CHF in English

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FOREWORD

First of all, lets thanks to Allah SWT, who has given us mercies and blessings,

the writer can finish this papers work which is about Congestive Heart Failure

(CHF) it purposes to complate english assignment that is given by lecturer.

Then a successive salawat not forget to send us to our great Prophet Muhamad

SAW, which has brought us from nature without the knowledge of the natural with

full knowledge of all powerful. So that spur us to further achievement in our lives.

The writer also wishes to say gratitude to Miss. Arma as the lecturer of english

who has guided, and given me an oppurtunity to make and to complate thisassignment. Writer realizes a lot of deficiencies in the writing of this paper. Criticism

and suggestions that are built, the author is expected for perfection this paper.

Jakarta, 26 April 2012

The writer

Groups of 1

iii

CONTENTS


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FOREWORD....iii

CONTENTS...iv

CHAPTER I INTODUCTION

A. Background.1B. The Purpose.1

1. General Purpose...12. Spesific Purpose...2

C. Plane of Problem.2D. Methode Of Writing2E. The Scope2F. Systemic Of Writing....2

CHAPTER II BASIC OF THEORY AND NURSING CARE

A. The Heart.4B. Heart Failure5C. Classifications.6D. Symptoms8E. Etiology...9F. Pathopysiology..11G. Pathoflow...18H. Test20I. Treatment...21J. Heart Failure Management21K. Congestive Heart Failure Intervension..23L. Complication of Heart Failure...24M.Physical examination.25

N.Nursing Care1. Patient Assessment Data Base.25

iv

2. Discharge plan.................................................................................................273. Diagnosis And Intervention.28

CHAPTER III CASE REPORT


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A. Case Report...44B. Fokus Data47C. Data Analysis....47D. Intervension...49E. Implementasion.49F. Evaluasion.52

CHAPTER IV CLOSING

A. Conclusion..53B. Suggestion..53

REFFERENCE54

v


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CHAPTER I

INTRODUCTION

A. BACKGROUNDCongestive Heart Failure (CHF) today is the only cardiovascular disease that has

increasing incidence and prevalence.Risk of death from heart failure ranged from 5-10% per

year in mild heart failure which will rise to 30-40% in severe heart failure. In addition, heart

failure is a disease that most often need a repeated treatment in the hospital (readmission)

although outpatient treatment has been given an optimal.

Congestive heart failure (CHF) is a complex clinical syndrome that can result from any

functional or structural cardiac disorder that impairs the ventricles ability to fill with or eject

blood. Since there is no definitive diagnostic test for heart failure, it remains a clinical

diagnosis that is largely based on a careful history and physical examination and supported by

ancillary tests such as chest radiograph, electrocardiogram, and echocardiography. The

diagnosis of heart failure is often determined by a careful history and physical examination

and characteristic chest radiograph findings.

Heart failure is a common disease, affecting approximately 5 million people in the United

States, and it occurs predominately in the elderly, with almost 80% of cases occurring in

patients over the age of 65. According to the research, the majority of elderly Heart Failure is

diagnosed can not live more than 5 years (Ebbersole, Hess, 1998).

With the background backs on these issues, the paper is made to find out more what it is

heart failure, how to handle it, until the nursing care to patient of heart failure.

B. THE PURPOSE1. General Purpose

The general purpose of this papers is aim to able to understand the definition, etiology,

classification, pathophysiology, diagnostic examination, treatment, and nursing care to

clients with congestive heart failure (CHF).


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2. Spesific PurposeSpesific purpose is of this papers is aim to :

a. Explain the definition of Congestive Heart failureb. Mention and explain the etiologyc. Mention the symptoms from Congestive Heart Failured. Explain the pathophysiology from congestive Heart Failuree. Mention the complication from Congestive Heart Failure

C. PLANE OF PROBLEM1. What is the definition of Congestive Heart Failure ?2. What is the etiology of Congestive heart failure ?3. What is the symptom of Congestive Heart Failure ?4. How is the pathophysiology of Congestive Heart Failure ?5. What is the treatment of Congestive Heart Failure ?6. What is the test of Congestive Heart Failure?7. What is the complication of Congestive Heart Failure?

D. METHODE OF WRITINGIn the writing of this paper we use books and internet as the source.

E. THE SCOPEThe scope of this paper is family and all the students. Students can explain the definition

of CHF, CHF etiology, pathophysiology of CHF, clinical manifestations of CHF, Medical

Management and Nursing Care should be given to clients with CHF.

F. SYSTEMIC OF WRITINGIn this papers, we used the systemic of write like this:

CHAPTER I INTODUCTION

G. BackgroundH. The Purpose


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3. General Purpose4. Spesific Purpose

I. Plane of ProblemJ. Methode Of WritingK. The ScopeL. Systemic Of WritingCHAPTER II BASIC OF THEORY AND NURSING CARE

O. The HeartP. Heart FailureQ. ClassificationsR. SymptomsS. EtiologyT. PathopysiologyU. PathoflowV. TestW.TreatmentX. Heart Failure ManagementY. Congestive Heart Failure IntervensionZ. Complication of Heart FailureAA. Physical examinationCHAPTER III CASE REPORT

G. Case ReportH. Fokus DataI. Data AnalysisJ. IntervensionK. ImplementasionL. EvaluasionCHAPTER IV CLOSING

C. CONCLUSIOND. SUGGESTION


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CHAPTER II

BASIC OF THEORY AND NURSING CARE

A. THE HEARTThe heart is responsible for pumping blood to all the organs in the body. It is highly

specialized muscle that is expected to work continously, without rest, for a lifetime. The heart

has aright and a left side. Each side has 2 chambers : the atrium and the ventricle. Special

valves divide the chambers and prevent blood from flowing backward.

Blood loaded with oxygen comes from the lungs and enters the left atrium. It stays there

until the mitral valve opens up and the atrium contracts. This forces the blood into the left

ventricle. The blood is then pumped to the rest of the body through the aortic valve into the

biggest blood vessel of the body, the aorta.

After the blood comes back from circulating through the body, it goes into the right

atrium. From there, it is pumped into the right ventricle through the tricuspid valve and then

to the lung through the pulmonic valve. In the lung, the blood picks up oxygen and returns to

the left atrium, where the whole cycle starts again. The heart needs a continous supply of


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oxygen and sugar to be able to function. Oxygen-rich blood is delivered to the heart through

the coronary arteries. These arteries branch off from the aorta.

B. HEART FAILURE

Heart failure is a condition where the heart is not able to pump blood to the rest of the

body at a normal rate. When the heart cannot pump all the blood it receives, excess fluidcould back up into the lungs and other parts of the body. The lack of blood being supplied to

the body in addition to the buildup of fluids causes symptoms of heart failure. When fluids

collect in the lungs, it is called congestion. That is why this disease is called congestive heart

failure.

There are 2 mechanisms of reduced cardiac output and heart failure: systolic dysfunction

and diastolic dysfunction.The most common causes of systolic dysfunction(defined by a left-

ventricular ejection fraction of_50%) are ischemic heart disease, idiopathic dilated

cardiomyopathy, hypertension, and valvular heart disease. Diastolic dysfunction (defined as

dysfunction of left-ventricular filling with preserved systolic function) may occur in up to 40

50% of patients with heart failure, it is more prevalent in women, and it increases in

frequency with each decade of life. Diastolic dysfunction can occur in many of the same

conditions that lead to systolic dysfunction. The most common causes are hypertension,

ischemic heart disease, hypertrophic cardiomyopathy, and restrictive cardiomyopathy. Many

patients who have symptoms suggestive of heart failure (shortness of breath, peripheraledema, paroxysmal nocturnal dyspnea) but also have preserved leftventricular function may


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not have diastolic dysfunction; instead, their symptoms are caused by other etiologies, such as

lung disease, obesity, or occult coronary ischemia.

There are several levels of congestive heart failure :

a. Mildb. Averagec. Severed. Very severeEach level may limit a persons activities more and more. With very severe heart failure, a

person may be short of breath or feel fatigued even at rest.

C. CLASSIFICATIONSThe New York Heart Association developed a system that has been used for many years

to provide a standardized set of criteria for the classification of heart failure based on the

severity of the condition. This is evaluated by symptoms and ability to function.

1. Class I: no undue symptoms associated with ordinary activity and no limitation ofphysical activity

2. Class II: slight limitation of physical activity; patient comfortable at rest3. Class III: marked limitation of physical activity; patient comfortable at rest4. Class IV: inability to carry on any physical activity without discomfort; symptoms of

cardiac insufficiency or chest pain possible even at rest.

Ef fects of Heart Failu re

1. Strength of muscle contractions is reduced.2.

Ability of the heart chambers to fill with blood is limited, so there is less blood to

pump out to tissues in the body.

3. The pumping heart chambers fill with too much blood; the the heart muscle is notstrong enough to pump out all the blood it receives.


