The heart is a roughly cone – shaped hollow muscular organ .

it is about 10 com long and

about the size of the owner’s fist. It weighs 225gms in women and heavier in men
approximately 310gms. The heart lies in the thoracic cavity in the mediastinum between
the lungs .

It is enclosed in a double-walled sac called the pericardium. The superficial part of this sac is
called the fibrous pericardium. This sac protects the heart, anchors its surrounding
structures, and prevents overfilling of the heart with blood.
The outer wall of the human heart is composed of three layers. The outer layer is
called the epicardium, or visceral pericardium since it is also the inner wall of the
pericardium. The middle layer is called the myocardium and is composed of muscle which
contracts. The inner layer is called the endocardium and is in contact with the blood that the
heart pumps. Also, it merges with the inner lining (endothelium) of blood vessels and covers
heart valves.

The human heart has four chambers, two superior atria and two inferior ventricles. The atria
are the receiving chambers and the ventricles are the discharging chambers. The pathway of
blood through the human heart consists of a pulmonary circuitand a systemic circuit.
Deoxygenated blood flows through the heart in one direction, entering through the superior
vena cava into the right atrium and is pumped through the tricuspid valve into the right
ventricle being pumped out through the pulmonary valve to the pulmonary arteries into the
lungs. It returns from the lungs through the pulmonary veins to the left atrium where it is
pumped through the mitral valve into the left ventricle before leaving through the aortic
valve to the aorta

PERICARDIUM:
The pericardium (pericardial complex) serves as a protective barrier from the spread of
infection or inflammation from adjacent structures. It is composed of the parietal
pericardium (an outer fibrous layer) and the visceral pericardium (an inner serous
membrane made of a single layer of mesothelial cells). The fibrous pericardium is a flask-
shaped, tough outer sac with attachments to the diaphragm, sternum, and costal cartilage.
The visceral pericardium is thin, adjacent to the surface of the heart, and attached to the
epicardial fat; it reflects back on itself to form the parietal pericardium.

The pericardium normally contains as much as 20-50 mL of an ultrafiltrate of plasma.

Approximately 90-120 mL of additional pericardial fluid can accumulate in the pericardium
without an increase in pressure. The capacity of the atria and ventricles to fill is
mechanically compromised with further fluid accumulation, which can result in marked
increases in pericardial pressure, eliciting reduced stroke volume, decreased cardiac output,
and hypotension (cardiac tamponade physiology). The rapidity of fluid accumulation
influences the hemodynamic effect. Drainage occurs via the thoracic duct and the right
lymphatic duct into the right pleural space.

CARDIOMYOPATHY
DEFINITION:

Cardiomyopathy constitutes a group of diseases that directly affect the structural or

functional ability of the myocardium. Cardiomyopathies can lead to cardiomegaly and heart
failure and are the leading cause of heart transplantation.

RISK FACTORS:

 Chronic alcoholic.
 Pregnancy.
 Systemic hypertension.
 Infections.

CLASSIFICATION:

Cardiomyopathy are classified as primary or secondary. Primary cardiomyopathy refers

to those conditions in which the etiology of the heart disease is unknown (idiopathic). The
heart muscle in this case is the only portion of the heart involved, and other cardiac
structures are unaffected.

Secondary cardiomyopathy the cause of the myocardial disease is known and is secondary
to another disease process.

The World Health Organization classified cardiomyopathy conditions into three major
types:
  Dilated cardiomyopathy.
 Hypertrophic
 Restrictive.

1. DILATED CARDIOMYOPATHY:
This is the most common form i.e. it accounts for 60% of cases. This type is
characterised by ventricular dilation, contractile dysfunction and heart failure. It
causes heart failure in 25% to 40% of cases, occurs more frequently in middleaged
African American men, and has a genetic link in 30% of cases.

ETIOLOGY:

 Cardiotoxic agents like alcohol,cocaine,etc.

