V.S.P.

M’s COLLEGE OF NURSING AND RESEARCH

CENTER, DIGDOH HILLS, HINGNA ROAD, NAGPUR

SEMINAR

ON

CONGESTIVE CARDIAC FAILURE

SUBMITTED TO,
Mrs. Lata sukare

professor

V.S.P.M.’S

College of Nursing and R.C

SUBMITTED BY,

Miss. Manmeet Kaur Babra

MSC Nursing IIndyear

V.S.P.M.’S

College of Nursing and R.C

Submission date:

10/01/2018
GENERAL OBJECTIVE :

At the end of the seminar the student will be able to gain in depth of knowledge
regarding congestive cardiac failure and will able to apply in teaching as well as clinical areas.

SPECIFIC OBJECTIVE :

At the end of the seminar the student will able to know about:

 define congestive cardiac failure

 review anatomy and physiology of cardiovascular system
 discuss the incidence and prevalence rate of congestive cardiac failure.
 enlist the etiological factors of congestive cardiac failure.
 classify the category of congestive cardiac failure.
 discuss the decompensated mechanism of heart failure.
 explain the pathophysiology of congestive cardiac failure.
 elaborate the clinical manifestation of congestive cardiac failure.
 explain the diagnostic evaluation of congestive cardiac failure.
 list down the complication of congestive cardiac failure.
 explain the management of congestive cardiac failure.
 discuss the preventive measures of congestive cardiac failure.
OUTLINE

1) Introduction.
2) Definition.
3) Anatomy and physiology of heart.
4) Incidence and prevalence rates.
5) Etiological factors.
6) Category of congestive cardiac failure.
7) Decompensated mechanism of heart failure.
8) Pathophysiology.
9) Clinical manifestation.
10) Diagnostic evaluation.
11) Complications.
12) Management.
 Medical management.
 Surgical management.
 Nursing management.
13) Preventive measures.
14) Research articles
15) Conclusion.
16) Summary.
17) Bibilograpy
INTRODUCTION

Congestive cardiac failure is as a physiologic state in which the heart cannot pump enough
blood to meet the metabolic need of the body ( determined as oxygen consumption ). Congestive
cardiac failureresults from changes in systolic or diastolic function of the left ventricle . the
heart fails when , because of structural defect, it cannot handle normal blood volume or in the
absence of the diseases cannot tolerate a sudden expansion in blood volume ( e.g during the
exercise ) . Congestive cardiac failureis not a disease itself ; instead the term refers to a clinical
syndrome characterized by manifestation of volume overload , inadequate tissue perfusion and
poor exercise tolerance . Whatever the cause , pump failure result in hypoperfusion of tissues ,
followed by pulmonary and systemic venous congestion, it is often called congestive cardiac
failure, although most cardiac specialist no longer use this term . other term used to denote heart
failure include chronic heart failure, cardiac decompensation , cardiac insuffiency, and
ventricular failure.
DEFINATION

Congestive cardiac failure in which the heart’s function as a pump is inadequate to deliver the
oxygen rich blood to the body .It is a serious , progressive condition that is usually chronic and
can be life- threatening.
ANAOMY AND PHYSIOLOGY OF HEART

Location of the heart

 The heart is relatively small, roughly the same size (but not the same shape) as close fist.

 It is about 12cm (5 in.) long, 9cm (3.5 in.) wide at its broadest point, and 6cm (2.5 in.)
thick, with an average mass of 250 g. (8 oz) in adult females and 300g. (10 oz) in adult
males.

 The heart rest on the diaphragm, near the midline of the thoracic cavity.

 The pointed apex is formed by the tip of the left ventricle (a lower chamber of the heart)

 The base of the heart is its posterior surface. It is formed by the atria (upper chamber) of
the heart, mostly the left atrium

PERICARDIUM

 The membrane that surrounds and protects the heart is the pericardium

 It confines the heart to its position in the mediastinum, while allowing sufficient freedom
of movement for vigorous and rapid contraction.

 The pericardium consist of two main parts

• The fibrous pericardium

• The serious pericardium

• The fibrous pericardium is composed of tough, inelastic, dense irregular connective

tissue. Its resembles a bag that rest on and attaches to the diaphragm; its open end is fused
to the connective tissue of the blood vessels entering and leaving the heart

• The serious pericardium is a thinner, more delicate membrane that forms a double layer
around the heart

• Outer parietal layers

• Inner visceral layer

CONDUCTIVE SYSTEM OF THE HEART

The heart possesses the property of autorhythmicity, which means it generate its own electrical
impulses and beats independently of nervous or hormonal control, i.e. it is not reliant on external
mechanism to initiates each heartbeat. However, it is supplied with both sympathetic and
parasympathetic nerve fibres, which increase and decrease respectively the intrinsic heart rate. In
addition, the heart responds to a number of circulating hormones, including adrenaline
(epinephrine) and thyroxine. Small group of specialized neuromuscular cells in the myocardial
initiate and conduct impulses, causing coordinated and synchronised contraction of the heart
muscle.