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LEFT-SIDED AND RIGHT-SIDED HEART FAILURE

Heart failure can affect the left, right, or both

sides of the heart. The heart is made up of four

chambers. The leftatrium and the right atrium on

top mainly collect the blood, and the left ventricle

and right ventricle on the bottom pump the blood.

The right side of the heart receives oxygen-

depleted or used blood from the body and

pumps it to the lungs to be replenished with

oxygen. The left side receives oxygen-rich blood from the lungs and pumps it to the rest of

the body.

Left-sided heart failure is the most

common type of heart failure.1 The left

ventricle on the lower left side of the heart is

the main pumping chamber. When it fails,

oxygen-rich blood is not pumped to the rest of

the body; instead, it can back up into the left

atrium and into the lungs, where it builds up.

Left-sided heart failure causes fatigue because

the body is not receiving enough blood and

shortness of breath because of the buildup of

fluid (congestion) in the lungs.

Right-sided heart failure usually happens as a result of left-sided heart failure. As the

failing left ventricle causes blood to build up in the lungs, the right ventricle finds it harder

and harder to pump blood to the lungs to pick up oxygen. Less commonly, right-sided heart

failure can also occur on its own, for example, when caused by lung disease (such as

emphysema) or heart valve problems. Right-sided heart failure can cause blood to back up in

theveins,resulting in swelling in the legs, ankles or belly, and can lead to shortness of breath

when the belly is enlarged. Right-sided heart failure can also cause fatigue when the left
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ventricle doesn't fill with enough blood and can't supply the body with enough oxygen-rich

blood.

D. SYMPTOMSa. Shortness of breath (dyspnea)b. Shortness of breath when lying down (orthopnea)c. Shortness of breath while sleeping (paroxysmal or intermittent nocturnal dyspnea)d. Buildup of fluid in the lungs (pulmonary edema), frequently causing a person to

cough up blood-tinged sputum

e. Buildup of excess fluid (edema) in other parts of the body, causing weight gain,swelling of the ankles, legs, and back, and in extreme cases fluid accumulation in

the abdomen (ascites)f. Fatigue, weakness, and an inability to exert oneself physically or mentallyg. Blueness of the skin (cyanosis)

1. Symptoms of left-side heart failurea. Fatigue

b. Shortness of breath (dyspnea)c. Shortness of breath when lying down (othopnea)d. Paroxysmal (intermittent) nocturnal dyspneae. Accumulation of fluid in the lungs (pulmonaryedema), frequently causing a person

to cough up blood-tinged sputum

2. Symptoms of right-side heart failurea. Swelling (edema)

b. Dependent edema (edema that travels by gravity to the lowest portions of thebody)

c. Enlargement or swelling of the liver (hepatomegaly)d. Buildup of fluid in the abdominal cavity (ascites)e. Edema of the skin and soft tissues, causing swelling of the feet, ankles, and legsf. Excessive urination at night caused by fluid redistribution while a person is

sleeping lying down (nocturia)


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E. ETIOLOGYCongestive heart failure (CHF) is a syndrome that can be brought about by several causes.

Congestive heart failure is a weakening of the heart caused by an underlying heart or blood

vessel problem, or a combination of several different problems, including the following:

1. Weakened heart muscle (cardiomyopathy)2. Damaged heart valves3. Blocked blood vessels supplying the heart muscle (coronary arteries), which may lead

to a heart attack (This is known as ischemic cardiomyopathy. If there are other,

noncoronary causes, these are collectively termed nonischemic cardiomyopathy.)

4. Toxic exposures, such as alcohol or cocaine5. Infections, commonly viruses, which for unknown reasons affect the heart in only

certain individuals

6. High blood pressure that results in thickening of the heart muscle (left ventricularhypertrophy)

7. Congenital heart diseases8. Certain genetic diseases involving the heart9. Prolonged, serious arrhythmias10.

A variety of less common disorders in which the heart muscle is infiltrated by adisease process.

11.Heart failure can happen at any age, but it is more common in older people. As weage, our heart becomes a little weaker and the blood vessels get narrower.

12.Heart valve disease can also cause heart failure. The blood may leak back through adefective valve, causing the heart to work harder and blood and fluids to collect in the

lungs

13.Hypertension, or high blood pressure, increases the workload of the heart over time.This can lead to heart failure, as well.

14.Coronary artery disease can cause heart failure. Coronary artery disease developswhen fatty materials deposit in the coronary arteries. This causes the blood vessels of

the heart to become narrow and clogged.

15.Heart attacks may cause heart failure. Because part of the heart muscle is damaged ina heart attack, the heart pumps less effectively, which in turn may lead to congestive

heart failure.

16.In some cases, the heart gets infected or infalmed; this causes it to weaken, a conditioncalled cardiomyopathy. This may also result in congestive heart failure.
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17.Other causes of heart failure include :a. Diabetes

b. Cancer treatment, radiation and some chemotherapy drugsc. Thyroid diseases, too much or too little thyroid hormonesd. Alcohol abuse.

There are over a hundred other less common causes of heart failure, which include a

variety of infections, exposures (such as radiation or chemotherapy), endocrine disorders

(including thyroid disorders), complications of other diseases, toxic effects, and genetic

predisposition. However, the cause of congestive heart failure is often idiopathic, or unknown.

People who have diabetes are at increased risk for both ischemic and nonischemic heart

failure. Congestive heart failure may be exacerbated by the following lifestyle habits:

1. Unhealthy habits, such assmoking and excessive use of alcohol2. Obesity and lack ofexercise (May contribute to congestive heart failure, either directly

or indirectly through accompanying high blood pressure, diabetes, and coronary artery

disease.)

3. High salt intake, which may cause more fluid retention4. Noncompliance with medications and other therapies

Whether through disease and/or complicating lifestyle choices, the pumping action of the

heart can be impaired by several physiologic mechanisms:

1. Direct heart muscle damage (cardiomyopathy):The heart muscle can become weakbecause of damage or disease and thus does not contract or squeeze as forcefully as it

should. This damage to the muscle can occur from any of the diseases mentioned

above, but sometimes, the cause is unknown.2. Damage to heart muscle due to blockage: When the coronary blood supply is

blocked, this results in a heart attack (myocardial infarction). A heart attack commonly

causes severe pain in the chest, shortness of breath, nausea, sweating, and/or a feeling

of impending doom. A heart attack may rapidly lead to either cardiac arrest (no

heartbeat) or permanent damage to the left ventricle. If this damage is bad enough, that

part of the heart will not work properly, which leads to heart failure. Prompt

(emergency) medical attention is critical for all heart attacks.
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3. High blood pressure (hypertension):Abnormally high blood pressure increases theamount of work the left ventricle has to do to pump blood out to the circulatory

system. Over time, this greater workload can damage and weaken the heart, leading to

heart failure. Proper treatment of high blood pressure can prevent left ventricular

failure.

4. Heart valve problems:The valves of the heart normally keep the blood flowing inthe proper direction through the heart. Abnormal heart valves impede this forward

flow in one of two ways:

a. An incompetent valve is a valve that does not close properly when it should andallows blood to flow backward in the heart, "against the current." When blood

flows the wrong way across a valve, the heart has to work harder to keep up its

output. Eventually, this backed up blood accumulates in the lungs and the bodyand the heart muscle weakens.

b. A stenotic valve is a valve that does not open properly. Blood flow through thenarrowed opening is blocked, creating an increased workload on the heart that can

also lead to heart failure.

5. Abnormal rhythm or irregular heartbeat:Abnormal heart rhythms can lower theheart's effectiveness as a pump. The rhythm may be too slow or too fast, or irregular.

The heart has to pump harder to overcome these rhythm disorders. If this excessively

slow or fast heartbeat is sustained over hours, days, or weeks, the heart can weaken,

which may lead to heart failure.

F. PATHOPHYSIOLOGYHeart failure is caused by any condition which reduces the efficiency of the myocardium,

or heart muscle, through damage or overloading. As such, it can be caused by as diverse an

array of conditions as myocardial infarction (in which the heart muscle is starved of oxygen

and dies), hypertension (which increases the force of contraction needed to pump blood) and

amyloidosis (in which protein is deposited in the heart muscle, causing it to stiffen). Over

time these increases in workload will produce changes to the heart itself:

1. Reduced contractility, or force of contraction, due to overloading of the ventricle. Inhealth, increased filling of the ventricle results in increased contractility (by the Frank-

Starling law of the heart) and thus a rise in cardiac output. In heart failure this

mechanism fails, as the ventricle is loaded with blood to the point where heart muscle
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contraction becomes less efficient. This is due to reduced ability to cross-link actin

and myosin filaments in over-stretched heart muscle.

2. A reducedstroke volume, as a result of a failure of systole, diastole or both. Increasedend systolic volume is usually caused by reduced contractility. Decreased end diastolic

volume results from impaired ventricular filling as occurs when the compliance of

the ventricle falls (i.e. when the walls stiffen).

