NURSING

MANAGEMENT
OF PATIENT
WITH
CONGESTIVE
HEART FAILURE

SUBMITTED TO SUBMITTED BY
MRS.SREEJA P MISS. NICE MATHEW
ASST. PROFESSOR 1ST YEAR MSc (N)
BMCON BMCON
CALICUT CALICUT

SUBMITTED ON 2/1/2012
NURSING MANAGEMENT OF PATIENT WITH CCF
INTRODUCTION

Heart failure does not mean the heart has stopped working. Rather, it means that the
heart's pumping power is weaker than normal. With heart failure, blood moves through the
heart and body at a slower rate, and pressure in the heart increases. As a result, the heart
cannot pump enough oxygen and nutrients to meet the body's needs. The chambers of the
heart respond by stretching to hold more blood to pump through the body or by becoming
stiff and thickened. This helps to keep the blood moving for a short while but, in time, the
heart muscle walls weaken and are unable to pump as strongly. As a result, the kidneys often
respond by causing the body to retain fluid (water) and sodium. If fluid builds up in the arms,
legs, ankles, feet, lungs, or other organs, the body becomes congested, and congestive heart
failure is the term used to describe the condition.

MEANING

Heart failure is an abnormal clinical condition involving impaired cardiac pumping.

It results in the characteristic pathophysiologic changes of vasoconstriction and fluid
retention. Heart failure, formerly called congestive heart failure, is the terminology preferred
today since not all patients with heart failure have pulmonary congestion. HF is not a disease.
It is associated with numerous types of CVD, particularly long standing HTN, CAD, and MI.
HF is characterized by ventricular dysfunction, reduced exercise tolerance, diminished
quality of life, and shortened life expectancy.

DEFINITION
“CHF , is the inability of the heart to pump sufficient blood to meet the needs of the tissues
for oxygen and nutrients.”
HF guidelines panel(1994) ,defined HF as a “clinical syndrome characterized by signs and
symptoms of fluid overload or of inadequate tissue perfusion. These signs and symptoms
result when the heart is unable to generate a CO sufficient to meet the body’s demands.”

INCIDENCE/ EPIDEMIOLOGY

CHF, one of the fastest growing diagnoses in the world today. Over 5 million individuals
worldwide have a diagnosis of CHF. As this diagnosis becomes more prevalent , over
400,000 new cases will be seen every year.20% of these patients will die in the first year, and
50% will die within a 5-year period. Blacks are more prone to this disease.
Gender differences

MEN
Men experience systolic dysfunction more
frequently than women.
Men with asymptomatic systolic dysfunction
experience greater mortality benefit from
ACE inhibitor therapy than women.
WOMEN
Women experience diastolic dysfunction
more frequently than women.
Women have a higher risk of ACE inhibitor –
related cough than men.
 Benefits of long term use of digitalis in
women may not justify the risks.
Women with heart failure experience major
depression more frequently than men.

CAUSES OF HEART FAILURE

CAD and advancing age are the primary risk factors for HF. Other
factors, such as HTN, DM, cigarette smoking, obesity and high serum cholesterol, can also
contribute to the development of HF. The major causes of HF may be divided into two
subgroups;

1. Primary causes (underlying disease conditions)

Chronic heart failure

 Cardiomyopathy----In which the ventricular muscle becomes enlarged, thickened, or

rigid can contribute to CHF. Dilated cardiomyopathy causes diffuse cellular necrosis,
leading to decreased contractility (systolic failure). Hypertrophic cardiomyopathy and
restrictive cardiomyopathy lead to decreased distensibility and ventricular filling
(diastolic failure). As with hypertension, the cause of cardiomyopathy can be either
idiopathic (unknown) or a result of alcohol/drug misuse, heart/ valve disease,
hypertension, or a viral disease affecting heart.
 Hypertension----Whether primary (no known case) or secondary (underlying causes
such as too much salt and/ or fluid in the body, CKD, diabetes, and heart valve
issues),hypertension leads to CHF due to an overstretching of the myocardial fibers in
the ventricle.
 Coronary artery disease-----Ischemia causes myocardial dysfunction because of
resulting hypoxia and acidosis from the accumulation of lactic acid.
 Congenital heart disease
 Cor pulmonale -----Hypoxia and hypercapnia cause pulmonary arterial
vasoconstriction and possibly reduction of the pulmonary vascular bed, as in
emphysema or pulmonary emboli. The result is increased resistance in the pulmonary
circulatory system, with a subsequent rise in pulmonary blood pressure. It results in
right ventricular hypertrophy followed by right ventricular failure.
 Bacterial endocarditis
 Anemia---It require an increase in CO to satisfy the systemic oxygen demand.
Anemia decreases the supply of oxygen to the myocardium.
 Valvular disorders---The valves ensure that the blood flows in one direction. With
valvular dysfunction, blood has increasing difficulty moving forward, increasing
pressure within the heart and increasing cardiac workload, leading to diastolic heart
failure.
Acute heart failure
 Acute myocardial infarction----It causes focal heart muscle necrosis, the death of
heart muscle cells, and loss of contractility; the extent of the infarction correlates with
the severity of heart failure.
 Dysrhythmias----Heart dysrhythmias may also be the culprit. Atrial fibrillation and
atrial flutter cause the atrium to contract suboptimally. This results in the loss of atrial
klick, in which upto 30% of the atrium’s volume doesn’t get to the ventricles and is
 n’t pumped out to the lungs and/ or the aorta. Bradycardiac rhythms, whether
electrical / physiologic (sinus bradycardia, junctional, and AV blocks) or
pharmacologic (digoxin, beta blockers, and calcium- channel blockers in particular)
in nature, are also suspects.
 Rheumatic heart disease
 Thyrotoxicosis---- It require an increase in CO to satisfy the systemic oxygen
demand.
 Pulmonary emboli---Same as cor pulmonale.
 Hypertensive crisis
 Ventricular septal defect
 Myocarditis----can lead to cardiomyopathy.

2. Precipitating causes

CAUSES MECHANISM
Anemia O2-carryingcapacity of the blood stimulating in CO to meet
tissue demands.
Infection O2 demand of tissues, stimulating CO
Thyrotoxicosis Changes the tissue metabolic rate, HR and workload of the
heart.
Hypothyroidism Indirectly predisposes to atherosclerosis; severe
hypothyroidism decreases myocardial contractility
Dysrhythmias May CO and workload and o2 requirements
Bacterial endocarditis Infection; metabolic demands and o2 requirements
Pulmonary disease Valvular dysfunction; causes stenosis and regurgitation
Paget’s disease Workload of the heart by vascular bed in the skeletal muscle
Nutritional deficiencies May cardiac function by myocardial muscle mass and
myocardial contractility
Hypervolemia Preload causing volume overload on the RV

CLASSIFICATIONS OF CONGESTIVE HEART FAILURE

 Right-sided CHF----It is the inability of the heart to adequately pump. In this case,
however , the blood backs up into the body. It is due to the increased pressure in the
lung.
 Left- sided CHF----In left-sided CHF, blood and fluid back up into the lungs. The
root cause of this is the left ventricle’s inability to propel the blood forward. There are
several factors that can lead to this condition;CAD is the most common. A lack of O2
carrying blood to the myocardial muscle leads to ischemia. If untreated, the ischemic
areas dies. The end result is weakened or dead heart muscle, which limits the
ventricle’s contracting ability. Left-sided CHF can further be broken down into 2
subdivisions;

Systolic Heart Failure –In systole, the ventricles are contracting, which forces the blood
forward into the system. This refers to the hearts inability to contract effectively. The
problem begins when the left ventricle undergoes an insult and both the CO and BP decrease.
Then the neurohormonal activation occurs, including stimulation of the SNS, and the arginine
vasopressin system, the rennin- angiotensin –aldosterone system. These mechanisms are all
designed to increase both CO and BP. They do so, however, at the cost of increasing the
amount of fluid in the blood stream and the heart rate.
The Frank- Starling law shows that stroke volume increases with an increase
of blood filling the heart, known as the end- diastolic filling volume. Over time, this leads to
an” overstretched rubber band” syndrome in which the rubber band loses its “snap”. The
ventricle is unable to eject blood efficiently out to the aorta as it becomes overstretched. This
leads to apoptosis, or programmed cell death, within the ventricle, as well as an actual
remodeling of theventricular shape itself. The end result is a decrease in blood ejected from
the ventricle.
Characteristics of systolic heart failure include an ejection fraction (EF) that is less
than 35% to 40%. The gold standard for treatment of systolic heart failure is ACE inhibitors,
Beta Blockers and Diuretics (Digoxin is added if the patient remains symptomatic after the
gold standard treatment).