 Genetic disorder i.e. autosomal dominant or familial.
 Hypertension.
 Ischaemia(coronary artery disease)
 Metabolic disorders.
 Myocarditis.
 Pregnancy.
 Valve disorders.

PATHOPHYSIOLOGY:

Diffuse inflammation (myocarditis)

Rapid degeneration of myocardial fibres.

Fibrous tissues replace viable tissue.

Reduced contractility and decreased cardiac output.

Compensatory increase in the heart rate.

 Ventricular dilation.

CLINICAL MANIFESTATION:

The signs and symptoms may develop acutely or insidiously over a period of time.

 Decreased exercise tolerance.

 Fatigue.
 Dry cough
 Dyspnea.
 Paroxysmal nocturnal dyspnea.
 Orthopnoea
 Palpitations.
 Anorexia.
 S3 and S4 are audible.
 Tachycardia.
 Crackles.
 Edema
 Weak peripheral pulse.
 Pallor
 Hepatomegaly.
 Jugular vein distension.

DIAGNOSTIC EVALUATION:

 History and physical examination.

 Chest x- ray may show cardiomegaly with signs of pulmonary hypertension, as well
as pleural effusion.
 ECG may show tachycardia, arrhythmia.
 Echocardiography.
 Cardiac catheterization.
 Coronary angiography.
 Left ventriculogram may reveal a thin walled ventricle that is dilated.
 Endomyocardial biopsy .

MANAGEMENT:

 COLLABORATIVE CARE:
 REST AND ACTIVITY: the activity level of the patient is determined by the
severity of the condition. A balance of rest and activity that does not
produce signs and symptoms of oxygen deprivation is essential.
 Avoid alcohol: as it depresses the myocardial contractility.

The treatment is usually palliative than curative.

 MEDICAL MANAGEMENT:

 Angiotensin – converting enzyme inhibitors:

Examples: Captopril, enalapril, benazepril.
It inhibits angiotensin converting enzyme resulting in decreased
levels of angiotensin II. As a result, plasma aldosterone level are also
reduced.

 Diuretics: they are used to mobilise edematous fluid, reduce

pulmonary venous pressure.

Diuretics act on the kidney by promoting excretion of sodium and

water .

Examples: thiazide, furosemide,

 Inotropic Drugs:

o Beta adrenergic Agonist: it includes dopamine,

dobutamine,etc. This result in an increase in the cyclic
monophosphate within the myocardial cells and an increase in
contractility. The patients are usually admitted for a 72 hours
period or infusion is done as an outpatient procedure for an 8
hour period. Patients report relieve in symptoms.
o Digitalis: they increase force or strength of cardiac
contraction.they also decrease the conduction speed of the
myocardium and slow the heart rate.

 Vasodilator drugs:
 Sodium nitroprusside
  Nitrates.

 Beta adrenergic blockers: example – carvedilol and long acting

metrolpolol. It blocks the sympathetic nervous system’s effect on the
failing heart like increased heart rate.

 Anticoagulants if indicated.

 Anti arrhythmic drugs.

 SURGICAL MANAGEMENT:

VENTRICULAR ASSIST DEVICE:

These devices are implanted mechanical device which maintain
cardiac output and allow a failing ventricle to rest. They are used temporarily
as a bridge to transplantation or as permanent therapy for those who are not
candidates for transplantation therapy.
They are referred to as left ventricle assist device if used in the left
ventricle, and right ventricle assist device if used in right ventricles or bi –VAD
if used in both ventricles.

A left ventricular assist device (LVAD)

pumping blood from the left ventricle to the aorta, connected to an externally
worn control unit and battery pack.
CARDIAC TRANSPLANTATION: it is usually done for patients with
end stage cardiac failure, who are less than 55 years of age, having
class IV cardiac disease, no irreversible pulmonary hypertension,
 unresolved pulmonary infarcts, no systemic disease limiting
survival.