The main components of the cardiac conduction system are :

1. Sinoatrial node
2. Atrioventricular node
3. Bundle of his
4. Bundle branches
5. Purkinje fiber

Sinoatrial node (SA node)

The small mass of specialized cells lies in the wall of the right arium near the opening of the
superior vena cava.

The sinoatrial cells generate these regular because they are electrically unstable. This instability
leads them to discharge (depolarise) regularly, usually between 60 and 80 times a minute. This
depolarisation is followed by recovery (repolarization), but almost immediately their instability
leads them to discharge again, setting the heart rate. Because the sinoatrial node discharges faster
than any other part of the heart. Firing of the sinoatrial node triggers atrial contraction.
Atrioventricular node (AV node)

This small mass of neuromuscular tissue is situated in the wall of the atrial septum near the
atrioventricular valves. Normally, the atroventricularnode merely transmit the electrical signals
from the atria into the ventricles. There is a delay here; the electric signal takes 0.1 of a second to
pass through into theventricles. This allows the atria to finish contracting before the ventricles
start.

The atrioventricular node also has a secondary pacemaker a function and takes over this role if
there is problem with the sinoatrial node itself, or with the transmission of impulse from the atria.
Its intrinsic firing rate, however, is slower than that set by the sinoatrial node (40-60 beats per
minute).

Bundle of his

The distal portion of the atrioventricular node is known as the bundle of his. The bundle of His is
a collection of heart muscle cells specialized for electrical conduction. As part of the electrical
conduction system of the heart, it transmits the electrical empulsesfrom the atrioventricular node
(located between the atria and the ventricle) to the point of the apex of the fascicular branches
via the bundle branches.

Bundle branches

Bundle branches which arises from the bundle of his, it divided into right and left branches.The
left bundle branch which activate the left ventricle, while the right bundle branch activates the
right ventricle. The left bundle branch is short, splitting into the left anterior fascicle and the left
posterior fascicle. The left posterior fascicle is relatively short and broad, with dual blood supply,
making it particularly resistant to ischemic damage. The left posterior fascicle transmits impulses
to the papillary muscles, leading to mitral valve closure. As the left posterior fascicle is shorter
and broader than the right, impulse reach to the papillary muscles just prior to the depolarization,
and therefore the contraction, of the left ventricular myocardium. This allows pre-tensioning of
the chordae tendinea, increasing the resistance to flow through the mitral valve during left
ventricular contraction. This mechanism works in the same manner as pretensioning of car
seatbelts.

Purkinje fiber

The two bundle branches taper out to produce numerous purkinje fibers, which stimulate
individual groups of myocardial cells to contract. The spreads of electrical activity through the
ventricular myocardium produces the QRS complex on the ECG.

The process by which the heart is stimulated to contract is called “depolarization”. And the
process by which the heart recovers from the effects of previous contraction is called
“repolarization”. The depolarization and repolarization activity of the atria and ventricles is
electrical energy that can be sensed on the surface of the body by skin electrodes. A
representation of the heart’s electrical activity is known as electrocardiogram (ECG).
INCDENCE AND PREVALENCE RATES OF CONGESTIVE CARDIAC FAILURE

Heart failure affect 5 million people in the population , with 500,000 new cases diagnosed each
year. In contrast to decreases in mortality associated with other cardiovascular diseases , the
incidence of heart failure and the mortality associated withit have increased steadily since 1975.
Annually about 300, 000 clients die from direct or indirect consequences of heart failure ,and the
number of deaths attributed to heart failure has increased six- fold over the past 40 years.

ETIOLOGICAL FACTORS

1) Coronary artery diseases (CAD):

A diseases of the arteries that supply blood and oxygen to the heart, causes decreased
blood flow to the heart muscle. If the arteries become blocked or severely narrowed, the
heart becomes starved for oxygen and nutrients.

2) Heart attack:
A heart attack occur when coronary artery become suddenly blocked, stopping the flow
of blood to the heart muscle. A heart attack damages the heart muscle, resulting in a
scarred area that does not function properly.

3) Cardiomyopathy:
Damage to the heart muscle from causes other than artery or blood flow problems, such
as from infection or alcohol or drugs abuse.

