SEMINAR

ON

Heart FAILURE
SUBMITTED TO SUBMITTED BY
SUMI.G
2nd YR MSc (N)

SUBMITTED ON
CENTRAL OBJECTIVES:

After the completion of the class the students acquire knowledge regarding heart
failure, appreciate its importance and apply the acquired knowledge in clinical practice.

SPECIFIC OBJECTIVES:

 Define heart failure

 Describe the incidence of heart failure
 Explain the etiology and risk factors
 Explain the pathophysiology of heart failure
 List down the clinical features of heart failure
 Describe the diagnostic measures of heart failure
 Describe the medical management of heart failure
 Explain the surgical management of heart failure
 Explain the nursing management of heart failure
SL. NO: CONTENT PAGE NO:
1 Introduction

2 Definition

3 Incidence

4 Etiology & risk factors

5 Pathophysiology

6 Clinical features

7 Diagnostic measures

8 Medical management

9 Surgical management

10 Nursing management

11 Conclusion

12 Bibliography
 HEART FAILURE
INTRODUCTION
The human heart, through rhythmic contraction, provides the pressure necessary to
propel blood through the body. Blood flow is essential to deliver nutrients to the tissues
of the body and to transport metabolic wastes, including heat, to removal sites. The
presence of an arterial pulse caused by the beating of the heart is appropriately
designated as a vital organ. This seminar provides a detailed discussion of a condition in
which cardiac muscles are not able to pump enough amount of blood to vital organs and
to meet the metabolic need of the body.

DEFINITION
Heart failure (HF) is a clinical syndrome that occurs in patients who, because of an
inherited or acquired abnormality of cardiac structure and/or function, develop a
constellation of clinical symptoms (dyspnea and fatigue) and signs (edema and rales)
that lead to frequent hospitalizations, a poor quality of life, and a shortened life
expectancy.

-Harrison

Heart failure is a physiological state in which the heart cannot pump enough blood to
meet the metabolic needs of the body.

- Joyce M Black

Heart failure, often referred to as congestive heart failure (CHF), is the inability of the
heart to pump sufficient blood to meet the needs of the tissues for oxygen and
nutrients.
-Brunner and Suddharth
Heart failure is a complex clinical syndrome manifested by shortness of breath, fatigue,
and abnormal heart function.
-Woods
Heart failure is a condition in which the heart fails to discharge its contents adequately.
-Lewis

Systole and Diastole

Systole means contraction and diastole means to send apart. The start of systole can be
regarded as

(1) The beginning of isovolumic contraction, when LV pressure exceeds the atrial
pressure, or

(2) Mitral valve closure. These correspond reasonably well, because mitral valve closure
actually occurs only about 20 milliseconds after the crossover point of the pressures.

STARLING'S LAW OF THE HEART

VENOUS FILLING PRESSURE AND HEART VOLUME

Starling, in 1918, related the venous pressure in the right atrium to the heart volume in
the dog heart-lung preparation. He proposed that within physiological limits, the larger
the volume of the heart, the greater the energy of its contraction and the amount of
chemical change at each contraction. Starling did not, however, measure sarcomere
length but could only relate LV volume to cardiac output. This holds true in normal,
compliant hearts. One modern version of Starling's law is that stroke volume is related
to the end-diastolic volume.

The LV volume can now be directly measured with two-dimensional echocardiography.

However, the value determined depends on a number of simplifying assumptions, such
as a spherical LV shape, and neglects the confounding influence of the complex anatomy
of the left ventricle. From the investigational point of view, real-time three-dimensional
echocardiographic recordings can now indicate global LV volume and endocardial
function. In practice, LV volume is not often measured, but instead uses various
surrogate measures, such as LV end-diastolic pressure and pulmonary capillary wedge
pressure. The relationship between LV end-diastolic volume and LV end-diastolic
pressure is curvilinear, depending on LV compliance.

The left ventricular diastolic filling pressure, the difference between the left atrial
pressure and the left ventricular diastolic pressure, is easier to measure and, in diseased
noncompliant hearts, may be used as a surrogate for heart volume. The venous filling
pressure can indirectly be measured in humans by the technique of Swan-Ganz
catheterization, as can the stroke volume. The left ventricular pressure and volume are,
however, not linearly related because of variations in the compliance of the
myocardium. Therefore, a jump from pressure to volume is required to apply the
Starling concept to the hemodynamic management of those critically ill who are
undergoing Swan-Ganz catheterization.

FRANK AND ISOVOLUMIC CONTRACTION

If a larger heart volume increases the initial length of the muscle fiber to increase the
stroke volume and hence the cardiac output, then diastolic stretch of the LV actually
increases contractile function. Frank, in 1895, had already reported that the greater the
initial LV volume, the more rapid the rate of rise, the greater the peak pressure reached,
and the faster the rate of relaxation. He described both a positive inotropic effect and
an increased lusitropic effect. These complementary findings of Frank and Starling are
often combined into the Frank-Starling law, which can account for two of the
mechanisms underlying the increased stroke volume of exercise—namely, increased
diastolic filling (Starling's law) and increased inotropic state (Frank's findings).

AFTERLOAD

This is the systolic load on the left ventricle after it has started to contract. In the
nonfailing heart, the left ventricle can overcome any physiological acute increase in
load. Chronically, however, the LV must hypertrophy to overcome sustained arterial
hypertension or significant aortic stenosis. In clinical practice, the arterial blood pressure
is often taken to be synonymous with the afterload while ignoring the aortic compliance
—the extent to which the aorta can yield during systole. A stiff aorta, as in isolated
systolic hypertension of the elderly, increases the afterload.