3. Reduced spare capacity. As the heart works harder to meet normal metabolicdemands, the amount cardiac output can increase in times of increased oxygen demand

(e.g. exercise) is reduced. This contributes to the exercise intolerance commonly seen

in heart failure. This translates to the loss of one's cardiac reserve. The cardiac reserve

refers to the ability of the heart to work harder during exercise or strenuous activity.

Since the heart has to work harder to meet the normal metabolic demands, it isincapable of meeting the metabolic demands of the body during exercise.

4. Increasedheart rate,stimulated by increased sympathetic activity in order to maintaincardiac output. Initially, this helps compensate for heart failure by maintaining blood

pressure and perfusion, but places further strain on the myocardium, increasing

coronary perfusion requirements, which can lead to worsening of ischemic heart

disease. Sympathetic activity may also cause potentially fatal arrhythmias.

5. Hypertrophy (an increase in physical size) of the myocardium, caused by theterminally differentiated heart muscle fibres increasing in size in an attempt to

improve contractility. This may contribute to the increased stiffness and decreased

ability to relax during diastole.

6. Enlargement of the ventricles, contributing to the enlargement and spherical shape ofthe failing heart. The increase in ventricular volume also causes a reduction in stroke

volume due to mechanical and contractile inefficiency.

The general effect is one of reduced cardiac output and increased strain on the heart. This

increases the risk ofcardiac arrest (specifically due to ventricular dysrhythmias), and reduces

blood supply to the rest of the body. In chronic disease the reduced cardiac output causes a

number of changes in the rest of the body, some of which are physiological compensations,

some of which are part of the disease process:

1. Arterial blood pressure falls. This destimulates baroreceptors in the carotid sinus andaortic arch which link to the nucleus tractus solitarius. This center in the brain

increases sympathetic activity, releasing catecholamines into the blood stream.
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Binding to alpha-1 receptors results in systemic arterial vasoconstriction. This helps

restore blood pressure but also increases the total peripheral resistance, increasing the

workload of the heart. Binding to beta-1 receptors in the myocardium increases the

heart rate and make contractions more forceful, in an attempt to increase cardiac

output. This also, however, increases the amount of work the heart has to perform.

2. Increased sympathetic stimulation also causes thehypothalamus to secrete vasopressin(also known as antidiuretic hormone or ADH), which causes fluid retention at the

kidneys. This increases the blood volume and blood pressure.

3. Reduced perfusion (blood flow) to the kidneys stimulates the release of renin anenzyme which catalyses the production of the potent vasopressor angiotensin.

Angiotensin and itsmetabolites cause further vasocontriction, and stimulate increased

secretion of the steroid aldosterone from the adrenal glands.This promotes salt andfluid retention at the kidneys, also increasing the blood volume.

4. The chronically high levels of circulating neuroendocrine hormones such ascatecholamines, renin, angiotensin, and aldosterone affects the myocardium directly,

causing structural remodelling of the heart over the long term. Many of these

remodelling effects seem to be mediated by transforming growth factor beta (TGF-

beta), which is a common downstream target of the signal transduction cascade

initiated by catecholamines and angiotensin II, and also by epidermal growth factor

(EGF), which is a target of the signaling pathway activated by aldosterone

5. Reduced perfusion of skeletal muscle causes atrophy of the muscle fibres. This canresult in weakness, increased fatigueability and decreased peak strength - all

contributing to exercise intolerance.

The increased peripheral resistance and greater blood volume place further strain on the

heart and accelerates the process of damage to the myocardium. Vasoconstriction and fluid

retention produce an increased hydrostatic pressure in the capillaries. This shifts of the

balance of forces in favour of interstitial fluid formation as the increased pressure forces

additional fluid out of the blood, into the tissue. This results inedema (fluid build-up) in the

tissues. In right-sided heart failure this commonly starts in the ankles where venous pressure

is high due to the effects of gravity (although if the patient is bed-ridden, fluid accumulation

may begin in the sacral region.) It may also occur in the abdominal cavity, where the fluid

build-up is called ascites. In left-sided heart failure edema can occur in the lungs - this is

called cardiogenic pulmonary oedema. This reduces spare capacity for ventilation, causesstiffening of the lungs and reduces the efficiency of gas exchange by increasing the distance
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Systolic dysfunction

Heart failure caused by systolic dysfunction is more readily recognized. It can be

simplistically described as failure of the pump function of the heart. It is characterized by a

decreased ejection fraction (less than 45%). The strength of ventricular contraction is

attenuated and inadequate for creating an adequate stroke volume, resulting in inadequate

cardiac output. In general, this is caused by dysfunction or destruction of cardiac myocytes or

their molecular components. In congenital diseases such as Duchennemuscular dystrophy,the

molecular structure of individual myocytes is affected. Myocytes and their components can be

damaged by inflammation (such as inmyocarditis)or by infiltration (such as in amyloidosis).

Toxins and pharmacological agents (such as ethanol, cocaine, and amphetamines) causeintracellular damage and oxidative stress. The most common mechanism of damage is

ischemia causing infarction and scar formation. After myocardial infarction, dead myocytes

are replaced by scar tissue, deleteriously affecting the function of the myocardium. On

echocardiogram, this is manifest by abnormal or absent wall motion.

Because the ventricle is inadequately emptied, ventricular end-diastolic pressure and

volumes increase. This is transmitted to the atrium. On the left side of the heart, the increased

pressure is transmitted to the pulmonary vasculature, and the resultant hydrostatic pressure

favors extravassation of fluid into the lung parenchyma, causing pulmonary edema. On the
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right side of the heart, the increased pressure is transmitted to the systemic venous circulation

and systemic capillary beds, favoring extravassation of fluid into the tissues of target organs

and extremities, resulting in dependent peripheraledema.

Diastolic dysfunction

Heart failure caused by diastolic dysfunction is generally described as the failure of the

ventricle to adequately relax and typically denotes a stiffer ventricular wall. This causes

inadequate filling of the ventricle, and therefore results in an inadequate stroke volume. The

failure of ventricular relaxation also results in elevated end-diastolic pressures, and the end

result is identical to the case of systolic dysfunction (pulmonary edema in left heart failure,

peripheral edema in right heart failure.)

Diastolic dysfunction can be caused by processes similar to those that cause systolic

dysfunction, particularly causes that affect cardiac remodeling.

Diastolic dysfunction may not manifest itself except in physiologic extremes if systolic

function is preserved. The patient may be completely asymptomatic at rest. However, they are

exquisitely sensitive to increases in heart rate, and sudden bouts of tachycardia (which can be

caused simply by physiological responses to exertion, fever, or dehydration, or by

pathological tachyarrhythmias such asatrial fibrillation with rapid ventricular response) may

result in flash pulmonary edema. Adequate rate control (usually with a pharmacological agent

that slows down AV conduction such as a calcium channel blocker or a beta-blocker) is

therefore key to preventing decompensation.

Left ventricular diastolic function can be determined through echocardiography by

measurement of various parameters such as the E/A ratio (early-to-atrial left ventricular filling

ratio), the E (early left ventricular filling) deceleration time, and the isovolumic relaxationtime.
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G. PATHOFLOWNon modifiable factors : modifiable factor :

Increase in age 55 years old in above sedentary lifestyle Gender

Decreased elasticity of blood and formation of plaques on blood vessels

Narrowing of the blood vessels

Necrosis and scarring of the vascular endothelium

Im ediment of blood flow to the bod

Increased work load of the heart

Dilatation of ventricles

Increased in reload

Increased stretchin of m ocardial muscle

Excessive stretchin of m ocardial muscle

Ineffective cardiac muscle contraction

Decreased contraction of cardiac muscle

Activation of neurohormonal pathways in order to increase circulating blood

Continued neurohormonal stimulation

Cardiac remodeling

Decreased blood filling


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H. TEST1. Laboratory tests. Low serum sodium is common (dilutional hyponatremia from

expansion of extracellular fluid volume) and predictive of poor outcome; elevated

creatinine and liver function tests also are predictors of poor outcome.

2. Chest radiograph. Finding of increased pulmonary capillary pressure are seen inapproximately 50% of patients; bilateral pleural effusion and cardiomegaly also may

be present.

3. Electrocardiography (ECG). Q waves and left bundle branch block are good predictorsof systolic dysfunction. A wide QRS (more than 220 milliseconds) is predictive of

increased mortality.

4. Echocardiogram. A simple and useful tool, echocardiography can help determinesystolic versus diastolic dysfunction and left and/or right ventricular impairment.

5. Six minute walk test. Short distance correlates with higher mortality and increasedHF-related hospitalizations

6. Metabolic stress testing. Used to measure oxygen consumption; a peak oxygenconsumption of less than 12 to 14 mL/kg/min portends a poor prognosis.


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7. Endomyocardial biopsy. Biopsy may be useful in selected cases, such as suspectedamyloidosis, sarcoidosis, and giant cell myocarditis.