4) Condition that overwork the heart :

Condition including high blood pressure, valve diseases , thyroid diseases, kidney
diseases ,diabetes , or heart defect present at can all cause heart failure.
Others factors:

1) High blood pressure

2) Irregular heart beats( arrhymia)
3) Heart valve diseases
4) Overweight weight , diabetes , alcoholic.
5) Large salt intake in diet
6) Congenital heart diseases
7) Infection of the heart muscle
8) Conduction defect
9) Hemochromatosis
10) Amyloidosis
CATEGORIES OF CONGESTIVE CARDIAC FAILURE:

New York Heart Association ( NYMA) Heart Failure Symptoms Classification

NYHA Level of Impairment

Class I Patients in this category feel no symptoms and can perform ordinary physical
activities without any limitations.
Class II Ordinary physical activity somewhat limited by dyspnea(e.g , long- distance
walking , climbing two flights of stairs). No symptoms at rest .
Class III Exercise limited by dyspnea with moderate work load (e.g , short –distance
walking , climbing one flight of stairs).
Class IV Symptoms of cardiac insufficiency with any physical activity or even at
rest.Dyspnea at rest or with very little exertion.

TYPES OF HEART FAILURE:

 Right – sided failure.

 Left – sided failure.

1) Right sided heart failure:

When the right ventricles is unable to empty or eject blood volume adequately . In this
type, increased right ventricular pressure or volume leads to increased right atrial
pressure which increases systemic venous pressure resulting in peripheral edema and
hepatic congestion.
 Swollen legs or peripheral edema of lower extremities
 Liver and spleen enlargement
 Right upper quadrant pain
 Swollen or distended jugular vein ( jugular venous distension)
 Fluid building in the stomach ( ascites)
 Nausea , vomiting ,appetite loss
 Weakness , fatigue , dizziness, and fainting episodes
 Slow weight gain
 Irregular heart rhythm
2) Left sided heart failure: Pulmonary congestion occur when left ventricle cannot pump
the blood out of the chamber. This increases pressure in the left ventricle and decreases
the blood flow from the left atrium, The pressure in the left atrium increases which
decreases the blood flow coming from the pulmonary tissues and alveoli which impairs
gas exchange.
 Fatigue and shortness of breath, dyspnea on exertion
 Paroxysmal nocturnal dyspnea
 Orthopnea
 Pulmonary edema
 Asthma – like wheezing or a dry hacking cough often occurs at night
 Wheezing
 Pale or bluish skin
 Palpitation , irregular heart rhythm, and increased blood pressure
 Weakness , insomnia and restlessness.
DECOMPENSATED HEART FAILURE :

Remodeling

Several structural changes, known as remodeling occur in the ventricle during decompensated
heart failure. Remolding is thought to result from hypertrophy of the myocardial cells and
sustained activation of the neuro-hormonal compensatory system. Recall that one of the initial
compensatory responses to a decrease in cardiac output is dilatation of the ventricles. This
dilation increases cardiac output but also increases wall stress in the ventricle. To reduce wall
stress, the myocardial cells hypertrophy, resulting in a thickening of the ventricular wall.
According to Laplace’s law, an increase in wall thickness reduce wall stress.

When used over time , theses compensatory response produces in the structure , function , and
gene expression of the myocardial cell . Changes in the myocardial cells eventually increases
failure by reducing myocardial contractility, increasing ventricular wall stress, and increasing
oxygen demand .In addition to increasing myocardial dysfunction, the genetically abnormal
myocytes die prematurely and at an accelerated rate through the process of
apptosis( programmed cell death).Apoptosis affects cells scattered throughout the myocardium
and causes a future reduction in cardiac function.

Sustained Neurohormonal Activation

Remolding changes continue to increase wall stress and future stimulate neurohormonal activity.
Long term sympathetic activation exerts a directs toxic effect on the heart that promotes myocyte
hypertrophy and apoptosis. Prolonged activation of the renin- angiotensin system and system
also stimulates myocyte hypertrophy and myocardial fibrosis. This creates a self- perpeutuating
cycle of cell death and further hypertrophy.

In addition , if renal artery pressure falls, a lowered glomerular filtration rate ( GFR ) increases
retention of sodium and water. In response to a continued reduction in renal blood flow, the
renin-angiotensin- aldosterone mechanism is activated. Aldosterone, released from the adrenal
cortex, promotes future retention of sodium and water by the renal tubule. This results in an
expansion in blood volume of upto 30% and edema. As the sodium concentration in the
extracellular fluids increases, so does the osmotic pressure of the plasma. The hypothalamus
responds to the higher osmotic pressure by releasing antidiuretic hormone (ADH) from the
posterior pituitary. This in turn promotes renal tubular reabsorption of water .Aldosterone,
however is more important than ADH in the production of edema because it promotes sodium
retention
PATHOPHYSIOLOGY

The healthy heart can meet the demand for oxygen delivery through the use of cardiac reserve.
Cardiac reserve is the heart’s ability to increase output in response to stress the normal heart can
increase its out put up to five times the resting level .The failing heart , even at rest , however , is
pumping near its capacity and thus has lost much of its reserve .The compromised heart has a
limited ability to respond to the body’s needs for increase output in situations of stress.