 
Diastolic Heart Failure – Diastole is the resting or relaxation phase of the cardiac cycle.
With diastolic heart failure the heart can contract effectively (EF > 40%), but the ventricle
has increased resistance to filling and causes a reduction in stroke volume. This can be due to
a “stiffer” ventricular wall, which then results in a lowered stroke volume and a decrease in
CO. Treatment for diastolic heart failure (according to the American Heart Association
Guidelines 2001) includes management of blood pressure, heart rate and fluid
retention/overload with ACE inhibitors, Beta Blockers and Calcium Antagonists.
 Functional Classification of Heart Disease

In the management of patients with heart disease, it is important to quantify and monitor the
severity of symptoms. A commonly used classification system is that of the New York Heart
Association (NYHA), shown below.

 Class I (Mild):    No limitation of physical activity. Ordinary physical activity does

not cause undue fatigue, dyspnea, or anginal pain.

 Class II (Mild):   Slight limitation of physical activity. Ordinary physical activity

results in symptoms.

 Class III (Moderate):  Marked limitation of physical activity. Comfortable at rest, but
less than ordinary activity causes symptoms.

 Class IV (Severe):  Unable to engage in any physical activity without discomfort.

Symptoms may be present even at rest.

Recent recommendations propose that patients with heart failure be classified into four
stages: (ACC/ AHA stages of heart failure )

 Stage A (High risk of developing heart failure): Those at high risk for congestive
heart failure (CHF) but no structural heart disease (ie, hypertension, coronary artery
disease [CAD]) and no symptoms. Patients at high risk for developing heart failure
because of the presence of conditions that are strongly associated with the
development of heart failure. Such patients have no identified structural or functional
 abnormalities of the pericardium, myocardium, or cardiac valves and have never
shown symptoms or signs of heart failure.

 Stage B (Asymptomatic heart failure): Those with structural heart disease associated
with CHF and no symptoms. Patients who have developed structural heart disease that
is strongly associated with the development of heart failure but who have never
shown symptoms or signs of heart failure.

 Stage C (Symptomatic heart failure): Those with structural heart disease who have
current or prior symptoms. Patients who have current or prior symptoms of heart
failure associated with underlying structural heart disease.

Stage D (Refractory end stage heart failure): Those with refractory CHF requiring
some device or special intervention. Patients with advanced structural heart disease
and marked symptoms of heart failure at rest despite maximal medical therapy and
who require specialized interventions.

PATHOLOGY OF VENTRICULAR FAILURE

Heart failure is classified as systolic or diastolic failure.

Systolic failure; the most common cause of HF, results from an inability of the heart to
pump blood. I t is a defect of the ventricle to contract. The left ventricle loses its ability to
generate enough pressure to eject blood forward through the aorta. Overtime, the LV
becomes thin walled , dilated, hypertrophied. The hallmark of systolic dysfunction is a
decrease in the left ventricular ejection fraction (the percentage of total ventricular filling
volume that is ejected during each ventricular contraction ). Systolic failure is caused by
impaired contractile function, increased afterload, and mechanical abnormalities.

Diastolic failure; It is an impaired ability of the ventricles to relax and fill during diastole.
Decreased filling of the ventricles will result in decreased stroke volume and CO. Diastolic
failure is characterized by high filling pressures due to stiff or noncompliant ventricles and
result in venous engorgement in both the pulmonary and systemic vascular resistance. The
diagnosis of diastolic failure is made on the basis of the presence of pulmonary congestion,
pulmonary hypertension, ventricular hypertrophy, and a normal EF.
Diastolic failure is usually the result of left ventricular hypertrophy from chronic
systemic hypertension,aortic stenosis, or hypertrophic cardiomyopathy. Diastolic failure is
commonly seen in older adults, and predominantly women, as a result of myocardial fibrosis,
and hypertension

Mixed systolic and diastolic failure; Systolic and diastolic failure of mixed orgin is seen in
disease states such as dilated cardiomyopathy. These .patients often have extremely poor EFs,
high pulmonary pressures, and biventricular failure( both ventricles may be dilated and have
poor filling and emptying capacity).

Compensatory mechanisms

. The main compensatory mechanisms include (1) sympathetic nervous system activation
(2) neurohormonal responses (3) ventricular dilation (4) ventricular hypertrophy
Sympathetic nervous system activation; It is the first mechanism triggered in low CO
states. However, it is the least effective compensatory mechanism. In response to an
inadequate stroke volume and CO, there is increased SNS activation, resulting in the
increased release of catecholaminnes( epinephrine and norepinephrine ).This results in an
increased HR and myocardial contractility, and peripheral vasoconstriction. Initially this
increase in HR and contractility improves CO. However, overtime these factors act in a
detrimental fashion by increasing the myocardium’s need for oxygen and workload of the
already failing heart. The vasoconstriction causes an immediate increase in preload, which
may initially increase CO. However, an increase in venous return to the heart, which is
already volume overloaded, actually worsens ventricular performance.

Neurohormonal responses; As the CO falls, blood flow to the kidneys decreases. This is
sensed by the juxtraglomerular apparatus in the kidneys as decreased volume. In response,
the kidneys release rennin, which converts angiotensin to angiotensin 1. Angiotensin 1 is
subsequently converted to angiotensin 2 by a converting enzyme made in the lungs.
Angiotensin 2 causes (1) the adrenal cortex to release aldosterone, which results in sodium
water retention, and (2) increased peripheral vasoconstriction, which increases BP. This
response is known as the rennin-angiotensin-aldosteron systems. (RASS).

Low CO causes a decrease in cerebral perfusion pressure. The posterior pituitary then
secretes ADH. ADH increases water reabsorption in the renal tubules, causing water retention
and therefore increased blood volume. As a result, blood volume is increased in a person who
is already volume overloaded.

Other factors also contribute to the development of HF. The production of endothelin,
produced by vascular endothelial cells, is stimulated by ADH, catecholamines, and
angiotensin 2. Endothelin results in further arterial vasoconstriction and an increase in cardiac
contractility and hypertrophy.

Locally, proinflammatory cytotokines are released by cardiac myocytes in response

to various forms of cardiac injury. Two cytokines and tumor necrosis factor (TNF) and
interleukin-1 (IL-1), further depress cardiac function by causing cardiac hypertrophy,
contractile dysfunction, and myocyte cell death. Over time, a systemic inflammatory response
is also mounted and accounts for the cardiac wasting, muscle myopathy, fatigue that
accompany advanced HF.

Activation of the SNS and the neurohormonal response lead to elevated levels of
norepinephrine, angiotensin 2, aldosterone, ADH, endothelin, and proinflammatory
cytokines. Together, these factors result in an increase in cardiac workload, myocardial
dysfunction, and ventricular remodeling. Remodeling involves hypertrophy of thee cardiac
myocytes, resulting in large, abnormally shaped contractile cells. This eventually leads to
increased ventricular mass, changes in ventricular shape, and impaired contractility. Although
the ventricles become larger, they become less effective pumps. All of these facors are over
expressed in HF and eventually perpetuate the downward spiral of progressive HF syndrome.

Dilation; Dilation is an enlargement of the chambers of the heart. It occurs when pressure in
the heart chambers (usually the left ventricle) is elevated over time. The muscle fibers of the
heart stretch in response to the volume of blood in the heart at the end of the diastole. The
degree of stretch is directly related to the force of the contraction (systole) (Frank- Starling
law). Initially this increased contraction leads to increased CO and maintenance of arterial BP
and perfusion. Initially dilation is an adaptive mechanism to cope with increasing blood
volume. Eventually this mechanism becomes inadequate because the elastic elements of the
muscle fibers are overstretched and can no longer contract effectively, thereby decreasing the
CO.

Hypertrophy; In chronic HF, hypertrophy is an increase in the muscle mass and cardiac wall
thickness in response to overwork and strain. It occurs slowly because it takes time for this
increased muscle tissue to develop. Hypertrophy generally follows persistent or chronic
dilation and thus further increases the contractile power of the muscle fibers. This will lead to
an increase in CO and maintenance of tissue perfusion. However, hypertrophic heart muscle
has poor contractility, require more oxygen to perform work, has poor coronary artery
circulation (tissue becomes more easily ischemic), and is prone to ventricular dysrhythmias.

Counterregulatory mechanisms;

The body’s ability to try to maintain balance is demonstrated by several

counterregulatory processes. Natriuretic peptides are hormones produced by the heart muscle
that promote venous and arterial vasodilation. Natriuretic peptides are endothelin and
aldosterone antagonists and enhance diuresis by increasing GFR and blocking the effects of
RASS. In addition, they inhibit the development of cardiac hypertrophy and may have anti-
inflammatory effects. ANP is produced by the atrium, and BNP is produced by the ventricles.
ANP is primarily triggered by increases in volume. BNP is primarily triggered by increased
pressure. Prolonged atrial and ventricular distention leads to a depletion of these factors.
Nitric oxide is another substance released from the vascular endothelium in response to the
compensatory mechanisms activated in HF. Like the natriuretic peptides, NO works to relax
the arterial smooth muscle, resulting in vasodilation and decreased afterload.

Cardic compensation occurs when compensatory mechanisms succeed in

maintaining an adequate CO that is needed for tissue perfusion. Cardiac decompensation
occurs when these mechanisms can no longer maintain adequate CO and inadequate tissue
perfusion results.