2. HYPERTROPHIC CARDIOMYOPATHY:

It is an asymmetric myocardial hypertrophy without ventricular dilation. About one

half of the cases of hypertrophic cardiomyopathy have a genetic basis.
It is characterised by:
i. Massive ventricular hypertrophy.
ii. Rapid and forceful contraction of the left ventricle.
iii. Impaired relaxation.
iv. Obstruction of aortic flow.

HCM occur less commonly than dilated cardiomyopathy. It occurs more in men than
women. It is the common cause of death in otherwise healthy young adults, usually seen in
active and athletic individuals.

ETIOLOGY:

 Aortic stenosis.
 Genetic.
 Hypertension.

PATHOPHYSIOLOGY:

Genetic predisposition or underlying cardiac disorders

Disproportionate thickening of the interventricular septum

Ventricular wall rigidity.

Increases resistance to blood flow from the left atrium and ventricle during diastolic filling.

Increases the left ventricular end diastolic pressure.

Elevation of left pulmonary venous and capillary pressure.

CLINICAL MANIFESTATION:

Patients are usually asymptomatic. The client may present the following:

 Exertional dyspnea.
 Fatigue.
 Angina.
 Syncope.
 Arrhythmia.
 Unconsciousness
 Sudden cardiac death.

DIAGNOSTIC EVALUATION:

 History and physical examination.

 ECG.
 Chest x- ray which is usually normal.
 Echocardiography.
 Cardiac catheterization.

COLLABORATIVE MANAGEMENT:

The goals of intervention for hypertrophic cardiomyopathy are to alleviate symptoms,

prevent complication and reduce risk of sudden death.

 REST AND ACTIVITY: the activity level of the patient is determined by the
severity of the condition. A balance of rest and activity that does not
produce signs and symptoms of oxygen deprivation is essential.
  Avoid alcohol: as it depresses the myocardial contractility.

MEDICAL MANAGEMENT:

o Beta adrenergic blockers.

o Calcium channel blockers.
o Anti arrhythmic.
o Drugs like nitrates, diuretics and digitalis should be avoided.
o Anti coagulants are used if indicated.

SURGICAL MANAGEMENT:

 Ventriculomyotomy and myectomy: incision and resection of the hypertrophied

muscles.

Flat, narrow, malleable retractors are placed over the mitral valve to protect leaflet
and chordae. External pressure is placed on the right ventricle, and thus the septum, to
push the septal bulge into view. A knife with a bent handle is used, to facilitate
exposure of the septal bulge.
 Alcohol septal ablation or nonsurgical reduction: it is performed in cardiac
catheterization laboratory. It involves administering absolute alcohol into the septal
artery branching off the left descending artery. Ablation of the septal wall will
decrease the obstruction to flow and patient’s symptoms will decrease.
 

3. RESTRICTIVE CARDIOMYOPATHY:
Any condition of the heart that results in fibrosis and and thickening can cause restrictive
cardiomyopathy. It is the least common of all the cardiomyopathies.
ETIOLOGY:

The specific cause is unknown. The following conditions can lead to restrictive
cardiomyopathy

 Myocardial fibrosis.
 Hypertrophy.
 Infiltration.
 Amyloidosis( deposition of eosinophilic fibrous protein in the heart)
 Hemochromatosis.

PATHOPHYSIOLOGY:

Any fibrotic infiltration into the myocardium, endocardium

Stiffening or rigid ventricular walls

Ventricles lose their ability to stretch.

Diastole filling is decreased.

Ventricular hypertrophy.

Decreased cardiac output.

CLINICAL MANIFESTATIONS:

 Exertional dyspnea.
 Fatigue.
  Angina.
 Syncope
 Peripheral edema.
 Ascites.

DIAGNOSTIC EVALUATION:

 Chest x- ray.
 ECG.
 Echocardiogram
 CT scan.
 Nuclear imaging.