INTERLINKED PRELOAD AND AFTERLOAD

These distinctions between preload and afterload do not allow for those situations
when the two change concurrently. By the Frank-Starling law, an increased LV volume
leads to increased contractile function, which in turn will increase the systolic blood
pressure and hence the afterload. Nonetheless, in general, the preload is related to the
degree to which the myocardial fibers are stretched at the end of diastole, and the
afterload is related to the wall stress generated by those fibers during systole.

FORCE-LENGTH RELATIONSHIPS AND CALCIUM TRANSIENTS

Evidence that there is no increase in the calcium transient as the sarcomere length
increases has been provided by direct measurements .The favored explanation for the
steep length-tension relationship of cardiac muscles is length-dependent activation,
whereby an increase in calcium sensitivity is the major factor explaining the steep
increase of force development as the initial sarcomere length increases. This change
may be explained by stretch of the titin molecule.

ANREP EFFECT: ABRUPT INCREASE IN AFTERLOAD.

When the aortic pressure is elevated abruptly, a positive inotropic effect follows within
1 or 2 minutes. This was formerly called homeometric autoregulation (homeo, the same;
metric, length), because it was apparently independent of muscle length and, by
definition, a true inotropic effect. A reasonable speculation would be that increased LV
wall tension could act on myocardial stretch receptors to increase the cytosolic sodium
level and then, by Na+/Ca2+ exchange, the cytosolic calcium level. Thus, this effect would
be different from that of an increase in preload, which acts by length activation.

INCIDENCE
Approximately 1 in every 100 older adults has HF. 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 6 fold over the past 40 years. Heart failure
affects both men and women although the mortality is higher among women. There are
also racial differences at all ages. It is also the leading cause of hospitalization in older
people.

ETIOLOGY AND RISK FACTORS

The performance of heart depends on four essential components:

 Contractility (inotropic state) of the muscle.

 Preload(amount of blood in the ventricle at the end of diastole)
 Afterload(the pressure against which the left ventricle ejects)
 Heart rate.
Terms used to describe cardiac function:

Preload:-the stretch of the ventricular myocardial fibers just before ventricular

contraction

Afterload:-the amount of tension the heart must generate to overcome systemic

pressure and to allow adequate ventricular emptying.

Inotropic state:-a measure of contractility.

Cardiac output:-stroke volume X heart rate

Adverse change in these determinants of myocardial performance ultimately causes the

heart to fail. CHD is the primary cause of heart failure in two thirds of clients with
decreased ventricular dysfunction; however, heart failure can also be caused by other
disorders. The causes of heart failure can be divided into three sub groups.

 Abnormal loading conditions

 Abnormal muscle function
 Conditions or diseases that limit ventricular filling.

Abnormal loading conditions:

Abnormal loading is associated with any condition that increases either the pressure or
the volume load of the ventricle. The effect of increasing volume on the ventricle can be
explained by the analogy that the heart muscle is like a stretched rubber band. When
the rubber band id stretched, it contracts with more force. The heart muscle does the
same. Venous return stretches the heart and improves contractility. When the rubber
band is over-stretched, however, it becomes limp and cannot contract. Likewise, when
the heart is overloaded with blood, excessive stretch and decreased contraction occur.
Overload develops because blood does not leave the ventricles during contraction.
Therefore cardiac workload increases in an effort to move blood.

Preload refers to the stretch of the ventricular myocardial fibers just before ventricular
contraction. The load or stretch placed on the ventricular fibers corresponds to the end-
diastolic ventricular volume and pressure. Preload is determined by the condition of the
heart valves (especially mitral valve), blood volume, ventricular wall compliance and
venous tone.
Conditions that increase preload:

 Regurgitation of mitral or tricuspid valve

 Hypervolemia
 Congenital defects(left-to-right shunts)
 Ventricular septal defect
 Atrial septal defect
 Patent ductus arteriosus.

Increased preload usually increases contractility (more stretch on the rubber band) and
stretch because of filling pressures from venous return and previous volume. Stretch
and filling pressures may rise beyond the capabilities of the normally compliant heart.
This increased preload lessens the force and efficiency of ventricular contraction.
Cardiac output decreases. Under the strain of this load, the heart will fail.

Increased pressure load in the ventricle is related to afterload, the amount of tension
the heart must generate to overcome systemic pressure and to allow adequate
ventricular emptying. Thus afterload indicates how hard the heart must pump to force
blood into circulation. The tone of systemic arterioles, the elasticity of the aorta and
large arteries, the size and thickness of the ventricles, the presence of aortic stenosis,
and the viscosity of the blood all determine afterload. High peripheral vascular
resistance and high blood pressure force the ventricle to work to work harder to eject
blood. Subjected to prolonged high pressures, the ventricle eventually fails.

Conditions that increase afterload:

 Hypertension-pulmonary or systemic
 Aortic or pulmonic stenosis
 High peripheral vascular resistance.

Abnormal muscle function

Disorders that impair the contractile function of the myocardial fibrils and reduce
ventricular filling and stroke volume affect the cardiac muscle’s ability to pump
effectively.

Abnormal muscle function-causes:

 MI
  Myocarditis
 Cardiomyopathy
 Ventricular aneurysm
 Long term alcohol consumption
 Coronary heart disease
 Metabolic heart disease
 Endocrine heart disease.