PATHOLOGY AND CLINICAL FEATURES

1.Increased workload and end-diastolic volume enlarge the left ventricle. You may note
increased heart rate, pale and cool skin, tingling in the extremities, decreased cardiac output,
and arrhythmias.

2.Blood pools in the ventricle and atrium and eventually backs up into the pulmonary veins
and capillaries.—You may note dyspnea on exertion, confusion, dizziness, orthostatic
hypotension, decreased peripheral pulses and pulse pressure, cyanosis, and an s3 gallop.

3.Rising capillary pressure pushes sodium and water into the interstitial space, causing
pulmonary edema. You may note coughing, subclavian retractions. crackles, tachypnea,
elevated pulmonary artery pressure, diminished pulmonary compliance, and increased partial
pressure of CO2.

4.Because the left ventricle can’t handle the increased venous return, fluid pools in the
pulmonary circulation, worsening pulmonary edema. You may note decreased breath sounds,
dullness on percussion, crackles and orthopnea.
5. The right ventricle may now become stressed because it’s pumping against greater
pulmonary vascular resistance and left ventricular pressure. You may note worsening
symptoms.

6.The stressed right ventricle enlarges with the formation of stretched tissue. You may note
increased heart rate,cool skin, cyanosis, decreased cardiac output, dyspnea and palpitation.

7. Blood pools in the right ventricle and right atrium. The backed up blood causes pressure
and congestion in the vena cava and systemic circulation. You may note increased CVP,
jugular vein distension and hepatojugular reflux.

8. Backed up blood distends the visceral veins, especially the hepatic vein. As the liver and
spleen become engorged, their function is impaired. You may note anorexia, nausea,
abdominal pain, palpable liver and spleen, weakness, and dyspnea secondary to abdominal
distention.

9. Rising capillary pressure forces excess fluid from the capillaries in to the interstitial space.
You may note edema, weight gain, and nocturia.

TYPES OF HEART FAILURE

HF is usually manifested by biventricular failure, although one ventricle may precede the
other in dysfunction. Normally the pumping actions of the left and right sides of the heart are
synchronized, producing a continuous flow of blood. However, as a result of pathologic
conditions, one side may fail while the other side continues to function normally for a period
of time. Because of the prolonged strain, both sides of the heart will eventually fail, resulting
in biventricular failure.

Left sided failure; The most common form of HF is left sided failure. Left- sided failure
results from left ventricular dysfunction, which prevents normal blood flow and causes blood
to back up into the left atrium and in to the pulmonary veins. The increased pulmonary
pressure causes fluid extravasation from the pulmonary capillary bed into the interstitium and
then the alveoli, which is manifested as pulmonary congestion and edema.

systemic
vascular resiatance

Peripheral artery
constriction Force of LV
contraction

Norepinephrine and
epinephrine release.
LV oxygen
demand

Systemic
blood pressure
LV hypoxia
 ADH Renal blood
flow
Force of LV
contraction
Renin

LVEDP

Angiotensin

LV preload

Aldosterone

LA preload
Sodium and water
retention

Pulmonary
Peripheral edema
edema
Pulomonary
vacular resistance

RV failure

RV preload

Right sided failure; Right sided failure causes a backup of blood into the right atrium and
venous circulation. It is a result of increased pressure in the lungs. Because the lung pressure
are lower than the aorta, the right ventricle does not need to pump as hard as the left.
Conditions such as pulmonary hypertension, COPD, pulmonic valve stenosis, and chronic
blood clots can lead to an enlargement of the jugular veins and swelling in the abdomen/
sacrum, lower legs and fee.
Venous congestion in the systemic circulation results in jugular venous
distention, hepatomegaly, splenomegaly, vascular congestion of the GIT and peripheral
edema. Jugular venous distension is reflective of the retrograde flow seen in elevated right
atrial pressures. The blood backs up through the superior vena cava in to the jugular vein.
With the patient lying at a less than 45 degree angle, the distended vein can be seen best over
the sternocleidomastoid muscle. The primary cause of right sided failure is the left sided
failure. In this situation, left-sided failure results in pulmonary congestion and increased
pressure in the blood vessels of the lung. Eventually chronic pulmonary hypertension results
in right- sided hypertrophy and failure. Cor pulmonale (right ventricular dilation and
hypertrophy caused by pulmonary disease ) can also cause right sided heart failure.

Hepatomegaly, or liver enlargement, is n’t in itself a disease, but rather a

sign of one. In CHF, this is due to the back up of blood from the inferior vena cava to the
portal blood system. An enlarged liver won’t be seen, but may be felt by palpating the right
upper abdominal quadrant just under the ribs as the patient takes in and lets out a deep breath.
Ascitis is excess fluid found in the peritoneal cavity. This, too, is a result of backflow through
the inferior vena cava. It may or may not be associated with hepatomegaly. In bedridden
patients, this excess fluid may also be seen pooling in the sacral area.

SIGNS AND SYMPTOMS OF CONGESTIVE HEART FAILURE

Left Sided Heart Failure:

 Capillary refill > 3 seconds

 LV heaves
 Tachypnea
 Diaphoresis
 Basilar crackles or rhonchi
 Cyanosis
 Hypoxia (respiratory acidosis)
 Elevated pulmonary artery pressures
 Elevate pulmonary artery occlusive pressures
 Audible S3 and S4 heart tones
 Mental confusion
 Weight gain
 Murmur or mitral insufficiency
 Enlarged left ventricle on X-ray
 Enlarged left atrium on X-ray
 Narrowing pulse pressure
 Pulsus alternans (alteration of weak and strong beats)

Symptoms

 Fatigue/weakness/lethargy
 Anxiety, depression
 Orthopnea
 Dyspnea on exertion
 Nocturnal dyspnea
 Cough with frothy sputum (indicative of pulmonary edema)
 Shallow respirations upto 32-40/min
 Nocturia

Right Sided Heart Failure:

 Hepatomegaly
 Splenomegaly
  RV heaves
 Jugular venous distension
 Dependant pitting edema
 Hepatojugular reflux
 Oliguria
 Arrhythmias
 Elevated CVP
 Elevated right atrial pressure
 Elevated right ventricular pressure
 Narrowing pulse pressure
 Kussmaul’s sign
 Murmur or tricuspid insufficiency
 Audible S3 and S4 heart tones
 Enlarged right atrium on X-ray
 Enlarged right ventricle of X=ray
 Ascites
 Weight gain
 Anasarca

Symptoms

 Anxiety
 Depression
 Fatigue/weakness
 Abdominal pain
 Anorexia, GI bloating
 Dependent bilateral edema
 Nausea

CLINICAL MANIFESTATIONS OF CHRONIC HEART FAILURE

 Ftigue
 Dyspnea
 Tachycardia
 Edema
 Nocturia
 Skin changes
 Behavioural changes
 Chest pain
 Weight changes

DIAGNOSIS

History;

 Note the presence of symptoms of heart failure.

 Obtain a detailed description of each symptom. Symptoms such as dyspnea or
weakness may occur in response to other diseases.
  Try to determine the possible underlying cause of HF .
 Try to determine the precipitating factors in this episode of heart failure.

Physical examination;

 General appearance

 The person may appear breathless at rest, with activity, or be unable to lie flat.
 The person with chronic severe heart failure, especially right sided, may appear thin
and undernourished.
 Distended neck veins may be evident in right sided failure.

 Vital signs,

 Respirations may be rapid and shallow. Chyne Stokes pattern may be observed.
 Pulse- Tachycardia may occur as a compensatory mechanism or be a precipitating
factor .Pulse alternans is a sign of heart failure
 Assess the lungs for rales, cough, pink- tinged sputum, or decreased breath sounds
due to pleural effusions or pulmonary edema.
 Heart- Palpate point of maximal impulse, which may be displaced to left.
Auscultation may reveal an S3, a sign of heart failure. An S4 may occur in people with
CAD. A murmer may indicate valvular problem.
 Assess the abdomen for hepatomegaly and ascitis.
 Edema- Assess the patient for the presence of edema in the dependent areas. If the
person is upright, edema starts in the feet or ankles and moves upward. If the person is
in the bed, edema accumulates in the sacral,lumbar, and posterior thigh region.
 Assess the extremities for color and temperature.

Lab Tests:

 Beta Natriuretic peptide (BNP) – this laboratory study can help to identify CHF as the
origin for unclear dyspnea. When serum levels of BNP are less than 100pg/ml the
diagnosis of CHF is unlikely. Serum levels of BNP that range between 100 – 500
pg/ml is probably caused by CHF and BNP levels that are > 500 pg/ml are considered
to be definitely consistent with a diagnosis of CHF.
 Serum lab values that positively identify pre-renal apothecia, elevated alanine-
aminotransferase (ALT), elevated Aspartate Aminotransferase (AST) or elevated
bilirubin are suggestive of congestive hepatomegaly (which is consistent with CHF).
 Cardiac enzymes and other serial markers for cardiac ischemia or injury should also
be drawn and analyzed.
 Arterial blood gases (ABG’s) should be drawn when there is evidence of hypoxia,
dyspnea or pulmonary edema.
 A decreased erythrocyte sedimentation rate (ESR) can help to diagnose early mild to
moderate CHF.
 Elevated creatinine levels and dilutional hyponatremia may be observed in severe
cases of CHF.