I. TREATMENTAcute

1. Nitrates. Nitrates are given sublingually or intravenously in cases in which preloadreduction is necessary. In the case of severe HF, nitroprusside administration should

be considered if both PCWP systemic vascular resistance (SVR) are elevated

2. Nesiritide. This from of human B-type natriuretic peptide causes vasodilation andincrease renal blood flow and urine output and has resulted in rapid symptomatic and

hemodynamic improvement in patiens with acutely decompenseted HF.

3.

Diuretics. Furosemide, 20 to 200 mg, is administered intravenously to alleviate lungedema due to volume overload, again by reducung preload. Addition of a thiazide (e.g

metolazone or chlorothiazide) may help potentiate diuresis. In cases of massive fluid

overload that spon poorly to diuretics, ultrafiltration may be effective.

4. Inotropic agents. No single agent has been found to be clinically superior, butadrenegric agents (such as dobutamine and dopamin and the phosphodiesterase

inhibitor, milrinone) each may have a role in certain hemodynamic states. Dopamin

may be preferable in those with low blood pressure because dobutamine reduces SVR

to a greater extent. (evidence based cardiology, peter J sharis,2003, lippincot william

and wilkins, philadelphia, USA).

J. HEART FAILURE MANAGEMENTTreatment focuses on improving the symptoms and preventing the progression of the

disease. Reversible causes of the heart failure also need to be addressed: (e.g. infection,

alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, hypertension). Treatments includelifestyle and pharmacological modalities.
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Acute decompensation

In acute decompensated heart failure (ADHF), the immediate goal is to re-establish

adequate perfusion and oxygen delivery to end organs. This entails ensuring that airway,

breathing, and circulation are adequate. Immediated treatments usually involve some

combination of vasodilators such as nitroglycerin,diuretics such as furosemide, and possibly

non invasive positive pressure ventilation (NIPPV).

Chronic management

The goal is to prevent the development of acute decompensated heart failure, to counteract

the deleterious effects of cardiac remodeling, and to minimize the symptoms that the patient

suffers. In addition to pharmacologic agents (oral loop diuretics, beta-blockers, ACE

inhibitors or angiotensin receptor blockers, vasodilators, and in severe cardiomyopathy

aldosterone receptor antagonists), behavioral modification should be pursued, specifically

with regards to dietary guidelines regarding salt and fluid intake. Exercise should be

encouraged as tolerated, as sufficient conditioning can significantly improve quality-of-life.

In patients with severe cardiomyopathy, implantation of an automatic implantable

cardioverterdefibrillator(AICD) should be considered. A select population will also probably

benefit from ventricular resynchronization. In select cases, cardiac transplantation can be

considered. While this may resolve the problems associated with heart failure, the patient

generally must remain on an immunosuppressive regimen to prevent rejection, which has its

own significant downsides.

Palliative care and hospice

Without transplantation, heart failure caused by ischemic heart disease is not reversible,

and cardiac function typically deteriorates with time. (In particular, diastolic function worsensas a function of age even in individuals without ischemic heart disease.) The growing number

of patients with Stage Dheart failure (intractable symptoms of fatigue, shortness of breath or

chest pain at rest despite optimal medical therapy) should be considered forpalliative care or

hospice, according to American College of Cardiology/American Heart Association

guidelines.
http://www.news-medical.net/health/Diuretic-What-is-a-Diuretic.aspxhttp://www.news-medical.net/health/What-are-Beta-Blockers-Used-for.aspxhttp://www.news-medical.net/health/ACE-Inhibitors-What-are-ACE-Inhibitors.aspxhttp://www.news-medical.net/health/ACE-Inhibitors-What-are-ACE-Inhibitors.aspxhttp://www.news-medical.net/health/What-is-Cardiomyopathy.aspxhttp://www.news-medical.net/health/Defibrillator-What-is-a-Defibrillator.aspxhttp://www.news-medical.net/health/Heart-Failure.aspxhttp://www.news-medical.net/health/Palliative-Care-What-is-Palliative-Care.aspxhttp://www.news-medical.net/health/Cardiology-What-is-Cardiology.aspxhttp://www.news-medical.net/health/Cardiology-What-is-Cardiology.aspxhttp://www.news-medical.net/health/Palliative-Care-What-is-Palliative-Care.aspxhttp://www.news-medical.net/health/Heart-Failure.aspxhttp://www.news-medical.net/health/Defibrillator-What-is-a-Defibrillator.aspxhttp://www.news-medical.net/health/What-is-Cardiomyopathy.aspxhttp://www.news-medical.net/health/ACE-Inhibitors-What-are-ACE-Inhibitors.aspxhttp://www.news-medical.net/health/ACE-Inhibitors-What-are-ACE-Inhibitors.aspxhttp://www.news-medical.net/health/What-are-Beta-Blockers-Used-for.aspxhttp://www.news-medical.net/health/Diuretic-What-is-a-Diuretic.aspx


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since these patients are at higher risk for serious ventricular arrhythmias. In these

circumstances, an ICD may be implanted as part of a pacemaker device. This

defibrillator can detect and electrically shock a life-threatening arrhythmia back to

normal.

Cardiac Resynchronization Therapy (CRT):This involves a biventricular pacemaker

that is used to synchronize the pumping action of the left and right ventricles. Synchronization

improves the effectiveness of the heart as a pump, since with heart failure the pumping action

is sometimes uncoordinated.

1. One pacer lead is placed in a coronary vein on the back side of the heart, overlying theleft ventricle. The other pacer is placed in the usual right ventricular position. This

improves the coordination of contraction between the left and right ventricle,

especially if the patient has left bundle branch block (LBBB). In LBBB, the electrical

signal to the left ventricle is delayed.

2. Biventricular pacing has been shown to improve exercise capacity, preventprogression of heart failure symptoms, and prolong life in certain patients.

3. Cardiac resynchronization therapy is frequently combined with an ICD to shock aperson out of life-threatening arrhythmias, such as ventricular tachycardia or

ventricular fibrillation. The worse the function of the left ventricle, the higher the risk

for sudden death secondary to these arrhythmias.

Temporary Cardiac Support: An intra-aortic balloon pump is used as a temporary

support of left ventricle function, such as in a large heart attack, waiting for the heart to

recover. There are other similar devices that can be used to temporarily support the heart if

there is something that can be done for the underlying heart failure.

L. COMPLICATIONS OF HEART FAILURECongestive heart failure is caused by circulatory congestion myocardium dysfunction.

Place of congestion depends on the involved ventricle. Left ventricular dysfunction or heart

failure, left, causing congestion in the pulmonary vein, whereas right ventricular dysfunction

or right heart failure resulting in systemic venous congestion. Failure in both ventricles called

biventricular failure. Left heart failure is a mechanical complication of the most common after

myocardial myocardium,


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M.PHYSICAL EXAMINATION

N. NURSING CARE1. PATIENT ASSESSMENT DATA BASE

a. ACTIVITY/REST1)May report: Fatigue/exhaustion progressing throughout the day, Insomnia,

Chest pain with activity, Dyspnea at rest or with exertion

2)May exhibit: restlessness, mental status changes, e.g., lethargy, Vital signchanges with activity.

b. CIRCULATION1)May report: History of hypertension, recent/acute multiple Mls, previous

episodes of CHF, valvular heart disease, cardiac surgery, endocarditis, SLE,

anemia, septic shock. Swelling of feet, legs, abdomen, belt too tight (right-

sided failure).

2)May exhibit: BP: May be low (pump failure); normal (mild chronic CHF); orhigh (fluid overload/increased SVR). Pulse pressure: May be narrow, reflectingreduced stroke volume. Heart rate: Tachycardia (left-sided failure). Heart


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rhytm: Dysrhytmias; e.g., atrial fibrillation, premature ventricular

contractions/tachycardia, heart blocks. Apical pulse: PMI msy be diffuse and

displaced inferiorly to the left. Heart sounds: S3 (gallop) is diagnostic; S4 may

occur; S1 and S2 may be softened.

Systolic and diastolic murmur may indicate the presence of valvular stenosis or

insufficiency. Pulse : Peripheral pulses diminished; alteration in strength of

beat may be noted; central pulses may be bounding, e.g., visible jugular,

carotid, abdominal pulsations.

Color: Ashen, pale, dusky, cyanotic. Nailbeds: Pale or cyanotic with slow

capillary refill. Liver: Enlarged/palpable, positive hepatojugular reflex. Breath

sound: Crackles, ronchi. Edema: May be dependent, genelized, or pitting,

especially in extremities; JVD.c. EGO INTEGRITY

1)May report: Anxiety, apprehension, fear. Stress related to illness/financialconcerns (job/cost of medical care).

2)May exhibit: Various behavioral manifestations, e.g., anxiety, anger, fearful,irritable.

d. ELIMINATION1)May report: Decreased voiding, dark urine Night voiding (nocturia).

Diarrhea/constipation.

e. FOOD/FLUID1)May report: Loss of appetite. Nausea/vomiting. Significant weight gain.