MANAGEMENT:

Currently no specific treatment for restrictive cardiomyopathy exists. Treatment includes

conventional therapy for congestive heart failure and arrhythmia. Heart transplant may be
considered.

NURSING MANAGEMENT:

 ASSESSMENT:

Subjective Assessment:
 Important health information:
Past health history: CAD, hypertension, valvular or congenital heart
disease.

 Medications: use of diuretics, estrogens, corticosteroids, NSAID, over the

counter drugs.

Functional Health patterns:

 Health perception and health management.

 Nutritional status.
 Elimination.
 Activity – exercise.
 Sleep – rest.
  Cognitive – perceptual.

ASSESSMENT NURSING GOAL NURSING RATIONALE EXPECTED

DIAGNOSIS INTERVENTION OUTCOME
Subjective data: Decreased To maintain Assess the patient Helps plan Maintains
cardiac output cardiac nursing care. cardiac output.
Patient says that related to cardiac output. Monitor vital
“ sister i am structural signs, blood Monitor any
feeling weak alterationas pressure. change in
and having evidenced by cardiac
difficulty in increased heart Auscultate heart function.
breathing” rate, dyspnea, rate.
decreased blood
Objective data: pressure. Monitor lung To monitor
sounds. respiratory
Tachycardia, function.
decreased blood Monitor intake
pressure, output. Monitor renal
Shortness of function and
breath. perfusion.

Administer Increase
prescribed contractility
medications.
Decreases
Encourage rest. oxygen
demand.
Subjective data:Impaired gas Maintain Assess the patient Helps to plan Oxygen
Patient says”exchange related proper out care. saturation and
sister im havingto increased respiratory respiration
difficulty in
preload and functioning Monitor the vital Helps to within normal
breathing” mechanical signs . detect limits
failure as deterioration .
Objective data: evidenced by in
creased
Tachypnoea, respiratory rate Auscultate breath To detect any
low oxygen shortness of sounds. abnormal
saturation, breath. breath sounds.
shortness of
breath. Administer Promotes
supplemental oxygenation of
oxygen as the tissue.
prescribed.

Position the client Facilitates gas

in semifowler’s or exchange.
fowler’s position
Detects
Monitor SPO2 response to
oxygen
therapy

Subjective data: Excess fluid Maintain Assess the Helps to plan Maintain
volume related adequate patient. out care. adequate fluid
Patient says” to cardiac intake and balance.
sister i feel weak failureas output.
and my feet are manifested by Monitor weight Helps to check
swollen” edena, dyspnea daily. for fluid
on exertion accumulation
Objective data: weight gain
Edema, Monitor serum Assess as a
shortness of and electrolytes. response to
breath. treatment.

Monitor For early

symptoms of recognition of
respiratory pulmonary
difficulty. congestion.

Monitor renal To monitor

function and fluid balance.
intake and
output.

Administer To enhance
diuretics excretion of
fluid.
subjective data: Activity tolerance Promote Assess the patient Helps to plan Respiratory rate
Patient says “ related to fatigue comfort effective within normal
sister i get tired secondary to nursing care. limits during
very easily” cardiac activity.
insufficiency as Encourage Helps reduce
Objective data: evidenced by alternate rest and cardiac
Weakness, dyspnea, activity period workload.
shortness of shortness of
breath breath ,
weakness. Monitor vitals. Determine’s
level of activity
tolerance.

Assist client with Promote

activities of daily hygiene.
living.

Encourage
relatives to assist
with daily care.
Subjective data: Disturbed sleep Promote Assess the Helps to Patient gets
pattern related rest and patient’s sleeping estasblish a uninterrupted
Patient says “ to nocturnal sleep pattern. routine. sleep
sister i can’t dyspnea as
sleep properly evidenced by
at night” inability to sleep Adjust the Promotes
through the environment. sleep.
Objective data: night.

Patient looks Adjust medication Helps support

weak and administration patient’s sleep
drowsy. schedule cycle.