Imaging Studies:
  Chest X-ray – Although diagnosis of congestive heart failure may be limited by chest
X-ray, it is one of the most useful tools available. Cardiomegaly can be seen if the
cardiothoracic ratio is greater than 50%. Bilateral pleural effusions can be viewed by
X-ray (if unilateral, they are more commonly found on the right side of the chest). Of
note: A 12 hour radiographic lag time from onset of symptoms to demonstration on
chest X-ray may be present making a diagnosis of congestive heart failure difficult by
X-ray alone.
 Echocardiography (ECHO) – Identifying the regional wall motion abnormalities that
are associated with congestive heart failure can be accomplished with an
echocardiogram. An ECHO can also help identify cardiac Tamponade, pericardial
constriction and possible valvular heart disease.

Other Tests/Procedures:

 Electrocardiogram (ECG) – This is a non-specific test that may be useful in

diagnosing cardiac ischemia that is caused by congestive heart failure. ECG can also
diagnose dysrhythmias that are caused by left ventricular hypertrophy (which often
occurs in left sided failure).
 Cardiac catheterization may be indicated for severe cases of CHF in an attempt to
assess and evaluate the progression and prognosis of the syndrome.
 A pulmonary artery catheter may be placed in order to provide initial and continual
monitor of heart pressures and responses to diuretic therapy (this is not a required
intervention).

COMPLICATIONS

Pleural effusion; Pleural effusion results from increasing pressure in the pleural capillaries.
A transudation of fluid occurs from these capillaries into the pleural space.

Dysrhythmias; Chronic HF causes enlargement of the chambers of the heart. This

enlargement may cause an alteration in the normal electrical pathway, especially in the atria.
Whennumerous sites in the atria fire spontaneously and rapidly, the organized spread of atrial
depolarization no longer occurs. This loss of the atrial contraction can reduce CO by 10% to
20%. Atrial fibrillation also promotes thrombus formation within the atria, which may break
loose and form emboli. Patients with atrial fibrillation are at risk for stroke and require
treatment with cardioversion, antidysrhythmics, and /or anticoagulants.

Patients with HF and an EF less than 35% have a high risk of fatal dysrhythmias;
nearly one half experience sudden cardiac death, usually due to ventricular ischemia causing
ventricular tachycardia or fibrillation.

Left ventricular thrombus; With ADHF or chronic HF, the enlarged LV and decreased CO
combine to increase the chance of thrombus formation in the LV. Once a thrombus has
formed, it may also decrease left ventricular contractility, decrease CO, and further worsen
the patient’s perfusion. The development of emboli from the thrombus also places the patient
at risk for stroke.
Hepatomegaly; The liver lobules become congested with venous blood. The hepatic
congestion leads to impaired liver function. Eventually liver cells die, fibrosis occurs, and
cirrhosis can develop.

Renal failure; The decreased CO that accompanies chronic HF results in decreased perfusion
to the kidneys and can lead to renal insufficiency or failure.

MANAGEMENT

Medical Treatment Options

Because congestive heart failure is considered to be “syndrome” rather than a disease

process; the most appropriate treatment regimen is one that focuses on treating the symptoms
and processes that present such as ischemia, atherosclerosis, inadequate systolic/diastolic
function, chest pain, excessive preload and renal artery stenosis. The goals of treating heart
failure are primarily to decrease the likelihood of disease progression (thereby decreasing the
risk of death and the need for hospitalization), to lessen symptoms, and to improve quality of
life.

The following medical treatment modalities should be considered for effective treatment of
congestive heart failure:

 CAB’s ( circulation, airway, breathing).

 Oxygen therapy as needed (100% non-rebreather mask or intubation with mechanical
ventilation may be initially required).
 Continuous cardiac/Pulse oximetry monitoring.
 Head of bed @ 30 degrees (this helps to reduce venous return).
 Pharmaceutical therapy often begins with nitrates and diuretics (appropriate
medication regimens are the major focus of treatment).
 Restrict sodium and fluid intake (strict I&O)
 Bed rest is tolerated (patients may not tolerate bed rest and may wish to sit up with
legs dangling off the bed).
 Pain relief (Morphine for chest pain).
 If a pulmonary artery catheter is placed; the following hemodynamic pressures should
be monitored for patients with congestive heart failure.

1. Cardiac Output (the amount of blood ejected from the heart per minute).
2. Cardiac Index (the cardiac output divided by the body surface area).
3. Central Venous Pressure (the pressure in the right atrium).
4. Preload/PAWP (the volume of blood in the ventricle at the end of diastole).
5. Afterload/SVR (the amount of work or resistance that the ventricles must over come
to eject stroke volume).
6. Pulmonary Artery Pressure (this is the pressure within the pulmonary bed).

Normal Hemodynamic Pressures

Hemodynamic Pressure Normal Value
Cardiac Output 4-8 L/min
 Cardiac Index 2.5-4 L/min
Central Venous Pressure (CVP) 2-8 mm Hg
Preload (PAWP) 8-12 mm Hg
Afterload (SVR) 800-1200 dynes
Pulmonary Artery Systolic Pressure 20-30 mm Hg
Pulmonary Artery Diastolic Pressure 6-12 mm Hg

Pharmaceutical Treatment Options

1. Vasodilator therapy decreases the workload of the heart by dilating peripheral

vessels.

Captopril (Capoten), Ramapril (Altace), or Zestril (Lisnopril) – Angiotensin

converting enzymes (ACE) inhibitors such as captopril are recommended for the
treatment of congestive heart failure because they produce vasodilation and
blockage of the RAAS process. By blocking the RAAS compensatory mechanism
Aldosterone and ADH are also blocked which prevents fluid retention. As a result
of these actions, captopril reduces preload and left ventricular filing pressures which
increase cardiac output. Dosage-12.5mg 2-3 times daily may be increased upto 50-
100mg 3 times daily. Side effects are hypotension, dizziness, loss of taste, cough,
hyperkalemia, acute renal failure, skin rash, angioedema.

Nitroglycerin – Nitrates such as Nitroglycerin cause vasodilation of the vessels and

help to decrease cardiac oxygen demand, cardiac preload and afterload while
increasing cardiac output. This in return helps to decrease venous return and
alleviates the heart from overworking. Dosage- SL- 0.3-0.6mg; may repeat qmin for
15min for acute atteack. PO; extended release capsules- 2.5-9mg q 8-12hr. IV-
5mcg/min .Side effects are hypotension, head-ache, vomiting and flushing.

Sodium nitroprusside---Direct arterial vasodilation reduces SVR and BP.. Side

effects are acute hypotension, N, V, muscle twitching. 
Human B-type natriuretic peptide (Nesiritide) used in patients with
decompensated heart failure. Dosage-IV-2mcg/kg bolus followed by
0.01mcg/kg/min as a continuous infusion. Side effects are hypotension , elevated
creatinine.

RESEARCH STUDY

effect of Vasodilator Therapy on Mortality in Chronic Congestive Heart Failure

 Jay N. Cohn, M.D., Donald G. Archibald, M.Phil.,

 Abstract
 To evaluate the effects of vasodilator therapy on mortality among patients with
chronic congestive heart failure, we randomly assigned 642 men with impaired
cardiac function and reduced exercise tolerance who were taking digoxin and a
diuretic to receive additional double-blind treatment with placebo, prazosin (20 mg
per day), or the combination of hydralazine (300 mg per day) and isosorbide dinitrate
(160 mg per day). Follow-up averaged 2.3 years (range, 6 months to 5.7 years).
 Mortality over the entire follow-up period was lower in the group that received
hydralazine and isosorbide dinitrate than in the placebo group. This difference was of
borderline statistical significance. For mortality by two years, a major end point
specified in the protocol, the risk reduction among patients treated with both
hydralazine and isosorbide dinitrate was 34 percent (P<0.028). The cumulative
mortality rates at two years were 25.6 percent in the hydralazine–isosorbide dinitrate
group and 34.3 percent in the placebo group; at three years, the mortality rate was
36.2 percent versus 46.9 percent. The mortality-risk reduction in the group treated
with hydralazine and isosorbide dinitrate was 36 percent by three years. The mortality
in the prazosin group was similar to that in the placebo group. Left ventricular
ejection fraction (measured sequentially) rose significantly at eight weeks and at one
year in the group treated with hydralazine and isosorbide dinitrate but not in the
placebo or prazosin groups.
 Our data suggest that the addition of hydralazine and isosorbide dinitrate to the
therapeutic regimen of digoxin and diuretics in patients with chronic congestive heart
failure can have a favorable effect on left ventricular function and mortality. (N Engl J
Med 1986; 314:1547–52.)