Lower extremity swelling. Tight clothing/shoes. Diet high in salt/processed

foods, fat, sugar, and caffeine. Use of diuretics.

2)May exhibit: Rapid weight gain. Abdominal distention (ascites); edema(general, dependent, brawn, pitting).

f. HYGIENE1)May report: Fatigue/weakness, exhaustion during self-care activities.2)May exhibit: Appearance indicative of neglect of personal care.

g. NEUROSENSORY1)May report: Weakness, dizziness, fainting episodes.2)May exhibit: Lethargy, confusion, disorientation. Behavior changes,

irritability.


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h. PAIN/ DISCOMFORT1) May report: Chest Pain, chronic or acute angina. Right upper abdominal

pain (RVF). Muscle aches.

2) May exhibit: Nervousness, restlessness.. Narrowed focus (withdrawal)i. RESPIRATION

1) May report: Dyspnea on exertion, sleeping sitting up, or with severalpillows. Cough with/ without sputum production. History of chronic lung

disease. Use of respiratory aids, e.g., oxygen or medications.

2) My exhibit: Respiration: Tachypnea; shallow, labored breathing; use ofaccessory muscles, nasal flaring. Cough: Dry/ hacking/ nonproductive or may

be gurgling with/ without sputum production. Sputum: may be blood-tinged,

pink/ frothy (pulmonary edema). Breath sounds: may be diminished, withbibasilar crackles and wheezes. Mentation: may be diminished; lethargy;

restlessness. Color: pallor or cyanosis.

j. SAFETY1) May exhibit: Changes in mention. Loss of strength/ muscle tone. Skin

excoriations.

k. SOCIAL INTERACTION1) May report: Decreased participation in usual social activities.

l. TEACHING/ LEARNING1) Mar report: Use/ misuse of cardiac medication, e.g.; -blockers, calcium

channel blockers. Recent/ recurrent hospitalizations.

2) May exhibit: evidence of failure to improve.

2. Discharge planConsiderations: DRG projected mean length of stay: 8.2 days

a. Assistance with shopping, transportation, self-care needs, homemaker/maintenance tasks.

b. Alteration in medication use/ therapy.c. Changes in physical layout of home.


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Rationale: s and may be weak because of diminished pumping

action. Gallop rhythms are common and ), produced as blood flows

into noncompliant / distended chambers. Murmurs may reflect valvular

incompetence / stenosis.

c) Palpate peripheral pulsesRationale : decreased cardiac output may be reflected in diminished radial,

popliteal, dorsalis pedis, and posttibial pulses. Pulses may be fleeting or

irregular to palpitation, and pulsus alternans (strong beat alternating with

weak beat) may be present.

d) Monitor BPRationale: in early, moderate, or chronic CHF, BP may be elevated due to

increased SVR. In advanced CHF, the body may no longer be able tocompensate, and profound / irrefersible hypotension may occur.

e) Inspect skin for pallor, cyanosisRationale: pallor is indicative of diminished peripheral Perfusion

secondary to inadequate cardiac output, vasoconstriction, and anemia.

Cyanosis may develop min refractory CHF. Dependend areas are often

blue or mottled as venous congestion increases.

f) Monitor urine output, nothing decreasing output and dark / concentratedurine.

Rationale:, kidneys respond to reduced cardiac output by retaining water

and sodium. Urine output is usually decreased during the day because of

fluid shifts into tissues but may be increased at night as fluid returns to

circulation when patient is recumbent.

g) Assess changes in sensorium, e, g, lethargy, perfusion con-Fusion,disorientation, anxiety, and depression.

Rationale :may indicate inadequate cerebral perfusion secondary to

decreased cardiac output.

h) Provide rest semirecubent in bed chair. Assist with physical rest asindicated.

Rationale : physical rest should be maintained during acute Or refractory

CHF to improve efficiency of Cardiac contraction and to decrease

myocardial Oxygen demand / consumption and workload.


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i) Provide for psychologic rest by quit environment; Explaining medical /nursing management; helping patient avoid stressful situations, listening /

responding to expressions of feelings / fears.

Rationale :emotional stress produces vasoconstriction, which elevates BP

and increases heart rate / work.

j) Provide bedside commode. Have patient avoid Activities eliciting avalsalve response, e.g., Straining during defecation, holding breath During

position changes.

Rationale : commode use decreases work of getting to bathroom or

struggling to use bedpan.Valsalva maneuver causes vegal stimulation

followed by rebound tachycardia, which further compromises cardiac

function/output.k) Elevate legs, avoiding pressure under knee. Encourage active/passive

exercises. Increase ambulation/ activity as tolerated.

Rationale : Decreases venous stasis and may reduce incidence of

thrombus/embolus formation.

l) Check for calt tenderness, diminished pedal pulse Swelling . local redness,or pallor of extremity.

Rationale :reduced cardiac output, venous pooling/stasis and enforced

bedrest increases risk of trombohlebitis.

m)Withhold digitalis preparation and notify physician It marked changesoccur in cardiac rate or rhythm Or signs of digitalis toxicity occur.

Rationale : incidence of toxicity is high (20%) because of narrow

margin between therapeutic and Toxic ranges. Digoxin may have to be

disontinued in the presence of toxic drug levels, a slow heart rate or low

postassium level.

Collaborative

a) Administer supplemental oxgen by nasal can- uptake Nula/mask asindicated.

Rationale :increases avaible oxygen for myocardial To combat effects

of hypoxia/ ischemia.

b) Administer medications as indicated:Rationale :a variety of medications may be used to increase stroke

volume, improve contractility, and reduce congestion.


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1. diuretics, e.g., furosemide (lasix); ethacrynic acid (Edecrin);bumetanide (Bumex); supironolactone (Aldoctone)

Rationale :type and dosage of diuretic depends on degree of heart

failure and state of renal function. Preload reduction is most useful in

treating patients with a relatively normal cardiac output accompanied

by congestive symptoms. loop diuretics block chloride reabsorption,

thus interfering with the reabsorption of sodium and water.

2. vasodilators, e.g, nitrates (Nitro-Dur, Isordil);arteriodilators, e.g.,hydralazine (Apresoline); combination drugs, e.g., prazosin

(Minipress);;

Rationale :vasodilators are used to increase cardiac output, reducing

circulating volume (venodilators) and decreasing systemic vascularresistence (arteriodilators), thereby reducing ventricular workload.

3. digoxin (lanoxin);Rationale : increases force of myocardial contraction and slows heart

rate by decreasing conduction velocity and prolonging refractory period

of the AV junction to increase cardiac efficiency/output.

4. captopril (Capeton); lisinopril (prinvil); enalapril (vasotec);Rationale :ACE inhibitors may be used to control heart failure by

inhibiting angiotension conversion in the lungs and reduce

vasoconstriction, SVR, and BP.

5. Morphine sulfate;Rationale :decreases vascular resistance and venous return reducing

myocardial workload. Allays anxiety and breaks the feedback cycle of

anxiety/catecholamine release/anxiety.

6. Tranquilizers/sedatives;Rationale : promotes rest/relaxation reducing oxygen demand and

myocardial workload. note ; There is an ontrial oral analogue of

amrinone (inocor) a positive inotropic agent, called milrinone, which

may be suitable for longterm use.

7. Anticoagulants, e.g., low-dose heparin; warfarin (coumadin)Rationale :may be used prophylactically to prevent thrombus/emboli

formation in presence of risk factors such as venous stasis, enforced

bed rest, cardiac dysrhythmias, and history of previous thrombolic

episodes.


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c) Administer IV solutions, restricting total amount as indicated. Avoid salinesolutions

Rationale : because of existing elevated left ventricular pressure, patient

may not tolerate increased fluid volume (preload). CHF patients also

execrate less sodium, which cause fluid retention and increases myocardial

workload.

d) Monitor/replace electrolytes.Rationale :fluid shifts and use of diuretics can alter electrolytes (especially

potassium and chloride), which affect cardiac rhythm and contractility.

e) Monitor serial EGC and chest x-ray changesRationale : ST segment depression and T wave flattening can develop

because of increased myocardial oxygen demand, even if no coronaryartery disease is present. Chest x-ray may show enlarged heart and

changes of pulmonary congestion.

f) Monitor laboratory studies, e.g., BUN, creatinine;Rationale : Elevation of BUN/creatinine reflects kidney

hypoperfusion/failure.

1. liver function studies (AST, LDH);Rationale : AST/LDH may be elevated due to liver congestion and

indicate need for smaller dosages of medications that are detoxified by

the liver.

2. PT/APT/coagulation studies.Rationale :measure changes in coagulation processes or effectiveness

of anticoagulant therapy.

g) Prepare for insertion/maintain pacemaker, if indicated.Rationale :may be necessary to correct bradydysrhythmias unresponsive

to drug intervention, which can aggravate congestive failure/produce

pulmonary edema.

h) Prepare for surgery as indicated.Rationale :congestive failure due to ventricular aneurysm or valvular

dysfunction may require aneurysectomy or valve replacement to improve

myocardial contractility/function.