Myocardial fibrils are injured during an MI and during the healing phase some of the
heart muscle is replaced by non-contracting scar tissue. Scar tissue does not move
during contraction and the ventricles pump less efficiently. Some degree of heart failure
either chronic or transient appears in more than half of clients after MI.

Certain conditions that externally compress the heart, thereby limiting ventricular filling
and myocardial contractility. Disorders that greatly restrict cardiac chamber filling and
myocardial fiber stretch include constrictive pericarditis, an inflammatory and fibrotic
process of the pericardial sac; and cardiac tamponade, which involves the accumulation
of fluid or blood within the pericardial sac. Because the pericardium encloses all four
heart chambers, compression of the heart both decreases diastolic relaxation, thereby
elevating diastolic pressure, and hampers forward blood flow through the heart.

Conditions that precipitate heart failure

Some clients have preexisting mild to moderate heart disease with no evidence of heart
failure. In these clients adequate cardiac output depends on functional compensatory
mechanisms. When the heart undergoes undue stress these compensatory mechanisms
may prove inadequate and heart fails.

Heart failure can be precipitated by conditions that increase cardiac and systemic
oxygen demand reduces the ability of the heart to contract or increase the work load of
the heart. Some of the conditions include:

 Dysrhythmias, especially tachycardia

 Systemic infections or sepsis
 Anemia
 Thyroid disorders
 Pulmonary embolism
 Thiamine deficiency
  Chronic pulmonary disease
 Medication dose change
 Physical or emotional stress
 Endocarditis, myocarditis, or pericarditis
 Fluid retention from medication or salt intake
 A new cardiac condition

PATHOPHYSIOLOGY
The healthy heart can meet the demands for oxygen delivery through the use of cardiac
reserve. Cardiac reserve is the heart’s ability to increase the output in response to
stress. The compromised heart has a limited ability to respond to body’s needs to
increased output in situation of stress. When cardiac output is not sufficient to meet the
metabolic needs of the body, compensatory mechanisms, including neuro hormonal
responses, become activated. These mechanisms initially help to improve contraction
and maintain integrity of the circulation but, if continued abnormal cardiac muscle
growth and reconfiguration (remodeling) of the heart. The compensatory responses to a
decrease in cardiac output are ventricular dilatation, increased sympathetic nervous
system stimulation, and activation of the renin angiotensin system.

Ventricular dilation

Ventricular dilation refers to lengthening of the muscle fibers that increase the volume
in the heart chambers. Dilation causes an increase in pre load, and thus cardiac output,
because a stretched muscle contracts more forcefully (Starling’s law) however dilation
has limits as a compensatory mechanism. Muscle fibers, if stretched beyond a certain
point, become ineffective. Second a dilated heart requires more oxygen. Thus the
dilated heart with a normal coronary blood flow can suffer from a lack of oxygen.
Hypoxia of the heart further decreases the muscle’s ability to contract.

Increased sympathetic nervous system stimulation

Sympathetic activity produces venous and arteriolar constriction, tachycardia, and

increased myocardial contractility all of which work to increase cardiac output and
improve delivery of oxygen and nutrients to tissues. This compensatory effect occurs at
the cost of increasing peripheral vascular resistance (afterload) and myocardial
workload, however. Sympathetic stimulation reduces renal blood flow and stimulates
the renin angiotensin system.
Stimulation of renin angiotensin system

When blood flow through the renal artery is decreased the baroreceptor reflex is
stimulated, and renin is released into the blood stream. Renin interacts with the
angiotensinogen to produce angiotensin I. When angiotensin I comes into contact with
ACE it is converted to angiotensin II, a potent vasoconstrictor. Angiotensin II increases
arterial vasoconstriction, promotes the release of norepinephrine from sympathetic
nerve endings and stimulates the adrenal medulla to secrete aldosterone, which
enhances sodium and water absorption. Stimulation of renin angiotensin system causes
plasma volume to expand and preload to increase.

When compensatory mechanisms fail, the amount of blood remaining in the left
ventricle at the end of diastole increases. This increase in residual blood in turn
decreases the ventricle’s capacity to receive blood from the left atrium. The left atrium
having to work harder to eject blood dilates and hypertrophies. It is unable to receive
the full amount of incoming blood from the pulmonary veins and left atrial pressure
increases this leads to pulmonary edema. Left ventricular failure results.

The right ventricle because of the increased pressure in the pulmonary vascular system,
must now dilate and hypertrophy to meet its increased workload. It too eventually fails.
Engorgement in the venous system then extends backward to produce congestion in the
gastrointestinal tract, liver, viscera, kidneys, legs and sacrum; edema is the main
manifestation. Right ventricular failure results. This usually follows LVF.

Decompensated heart failure

Remodeling: several structural changes known as remodeling occur in the ventricle

during decompensated heart failure. Remodeling is thought to result from hypertrophy
of the myocardial cells and sustained activation of the neurohormonal compensatory
system. One of the initial compensatory responses to decrease in cardiac output is
dilatation of the ventricle. This dilatation increase cardiac output but also increases wall
stress in the ventricle. To reduce the wall stress the myocardial cells hypertrophy,
resulting in a thickening of the ventricular wall. Gradually these compensatory
responses produce changes in the structure, function, and gene expression of the
myocardial cells. Changes in the myocardial cells eventually increase failure by reducing
myocardial contractility, increasing ventricular wall stress, increasing oxygen demand.in
addition to increasing myocardial dysfunction, the genetically the genetically abnormal
myocytes die prematurely and at an accelerated rate through the process of
apoptosis(programmed cell death). Apoptosis affects cells scattered throughout the
myocardium and causes a further reduction in cardiac function.