 Participants: VA Medical Centers, participating investigators, nurses, and technicians

2. Diuretics; It is used in HF to mobilize edematous fluid, reduce pulmonary venous

pressure, and reduce preload. Diuretics act on the kidney by promoting excretion of
sodium and water.

Loop diuretics (e.g furesemide, bumetanide, torsemide) are potent diuretics. These
drugs act on the ascending loop of Henle to promote sodium, chloride, and water
excretion.

Lasix-20-600mg as single daily dose.

Spironolactone is an expensive is an expensive , potassium- sparing diuretic that

promotes sodium and water excretion but blocks potassium excretion by blocking
receptors for aldosterone in the distal renal tubules. Dosage- 25-400mg as single
dose or divided upto 4 doses.

3. Beta-adrenergic blockers decrease myocardial workload and protect against

fatal dysrhythmias by blocking norepinephrine effects of the sympathetic nervous
system. Carvedilol (Coreg) – Coreg is a non-selective B-blocker that improves left
ventricular function and increases survival rates by increasing the force of
contraction. Because B-blockers have a negative inotropic effect, it is recommended
that they be titrated slowly after the patient has been stabilized with ACE inhibitors
and diuretics. Dosage- 3.125mg dailyfor 2wk; may be increases upto6.25mg twice
daily. Side effects are fluid and electrolyte imbalances and ototoxicity.
4. Positive inotropic agents increase the heart’s ability to pump more effectively
by improving the contractile force of the muscle.

Digitalis (Digoxin) – Digoxin is a cardiac glycoside that works by inhibiting the

sodium-potassium pump system. The result of this action is increased cardiac
contractility. Slows cardiac conduction through the AV node and therefore slows
the ventricular rate in instances of supraventricular dysrhythmias. Increases CO by
enhancing the force of contraction. Promotes dieresis by increasing CO.

Tablets-0.123, 0.25, 0.5mg

Capsules-0.05, 0.1, 0.2mg

Elixir-0.05mg/ml

Injection-0.25mg/ml, 0.1mg/ml

Digoxin toxicity---Fatigue, depression, malaise, N and V.

Changes in heart rhythm. ECG changes indicating SA or AV

block; new onset of irregular rhythm indicating ventricular dysrhythmias; and atrial
tachycardia with block, junctional tachycardia, and ventricular tachycardia.

Treatment----Digoxin immune FAB( Digibind)

Dopamine – Dopamine has both a and b-adrenergic effects (as well as dopaminergic
effects). At low doses (2-5 mcg/kg/min) it increases renal and mesenteric blood
flow. At moderate doses (5-10 mcg/kg/min) it has a positive inotrope affect which
increases blood pressure and cardiac output. At larger doses (10-20 mcg/kg/min) it
exhibits a pure alpha stimulation which causes peripheral vasoconstriction with both
increased systemic vascular resistance (SVR) and afterload.

1amp-200mg

A. 2ampule(400mg) in 500ml NS (1ml=800mcg)

2.5mcg/kg/min 1ml/hr
5 mcg/kg/min 20ml/hr
10 mcg/kg/min 40ml/hr
20 mcg/kg/min 80ml/hr
B. 2ampule(400mg) in 50ml NS (syringe pump) (1ml=800mcg)

2.5 mcg/kg/min 1ml/hr

5 mcg/kg/min 2ml/hr
10mcg/kg/min 4ml/hr
20mcg/kg/min 8ml/hr
C. 2ampule in 100ml NS (1ml=4000mcg)
 2.5 mcg/kg/min 2ml/hr
5 mcg/kg/min 4ml/hr
10 mcg/kg/min 8ml/hr
20 mcg/kg/min 16ml/hr
Side effects are arrhythmias, hypotension and dyspnea

Dobutamine – Dobutamine stimulates B-receptors of the heart and provide a direct

acting positive inotrope effect. Dobutamine increases stroke volume and cardiac
output by increasing cardiac contractility while decreasing SVR. By increasing
contractility and cardiac output; there is more oxygen rich blood available for
damaged tissue. 

1amp=250mg (dose 2.5 mcg/kg/min-40mcg)

A.2amp (500mg) in 500ml NS (1ml=1000mcg)

2.5 mcg/kg/min 9ml/hr

5 mcg/kg/min 18ml/hr

10 mcg/kg/min 36ml/hr

20 mcg/kg/min 72ml/hr

40 mcg/kg/min 144ml/hr

B. 2 amp in 100ml NS (1ml=5000mcg)

2.5 mcg/kg/min 2ml/hr

5 mcg/kg/min 4ml/hr

10 mcg/kg/min 8ml/hr

20 mcg/kg/min 15ml/hr

40 mcg/kg/min 30ml/hr

C.1amp(250mg) in 50ml NS (syringe pump) 1amp=20ml, hence only one ampule is

used, 1ml=5000mcg

2.5 mcg/kg/min 2 ml/hr

5 mcg/kg/min 4ml/hr

10 mcg/kg/min 8ml/hr

20 mcg/kg/min 15ml/hr

40 mcg/kg/min 30ml/hr
 Side effects are hypertension, increased heart rate and premature ventricular
contraction.

Β- adrenergic agonists ---Potential problems related to long term treatment include tolerance,
increased ventricular irritability, and increased need for oxygen by the myocardium.

Calcium sensitizers---These are the positive ionotropic agents. They improve

cardiac performance by interacting directly with contractile proteins without
affecting intracellular calcium concentrations or increasing myocardial oxygen
demand.eg Levosimendan…

5. Angiotensin II-receptor blockers (ARBs) similar to ACE inhibitors. Used

in patients who cannot tolerate ACE inhibitors due to cough or angioedema .Eg.
Cindesartan,Telmisartan---Prevent action of angiotensin 2 and produce vasodilation
and increased salt and water excretion. Dosage 50mg/day. Side effects are
Hyperekalemia, decreased renal function.

6. Morphine – Because catecholamines are released in response to the anxiety and pain
associated with suffering an acute MI (increasing the workload of the heart),
Morphine can be used to help reduce the pain that can be associated with congestive
heart failure. Morphine is also beneficial in reducing the hemodynamic workload by
increasing venous capacitance and reducing systemic vascular resistance (therefore
decreasing myocardial oxygen demand).

7. Milrinone (Incor) – Milrinone is a phosphodiesterase inhibitor that may be effective

in the treatment of exacerbations of congestive heart failure. Milrinone decreases or
inhibits the breakdown of cyclic AMP resulting in an increase in cardiac contraction
and arterial venous dilation.

NUTRITIONAL THERAPY; CHRONIC HEART FAILURE

Diet education and weight management are critical to the patient’s control of
chronic HF. The nurse or dietitian should obtain a detailed diet history, determining
not only what foods the patient eats and when, but also the socio- cultural value of
food to the patient.

 Dietary Recommendations

The Dietary Approaches to Stop Hypertension (DASH) diet is effective as a first-line

therapy for many individuals with isolated systolic hypertension. The average adult’s
daily dietary intake of sodium ranges from 7 to 15 g.
A 2-g sodium diet is frequently recommended. However, no studies have been
conducted to evaluate specific recommendations related to sodium restriction. A 2-g
sodium diet is unpalatable for some patients, whereas a 3-g sodium diet may be a
more realistic target for patients with mild to moderate heart failure. It can be
 achieved by avoiding salty foods (eg, canned or frozen foods) and by not adding salt
to foods after cooking. If patients require large doses of diuretics to prevent fluid
retention, sodium intake will have to be more severely restricted, which requires the
careful reading of food labels. Dietary instruction must take into account ethnic
preferences and may require individualized counseling by a dietitian.

SODIUM CONTENT IN DIFFERENT FOOD GROUPS

FOOD GROUPS SODIUM (Mg)

Grains and grain products
Cooked cereal, rice, pista, unsalted, ½ 0-5
cup
Bread, 1 slice 110-175
Vegetables
Fresh or frozen, cooked without salt, ½ 1-70
cup
Canned or frozen with sauce, ½ cup 140-460
Tomato juice, canned , ¾ cup 820
Fruit
Fresh, frozen, canned, ½ cup 0-5
Low- Fat or Fat- Free Dairy Foods
Milk, 1 cup 120
Natural cheeses, 1 ½ oz 110-450
Processed cheeses 1 ½ oz 600
Nuts , seeds, and dry beans
Peanuts, salted,1/3 cup 120
Peanuts, unsalted, 1/3 cup 0-5
Beans, cooked from dried or frozen, 400
without salt, ½ cup
Meats, fish, and poultry
Fresh meat, fish, poultry, 3 oz 30-90

 Similarly, patients who require large doses of diuretics or who have hyponatremia
may also have to restrict their fluids to ≤2 L/d. Anecdotally, a significant number of
patients with heart failure are under the misperception that taking diuretics requires
"flushing the kidneys" with large amounts of fluids; this misperception should be
quickly corrected. For some patients, fluid restrictions are difficult to follow because
of excessive thirst related to decreased cardiac output. Suggestions for satisfying their
thirst with sugarless hard candy or ice chips may prove helpful.