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b. Chest PainAcute (Chest) Pain related to myocardial ischemia resulting from coronary artery

occlusion with loss/restriction of blood flow to an area of the myocardium and

necrosis of the myocardium

1) Planning :STG : within 1 hour of nursing interventions, the client will have improved

comfort in chest as evidenced by :

a) States a decrease in the rating of chest painb) Is able to rest displays reduced tension, and sleeps comfortablyc) Requires decrease analgesia or nitroglycerinLTG : The client will have an improved feeling af control as evidenced by

verbalizing a sense of control over present situation and future outcomes

within 2 days of nursing interventions.

2) INTERVENTIONS :Independent:

a) Obtained resting vital signsRationale: Baseline data is important to help determine patients current

health status and evaluate efficacy of nursing interventions rendered.

b) Placed patient on complete bed rest during angina episodes.Rationale:Reduces mycocardial oxygen demand to minimize risk of tissue

injury.

c) Placed patient on semi-Fowlers position.Rationale : Relieves shortness of breath and decreases myocardial

workload.

d) Monitored vital signs q 5 minutes during initial anginal attack.Rationale:Blood pressure may initially rise and then fall if cardiac output

is compromised. Tachycardia also develops and may be sustained if cardiac

output falls.

e) Monitored heart rate and rhythmRationale : Patients with unstable angina have an increased risk of acute

life-threatening dysrhythmias

f) Maintained quiet, comfortable environment; restrict visitors as necessary.Rationale: Mental and emotional stress increases myocardial workload


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g) Provided light meals; encouraged patient to rest for 1 hr after mealsRationale: Decreases risk of myocardial attack by decreasing myocardial

workload.

h) Instructed patient to notify nurse immediately if chest pain occurs.Rationale: Pain and decreased cardiac output may complicate and prolong

an angina attack.

i) Provided emotional support.Rationale: Reduces anxiety.

j) Provided client teaching and discharge planning on:1. medication regimen2. ways to minimize

events that precipitate anginal attacks.Rationale :Patient must be taught on the proper use of medications along

with expected side effects (eg. Nitroglycerin). It is also important to

encourage patient to avoid stressful events, quit smoking, avoid

overexertion, have a regular exercise program, and maintain a low-fat, low

cholesterol diet and small, frequent meals.

Dependent:

a) Provided supplemental oxygen as orderedRationale : Increases oxygen available for myocardial uptake/reversal of

ischemia.

b) Administered antianginal medications as orderedRationale : Patients with angina pectoris are given medications that

promote vasodilation (e.g. nitroglycerin), reduce cardiac workload (e.g.

betablockers), reduce coronary artery spasms (e.g. calcium channel

blockers), and relieve pain (e.g. morphine sulfate)

Collaborative:

a) Monitored laboratory and serial ECG resultsRationale :Diagnostic studies such as ECG, ECG stress test, serum lipids,

cardiac enzymes, may be ordered to identify cause of angina pectoris and

other cardiac conditions.

b) Coordinated with dietary department regarding therapeutic diet for patientswith angina pectoris (low fat, low cholesterol).


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Rationale :Patients with angina pectoris are maintained on low-fat, low-

saturated cholesterol diet.

c. ACTIVITY INTOLERANCE1) May be related to : Imbalance between oxygen suplay/demand. Generalized

weakness. prolonged bed rest/immobility.

2) possibly evidenced by :Weaknes, fatigue. changes in vital signs, presencedysrhythmias. dyspnea. pallor. diaphoresis.

3) Desired outcomes/evaluation participate in desired activites; meet ownself-

4) Criteria patient will: care needs. Achieve measurable increase in activitytolerance, evidenced by reduced fatigue and weakness and vital signs withim

acceptable limita during activity.

5) Actions/interventionsIndependent

a) Check vital signs before and immediately after activity, especially if patientis on vasodilators, diuretics, or -blockers

Rationale :orthostatic hypotension can occur cause of medication effect

(va shift (dieresis) ; or compromised

b) Document cardiopulmonary response to activity. Note tachycardia,dysrhythmias, dyspnea, diaphoresis, pallor.

Rationale :compromised myocardium/inability to increase stroke volume

during activity may cause an immediate increase in heart rate and oxygen

demands, theraby aggravating weakness and fatigue

c)

Assess for other precipitators/causes of fatigue, e.g , treatments, pain,medications

Rationale :fatigue is aside of some medications (-blockers, tranquilizers,

and sedatives). Pain and stressful regimens also extract energy and produce

fatigue.

d) Evaluate accelerating activity intoleranceRationale : may denote increasing cardiac decompensation rather than

overactivity.


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d) Establish fluid intake schedule, incorporating beverage preferenceswhen possible. Give frequent mouth care/ice chips as part of fluid

allotment.

Rationale : involving patient in therapy regimen may enhancing sense

of control and cooperation with restriction.

e) Weigh dailyRationale : documents changes in/resolution of edema in response to

therapy. A gain of 5 lb represents approximately 2 L of fluid.

Conversely, diuretics can result in rapid/excessive fluid shifts and

weight loss.

f) Assess for distended neck and peripheral vessels. Inspect dependentbody areas for edema with/without pitting; note presence of generalizedbody edema (anasarca).

Rationale : excessive fluid retention may be manifested by venous

engorgement and edema formation.

g) Change position frequently. Elevate feet when sitting. Inspect skinsurface, keep dry and provide padding as indicated.

Rationale : edema formation, slowed circulation, altered nutional intake

and prolonged immobility/bed rest a cumulative stressor which affect

skin integrity arrequire close supervision/preventive intervention

h) Auscultate breath sounds, noting decreased and/ adventition sounds, e.gcrackles, wheezes. Not presence of increased dyspnea, tachypnea,

orthopnea, paroxysmal nocturnal dyspnea, persistent cough.

Rational: Excess fluid volume often leads to pulmonary cogestion.

Symptoms of pulmonary edema may reflect acute left-sided heart

failure. Right-side heart failures respitarory symptoms (dyspnea

cough, orthopnea) may have slower onset but a more difficult to

reverse.

i) Investigate complaints of sudden extreme dypsnea/ air hunger, need tosit stragight up, sensation of suffocation, feelings of panic or impending

doom.

Rational: May indicate development of complications (pulmonary

edema/ embolus) and differs from orthopnea and paroxysmal nocturnal

dyspnea in that develops much more rapidly and requires immetate

intervention.


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j) Monitor BP and CVP (if available).Rational: Hypertension and elevated CVP suggests fluid volume excess

and may reflect developing/ increasing pulmonary congestion, heart

failure.

k) Assess bowel sounds. Note complaints of anorexia, nausea, abdominaldistention, constipation.

Rational: Visceral congestion (occurring in progress CHF), can alter

gastric/ intestinal function.

l) Provide small, frequent easily digestible meals.Rational: Reduced gastric motility can adversely affect digestion and

absorption. Small, frequent meals mayenhance digestion/ prevent

abdominal discomfort.m)Measure abdominal girth, as indicated.

Rational: In progressive right-sided heart failure, fluid may shift into

the peritoneal space, causing increasing abdominal girth (ascites).

n) Encaourage verbalization of feelings regarding limitations.Rational: Expression of feelings/ concerns may decreases stress/

anxiety, which is an energy drain and can contribute to feelings of

fatigue.

o) Palpate for hepatomegaly. Note complaints of right upper quadrantpain/ tenderness.

Rational: Advancing heart failure leads to venous congestion, resulting

in andominal distention, liver engorgement, and pain. This can alter

liver function and impair/ prolong drug metabolism.

p) Note increased lethargy, hypotension, muscle cramping.Rational: Signs of potassium and sodium deficits that may occur due to

fluid shifts and diuretic therapy.

Collaborative

Administer medications as indicated:

a) Diuretics, e.g furosemide (Lasix); bumetanide (Bumex).Rational: Increases rate of urine flow and may inhibit reabsorption of

sodium/ chloride in the renal tubules.

b) Thiazides with pottasium-sparing agents, e.g., spironolactone(Aldactone).

Rational: Promotes diuresis without excessive potassium losses.


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c) Potassium supplements, e.g., K Dur.Rational : Replaces potassium that is lost as a common side effect of

diuretic therapy, which can adversely affect cardiac function.

d) Maintain fluid/sodium restrictions as indicated.Rational : Reduces total body water/prevents fluid reaccumulation.

e) Consult with dietitian.Rational : May be necessary to provide diet acceptable to patient that

meets caloric needs within sodium restriction.

f) Monitor chest x-ray.Rational : Reveals changes indicative of increase/resolution of

pulmonary congestion.

g)

Assist with rotating tourniquets/phlebotomy, dialysis, or ultrafiltrationas indicated.

Rational : Although not frequently used, mechanical fluid removal may

be carried out to rapidly reduce circulating volume, especially in

pulmonary edema refractory to other therapies.

e. GAS EXCHANGE, IMPAIRED, HIGH RISK FOR1) Risk factors may include : Alveolar-capillary membrane changes, e.g., fluid

collection/shifts into interstitial space/alveoli.