When cardiac output is not sufficient to meet metabolic needs of the body, compensatory
mechanism, including neurohormonal responses , become activated. These mechanism initially
help to improve contraction , but if continued lead to abnormal cardiac muscle growth and
reconfiguration ( remolding) of the heart .The compensatory response to decrease sympathetic
nervous system stimulation and activation of the renin-angiotensin system.
CLINICAL MANIFESTATION:
DIAGNOSTIC EVALUATION

Diagnosis of congestive heart failure is able to be accomplished by history and physical

examination. The health care professional often will ask question about the symptoms like
shortness of breath, swelling in the legs, chest pain, and what the patient does to make them
better (sit down, rest). It will also be important to know whether the symptoms have come on
gradually or over a shorter period of time.

1) History collection: A careful history is important to asceratain possible cause of heart

failure and identify patients at risk for heart failure .The history should include past
medical history and a through review of systemsincluding a history of coronary artery
diseases , hypertension, valvular heart diseases, congenital heart defects or diabetes.
Other endocrine abnormalities include a history of thyroid diseases or a family history of
cardiomyopathy or coronary artery diseases should be explored
2) Physical examination : A major goal in assessing the patient with heart failure is to
determine the type severity of the underlying diseases causing heart failure and the
extend of the heart failure syndrome .physical examination of the patient with heart
failure focuses on the cardiovascular and pulmonary system ,as well as relevant aspects
of the integumentary and gastrointestinal system.

a) Cardiac assessment : Determination of the rate , rhythm and character of

the pulse is important in patient with heart failure. The pulse rate is usually
elevated in response to a low cardiac output pulsusalternans is associated
( alternating pulse) is characterized by an alternating strong and weak pulse
with normal rate and interval Increase in heart size is more common in
heart failure. This cardiac enlargement is detected by pericardial
palpation ,with the apical impulse displaced laterally to the left and
downward .
 b) Pulmonary Assessment: Persistently elevated pulmonary assessment
pressure result in the transudation of fluid from the capillaries into the
interstitial spaces and eventually onto the alveolar spaces. The accumulated
fluid may result in pulmonary crackles.
c) Integumentary assessment: Patient with heart failure often present with
dependent edema. It is most often detected in the feet , ankles or sacral
area. Color and temperature of the skin are also assessed with major
findings begins pallor, decreased temperature, cyanosis and diphoresis.
d) Gastrointestinal assessment : Characteristically , heart failure results in
hepatomegaly. The liver span is increased and the liver is usually palpable
may also palpated in advance heart failure.

3) Laboratory and imaging studies:

a) Blood test: Blood test are used to evaluate kidney and thyroid function
as well as to check cholesterol level and the presence of anemia.
Anemia is a blood condition that occur when there is not enough
hemoglobin( the substance in red blood cells that enables the blood to
transports oxygen through the body) in a person’s blood .
b) B- type Natriuretic Peptide( BNP) : BNP is a substance secreted
from the heart in response to changes in blood pressure that occur
when heart failure develops or worsens BNP blood levels increases
when heart failure symptoms worsens, and decrease when the heart
condition is stable.
c) Chest X – ray : A chest x- ray show the size of our heart and whether
there is fluid build –up around the heart and lungs.
d) Echocardiogram : This test is an ultrasound which shows the heart’s
movement , structure and function .
e) Ejection Fraction ( EF): It is used to measure how well the heart
pumps with each beats to determined if systolic dysfunction or heart
failure with preserved left ventricular function is present.
f) Electrocardiogram( EKG or ECG): To help assess heart rate,
rhythm, and indirectly, the size of the ventricles and blood flow to the
heart muscle.
 g) Cardiac catheterization/ coronary arteriography: It is used in
patient with angina or large areas of ischemic myocardium .
h) Stress test : Noninvasive stress test provide information about the
likelihood of coronary artery diseases.

COMPLICATION

1) Right ventricular failure:

When right ventricle functioning decreases , peripheral edema and venous congestion of
the organ develop. Liver enlargement (hepatomegaly) and abdominal pain occur as the
liver becomes congested with venous blood.