 Alcohol is usually prohibited because its acute ingestion depresses myocardial

contractility in patients with known cardiac disease. However, no studies of the effect
of moderate ingestion of alcohol on functional status or death have been conducted. In
general, alcohol use should be discouraged and should be prohibited for patients with
alcohol-induced cardiomyopathy.
  Other dietary restrictions should be discouraged unless clearly indicated (eg, a low-
fat, low-cholesterol diet for hypercholesterolemia in patients with ischemic
cardiomyopathy or a reduced-calorie diet for obese patients). Although some heart
failure patients are obese, other patients with advanced heart failure experience a
syndrome of chronic wasting, which can be exacerbated by unnecessary dietary
restrictions. Frequent, small meals may combat the effect of anorexia caused by
congestion of the gastrointestinal tract.

Nursing Care and Management

Assessment/Interventions:

 Monitor vital signs/oxygenation/Neuro status (report changes in heart and respiratory

rate/patterns as well as changes in LOC).
 Daily weight (a 2.2 kg weight increase over a 1 day period is considered significant).
 Breath sounds (monitor for increased crackles, rhonchi or pulmonary congestion).
 Capillary refill (if greater than 3 seconds, assess for signs of peripheral edema).
 The presence of jugular vein distention (jugular vein distention can be a sign of
worsening right sided heart failure).
 The presence of hepatomegaly (also a sign of worsening right sided heart failure).
 The presence of ascites (also a sign of worsening right sided heart failure).
 EKG changes
 Evaluate electrolyte levels (sodium, potassium and creatinine)
 Digoxin levels (if patient taking Digoxin)
 Pain level (degree, quality, source, location, onset and relieving factors)
 Intake and Output (monitor effects of diuretic therapy and observe for signs and
symptoms of either fluid overload or deficit)
 Assess degree of discomfort associated with activity (provide a proper rest/activity
balance. Group nursing interventions when appropriate).
 Monitor for restless, anxious behavior and promote self care participation.
 Maintain adequate bowel function (stool softeners such as Colace should be ordered
to prevent constipation).

Patient Teaching:

 The following patient/family education should be provided prior to discharge and

should also be reiterated at post discharge office visits:

Health promotion;

 Obtain annual flu vaccination.

 Obtain pneumococcal vaccine and revaccination after 5yr.
 Consider smoking cessation and weight reduction if appropriate.

Rest;

 Plan a daily rest and activity program

  Avoid emotional upsets. Verbalize any concerns, fears , feelings of depression etc to
health care provider

Drug therapy

 Take each drug as prescribed daily.

 Develop a check-off system to ensure medication have been taken.
 Take pulse rate each day before taking medications.
 Know your target BP limits.
 Know signs and symptoms of orthostatic hypotension and how to prevent them.
 Know signs and symptoms of internal bleeding.(bleeding gums, increased bruises,,
blood in stool and urine.)
 Know own INR if taking warfarin and how often to have blood monitored.

Dietary therapy

 Consult the written diet plan and list of permitted and restricted foods
 Avoid to use too much salt.
 Weigh daily
 Report weight gain of 1.4kg in 2 days, or 2.3kg in a wk.
 Eat smaller, more frequent meals.

Activity program

 Increase walking and other activities gradually

 Avoid extremes of cold and heat.

Ongoing monitoring

 Know the signs and symptoms of recurring or progressing heart failure.

 Report immediately---Difficulty breathing, waking up breathless at night, Frequent
dry, hacking cough, fatigue, weakness, Edema, N and abdominal pain, dizziness or
fainting

Follow up regularly.

Stages of Heart Failure

In 2001, the American Heart Association (AHA) and American College of Cardiology (ACC)
developed the "Stages of Heart Failure."

Usual Treatments

Stage A

People at high risk of developing heart failure (pre-heart failure), including people with:

 High blood pressure

 Diabetes
 Coronary artery disease
  Metabolic syndrome
 History of cardiotoxic drug therapy
 History of alcohol abuse
 History of rheumatic fever
 Family history of cardiomyopathy

Exercise regularly.

 Quit smoking
 Treat high blood pressure
 Treat lipid disorders
 Discontinue alcohol or illegal drug use
 An angiotensin converting enzyme inhibitor (ACE inhibitor) or an angiotensin II
receptor blocker (ARB) is prescribed if you've had a coronary artery disease or if you
have diabetes, high blood pressure, or other vascular or cardiac conditions
 Beta blockers may be prescribed if you have high blood pressure or if you've had a
previous heart attack

Stage B

People diagnosed with systolic left ventricular dysfunction but who have never had
symptoms of heart failure (pre-heart failure), including people with:

 Prior heart attack

 Valve disease
 Cardiomyopathy

The diagnosis is usually made when an ejection fraction of less than 40% is found during an
echocardiogram test.

 Treatment methods above for Stage A apply

 All patients should take an angiotensin converting enzyme inhibitor (ACE inhibitors)
or angiotensin II receptor blocker (ARB)
 Beta-blockers should be prescribed for patients after a heart attack
 Surgery options for coronary artery repair and valve repair or replacement (as
appropriate) should be discussed

If appropriate, surgery options should be discussed for patients who have had a heart attack.

Stage C

Patients with known systolic heart failure and current or prior symptoms. Most common
symptoms include:

 Shortness of breath
 Fatigue
 Reduced ability to exercise
  Treatment methods above for Stage A apply
 All patients should take an angiotensin converting enzyme inhibitor (ACE inhibitors)
and beta-blockers
 African-American patients may be prescribed a hydralazine/nitrate combination if
symptoms persist
 Diuretics (water pills) and digoxin may be prescribed if symptoms persist
 An aldosterone inhibitor may be prescribed when symptoms remain severe with other
therapies
 Restrict dietary sodium (salt)
 Monitor weight
 Restrict fluids (as appropriate)
 Drugs that worsen the condition should be discontinued
 As appropriate, cardiac resynchronization therapy (biventricular pacemaker) may be
recommended
 An implantable cardiac defibrillator (ICD) may be recommended

Stage D

Patients with systolic heart failure and presence of advanced symptoms after receiving
optimum medical care.

 Treatment methods for Stages A, B & C apply

 Patient should be evaluated to determine if the following treatments are available
options: heart transplant, ventricular assist devices, surgery options, research
therapies, continuous infusion of intravenous inotropic drugs and end-of-life
(palliative or hospice) care

How Can I Prevent Heart Failure From Worsening?

 Keep your blood pressure low. In heart failure, the release of hormones causes the
blood vessels to constrict or tighten. The heart must work hard to pump blood through
the constricted vessels. It is important to keep your blood pressure as low as possible,
so that your heart can pump effectively without extra stress.
 Monitor your own symptoms. Check for changes in your fluid status by weighing
yourself daily and checking for swelling. Call your doctor if you have unexplained
weight gain (3 pounds in one day or 5 pounds in one week) or if you have increased
swelling.
 Maintain fluid balance. Your doctor may ask you to keep a record of the amount of
fluids you drink or eat and how often you go to the bathroom. Remember, the more
fluid you carry in your blood vessels, the harder your heart must work to pump excess
fluid through your body. Limiting your fluid intake to less than 2 liters per day will
help decrease the workload of your heart and prevent symptoms from recurring.
 Limit how much salt (sodium) you eat. Sodium is found naturally in many foods we
eat. It is also added for flavoring or to make food last longer. If you follow a low-
sodium diet, you should have less fluid retention, less swelling, and breathe easier.
 Monitor your weight and lose weight if needed. Learn what your "dry" or "ideal"
weight is. Dry weight is your weight without extra water (fluid). Your goal is to keep
your weight within 4 pounds of your dry weight. Weigh yourself at the same time
each day, preferably in the morning, in similar clothing, after urinating but before
 eating, and on the same scale. Record your weight in a diary or calendar. If you gain
two pounds in one day or five pounds in one week, call your doctor. Your doctor may
want to adjust your medications.
 Monitor your symptoms. Call your doctor if new symptoms occur or if your
symptoms worsen. Do not wait for your symptoms to become so severe that you need
to seek emergency treatment.
 Take your medications as prescribed. Medications are used to improve your heart's
ability to pump blood, decrease stress on your heart, decrease the progression of heart
failure, and prevent fluid retention. Many heart failure drugs are used to decrease the
release of harmful hormones. These drugs will cause your blood vessels to dilate or
relax (thereby lowering your blood pressure).
 Schedule regular doctor appointments. During follow-up visits, your doctors will
make sure you are staying healthy and that your heart failure is not getting worse.
Your doctor will ask to review your weight record and list of medications. If you have
questions, write them down and bring them to your appointment. Call your doctor if
you have urgent questions. Notify all your doctors about your heart failure,
medications, and any restrictions. Also, check with your heart doctor about any new
medications prescribed by another doctor. Keep good records and bring them with
you to each doctor visit.

LIFE STYLE MODIFICATIONS

In an effort to prevent further heart damage:

 Stop smoking or chewing tobacco.