Monitor patient’s
sleep pattern and
number of sleep
jours
Subjective data: Fear and anxiety Relieve fear Assess the level of Helps to plan
Patient says “ im related to and anxiety fear and anxiety. nursing care.
scared bout the perceived threat
disease of death Use calm Increase
outcome” secondary to lack reassuring confidence in
of information approach. care giver.
Objective data: ablout the
disease
Facial condition, as Explain all Reduces fear
expression, evidenced by procedures of unknown.
verbalization verbalization
Encourage client Facilitate
to ventilate coping.

HEALTH EDUCATION:

 Balance Activity and Rest

 Stop smoking
 Lose any excess weight. .
 Avoid alcohol.
Advice client to keep Track of their Weight:
Rapid weight gain may mean that clients are retaining fluid, which is one of the signs of
heart failure. Keeping track of their weight helps them to detect this weight gain early and
prevent further damage to the heart. To keep track of their weight advice them to:
 Weigh at the same time each day, after urinating. Wear the same thing each time.
Write down the weight each day.
 Don’t stop weighing . If client forgets one day, advice to weigh again the next
morning.
 Advice client to report if they gain 2 or more pounds in one day, or if they gain 3–5
pounds in one week.
Teach client to observe for the following and to seek immediate medical attention:
 Faint or have dizzy spells
 Notice new symptoms from your medication
 Have a new onset of coughing
 Have trouble breathing, especially if it occurs while at rest or lying down
 Get tired faster
 Begin urinating less often
 Find that your feet or ankles swell more than usual
 Have tightness or pain in your chest
 INFLAMMATORY DISORDER OF THE HEART

Inflammatory heart disease pertains to inflammation of the heart muscles because of an

infection that develops from a bacteria or virus or from an internal peculiarity. This type of
inflammation is often associated with episodes of rheumatic fever and kawasaki disease.
The condition may be classified as either myocarditis, pericarditis or endocarditis.
 A. MYOCARDITIS:
It is a focal or diffuse infection of the myocardium, with a wide range of clinical
presentation, from subtle to devastating.

ETIOLOGY:

Myocarditis is an uncommon disorder that is usually caused by viral, bacterial, or fungal

infections that reach the heart.
Viral infections:
 Coxsackie
 Cytomegalovirus
 Hepatitis C
 Herpes
 HIV
 Parvovirus
Bacterial infections:
 Chlamydia
 Mycoplasma
 Streptococcus
 Treponema
Fungal infections:
 Aspergillus
 Candida
 Coccidioides
 Cryptococcus
 Histoplasma
PATHOPHYSIOLOGY:

The pathophysiology is poorly understood.

The most common cause of myocarditis is infection of the heart muscle by a
virus. The virus invades the heart muscle to cause local inflammation. After the initial
infection subsides, the body's immune system continues to inflict inflammatory
damage to the heart muscle. This immune response actually prolongs the
myocarditis.

Myocardial damage has 2 main phases, as follows:

 Acute phase (first 2 wk): Myocyte destruction is a direct consequence of the
offending agent, which causes cell-mediated cytotoxicity and cytokine release,
 contributing to myocardial damage and dysfunction. Detection of the causal agent is
uncommon during this stage.
 Chronic phase (>2 wk): Continuing myocyte destruction is autoimmune in nature,
with associated abnormal expression of human leukocyte antigen (HLA) in myocytes
(and in the case of viral myocarditis, persistence of viral genome in myocardium).

TYPES:

 Fulminant myocarditis - Follows a viral prodrome; distinct onset of illness comprising

severe cardiovascular compromise with ventricular dysfunction and multiple foci of
active myocarditis; either resolves spontaneously or results in death
 Acute myocarditis - Less distinct onset of illness, with established ventricular
dysfunction; may progress to dilated cardiomyopathy
 Chronic active myocarditis - Less distinct onset of illness, with clinical and histologic
relapses; development of ventricular dysfunction associated with chronic
inflammatory changes.
 Chronic persistent myocarditis - Less distinct onset of illness; persistent histologic
infiltrate with foci of myocyte necrosis without ventricular dysfunction despite
symptoms (eg, chest pain, palpitations)
These terms are still used to describe the clinical presentation and progression of
myocarditis, particularly in the absence of ongoing histologic evaluation.