2) Possibly evidenced by : [Not applicable; presence of signs and symptomsestablishes an actual diagnosis.

3) Desired outcomes/evaluation criteria-patient will : Demonstrate adequateventilation and oxygenation of tissues by ABGs/oxymetry within patients

normal ranges and free of symptoms of respiratory distress. Participate in

treatment regimen within level of ability/situation.


a) Auscultate breath sounds noting crackles, wheezes.Rational : Reveals presence of pulmonary congestion/collection of

secretions indicating need for further intervention.

b) Instruct patient in effective coughing, deep breathing.Rational : Clears airways and facilitates oxygen delivery.

c) Encourage frequent position changes.Rational : Helps prevent atelectasis and pneumonia.


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d) Maintain chair/bedrest with head-of-bed elevated 20 to 30 degrees, semi-Fowlers position. Support arms with pillows.

Rational : Reduces oxygen consumption/demands and promotes maximal

lung inflation.

Collaborative

a) Monitor/graph serial ABGs, pulse oximetry.Rational : Hypoxemia can be severe during pulmonary edema.

Compensatory changes are usually present in chronic CHF.

b) Administer supplemental oxygen as indicated.Rational : Increases alveolar oxygen concentration, which may

correct/reduce tissue hypoxemia.

c)

Administer medications as indicated :Diuretics, e.g., furosemide (Lasix)

Rational : Reduces alveolar congestion, enhancing gas exchange.

Bronchodilators, e.g., aminophylline.

Rational : Increases oxygen delivery by dilating small airways and exerts

mild diuretic effect to aid in reducing pulmonary congestion.

f. SKIN INTEGRITY, IMPAIRED, HIGH RISK FOR1) Risk factors may include : Prolonged bed rest.2) Possibly evidenced by : [Not applicable; presence of signs and symptoms

establishes an actual diagnosis].

3) Desired outcomes/evaluation criteria-patient will: Demonstratebehaviors/techniques to prevent skin breakdown.


a) Inspect skin, noting skeletal prominences, presence of edema, areas ofaltered circulation/pigmentation, or obesity/emaciation.

Rational : Skin is at risk because of impaired peripheral circulation,

physical immobility, and alterations in nutritional status.

b) Massage reddened or blanched areas.Rational : Improves blood flow, minimizing tissue hypoxia.

c) Reposition frequently in bed/chair, assist with active/passive range ofmotion exercises.


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Rational : Improves circulation/reduces time any one area is deprived of

blood flow.

d) Provide frequent skin care, minimize contact with moisture/excretions.Rational : Excessive dryness or moisture damages skin and hastens

breakdown.

e) Check fit of shoes/slippers and change as needed.Rational : Dependent edema may cause shoes to fit poorly, increasing risk

of pressure and skin breakdown on feet.

f) Avoid intramuscular medication.Rational : Interstitial edema and impaired circulation impede drug

absorption and predispose to tissue breakdown/development of infection.

Collaborative :

a) Provide alternating pressure/eggcrate mattress, sheep skin, elbow/heelprotectores.

Rational : Reduces pressure to skin, may improve circulation.

g. KNOWLEDGE DEFICIT (LERNING NEED), REGARDING CONDITION,TREATMENT REGIMEN.

1) May be related to: Lack of understanding/ misconceptions aboutinterrelatedness of cardiac function/ disease/ failure.

2) Possibly evidenced by :a) Questions.

b) Statements of concern/misconceptions.c) Recurrent, preventable episodes of CHF.

3) Desired outcomes/evaluation criteria-patient will :a) Identify relationship of ongoing therapies (treatment program) to

reductionof recurrent episodes and prevention of complications.

b) List signs/symptoms that require immediate intervention.c) Identify own stress/risk factors and some techniques for handling.d) Initiate necessary lifestyle/behavioral changes.


a) Discuss normal heart function. Include information regarding patientsvariance from normal function. Explain difference between heart attack

and CHF.


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Rational : Knowledge of disease process and expectations can facilitate

adherence to prescribed treatment regimen.

b) Reinforce treatment rationale.Rational : Patient may believe it is acceptable to alter postdischarge

regimen when feeling well and symptom-free or when feeling below par,

which can increase the risk of exacerbation of symptoms. Understanding of

regimen, medications, and restrictions may augment cooperation with

control of symptoms.

c) Discuss importance of being as active as possible without becomingexhausted and to rest between activities.

Rational : Excessive physical activity can further weaken the heart,

exacerbating failure.d) Discuss importance of sodium limitation. Provide list of sodium content of

common foods that are to be avoided/limited. Encourage reading of labels

on food and drug packages.

Rational : Dietary intake of sodium above 3 g/d will offset diuretic effect.

Most common source of sodium is table salt and obviously salty foods,

although canned soups/vegetables, luncheon meats, and dairy products also

may contain high levels of sodium.

e) Discuss medications, purpose and side effects. Provide both oral andwritten instructions.

Rational : Understanding therapeutic needs and importance of prompt

reporting of side effects can prevent occurrence of drug-related

complications. Anxiety may block comprehension of input or details and

patient/SO may refer to written material at late date to refresh memory.

f) Recommend taking diuretic early in morning.Rational : Provides adequate time for drug effect before bed time to

prevent/limit interruption of sleep.

g) Instruct and receive return demonstration of ability to take and record dailypulse and when to notify health care provider, e.g., pulse above/below

preset rate, changes in rhythm/regularity.

Rational : Promotes self-monitoring of condition/drug effect. Early

detection of changes allows for timely intervention and may prevent

complications, such as digitalis toxicity.


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h) Explain and discuss patients role in control of risk factors (e.g., smoking)and precipitating or aggravating factors, (e.g., high salt diet,

inactivity/overexertion, exposure to extremes in temperature).

Rational : Adds to body of knowledge and permits patient to make

informed decisions regarding control of condition and prevention of

recurrence/complications. Smoking potentiates vasoconstriction; sodium

intake promotes water retention/edema formation improper balance

between activity/rest and exposure to extremes in temperature may result in

exhaustion/increased myocardial workload and increased risk of respiratory

infections.

i) Review signs/symptoms that require immediate medical attention, e.g.,rapid weight gain, edema, shortness of breath, increased fatigue, cough,hemoptysis, fever.

Rational : Self-monitoring increases patient responsibility in health

maintenance and aids in prevention of complication, e.g., pulmonary

edema, pneumonia.

j) Provide opportunities for patient/SO to ask questions, discuss concerns andto make necessary lifestyle changes.

Rational : Chronicity and reccurent/debilitating nature of CHF often

exhausts coping abilities and supportives capacity of both patient and SO,

leading to depression.

k) Stress importance of reporting signs/symptoms of digitalis toxicity, e.g.,development of GI and visual disturbances, changes in pulse rate/rhythm,

worsening of congestive failure.

Rational : Early recognition of developing complications and involvement

of health care provider may prevent toxicity/hospitalization.

Collaborative :

Refer to community resources/support groups and Visiting Nurse

Association as indicated.

Rational : May need additional assistance with self monitoring/home

management.


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CHAPTER III

CASE REPORT

A. CASE REPORTIdentity1. Client Identity

Name : Mr. F

Age : 57 years old

Address : Jl. Kenanga, No 57, Cilandak, Jakarta Selatan

Phone : 021- 7556432

Religion : Moslem

Education : S1 business management

Occupation/job tittle : CEO of rekayasa company

Nationality : Indonesian

Sex (M/F) : Male

Blood Group : B

Marital status : Married

Entrance Date :May 23, 2012

Reg Number : 238475

2. The Main Complaint : client complains of chest pain and shortness of breath3. Medical History

a. Medical Present History :1) The history of complaint :

He has 2 week history of progressive lower leg edema, chest pain, and

shortness of breath on exertion. He had also experienced a weight loss of

approxiamately 4 kilograms. Shortness of breath and general malaise hadincreased over the 3 days before admission.

2) Predisposing factor :He had a- 20 year history of cigarette smoking

3) Duration :Had chest pain for arround 10 minutes


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4) Appear Pattern :Chest pain occurs when the client is doing the activity

5) Bear-down efforts to overcome :Clients overcome the chest pain and shortness of breath with resting

6) Medical Past Historya) Allergy History (drugs, food, animal, environment) :

Clients has not allergy history

b) Accident History :Clients has not accident and hospitalized history

c) History of drugs taking :Clients has not history of drug all this time before he comes to the hospital

7) Medical Family History (genogram and explanation) :Clients families has no heart disease

4. Physical Assesmenta. Eyes system : clients has no problem with his eyes system

b. Ears system : clients has no problem with his ears systemc. Respiratory system : clients has complain that he has a shortness of breath

with respiratory rate 25 times per minute.

d. Cardiovascular system : Clients complain chest pain. He also has a high bloodpressure (140/100). Cardiac examination demonstrated a laterally displaced apex

and fast first and second heart sounds.

e. Hematology system : Clients has no problem with his hematology systemf. Nervous system : Clients has no problem with his nervous systemg. Digestive system : Clients has no problem with his digestive systemh. Endocrine system : Clients has no problem with his endocrine systemi. Urogenitalia system : Clients has no problem with his urogenitalia system

j. Integument system :Clients has no problem with his integument systemk. Musculoskeletal system : clients complain that he felt malaise increased over the

3 days before admission.