 Reach and maintain your healthy weight.
 Control high blood pressure, cholesterol levels, and diabetes.
 Exercise regularly.
 Do not drink alcohol.
 Have surgery or other procedures to treat your heart failure as recommended.

What Medications Should Avoid If the Patient Has Heart Failure?

There are several different types of medications that are best avoided in those with heart
failure including:

 Nonsteroidal anti-inflammatory medications such as Motrin or Aleve. For relief of

aches, pains, or fever take Tylenol instead.
 Most antiarrhythmic agents
 Most calcium channel blockers (if you have systolic heart failure)
 Some nutritional supplements, such as salt substitutes, and growth hormone therapies
 Antacids that contain sodium (salt)
 Decongestants such as Sudafed

If you are taking any of these drugs, discuss them with your doctor.

It is important to know the names of your medications, what they are used for, and how often
and at what times you take them. Keep a list of your medications and bring them with you to
each of your doctor visits. Never stop taking your medications without discussing it with your
doctor. Even if you have no symptoms, your medications decrease the work of your heart so
that it can pump more effectively.

How Can A Patient Improve His Quality of Life With Heart Failure?

There are several things you can do to improve your quality of life if you have heart failure.
Among them:

 Eat a healthy diet. Limit your consumption of sodium (salt) to less than 2,000
milligrams (2 grams) each day. Eat foods high in fiber. Limit foods high in fat,
cholesterol, and sugar. Reduce total daily intake of calories to lose weight if
necessary.
 Exercise regularly. A regular cardiovascular exercise program, prescribed by your
doctor, will help improve symptoms and strength and make you feel better. It may
also decrease heart failure progression.
 Don't overdo it. Plan your activities and include rest periods during the day. Certain
activities, such as pushing or pulling heavy objects and shoveling may worsen heart
failure and its symptoms.
 Weigh regularly.
 Restrict fluid intake to no more than 2L.
 Prevent respiratory infections. Ask your doctor about flu and pneumonia vaccines.
 Take your medications as prescribed. Do not stop taking them without first
contacting your doctor.
 Get emotional or psychological support if needed. Heart failure can be difficult for
your whole family. If you have questions, ask your doctor or nurse. If you need
emotional support, social workers, psychologists, clergy, and heart failure support
groups are a phone call away. Ask your doctor or nurse to point you in the right
direction.

 Activity and Exercise


Given current evidence, patients should be encouraged to stay as active as possible,
including sexual activity and a moderate exercise regimen. After many years of
restricting patients with heart failure from aerobic exercise, researchers have
demonstrated that aerobic exercise training in patients results in improved exercise
duration, less fatigue, faster pace of activities, and improved general well-being. To
date, there are no data on the benefit or harm of a strength or resistance exercise
program. Given the threat of complications related to increased myocardial oxygen
demand in the face of isometric exercise, patients are usually counseled to avoid
lifting a significant weight (eg, >20 lb) or performing exercises that cause a patient to
strain (eg, performing a Valsalva maneuver).

 Sexual problems are well documented and should be carefully assessed by the
practitioner. Fears about physical exertion or symptoms may contribute unnecessarily
to sexual difficulties. Sexual practices may have to be modified to accommodate
patients with limited exercise tolerance, and practitioners should be proactive in
raising this topic to avoid unnecessary anxiety on the part of the patient or partner.
RESEARCH STUDY

Health related quality of life in patients with congestive heart failure: comparison with
other chronic diseases and relation to functional variables

1. J Juenger1,
2. D Schellberg1

Abstract

Objective: To assess health related quality of life of patients with congestive heart failure; to
compare their quality of life with the previously characterised general population and in those
with other chronic diseases; and to correlate the different aspects of quality of life with
relevant somatic variables.

Setting: University hospital.

Patients and design: A German version of the generic quality of life measure (SF-36)
containing eight dimensions was administered to 205 patients with congestive heart failure
and systolic dysfunction. Cardiopulmonary evaluation included assessment of New York
Heart Association (NYHA) functional class, left ventricular ejection fraction, peak oxygen
uptake, and the distance covered during a standardised six minute walk test.

Results: Quality of life significantly decreased with NYHA functional class (linear trend: p <
0.0001). In NYHA class III, the scores of five of the eight quality of life domains were
reduced to around one third of those in the general population. The pattern of reduction was
different in patients with chronic hepatitis C and major depression, and similar in patients on
chronic haemodialysis. Multiple regression analysis showed that only the NYHA functional
class was consistently and closely associated with all quality of life scales. The six minute
walk test and peak oxygen uptake added to the explanation of the variance in only one of the
eight quality of life domains (physical functioning). Left ventricular ejection fraction,
duration of disease, and age showed no clear association with quality of life.

Conclusions: In congestive heart failure, quality of life decreases as NYHA functional class
worsens. Though NYHA functional class was the most dominant predictor among the
somatic variables studied, the major determinants of reduced quality of life remain unknown.

SURGICAL MANAGEMENT

In heart failure, surgery is aimed at stopping further damage to the heart and improving the
heart's function. Procedures used include:

 Coronary artery bypass grafting surgery. The most common surgery for heart
failure is bypass surgery. Your doctor will determine if your heart failure is caused by
coronary artery disease and if you have blockages that can be bypassed. Although
surgery is more risky for people with heart failure, new strategies before, during, and
after surgery have reduced the risks and improved outcomes.
 Heart valve surgery . Diseased heart valves can be treated both surgically
(traditional heart valve surgery) and non-surgically (balloon valvuloplasty).
  Implantable left ventricular assist device (LVAD). The LVAD is known as the
"bridge to transplantation" for patients who haven't responded to other treatments and
are hospitalized with severe systolic heart failure. This device helps your heart pump
blood throughout your body. It allows you to be mobile, sometimes returning home to
await a heart transplant. It may also be used as destination therapy for long-term
support in patients who are not eligible for transplant.
 Heart transplant- A heart transplant is considered when heart failure is so severe that
it does not respond to all other therapies, but the person's health is otherwise good.

NURSING MANAGEMENT

ASSESSMENT

The nursing assessment for the patient with HF focuses on observing for effectiveness of
therapy and for the patient’s ability to understand and implement self-management strategies.
Signs and symptoms of pulmonary and systemic fluid overload are recorded and reported
immediately so that adjustments can be made in therapy. The nurse also explores the patiet’s
emotional response to the diagnosis of HF, a chronic illness.

Patients Health History

 Obtain history of symptoms, limits of activity, response to rest, and history of

response to drug therapy.
 The nurse explores sleep disturbances, particularly sleep suddenly interrupted by
shortness of breath.
 The nurse also asks about the number of pillows needed for sleep (an indication of
orthopnea), activities of daily living, and the activities that cause shortness of breath.
 The nurse helps patients to identify things that they have lost because of the diagnosis,
their emotional response to that loss, and successful coping skills that they have used
previously.
 Family and significant others are often included in these discussions.

Physical Examination Nursing Care Plans for Congestive Heart Failure (CHF).

 Assess peripheral arterial pulses; note quality, character; assess heart rhythm and rate
and BP; assess edema.
 Inspect and palpate precordium for lateral displacement of PMI.
 Obtain hemodynamic measurements as indicated and note change from baseline.
 Assess weight and ask about baseline weight.
 Note results of serum electrolyte levels and other laboratory tests.
 Identify sleep patterns and sleep aids commonly used by patient.

Nursing Diagnosis Nursing Care Plans for Congestive Heart Failure

(CHF).

 Decreased Cardiac Output related to impaired contractility and increased

preload and afterload as manifested by increased HR, dysrhythmias, ECG
changes, Changes in BP, extra heart sounds, decreased urine output
 Desired outcome; Patient will display vital signs within acceptable limits,
dyrhythmias absent/controlled, and no symptoms of failure.

Place patient at physical and emotional rest to reduce work of heart.

o Provide rest in semi-recumbent position or in armchair in air-conditioned

environment reduces work of heart, increases heart reserve, reduces BP,
decreases work of respiratory muscles and oxygen utilization, improves
efficiency of heart contraction; recumbency promotes diuresis by improving
renal perfusion.
o Provide bedside commode to reduce work of getting to bathroom and for
defecation.
o Provide for psychological rest emotional stress produces vasoconstriction,
elevates arterial pressure, and speeds the heart.

 Evaluate frequently for progression of left-sided heart failure. Take frequent BP

readings.

 Auscultate heart sounds frequently and monitor cardiac rhythm.

 Observe for signs and symptoms of reduced peripheral tissue perfusion: cool
temperature of skin, facial pallor, poor capillary refill of nail beds.

 Administer pharmacotherapy as directed.

Monitor clinical response of patient with respect to relief of symptoms (lessening

dyspnea and orthopnea, decrease in crackles, relief of peripheral edema

 Impaired Gas Exchange related to alveolar edema due to elevated ventricular

pressure as manifested by decreased oxygen saturation level and changes in
ABGs.