CLINICAL MANIFESTATIONS :

 Fever.
 Fatigue.
 Malaise.
 Myalgia
 Pharyngitis.
 Dyspnea.
 Nausea and vomiting.
Early cardiac manifestations appear 7- 10 days after the viral infection and include
the following:
 Pericardial chest pain.
 Friction rub.
 Crackles.
 Jugular vein distension.
 Peripheral edema.
 Pericardial effusion.
  Syncope.

DIAGNOSTIC EVALUATION:

ECG.
Complete blood count : shows leukocytosis, elevated WBC count,
Elevated ESR.
Elevated myocardial enzyme like creatine kinase.
Endomyocardial biopsy

COLLABORATIVE MANAGEMENT:
The specific treatment for endo carditis is yet to be established.

 Oxygen therapy.
 Bed rest
 Restricted activities.
 Low sodium diet.
 Immunosuppressive theraphy: like prednisone,cyclosporine.
 Digoxin : to treat ventricular failure as it improves myocardial contractility.
 Intravenous immunoglobulin (epxperimental)
 Anti viral agents : like ribavarin are undergoing clinical investigation.

COMPLICATIONS:
 Cardiomyopathy
 Heart failure
 Pericarditis

PROGNOSIS:

It depends on the cause of the problem and the client’s overall health. The outlook varies.
Some people may recover completely. Others may have permanent heart failure. Promptly
treating conditions that cause myocarditis may reduce the risk

B. PERICARDITIS:
Pericarditis is an inflammation of the pericardium characterized by chest pain, pericardial
friction rub, and serial electrocardiographic (ECG) changes. Pericarditis involves the
potential space surrounding the heart or pericardium; pericarditis is one cause of fluid
accumulation in this potential space.

ETIOLOGY:

Pericarditis is usually a complication of viral infections, most commonly echovirus or

coxsackie virus. Less frequently, it is caused by influenza or HIV infection.
Infections with bacteria can lead to bacterial pericarditis (also called purulent pericarditis).
Some fungal infections can also produce pericarditis.
In addition, pericarditis can be associated with diseases such as:
 Autoimmune disorders
 Cancer (including leukemia)
 HIV infection and AIDS
 Hypothyroidism
 Kidney failure
 Rheumatic fever
 Tuberculosis
Other causes include:
 Heart attack (post-MI pericarditis)
 Injury (including surgery) or trauma to the chest, esophagus, or heart
 Medications that suppress the immune system
 Myocarditis
 Radiation therapy to the chest
Often the cause of pericarditis remains unknown. In this case, the condition is called
idiopathic pericarditis.
Pericarditis most often affects men aged 20 - 50. It usually follows respiratory infections. In
children, it is most commonly caused by adenovirus or coxsackie virus.
CLINICAL MANIFESTATION:
 Ankle, feet, and leg swelling (occasionally)
 Anxiety
 Breathing difficulty when lying down
 Chest pain, caused by the inflamed pericardium rubbing against the heart
o May radiate to the neck, shoulder, back, or abdomen
o Often increases with deep breathing and lying flat, and may increase with
coughing and swallowing
o Pleuritis type: a sharp, stabbing pain
o Usually relieved by sitting up and leaning forward
 o It is sharpest over the precordium or retrosternally.
 Dry cough
 Fatigue
 Fever
 Need to bend over or hold the chest while breathing
If the disorder is severe, there may be:
 Crackles in the lungs
 Decreased breath sounds
 Friction rub.

