cardiac Replacement Therapy

For Heart Failure with Preserved EF


The goals of therapy in heart failure with preserved EF include (1) the relief of pulmonary and systemic congestion,
and (2) addressing
correctable causes of the impaired diastolic function (e.g., hypertension, coronary artery disease). Diuretics reduce
pulmonary congestion and peripheral edema but must be used cautiously to avoid under filling of the left ventricle.
A stiffened left ventricle relies on higher-than-normal pressures to achieve adequate diastolic filling and excessive
diuresis could reduce filling and stroke volume

Acute Heart Failure


Patients with acute heart failure are those who present with urgent and often life-threatening symptomatology.
Acute heart failure may develop in a previously asymptomatic patient (e.g., resulting from an acute coronary
syndrome, severe hypertension, or acute valvular regurgitation), or it may complicate chronic compensated heart
failure following a precipitating trigger. Management of acute heart failure typically requires hospitalization and
prompt interventions
The classification of patients with acute heart failure, and the approach to therapy, can
be tailored based on the presence or absence of two major findings at the bedside:
(1) Volume overload (i.e., wet vs. dry) as a reflection of elevated LV filling pressures, and
(2) Signs of decreased cardiac output with reduced tissue perfusion (cold vs. warm extremities).
The goals of therapy in acute heart failure are to normalize ventricular filling pressures and restore
adequate tissue perfusion

DIFFERENTIAL DIAGNOSIS
Differential diagnosis for Heart Failure

Acute Renal Failure

Acute Respiratory Distress Syndrome

Chronic Obstructive Pulmonary Disease

Cirrhosis

Emphysema

Goodpasture syndrome

Myocardial Infarction

Nephrotic syndrome

Respiratory failure

Venous Insufficiency

Alya Putri Khairani / 130110110220 / B2

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.

Differential Diagnosis of Endocarditis

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)

Antiphospholipid Syndrome Thrombotic Endocarditis:

Atrial Myxoma
Infective endocarditis with septic emboli and a

Cardiac Neoplasms, Primary systemic vasculitis

Endocarditis

Lyme Disease

Polymyalgia Rheumatica

Reactive Arthritis

Systemic Lupus Erythematosus

References:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1079236/
http://emedicine.medscape.com/article/216650-differential

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