Sustained neurohormonal activation:

Remodeling changes continue to increase wall stress and further stimulate

neurohormonal activity. Long term sympathetic activation exerts a direct toxic effect on
the heart that promotes myocyte hypertrophy and apoptosis. Prolonged activation of
the rennin angiotensin system also stimulates myocyte hypertrophy and myocardial
fibrosis. This creates a self-perpetuating cycle of cell death and further hypertrophy. In
addition if renal artery pressure falls, a lowered GFR increase retention of sodium and
water. As a result the RAA mechanism is activated .Aldosterone released from the
adrenal cortex promotes further retention of sodium and water by the renal tubule. This
results in an expansion in blood volume of up to 30% and edema.

TYPES OF HEART FAILURE

Heart failure may be categorized as (1) LVF versus RVF, (2) backward versus forward and
(3) high output versus low output

1. Left ventricular versus right ventricular failure

It is based on the fact that fluid accumulates behind the chamber that fails first. Because
the circulatory system is a closed circuit, however, impairments of one ventricle
common progress to failure of the other. This is referred to as ventricular
interdependence.

Left ventricular failure

Left ventricular failure causes either pulmonary congestion or a disturbance in the

respiratory control mechanisms. These problems intern precipitate respiratory distress.
The degree of distress varies with the client’s position, activity and level of stress.

Dyspnea (difficult breathing) is a subjective problem, and it does not always correlate
with the extent of heart failure. To some degree exertional dyspnea occurs in all clients.
The mechanism of dyspnea may be related to the decrease in the lungs’ air volume (vital
capacity) as air is displaced by blood or interstitial fluid. Pulmonary congestion can
eventually reduce the vital capacity of the lungs to 1500 ml or less.
Orthopnea is a more advanced stage of dyspnea. The client often assumes a ‘‘three
point position” sitting up with both hands on the knees and learning forward.
Orthopnea develops because the supine position increases the amount of blood
returning from the lower extremities to the heart and lungs (preload). The clients learn
to avoid respiratory distress at night by supporting the head and thorax on pillows. In
severe heart failure the client may resort to sleeping upright in a chair.

Paroxysmal nocturnal dyspnea resembles the frightening situation of suffocation. The

client awakens with the feeling of severe suffocation and seeks relief by sitting upright
or opening a window for a “breath of fresh air”. Respirations may be labored and
wheezing (cardiac asthma). PND represents an acute exacerbation of pulmonary
congestion.it occurs due to combination of increased venous return to the lungs during
recumbency and suppression of the respiratory center to sensory input from the lungs
during sleep. Cheyn-stroke respirations sometimes occur in clients with severe form of
heart failure which probably results from the prolonged circulation time between the
pulmonary circulation and the central nervous system.

Cough is a common manifestation of LVF. The cough often hacking may produce large
amounts of frothy blood tinged sputum. The client coughs because a large amount of air
is trapped in the pulmonary tree, irritating the lung mucosa. On auscultation bilateral
crackles may be heard.

Cardiovascular manifestation also denotes LVF. Inspecting and palpating the precordium
may reveal an enlarged or left laterally displaced apical impulse. This occurs because the
left ventricle dilates in an effort to supplement ventricular contraction and emptying.
Heart gallop (S3-S4) sounds may be an early finding in heart failure as the left ventricle
becomes less compliant and its walls vibrate in response to filling during diastole.

Cerebral hypoxia may occur as a result of a decrease in cardiac output, causing

inadequate brain perfusion. Depressed cerebral function can cause anxiety, irritability,
restlessness, confusion, impaired memory, bad dreams, and insomnia. Impaired
ventilation with resultant hypercapnia may also be a precipitant. Fatigue and muscular
weakness are often associated with LVF. Inadequate cardiac output leads to hypoxic
tissue and slowed removal of metabolic wastes, which inturn cause the client to tire
easily.
Renal change can occur in both RVF and LVF but are more striking in LVF. Nocturia
occurs early in heart failure. During the day the client is upright, blood flow is away from
the kidneys, and the formation of urine is reduced. At night urine formation increase as
blood flow to the kidneys improves. Nocturia may interfere with effective sleep
patterns, which may contribute to fatigue. As cardiac output declines, decreased renal
blood flow may result in oliguria, a late manifestation of heart failure.

Complication of left ventricular failure

Acute pulmonary edema, a medical emergency, usually results from LVF. In clients with
severe cardiac decompensation, the capillary pressure within the lungs becomes so
elevated that fluid is pushed from the circulating blood into the interstitium and then
into the alveoli, bronchioles, and bronchi. The resulting pulmonary edema if untreated
may cause death from suffocation. Clients with pulmonary edema literally drown in
their own fluids.

Right ventricular failure

When right ventricle functioning decrease, peripheral edema and venous congestion of
the organs develop .Hepatomegaly and abdominal pain occurs as the liver becomes
congested with venous blood. In severe RVF the lobules of the liver becomes so
congested with the venous blood that may become anoxic. Anoxia leads to necrosis of
the lobules. In long standing heart failure these necrotic areas may become fibrotic and
then sclerotic. As a result a condition called cardiac cirrhosis develops, manifested by
ascites and jaundice.