DIAGNOSTIC EVALUATION:
 History and physic al examination.
 ECG.
 Chest X-ray.
 Echocardiogram.
 Complete blood count.
 Nuclear imaging.
 CT scan.
 Pericardiocentesis.
 Pericardial biopsy.

COLLABORATIVE MANAGEMENT:
 Treatment of the underlying disease.
 Bed rest.
 Non steroidal anti inflammatory drugs like ibuprofen, aspirin.
 Antibiotics for bacterial pericarditis.
 Pericardiocentesis:
 Pericardiotomy: Consider subxyphoid pericardiotomy for large effusions that do not
resolve. This procedure may be performed under local anesthesia and has a lower
risk of complications compared with pericardiectomy. Percutaneous balloon
pericardiotomy, which creates a pleuro-pericardial direct communication, allowing
for drainage of fluid into the pleural space. In large malignant pericardial effusions
and recurrent tamponade, it appears to be a safe and effective (90-97%)
intervention.
 Pericardiectomy: Pericardiectomy is the most effective surgical procedure for
managing large effusions, because it has the lowest associated risk of recurrent
effusions. This procedure is used for constrictive pericarditis, effusive pericarditis, or
recurrent pericarditis with multiple attacks, steroid dependence, and/or intolerance
to other medical management.
 Pericardiectomy requires general anesthesia and a thoracotomy; therefore,
pericardiectomy should be considered only if pericardiotomy cannot be performed or has
been unsuccessful.
COMPLICATIONS:
The following conditions are possible complications of acute pericarditis itself or treatment
used in its management:
 Recurrence in 15-32% of patients
 Cardiac tamponade
 Constrictive pericarditis.
 Combination of effusive and constrictive pericarditis.
 Cardiac perforation with pericardiocentesis.
PROGNOSIS:
Pericarditis can range from mild cases that get better on their own to life-threatening
cases. The condition can be complicated by significant fluid buildup around the heart
and poor heart function. The outcome is good if the disorder is treated promptly. Most
people recover in 2 weeks to 3 months. However, pericarditis may come recur.

C. INFECTIVE ENDOCARDITIS:

Infective endocarditis or bacterial endocarditis is an infection of the endocardial

surface of the heart. which may include one or more heart valves, the mural
endocardium, or a septal defect.

CLASSIFICATION:

Infective endocarditis may have an indolent, subacute course or a more acute, fulminant
course with greater potential for rapid decompensation.
 Subacute bacterial endocarditis (SBE), although aggressive, usually develops
insidiously and progresses slowly (ie, over weeks to months). Often, no source of
infection or portal of entry is evident. SBE is caused most commonly by streptococci
(especially viridans, microaerophilic, anaerobic, and nonenterococcal group D
streptococci and enterococci) and less commonly by S. aureus, Staphylococcus
epidermidis, Gemella morbillorum, Abiotrophia defectiva, Granulicatella sp, and
fastidious Haemophilus sp. SBE often develops on abnormal valves after
asymptomatic bacteremia due to periodontal, GI, or GU infections.
 Acute bacterial endocarditis (ABE) usually develops abruptly and progresses rapidly
(ie, over days). A source of infection or portal of entry is often evident. When
bacteria are virulent or bacterial exposure is massive, ABE can affect normal valves. It
 is usually caused by S. aureus, group A hemolytic streptococci, pneumococci, or
gonococci.
 Prosthetic valvular endocarditis (PVE) develops in 2 to 3% of patients within 1 yr
after valve replacement and in 0.5%/yr thereafter. It is more common after aortic
than after mitral valve replacement and affects mechanical and bioprosthetic valves
equally. Early-onset infections (< 2 mo after surgery) are caused mainly by
contamination during surgery with antimicrobial-resistant bacteria (eg, S.
epidermidis, diphtheroids, coliform bacilli, Candida sp, Aspergillus sp). Late-onset
infections are caused mainly by contamination with low-virulence organisms during
surgery or by transient asymptomatic bacteremias, most often with streptococci; S.
epidermidis; diphtheroids; and the fastidious gram-negative bacilli, Haemophilus sp,
Actinobacillus actinomycetemcomitans, and Cardiobacterium hominis.