In sever right ventricular failure , the lobules of the liver may becomes so congested with
venous blood that they become anoxic .Anoxic leads to necrosis of the lobules .In long
standing failure , these necrotic areas may become fibrotic and then sclerotic .As a
result , a condition called cardiac cirrhosis develops ,manifested by ascites and jaundice

2) Left ventricular failure :

Acute pulmonary edema: A medical emergency, usually result from left ventricular
failure. In client with severe cardiac decompensation, the capillary pressure within the
lungs becomes so elevated that fluid is pushed from the circulating blood into the bronchi
this resulting pulmonary edema .
MANAGEMENT

The management of heart failure is divided into two situations: the treatment of decompensated
heart failure and the treatment of stable chronic heart failure. Diuretics, nitrates, analgesia and
inotropic agents are indicated for the treatment of decompensated heart failure and pulmonary
edema.

Goal : The of that management is

1) To reduce myocardial workload

2) Improve ventricular pump performance
3) Perfuse essential organs
4) Prevent further heart failure by affecting the process of cardiac remodeling.

A] Medical Management:

I) General Measures:

1) Reduce myocardial workload:

Diuretic are an important aspect of treatment because of the central role of the kidney as
the target organ of many of the neurohormonal changes in response to the failing heart.
First- line therapy generally includes a loop diuretic such as furosemide, which will
inhibits sodium chloride reabsorption in the ascending loop of henle. Diuretic reduced the
circulating blood volume by diminished preload and lessen systemic and pulmonary
congestion.

2) Elevate the client’s head :

The client is placed in a high flower position or the chair to reduce the pulmonary venous
congestion and to relive the dyspnea. The legs are maintained in a dependent position as
much as possible . Even though the legs are edematous, they should not be elevated .
Elevated the legs are rapidly increase venous return.

3) Reduce Fluid Retention:

Controlling sodium and water retention improves cardiac performance. Sodium
restriction are placed on the diet to prevent ,control , or eliminate edema. Diet with 2 to 4
g of sodium are usually prescribed .

4) Improved Ventricular Pump Performance:

The most power full way to increase contractility of the heart is to use adrenergic agonist,
or inotropic medications. Angiotensin – converting enzymes (ACE) inhibitors also
commonly used in hemodynamic.
 5) Supply oxygen:
High concentration of oxygen by mask or cannula are provided to relieve hypoxia and
dyspnea and to improve oxygen carbon di oxide exchanges. For hypoxia , partial
rebrether mask with flow rate of 8 to 10 L / min can be used to deliver oxygen
concentration of 40% to 70 %.

6) Control dysrhythmias:
Atrial fibrillation with a rapid ventricular response is the most common dysrhythmias
seen in heart failure clients .Atrial fibrillation can lead to embolic stroke, so client are
given anticoagulants .The rhythm is often controlled with medication such as
amiodarone.

7) Reduce stress and Risk of injury:

To improve ventricular performance and reducing myocardial workload , the client also
needs to reduce physical and emotional stress .Sometimes clinicians overlook rest as an
intervention to diminished the work of the heart . The proper use of restas the initial steps
in management offers many benefits. Rest can promote diuresis , slow the heart rate and
relieve dyspnea all of which allows more conservative use of pharmacological agents( e.g
ACE inhibitor, diuretics, beta – blockers).

II) Pharmacological Management:

 Patient with left ventricular often present with exercise intolerance , shortness of breath
and or fluid retention. Incidental findings of dysfunction also may be found in
asymptomatic patients. All the patients presenting with heart failure should undergo a
detailed evaluation to:
1) Determine the type of cardiac dysfunction.
2) Uncover correctable causative factors
3) Determine prognosis .
4) Guide the treatment.

1) Anticoagulation : patients with increased left ventricular volume and reduced function
are at risk for left ventricular thrombous formation. Embolization of these thrombi into
the systemic circulation can result in transient ischemic attack and cerebrovascular
accidents.
Therefore, routine anticoagulation with warfarin is recommended only for patients with
atrial fibrillation, a previous history of systemic pulmonary embolism or mobile
ventricular thrombi.

2) Angiotensin converting enzymes inhibitors: The use of ACE-I has been conclusively
shown to improve long term prognosis in heart failure. ACE-I block the formation of
AT, which reverse vasoconstriction ( reducing the after load) and inhibit
endocrine ,paracrine and cellular growth effect of AT. ACE-I also diminished release of
aldosterone (inhibiting sodium retension ) and produce venodilations ( reducing preload) .
Drugs : Captopril ,Enapril, Lisinpril, Ramipril, Hydralazine etc.

3) B- Adrenergic Blockers: Cardiac myocytes have three adrenergic receptors( B1,B2and

x1) that are coupled with positive inotropic andchronotropic response , cardiac myocytes
growth toxicity , and apoptosis. Although B1 and B2 receptors are present in the normal
human myocardium , because B1 receptors are down regulate ,B2 receptor predominate in
the failing myocardium.
Drugs :Carvediol, Metoprolol succinate, Bisoprolol.