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5. Supportive Data (diagnostic tests) :a. Hb : 13.4b. HT : 39c. Leukosit : 9.9d. Eritrosit : 4.35e. Trombosit : 450f. Protobintine : 13.2g. Ureum : 30h. Kreatinin : 1.4i. Natrium : 141

j. Kalium : 3.43k.

Chlorida : 105

l. CPK : 161m. CKMB (Lab) : 15n. Troponin T :


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In the emergency room, his temperature was 36.3o c, irregular pulse rate 142 per

minute, respiratory rate 25 per minute and blood pressure 140/100 mmHg. Head and neck

examination revealed a symmetrically en large, non-tender thyroid gland. Jugular venous

dilatation was observed. Cardiac examination demonstrated a laterally displaced apex and

fast first and second heart sounds. Murmurs were heard at the apex and left sternal border.

Chest examination revealed few basilar crackles over both lung fields. Moderate ankle

pitting edema was noted bilaterally.

Twelve-lead electrocardiogram (ECG) showed atrial fibrillation (AF) with rapid

ventricular response and diffused ischemic change. His hematology parameters were

normal. The serum total protein and albumin were 6.4 and 3.79/dL respectively.

B.

FOCUS DATA

SUBJECTIVE DATA OBJECTIVE DATA

1. Clients complain chest pain2. Clients complain lower leg edema and it

does not go away

3. Clients complain shortness of breath ifhas a high activity

4. Clients complain malaise

1.Edema seen in the legs the client2.Has weight loss 4 kilograms in a week (65

kilograms to 61 kilograms)

3.Vital sign :

C. PROBLEM ANALYSISNo Data Problem Etiology

1. Subjective Data :

1. client complains of chest painObjective Data :

1. Vital signa. Blood pressure : 140/100

b.RR : 25 times/minutec. Pulse rate : 142 times/minuted.Temperature : 36,3oC

2. ECG : lead 12 (AF)3. Chest pain scale : 7

Chest pain Myocardial ischemia resulting

from coronary artery occlusion

with loss/ restriction of blood

flow to an area of the

myocardium


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2. Subjective Data :

1. clients complained of shortness ofbreath when doing strenuous

activities

Objective Data :

1. edema seen at the foot of the client2. Vital sign

a. Blood pressure : 140/100b.RR : 25 times/minutec. Pulse rate : 142 times/minuted.Temperature : 36,3oC

3.

Heard sound crackles in his bothlungs

4. There is pitting edema grade 3

Shortness of breath Decrease in lung expansion

(fluid accumulation)


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E. IMPLEMENTATIONTanggal/

Waktu

NO.

DxIMPLEMENTATION INITIALS

24/5/2012 1.

2.

INDEPENDENT

k) Obtainetion resting vital signsl) Placetion patient on complete bed rest during angina episodes.

m)Placetion patient on semi-Fowlers position.n) Monitoretion vital signs q 5 minutes during initial anginal attack

o) Monitoretion heart rate and rhythmCOLABORATION

c) Monitored laboratory and serial ECG results

INDEPENDENT

1.Auscultation breath sounds noting crackles, wheezes.

2.Instruction patient in effective coughing, deep breathing.

3.Encouragion frequent position changes.

4.Maintaining chair/bed rest with head-of-bed elevated 20 to 30 degrees,semi-Fowlers position. Support arms with pillows.

COLABORATION

d) Administering medications as indicated :a. Diuretics, e.g., furosemide (Lasix)

b. Bronchodilators, e.g., aminophylline.25/5/2012 1. INDEPENDENT

1. Obtainetion resting vital signs


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2.

2. Placetion patient on complete bed rest during angina episodes.

3. Placetion patient on semi-Fowlers position.4. Monitoretion vital signs q 5 minutes during initial anginal attack

5. Monitoretion heart rate and rhythmCOLABORATION

1. Monitored laboratory and serial ECG results

INDEPENDENT

1. Auscultation breath sounds noting crackles, wheezes.

2.Instruction patient in effective coughing, deep breathing.

3.Encouragion frequent position changes.

4.Maintaining chair/bed rest with head-of-bed elevated 20 to 30 degrees,semi-Fowlers position. Support arms with pillows.

COLABORATION

1. Administering medications as indicated :a. Diuretics, e.g., furosemide (Lasix)

b. Bronchodilators, e.g., aminophylline.

F. EVALUATIONDATE DX HOURS EVALUATION INITIALS

24/5/2012 DX 1 14.00 pm S: clients say the pain was reduced by a scale of 4

O: Vital sign

1. Blood pressure : 130/1002. RR : 25 times/minute


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DX 2

3. Pulse rate : 125times/minute4. Temperature : 36,3oC

Chest pain scale : 4

A: intervention resolved in part

P: continued intervention

1. Obtained resting vital signs2. Placed patient on complete bed rest during

angina episodes

3. Placed patient on semi-Fowlers position.4. Monitored vital signs q 5 minutes during initial

anginal attack

5.

Monitored heart rate and rhythm6. Maintained quiet, comfortable environment;

restrict visitors as necessary

7. Provided light meals; encouraged patient to restfor 1 hr after meals

S: the client says shortness of breath remained

O: edema seen at the foot of the client


b. RR : 25 times/minutec. Pulse rate : 125 times/minuted. Temperature : 36,3oC

2. Heard sound crackles in his both lungs3. There is pitting edema grade 3

A:intervention has not been resolved


1. Auscultation breath sounds noting crackles,wheezes

2. Instruct patient in effective coughing, deepbreathing

3. Encourage frequent position changes.


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4. Maintain chair/ bed rest with head-of-bedelevated 20 to 30 degrees, semi-Fowlers

position. Support arms with pillows

25/5/2012 DX 1

DX 2

S: clients say the pain is gone

O: Vital sign

1. Blood pressure : 125/1002. RR : 25 times/minute3. Pulse rate : 100 times/minute4. Temperature : 36,3oC

ECG : lead 12 (AF)

A: intervention resolved

P: the intervention is stopped

S: shortness of breath decreases the client says

O:


b. RR : 25 times/minutec. Pulse rate : 100 times/minuted. Temperature : 36,3oC

2. Heard sound crackles in his both lungs3. There is pitting edema grade 3

A: intervention resolved in part


1. Auscultation breath sounds noting crackles,wheezes


3. Encourage frequent position changes.4. Maintain chair/ bed rest with head-of-bed

elevated 20 to 30 degrees, semi-Fowlers


5. breath sounds noting crackles, wheezes


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7. Encourage frequent position changes.8. Maintain chair/ bedrest with head-of-bed

elevated 20 to 30 degrees, semi-Fowlers



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CHAPTER IV

CLOSING

A. CONCLUSION1. Heart failure is a condition where the heart as a pump pathophysiology unable to meet

the needs blood to tissue metabolism

2. Factors that can trigger the development of heart failure through the suppression of asudden circulation can be: arrhythmias, systemic infections and lung infections and

pulmonary embolism.

3. Complications caused by CHF include deep venous thrombosis, digitalis toxicity andcardiogenic shock. Investigations can be performed in patients with CHF is a chest

radiograph, ECG, EKG, and others. Management that can be done by health,

especially nurses and physicians include: pharmacological management, non-

pharmacological and health education.

4. Heart failure is handled by common action to reduce the workload of the heart andselective manipulation of the three major determinants of myocardial function, either

individually or a combination of: an initial load, contractility, and the load end.

B. ADVICEIt is desirable to avoid the disease congestive heart failure is performed by avoiding the

cause of the disease such as maintaining a healthy lifestyle, especially in the food consumed is

expected to not only look delicious but also consider the nutrients contained in, the food.


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REFFERENCE

1. http://www.emedicinehealth.com/congestive_heart_failure/page12_em.htm#Interventions

2. http://www.hearthealthywomen.org/cardiovascular-disease/heart-failure/heart-failure-4.html
http://www.emedicinehealth.com/congestive_heart_failure/page12_em.htm#Interventionshttp://www.emedicinehealth.com/congestive_heart_failure/page12_em.htm#Interventionshttp://www.emedicinehealth.com/congestive_heart_failure/page12_em.htm#Interventionshttp://www.emedicinehealth.com/congestive_heart_failure/page12_em.htm#Interventionshttp://www.emedicinehealth.com/congestive_heart_failure/page12_em.htm#Interventionshttp://www.emedicinehealth.com/congestive_heart_failure/page12_em.htm#Interventions

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