In chronic heart failure, the increased workload of the heart and the extreme work of
breathing increase the metabolic demands of the body. Anorexia, nausea and bloating
develop secondary to venous congestion of the GIT. The combination of increased
metabolic needs and decreased caloric intake results in a marked wasting of the tissue
mass, called cardiac cachexia. Anorexia and nausea may also result from digitalis
toxicity.

Dependent edema is one of the early manifestations of RVF. Venous congestion in the
peripheral vascular beds causes increased hydrostatic capillary pressure. This
overwhelms the opposing pressure of plasma proteins, and fluid shifts out of the
capillary beds and into the interstitial spaces, with resultant pitting edema. In
ambulatory clients edema begins in the feet and ankles and moves up the lower legs. It
is most noticeable at the end of the day and often subsides after a night’s rest. In the
recumbent client pitting edema may develop in the pre sacral area and as it worsens
progress to the genital region and medial thighs.

Anasarca, a late manifestation in heart failure, is substantial and generalized edema. It

can involve the upper extremities, genital area, and thoracic and abdominal walls.
Cyanosis of the nail beds appears as venous congestion reduces peripheral blood flow.

2. Backward versus Forward Failure

In 1832, James Hope first described backward failure as the failure that results as the
ventricle fails to pump its volume, causing blood accumulation and subsequent rise in
ventricular, atrial, and venous pressures. A primary etiology of backward failure is
mechanical cardiac obstruction.

The term forward failure, proposed by MacKenzie in 1913, is applied to a situation in

which the primary pathologic process is decreased cardiac output, which ultimately
leads to a decrease in vital organ perfusion. Both backward and forward failure are seen
in most patients with chronic HF.

3. High output versus low output failure

High output failure occurs when the heart, despite normal output to high output levels,
is simply not able to meet the accelerated needs of the body. Causes include sepsis,
Pager’s disease, beriberi, anemia, thyrotoxicosis, arterio venous fistula, and pregnancy.

Low output failure occurs in most forms of heart disease, resulting in hypo perfusion of
tissue cells.

4. Acute versus chronic heart failure

The onset of heart failure may be acute, as when a client experiences an MI, or gradual
as in chronic heart failure. In chronic heart failure there is a progression of
compensatory events: a decrease in contractility, neurohormonal activation, increased
preload and afterload, and finally cardiac remodeling.

CLINICAL MANIFESTATIONS
The manifestations of heart failure depends on the specific ventricles involved, the
precipitating causes of failure, the degree of impairment, the rate of progression, the
duration of the failure, and clients underlying condition.

1. Fatigue: - fatigue is one of the earliest symptoms of chronic HF. The patient
notices fatigue after activities that normally are not tiring. The fatigue is caused
by decreased CO, impaired perfusion to vital organs, decreased oxygenation to
tissues, and anemia. Anemia can result from poor nutrition, renal disease, or drug
therapy (e.g. ACE inhibitors).
2. Dyspnea: - it is caused by increased pulmonary pressures secondary to interstitial
and alveolar edema. Dyspnea can occur with mild exertion or at rest. Orthopnea
is shortness of breath that occurs when the patient is in a recumbent position.
Paroxysmal nocturnal dyspnea occurs when the patient is asleep. It is caused by
the reabsorption of fluid from dependent body areas when the patient is
recumbent.
3. Tachycardia:-it occurs as body’s first compensatory mechanism for a failing
ventricle. Because of diminished CO there is increased SNS stimulation which
increases heart rate.
4. Edema: - it is occur in dependent body areas (peripheral edema), liver
(hepatomegaly), abdominal cavity (ascites), and lungs (pulmonary edema and
pleural effusion).pressing the edematous part with the finger may leave a
transient indentation(pitting edema).
5. Nocturia:-when the person lies down at night fluid movement from interstitial
spaces to circulatory system is enhanced. This increases increased renal blood
flow and diuresis. The patient may complain of having to void 6 or seven times
during the night.
6. Skin changes: - the skin may appear dusky, cool and damp to the touch from
diaphoresis because tissue capillary oxygen extraction may increases. Lower
extrimities are shiny and swollen, with diminished or absent hair growth.
7. Behavioral changes: - due to decreased CO cerebral perfusion may impaired.
Patient exhibit unusual behavior, restlessness, confusion, decreased attention
span, or memory. It also occurs due to poor gas exchange and worsening HF.
8. Chest pain:-it occurs due to decreased coronary perfusion secondary to
decreased CO and increased myocardial workload.
9. Weigh changes:-initially there will be progressive weight gain from fluid
retention. But gradually. Patient becomes too sick to eat and due to
 hepatomegaly and ascites patient feels anorexia and nausea. In many cases
muscle fat loss is masked by edema.

Comparison of clinical manifestations in right and left heart failure

Right sided HF Left sided HF

Signs
RV heaves LV heaves
Murmurs Pulsus alternans
Jugular venous distention Increased HR
Edema Decreased PaO2,slight increased PaCO2
Weight gain crackles
tachycardia S3 and S4 heart sounds
Ascites Pleural effusion
Anasarca Changes in mental status
hepatomegaly Restlessness, confusion
symptoms
Fatigue Weakness, fatigue
Anxiety, depression Anxiety, depression
Dependent, bilateral dyspnea
edema
Right upper quadrant pain Shallow respirations
Anorexia and GI bleeding PND
Nausea Orthopnea, dry hacking cough, nocturia, frothy
sputum

New York Heart Association (NYHA) Classification Of Heart Failure

Class I

No limitation on physical activity. Ordinary physical activity does not cause undue
fatigue, palpitation, dyspnea, or angina pain

Class II

Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity
results in fatigue, palpitation, dyspnea, or angina pain.