4) Diuretics : The kidney is the target organ of many of the neurohormonal and
hemodynamic changes that occur in heart failure .Diuretics and diterary salt restriction
exert their primary benefit by decreasing extracellular fluid and intravascular blood
volume.
Drugs : Furosemide, Torsemide, Metolazone ,Spironolactone.

5) Digitalis Glycosides: The cardiac glycosides have important effects in heart failure
including augmenting contractility slowing of the sinus pacemaker
andatrioventricularconductionandneurohormonal modulating effects including a
sympathoinhibitory effect.
 6) Vasodilator therapy : The venous and arterial beds are often inappropriately
constricted.Venoconstriction tends to displace blood in the thorax causing pulmonary
congestion , whereas arteriolar constriction increases the impedance to left ventricular
emptying.

7) Venous dilators: Nitroglycerine and the closely related isosorbidedinitrate are primarily
reducers of preload because they dilate the systemic veins and reduce venous return,
ultimately to reduce left ventricular filling pressure.

8) Arterial dialtors: As a direct arteriolar vasodilators with direct inotropic effects ,

hydralazine can improve left ventricular function by reducing afterload and myocardium
oxygen consumptions , augumenting stroke volume and improve cardiac output.

9) Calcium clannel blockers: The net benefits of calcium channel blockers use rest in their
ability to decrease afterload and to exert anti –ischemic effect.

10) Natriueticpeptide : Natriuretic peptide such as nesitride are intravenously delivered

compound that promote diuresis and have vasodilators properties that suppress
neurohormoanl activation and directly improve myocardial performance.

B] Surgical Management:
1) Biventricular pacing: Cardiac resynchronization therapy ( CRT) is used to treat the delay in
heart ventricles contraction that occurs in some people with advanced heart failure. The CRT
pacing devices( also called as a bi ventricular pacemaker ) is an electronic device , battery
powered device that is surgically implanted under the skin . The device has 2 or 3 leads ( wires)
that are positioned in the heart to help the heart beat in a more balanced way. The leads are
implanted through a vein in the right atrium and right ventricle and into the coronary sinus vein
to place the left ventricle. The CRT device can be implanted using the endocardial or
epicardialapproach . With the endoacrdial( transvenous) approach , a local anesthetic ( pain –
reliving mediaction ) is injected to numb the area. The epicardial approach may also be used to
place the CRT if the person having the surgery to treat another heart condition.

3) Coronary artery bypass grafting surgery: The most common surgery for heart failure
caused by coronary artery diseases is bypass surgery. Althought surgery is more risky for
people with heart failure , new strategies before, during and after the surgery have
reduced the risk and i.mproved outcome

.
3) Heart valve surgery : Diseased heart valves can be treated both surgically (traditional heart
valve surgery) and nonsurgically (balloon valvuloplasty).
 4)Implantable left ventricular assist device( LVAD): The LVAD is know as the
‘bridge to transplantation’ for patient who have not responded to another treatment and
are hospitalized with severe systolic heart failure . This devices helps our heart pump
blood throught our body .It allows us to mobile ,sometime returning home to await a
heart transplants .It may also be used as destination therapy for long term supports in
patients who are not eligible for transplant.

5) Stem cell transplants: Stem cell transplantation represents a new therapeutic opportunity
for such patient . Peripheral stem cells were mobilized and collected by apheresis. They
were transplanted into areas of injury with open –heart surgery . To increases blood flow
to the engrafted areas, coronary artery bypass surgery was also performed. This
approaches opens a new window in the treatment of ‘no hope ‘ patients.
6) Heart transplantations.
III) Nursing Management:

1) Nursing Diagnosis: Decreased Cardiac Output related to heart failure or dysrthymias or

both.
Goal : The client will have an increased in cardiac out put as evidence by regular cardiac
rhythm, heart rate, blood pressure respirations, and urine output within in normal.
Interventions:
 Assess blood pressure for hypotension or hypertension and respiratory rates for
tachypnea for every 1 hourly.
 Assess the heart rate and rhythm for every 1 hourly for tachycardia. Continuously
monitors dysrhythmias.
 Reports dysrhythmias to the physicians or follow protocol for emergency
treatment.
 Monitor lab values for isoenzymes, atrial peptide, CK, BUN, cretanine , liver
function test ,CBC ,electrolyte, glucose, thyroid function, blood lipids.
 Monitor the lungs sounds every 2 hourly for any adventitious such as crackle, and
for the presence of coughing.
 Monitor the intake and out put chart and analyzed finding every 8 hourly. Note
amount and color of urine.
 Assess for changes in the mental status .
 Assess the peripherial pulse for strength and quality and for pulsusalternans