Desired outcome; Patient will demonstrate adequate ventilation and oxygenation of

tissues by ABGs/ oximetry within client’s normal ranges and free of symptoms of
respiratory dstress.

 Raise head of bed 8 to 10 inches (20 to 30 cm) reduces venous return to heart and
lungs; alleviates pulmonary congestion.
o Support lower arms with pillows to eliminate pull of their weight on shoulder
muscles.
o Sit orthopneic patient on side of bed with feet supported by a chair, head and
arms resting on an over-the-bed table, and lumbosacral area supported with
pillows.
 Auscultate lung fields at least every 4 hours for crackles and wheezes in dependent
lung fields (fluid accumulates in areas affected by gravity).

 Observe for increased rate of respirations (could be indicative of falling arterial pH).
 Observe for Cheyne-Stokes respirations (may occur in elderly patients because of a
decrease in cerebral perfusion stimulating a neurogenic response).
 Position the patient every 2 hours (or encourage the patient to change position
frequently) to help prevent atelectasis and pneumonia.
 Encourage deep-breathing exercises every 1 to 2 hours to avoid atelectasis.
 Offer small, frequent feedings to avoid excessive gastric filling and abdominal
distention with subsequent elevation of diaphragm that causes decrease in lung
capacity.

Administer oxygen as directed.

 Excess Fluid Volume related to sodium and water retention as manifested by

orthopnea, S3 heart sound, oliguria, edema, JVD, weight gain, HTN, respiratory
distress and abnormal breath sounds

Desired outcome; Patient will demonstrate stabilized fluid volume with balanced intake
and output, breath sounds clear/ clearing, vital signs within acceptable range, stable
weight, and absence of edema.

 Administer prescribed diuretic as ordered.

 Give diuretic early in the morning nighttime diuresis disturbs sleep.
 Keep input and output record patient may lose large volume of fluid after a single
dose of diuretic.
 Weigh patient daily to determine if edema is being controlled: weight loss should not
exceed 1 to 2 lb (0.5 to 1 kg)/day.
 Assess for signs of hypovolemia caused by diuretic therapy thirst, decreased urine
output, orthostatic hypotension, weak, thready pulse, increased serum osmolality, and
increased urine specific gravity.
 Be alert for signs of hypokalemia, which may cause weakening of cardiac
contractions and may precipitate digoxin toxicity in the form of dysrhythmias,
anorexia, nausea, vomiting, abdominal distention, paralytic ileus, paresthesias, muscle
weakness and cramps, confusion.
 Give potassium supplements as prescribed.
 Be aware of disorders that may be worsened by diuretic therapy including
hyperuricemia, gout, volume depletion, hyponatremia, magnesium depletion,
hyperglycemia, and diabetes mellitus. Also, note that some patients allergic to sulfa
drugs may also be allergic to thiazide diuretics.
 Watch for signs of bladder distention in elderly male patients with prostatic
hyperplasia.
 Administer I.V. fluids carefully through an intermittent access device to prevent fluid
overload.
 Monitor for pitting edema of lower extremities and sacral area. Use convoluted foam
mattress and sheepskin to prevent pressure ulcers (poor blood flow and edema
increase susceptibility).
 Observe for the complications of bed rest pressure ulcers (especially in edematous
patients), phlebothrombosis, pulmonary embolism.
 Be alert to complaints of right upper quadrant abdominal pain, poor appetite, nausea,
and abdominal distention (may indicate hepatic and visceral engorgement).
 Monitor patient’s diet. Diet may be limited in sodium to prevent, control, or eliminate
edema; may also be limited in calories.
 Caution patients to avoid added salt in food and foods with high sodium content

 Activity Intolerance related to oxygen supply and demand imbalance as

manifested by weakness, fatigue, changes in vital signs, presence of
dysrhythmias, dyspnea, pallor, diaphoresis.

Desired outcome; Patient will participate in desired activities; meet own self care needs.

 Increase patient’s activities gradually. Alter or modify patient’s activities to keep

within the limits of his cardiac reserve.
o Assist patient with self-care activities early in the day (fatigue sets in as day
progresses).
o Be alert to complaints of chest pain or skeletal pain during or after activities.
 Observe the pulse, symptoms, and behavioral response to increased activity.
o Monitor patient’s heart rate during self-care activities.
o Allow heart rate to decrease to preactivity level before initiating a new
activity.

Relieve nighttime anxiety and provide for rest and sleep patients with heart failure
have a tendency to be restless at night because of cerebral hypoxia with superimposed
nitrogen retention. Give appropriate sedation to relieve insomnia and restlessness.

Main Nursing interventions for Congestive Heart Failure CHF is To conserve her or his
energy and to maximize the oxygen that is available for body processes, below is examples
for Nursing interventions for Congestive Heart Failure CHF:

 Place the patient in Fowler's position and give him supplemental oxygen to help him
breathe more easily. Organize all activity to provide maximum rest periods.
 Weigh the patient daily, and check for peripheral edema. Also, monitor I.V. intake
and urine output especially for patient with diuretic
 Assess vital signs and mental status. Auscultation for abnormal heart and breath
sounds.
 Frequently monitor blood urea nitrogen and serum creatinine, potassium, sodium,
chloride, and magnesium levels.
 Provide continuous cardiac monitoring during acute and advanced stages to identify
and treat arrhythmias promptly.
 To prevent deep vein thrombosis from vascular congestion, help the patient with
range-of-motion exercises. Apply antiembolism stockings as needed. Check for calf
pain and tenderness.
 Monitor the patient for signs and symptoms of fluid overload, impaired gas exchange,
and activity intolerance
 explanation of the disease process helps the patient understand the need for the
prescribed medications, activity restrictions, diet, fluid restrictions, and lifestyle
changes.
 Helping the patient work through and verbalize these feelings may improve
psychological well-being
 assess abnormal response to increased activity
 Increase client activity each shift according to the indications
 Increase of activity when no complaint Dyspnea, or not perceived Dyspnea increases
  Increase the time down from the bed to 15 minutes per shift
 Neurological Monitoring
 Environmental management
 Oxygen therapy
 Fluid Management
 Respiratory Management
 Self care assistance

Deficient knowledge regarding condition, treatment regimen, self-care, and

discharge needs related to lack of understanding/ misconceptions about
interrelatedness of cardiac function/ disease/failure as manifested by questions,
statement of concern/misconceptions.

Desired outcome; Patient will identify relationship of ongoing therapies to reduction of

recurrent episodes and prevention of complications.

 Discuss normal heart function

 Reinforce treatment rationale
 Encourage developing a regular home exrcise program and provide guidelines for
sexual activity.
 Discuss importance of sodium limitation
 Review medications ,purpose, and side effects
 Recommend taking diuretic early in the morning.
 Instruct and receive return demonstration of ability to monitor pulse and BP
 Explain client’s role in control of risk factors.
 Review signs and symptoms which require immediate medical attention
 Provide opportunities to ask questions

CONCLUSION

The incidence of heart failure is increasing. It is therefore incumbent on healthcare

providers to evaluate their heart failure practices and to incorporate the most current knowledge of the
pathophysiology, assessment, and treatment modalities for heart failure into their patient care. Current
practice guidelines provide a basis for the treatment of patients with heart failure. Critical to the
success of heart failure management is the discharge planning process and follow-up in the outpatient
setting. Integration of medical care and patient education with close communication between inpatient
and outpatient care providers is essential. Monitoring and enhancement of patient compliance are the
responsibility of both in-hospital and outpatient heart failure team members. An integrated and
innovative approach to the management of heart failure patients based on consensus recommendations
can contribute to improved patient outcomes, including reduced morbidity rates, improved functional
status and quality of life, enhanced compliance, reduced rates of rehospitalization, reduced costs, and
prolonged survival.

BIBLIOGRAPHY

Lewis, Heitkemper, Dirksen, O’Brien, Bucher, ‘Lewis’s medical surgical nursing’, Mosby-Elsevier,
page no;820-830

Linton, ‘Introduction to medical- surgical nursing’, Saunders- Elsevier’4th edition, Page no; 660-665
BOOK REFERENCE

Joan Luckmann, ‘Saunders manual of nursing care’ w.b saunders company, 9th edition,page no;1068-
1080

Joyce M Black, Jane Hokanson,’Medical surgical nursing’ ,Saunders-Elsevier,7th edition, page

no;1648-1668

Suzanne C Smeltzer, Brenda Bare,’Brunner $ Suddath’s textbook of medical surgical

nursing’,Lippincott Williams $ Wilkins,10th edition,page no;789-806

JOURNEL REFERENCE

V. Bhavani ,Indian journel of holistic nursing,’ Cardiac rehabilitation’ June 2011, Volume 7, Number
1, page no;3-7

Lacey Buckler, Nursing Made Incredibly Easy, May/ June 2009, page no;12-20

Nursing made incredibly easy, March- April 2012, Page no;15-20

WEB REFERENCE

 dynamicnursingeducation.com/class.php?class_id=130&pid=23
www.lifenurses.com › Nursing Care Plans