Class III
Marked limitation of physical activity. Comfortable at rest, but less than ordinary
physical activity causes fatigue, palpitation, dyspnea, or angina pain.

Class IV

Unable to carryout any physical activity without discomfort. Symptoms of cardiac

insufficiency or of the angina syndrome may be present even at rest. If any physical
activity is undertaken, discomfort is increased.

DIAGNOSTIC FINDINGS
The diagnosis of heart failure depends primarily on the history and physical examination
datas. Other diagnostic modalities include:

Echocardiogram: two- dimensional echocardiogram, coupled with Doppler flow studies,

provides information about cardiac chamber size and ventricular function. These tests
aids in assessing myocardial, valvular, congenital, endocardial, and pericardial heart
disease, allowing the clinician to determine whether the dysfunction is systolic or
diastolic.

Chest X-ray:- reveals an enlarged cardiac silhouette, pulmonary and venous congestion,
and interstitial edema. On X-ray interstitial edema produces images called Kerley’s
Blines. Pleural effusions may develop and generally reflect biventricular failure.

Arterial blood gas analysis:-

Early hear failure with pulmonary edema may lead to respiratory alkalosis that is due to
hyperventilation. As the disorder progresses and oxygenation becomes more impaired,
acidosis develops. Pulse oximetry values show decreased oxygen levels.

Liver enzymes: may reflect the degree of liver. Elevated blood urea nitrogen and
creatinine levels reflect decreased renal perfusion.

ECG:- gives clues to the cause of LVF. Abnormality in the ECG occurs from the underlying
cardiac disorder and from therapeutic agents. It may demonstrate evidence of a prior
MI, dysrhythmias, or left ventricular dysfunction.

B-type natriuretic peptide: it is a protein secreted from the ventricles in response to

overload. As the degree of heart failure worsens, the level of BNP secreted in to the
blood increases. Higher levels of BNP are correlated with a diagnosis of heart failure.
MANAGEMENT
Medical management

The goals of management are to

 Improve cardiac pump performance

 Reduce myocardial workload
 Prevent further heart failure by affecting the process of cardiac remodeling

Improve ventricular pump performance

a) Supplemental oxygen: - high concentrations of oxygen by mask or cannula is

providing to relieve dyspnea or hypoxia and to improve oxygen-carbon dioxide
exchange. For hypoxemia partial rebreather mask with a flow rate of 8-10L /min can be
used to deliver oxygen concentrations of 40%-70%.If arterial oxygen tension is not
raising above 60 mmHg the client may need intubation and ventilator management.

B) Digoxin: - digoxin is used in clients who remain symptomatic despite ACE inhibitor
and beta blocker therapy. It is very effective in heart failure associated with low cardiac
output caused by ischemic, rheumatic, hypertensive, or congenital heart disease.
Digoxin is contraindicated in constricted pericarditis or cardiac tamponade and should
be used with caution in clients who have had acute MI because it increases myocardial
oxygen demand.

c) Inotropes: - inotropic agents like dopamine, dobutamine and amrinone may be

ordered for clients with severe low-output heart failure. These medications facilitate
myocardial contractility and enhance stroke volume. Dopamine is given in small doses
(<4 microgram/kg/min), stimulates the dopaminergic receptors in the renal, mesenteric,
cerebral, and coronary vascular beds. Although Dopamine may improve cardiac output
it leads to tachycardia, which increases myocardial oxygen demand and decreases
myocardial oxygen supply.

Dobutamine is a synthetic derivative of Dopamine that produces strong beta stimulatory

effects within the myocardium; it increases heart rate, AV conduction, and myocardial
contractility. Dopamine increases cardiac output without increasing myocardial oxygen
demand or reducing coronary blood flow.
Amrinone is also used to increase cardiac output in severe heart failure. In addition to
the positive ionotropic effects, it increases renal blood flow and GFR.

Reduce workload

Reduce after load: - vasodilating agents are used here. Vasodilator helps in

 Direct dilation of veins

 Dilation of arterioles
 Combined action on veins and arterioles
 Inhibition of ACE

Direct dilation of veins: venous dilators relax venous smooth muscle and increase the
capacity of the systemic venous bed; blood is trapped in the veins, and venous return to
the heart is reduced. This increased venous capacity reduces preload. E.g.:-
nitroglycerin, isosorbide dinitrate.

Dilation of arterioles: - arteriolar dilators reduce systemic arteriolar tone, which

decreases peripheral vascular resistance and afterload. Reduction in afterload reduces
the left ventricular workload and increases cardiac output. Improved renal perfusion
may initiate diuresis. ACE inhibitors are commonly used. E.g.:- Ramipril.

Combined action on veins and arterioles

Combined venous and arteriolar dilators decrease both preload and afterload.

Eg: - Sodium nitroprusside- it does not directly affect heart muscle or heart rate, but it
relaxes smooth muscles of veins and arterioles.

Inhibition of angiotensin converting enzyme inhibitors

ACE inhibitors are now considered as first choice treatment and are the cornerstone of
heart failure drug therapy. ACE inhibitors reduce afterload by blocking the production of
angiotensin a potent vasoconstrictor. They also increase renal blood flow and decreases
renal vascular resistance, which enhances diuresis.

Eg: - LIsinopril, Ramipril

Beta blockers: - they are used to inhibit the effect of the sympathetic nervous system.