2) Nursing Diagnosis: Excess fluid volume related to reduced glomerular filtration ,

decreased cardiac out put , increased antidiuretic hormone (ADH) and aldosterone
production and sodium and water retention.
Goal:The client will demonstrate adequate fluid balanced as evidenced by equal to or
exceeding intake, clearing breath sound and decreasing edema.
Interventions:
 Monitor intake and out put chart every 4 hourly.
 Weight the client daily and compare to previous weight.
 Assess for presence of peripheral edema. Do not elevate the legs if the client is
dyspneic.
 Assess the jugular vein distension , hepatomegaly , and abdomen pain.
 Follow low sodium diet and or fluid restriction.
 Administered diuretic therapy as ordered and evaluate the effectiveness of that
therapy.
 Encourage or provide oral care to the patient every 2 hourly.

3) Nursing Diagnosis:Impaired gas exchange related to fluid in alveoli.

 Goal : The client will have improved gas exchange as evidenced by decreased dyspnea,
no cyanosis, normal arterial blood gases and a decreased in pulmonary congestion on
auscultation.
Interventions:
 Auscultate breath sound every 2 hourly.
 Encourage the client to turn , cough and deep breath and the use of incentive
spirometry every 2 hourly.
 Administer the oxygen as ordered by the physicians.
 Assess the respiratory rate and rhythm every 2 hourly.
 Assess for cyanosis every 4 hourly.
 Position the client to facilitates breathing and observe for paroxysmal nocturnal
dyspnea.
 Monitor the pulse oximetry.
 Obtained the atrial blood gases if ordered.
 Administration of diuretic therapy as ordered and monitor for effectiveness.

4) Nursing Diagnosis: Infective tissue perfusion related to decreased cardiac output.

Goal : The client will have adequate tissue perfusion as evidenced by warm , dry skin ,
peripheral pulses and adequate urine output.
Interventions:
 Note color and temperature of the skin every 4 hourly.
 Monitor peripheral pulses every 4 hourly.
 Provide a warm environment.
 Encourage active range of motion.
 Monitor urine output every 4 hourly.
 Protect the skin from trauma by applying cotton socks or fleece.

5) Nursing Diagnosis: Risk for activity intolerance related to the decreased cardiac output.
Goal : The client will have improved levels of activity without dyspnea.
Interventions:
 Space the nursing activity.
 Schedule rest period.
 Monitor the client response to activities .
 Assess vitals signs before and after an activity.
 Increases activity as ordered or according to the rehabilitation nurse’s directions.
 Instruct the client to avoid activities that increases cardiac workload.

6) Nursing Diagnosis:Risk for impaired skin integrity related to decrease tissue perfusion
and activities.
 Goal :The client have reduced risk of skin impairement.
Interventions:
 Reposition the client quarterly 2 hourly if the client moving self .Turn side to
side quarterly 2 hourly if client unable to turn self.
 Provide a therapeutic mattress or bed while the client is in the bed.
 Assess the skin , especially the bony prominences for redness each shift and as
needed . Use protective devices if redness is noted .Inspect between skin folder
in obese clients.
 Float the heels from the bed if the client has little spontaneous leg movement .
 Assist the client with morning care and lubricate the skin.

7) Nursing Diagnosis:Risk for anxiety related to decrease cardiac output, hypoxia,

diagnosis of heart failure , and fear of death or debilitation.
Goal :The client will not exhibit manifestation of anxiety and will be able to express
concerns.
Interventions:
 Provide a calm environment.
 Explain in advance all procedures and routine regimens.
 Encourage the client support to clients and their significant others.
 Encourage the client to use additional support system.

PREVENTION MEASURES
After congestive heart failure is diagnosed, treatment should be started immediately. Lifestyle
modification is one of the most important aspects a patient can incorporate to treat congestive
heart failure. Some of these lifestyle changes include diet, exercise, fluid regulation, and weight
maintenance.

1) Diet:

Sodium: Sodium causes an increase in fluid accumulation in the body's tissues.

Because the body is often congested with excess fluid, patients become very sensitive to the
levels of intake of sodium and water.Restricting salt and fluid intake is often recommended
because of the tendency of fluid to accumulate in the lungs and surrounding tissues.

 A "no added salt" diet can still contain 4 to 6 grams (4000 to 6000 milligrams) of sodium
per day.
 In individuals with congestive heart failure, an intake of no more than 2 grams (2000
milligrams) of sodium per day is generally advised.
 Reading food labels and paying close attention to total sodium intake is very important.
Severe restriction of alcohol consumption also is advised.
2) Exercise:

Aerobic exercise, once discouraged for congestive heart failure patients, has been
shown to be beneficial in maintaining overall functional capacity, quality of life, and perhaps
even improving survival. Each person's body has its own unique ability to compensate for the
failing heart. Given the same degree of heart muscle weakness, individuals may display
widely varying degrees of limitation of function. Regular exercise, when tailored to the
person's tolerance level, appears to provide significant benefits and should be used only when
the individual is compensated and stable.