Eg: - Atenelol, Propranolol.

Nesiritide: - it is newer medication for treatment of heart failure. It mimics the beta
natriuretic peptide secreted by the ventricles during heart failure, producing
vasodilation and diuresis. The medication is given intravenously and blood pressure
response is closely monitored.

Reduce preload

Diuretic enhances the renal excretion of sodium and water, which reduces circulating
blood volume, diminishes preload, and lessens systemic and pulmonary congestion.
Although they are effective they have so many side effects like electrolyte imbalance
especially hypokalemia potentiates digitalis toxicity and can cause myocardial weakness
and cardiac dysrhythmias. Also it produces hypo volemia and hypotension.

Position the client

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

Reduce fluid retention

Sodium is restricted on the diet to prevent, control or eliminate edema. Diets with 2-4g
of sodium are usually prescribed. Use of some loop diuretics produce electrolyte
imbalances especially hypokalemia that produce digitalis toxicity. So potassium
supplement and adequate dietary potassium are important. In mild to moderate heart
failures fluid restriction is not necessary. But in advanced cases it is beneficial to reduce
water to 1L/day.

Ventricular assist devices

The use of mechanical circulatory support in heart failure is to decompress the

hypokinetic ventricle, decrease myocardial workload reduce oxygen demands and
maintain adequate systemic perfusion to sustain end organ function. Ventricular assist
devices (VAD) are used as a bridge to heart transplantation and are used as a permanent
support. This may be right ventricular, left ventricular, or biventricular VADs.
Traditionally non pulsatile pumps have been used as VADs. Difficulties with these
devices include end organ dysfunction, thromboembolic complications, and the need for
full anticoagulation. These pumps can be used for a relatively short period about 10
days. Due to all these reasons their use in patients with heart failure is diminishing now.

Total artificial hearts are also used but its use is limited to smaller people because the
device may not fit for client’s small body. Initially these are limited to people awaiting
heart transplantation but currently it is used in patients who are not fit for
transplantation such as advanced age.

Extracorporeal membrane oxygenation (ECMO) systems are used for short term
hemodynamic stabilization. These devices remove blood from the inferior vena cava to
a centrifugal pump that pump the blood to an oxygenator. The oxygenated blood is
returned to the client via the femoral artery. Long term use does not promote recovery;
also bleeding is also a problem due to needed anticoagulation therapy.

Complications of any VAD includes: bleeding, hemolysis, thromboembolism, infection,

and multi organ failure.

Reduce stress and risk of injury

Rest is an important aspect in the management of heart failure. Rest can promote
diuresis, slow the heart rate, and relieve dyspnea, all of which allow more conservative
use of pharmacologic agents. The physician may prescribe a mild sedative or small doses
of barbiturates and tranquilizers to promote rest and overcome problems of
restlessness, insomnia, and anxiety.

Give specific guidelines to clients who are confined to bed rest to prevent harm full
effects of immobility. Client should perform passive leg exercises several times daily to
prevent venous stasis which may leads to venous thrombi formation and pulmonary
embolism.

SURGICAL MANAGEMENT
Heart transplantation:- when the heart is irreversibly damaged and no longer functions
adequately and when the client is at risk of dying, cardiac transplantation and use of an
artificial heart to assist or replace the failing heart to assist or replace the failing heart
measures of last resort. With the development of cyclosporine, and more recently FK-
506 and mycophenolate mofetil, and with improvements in the procurement and
preservation of donor hearts, cardiac transplantation has become an accepted
therapeutic procedure. One year survival rates after transplantation are greater than
85%. Although transplantation may not be appropriate for all clients, it may be the only
option available to some.

Cardiomyoplasty:-

For clients with low cardiac output who are not candidates for cardiac transplantation, a
procedure called cardiomyoplasty may support the failing heart. This procedure involves
wrapping the latismus dorsi muscle around the heart and electro stimulating it in
synchrony with ventricular systole. Continuous cardiac and hemodynamic monitoring is
initiated. Inotropic and vasopressor agents are administered to maintain cardiac output
until the pulse generator is activated (within 2-3 weeks). Because the muscle flap
obliterates the left upper lobe and can reduce vital capacity by as much as 20%,
aggressive pulmonary hygiene and judicious pain management are essential to prevent
atelectasis or pneumonia. In addition an upper-extremity exercise regimen is prescribed.

MODIFICATION FOR OLDER CLIENTS

Heart failure is becoming increasingly a disorder of the very old. Cardiac

decompensation can be triggered by seemingly minor illness and dietary indiscretions.
Medications commonly used by older people may have an impact on heart performance
even though they pose little risk of interaction with cardiovascular medications. NSAIDs
tend to worsen heart disease because they promote sodium retention tricyclic
antidepressants and neuroleptic agents leads to orthostatic hypotension.

NURSING MANAGEMENT
The goals of nursing management for clients with heart failure:

 To monitor for reduced cardiac output.

 To maintain adequate fluid balance.
 To reduce myocardial work load
 To assess response to medical therapies.
 To educate the client about self-care after discharge.

Nursing diagnosis and interventions

1) Decreased cardiac output related to heart failure or dysrhythmias or both.