3) Fluid regulation:

The total amount of fluid a patient consumes must be regulated. Although many
people with congestive heart failure take prescription diuretics to aid in the elimination of
excess fluid, the action of these medications can be overwhelmed by an excess intake of
water and other fluids. The maxim that "drinking eight glasses of water a day is healthy"
certainly does not apply to patients with congestive heart failure. Patients with more
advanced cases of congestive heart failure are often advised to limit their total daily fluid
intake from all sources to 2 quarts.

The above guidelines for sodium and fluid intake may vary depending on the severity
of congestive heart failure in any given individual and should be discussed with their
physician.
4) Weight maintenance

An important tool for monitoring an appropriate fluid balance is the frequent tracking
of the patient's body weight. An early sign of fluid accumulation is an increase in body
weight. This may occur even before shortness of breath or swelling in the legs and other
body tissues (edema) is detected. A weight gain of 2 to 3 pounds over 2 to 3 days should
prompt a call to the physician, who may order an increase in the dose of diuretics or other
methods designed to stop the early stages of fluid accumulation before it becomes more
severe.
RESEARCH ARTICLE

Arati A. Inamdar ,Ajinkya C .Inamdar(2016) : Despite the advancement in medicine,

management of heart failure (HF), which usually presents as a disease syndrome, has been a
challenge to healthcare providers. This is reflected by the relatively higher rate of readmissions
along with increased mortality and morbidity associated with HF. In this review article, they
first provide a general overview of types of HF pathogenesis and diagnostic features of HF
including the crucial role of exercise in determining the severity of heart failure, the efficacy of
therapeutic strategies and the morbidity/mortality of HF. Then they discuss the quality control
measures to prevent the growing readmission rates for HF. They also attempt to elucidate
published and ongoing clinical trials for HF in an effort to evaluate the standard and novel
therapeutic approaches, including stem cell and gene therapies, to reduce the morbidity and
mortality. Finally, they discuss the appropriate utilization/documentation and medical coding
based on the severity of the HF alone and with minor and major co-morbidities. They consider
that this review provides an extensivee overview of the HF in terms of disease pathophysiology,
management and documentation for the general readers, as well as for the
clinicians/physicians/hospitalists.

Aleza.M .Dalbe ,Jesa.k (2011):Chronic heart failure (CHF) remains the only cardiovascular
disease with an increasing hospitalization burden and an ongoing drain on health care
expenditures. The prevalence of CHF increases with advancing life span, with diastolic heart
failure predominating in the elderly population. Primary prevention of coronary artery disease
and risk factor management via aggressive blood pressure control are central in preventing new
occurrences of left ventricular dysfunction. Optimal therapy for CHF involves identification and
correction of potentially reversible precipitants, target-dose titration of medical therapy, and
management of hospitalizations for decompensation. The etiological phenotype, absolute
decrease in left ventricular ejection fraction and a widening of QRS duration on
electrocardiography, is commonly used to identify patients at increased risk of progression of
heart failure and sudden death who may benefit from prophylactic implantable cardioverter-
defibrillator placement with or without cardiac resynchronization therapy. Patients who
transition to advanced stages of disease despite optimal traditional medical and device therapy
may be candidates for hemodynamically directed approaches such as a left ventricular assist
device; in selected cases, listing for cardiac transplant may be warranted.
CONCLUSION

Congestive cardiac failure is a condition in which the heart can't pump enough blood to meet the
body's needs. Congestive cardiac failure does not mean that our heart has stopped or is about to
stop working. It means that our heart is not able to pump blood the way it should. It can affect
one or both sides of the heart.

SUMMARY

Today we have learned about the introduction, definition, anatomy and physiology of
cardiovascular system, incidence and prevalence rates, etiological factors,
category ,pathophysiology , clinical manifestation, diagnostic evaluation, medical management,
surgical management, nursing management, complication , preventive measures, research article
of congestive cardiac failure.
BIBILOGRAPHY

 Joyce Black, textbook of medical surgical nursing, 7th edition, volume 2, Elsevier
publications, page 229-236
 Levis Textbook of Medical Surgical nursing 7th edition2009, Elsevier publications, page
No.744-755
 Brunner textbook of medical surgical nursing 10th edition, volume 1 page No. 365-370
 Lippincott Williams and Wilkins, Lippincott manual of nursing practice, 10th edition,
2013, Wolter Kluwer publication, page no 632-639.
 https://en.wikipedia.org/wiki/Heart#Nerve_supply