Outcome: the client will have cardiac output as evidenced by regular cardiac rhythm,
heart rate, blood pressure, respirations, and urine output within normal limits

Interventions:

 Assess blood pressure for hypotension or hypertension and respiratory rate

for tachypnea q1 hr
 Assess heart rate and rhythm q 1 hr for tachycardia, or continue monitoring
for the presence of dysrhythmias.
 Document rhythm strips q 8 hr and if dysrhythmias occur.
 Report dysrhythmias to the physician, or follow protocol for emergency
treatment.
 Auscultate heart rate q 2 hr for changes in heart sounds
 Monitor lung sounds q 2 hr for adventitious lung sounds such as crackles and
for the presence of coughing.
 Monitor I& O and analyze findings q8h.
 Assess for changes in mental status. Assess peripheral pulses for strength and
quality and for pulses alternans.
 Administer prescribed medications and evaluate responses.
 Encourage physical and psychological rest. Encourage clients to eat small
meals and rest afterward.
2) Excess fluid volume related to reduced glomerular filtration, decreased cardiac
output, increased antidiuretic hormone and aldosterone production and sodium
and water retention
Outcomes: the client will demonstrate adequate fluid balance as evidenced by
output equal to or exceeding intake, clearing breath sounds, and decreasing
edema.
Interventions:
 Monitor I & O ratio q 4 h.
 Weigh the client daily
 Assess for peripheral edema.
 Assess for jugular venous distension, hepatomegaly and abdominal pain.
 Follow low sodium diet or fluid restriction
  Administer diuretic therapy as ordered and evaluate effectiveness of the
therapy.
3) Impaired gas exchange related to fluid in alveoli
Outcome: the client will have improved gas exchange as evidenced by decreased
dyspnea, no cyanosis, normal arterial blood gases, and a decrease in pulmonary
congestion on auscultation.
Interventions:
 Auscultate breath sounds q 2 hr.
 Encourage the client to turn, cough, and deep breathe and use the
incentive spirometer q 2 hr.
 Administer oxygen as ordered.
 Assess respiratory rate and rhythm q 2 hr and prn.
 Assess for cyanosis q 4 hr and prn.
 Position the client to facilitate breathing and observe for paroxysmal
nocturnal dyspnea.
 Monitor pulse oximetry.
 Administer diuretic therapy as ordered.
4) Ineffective tissue perfusion related to decreased cardiac output.
Outcomes: the client will have adequate tissue perfusion as evidenced by warm,
dry skin, peripheral pulses, and adequate urine output.
Intervention:
 Note color and temperature of skin q 4 h.
 Monitor peripheral pulses q 4 h.
 Provide a warm environment.
 Encourage active range of motion
 Monitor urine output q 4 h.
 Protect the skin from trauma by applying cotton socks.
5) Risk for activity intolerance related to decreased cardiac output.

Outcomes: the client will have improved levels of activity without dyspnea.

Interventions:

 Space nursing activities

 Schedule rest periods
 Monitor client’s response to activities.
  Increase activity as ordered or according to the rehabilitation nurse’s
directions.
 Instruct the client to avoid activities that increase cardiac workload.
6) Risk for impaired skin integrity related to decreased tissue perfusion and
activities.
Outcomes: the client will have reduced risk of skin impairment.
Interventions:
 Reposition the client q 2 hr.
 Provide a therapeutic mattress or bed while the client is in bed.
 Assess the skin especially bony prominences, for redness each shift and as
needed
 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) Risk for anxiety related to decrease cardiac output, hypoxia, diagnosis of heart
failure, and fear of death or debilitation.

Outcomes: the client will not exhibit manifestations 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 to ask questions.
 Provide emotional support.
 Encourage to use additional support systems.

RESEARCH STUDIES
1. Medicines currently being studied are aimed both at preventing cardiovascular
disease and treating the symptoms of those who already suffer from it. They
include 29 for lipid disorders, such as high cholesterol, 30 for heart failure, 17 for
hypertension, and 19 for stroke.
 
Many of the potential medicines use cutting-edge technologies and new scientific
approaches. For example:
  A gene therapy that uses a patient’s own cells to treat heart failure.
 A medicine that blocks the transfer of good (HDL) cholesterol to bad (LDL).
 A genetically-engineered medicine that dissolves clots to treat stroke.

These new medicines promise to continue the already remarkable progress against
heart disease and stroke and to raise the quality of life for patients suffering from these
diseases

2. Evidence linking vitamin D to cardiovascular (CV) health has accumulated in

recent years: numerous epidemiologic studies report deficiency as a significant
CV risk factor, and rodent models suggest that active vitamin D can modulate
critical remodeling processes, including cardiac hypertrophy and extracellular
matrix remodeling. The presence of vitamin D signaling machinery within the
human heart implies a direct role for this hormone in cardiac physiology and may
explain associations between vitamin D status and CV outcomes. Heart failure
(HF) represents a growing social and economic burden worldwide. Myocardial
remodeling is central to HF development, and in the context of emerging
evidence supporting mechanistic involvement of vitamin D, this review provides
critical appraisal of scientific literature related to the role of vitamin D in CV
disease, including data from epidemiologic and supplementation studies, as well
as novel findings from animal models and in vitro work. Although associative data
linking vitamin D and CV outcomes and evidence supporting a role for vitamin D
in relevant pathogenic processes are both substantial, there are limited
mechanistic data to indicate vitamin D supplementation as a viable therapeutic
adjunct for the prevention of HF development following myocardial injury.

CONCLUSION
Disorders of cardiac function are the leading cause of death in the industrialized world.
CHD is the precursor to several problems. Our role is to educate the client about risk
reduction. Heart failure is a frequent end point of cardiac disease. It is important to
maximize cardiac output and reduce system demands on the heart.

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