ETIOLOGY:

 Endocardial factors: Endocarditis usually involves the heart valves. Major predisposing
factors are
o congenital heart defects,
o rheumatic valvular disease,
o bicuspid or calcific aortic valves,
o mitral valve prolapse, and
o hypertrophic cardiomyopathy.
Prosthetic valves are a particular risk. Occasionally,
o mural thrombi,
o ventricular-septal defects, and
o patent ductus arteriosus sites become infected.

 Microorganisms:Microorganisms that infect the endocardium may originate from

distant infected sites (eg, cutaneous abscess, inflamed or infected gums, UTI) or have
obvious portals of entry such as a central venous catheter or a drug injection site.
Almost any implanted foreign material (eg, ventricular or peritoneal shunt,
prosthetic device) is at risk of bacterial colonization, thus becoming a source of
bacteremia and hence endocarditis. Endocarditis also may result from asymptomatic
bacteremia, such as typically occurs during invasive dental, medical, or surgical
procedures. Even toothbrushing and chewing can cause bacteremia (usually due to
viridans streptococci) in patients with gingivitis.
Causative microorganisms vary by site of infection, source of bacteremia, and host risk
factors (eg, IV drug abuse), but overall,
o streptococci and Staphylococcus aureus cause 80 to 90% of cases.
o Enterococci, gram-negative bacilli, and
 o fungi cause most of the rest.

PATHOPHYSIOLOGY:
Endocarditis has local and systemic consequences.
 Local consequences:Local consequences include formation of myocardial abscesses
with tissue destruction and sometimes conduction system abnormalities (usually
with low septal abscesses). Severe valvular regurgitation may develop suddenly,
causing heart failure and death (usually due to mitral or aortic valve lesions). Aortitis
may result from contiguous spread of infection. Prosthetic valve infections are
particularly likely to involve valve ring abscesses, obstructing vegetations, myocardial
abscesses, and mycotic aneurysms manifested by valve obstruction, dehiscence, and
conduction disturbances.
 Systemic consequences:Systemic consequences are primarily due to embolization of
infected material from the heart valve and, primarily in chronic infection, immune-
mediated phenomena. Right-sided lesions typically produce septic pulmonary
emboli, which may result in pulmonary infarction, pneumonia, or empyema. Left-
sided lesions may embolize to any tissue, particularly the kidneys, spleen, and CNS.
Mycotic aneurysms can form in any major artery. Cutaneous and retinal emboli are
common. Diffuse glomerulonephritis may result from immune complex deposition.

CLINICAL MANIFESTATION:
 Fever.
 Chills.
 Malaise.
 Fatigue.
 Anorexia.
 Arthralgia.
 Abdominal discomfort.
 Weight loss.
 Headache.
 Clubbing.
 Petechiae.
 Murmur.
 Osler nodes - Tender subcutaneous nodules usually found on the distal pads of the
digits
 Janeway lesions - Nontender maculae on the palms and soles
 Roth spots - Retinal hemorrhages with small, clear centers; rare and observed in
only 5% of patients.
 Stiff neck
 Delirium
  Paralysis, hemiparesis, aphasia
 Conjunctival hemorrhage
 Pallor
 Gallops
 Rales
 Cardiac arrhythmia
 Pericardial rub
 Pleural friction rub

DIAGNOSTIC EVALUATION:
 History and physical examination.
 Blood culture and sensitivity.
 Complete blood count shows leukocytosis.
 Elevated ESR
 Echocardiography.
 Chest x ray.
 ECG
 Cardiac catheterization.
COMPLICATIONS:
The following are potential complications of Infective endocarditis:
 Myocardial infarction, pericarditis, cardiac arrhythmia
 Cardiac valvular insufficiency
 Congestive heart failure
 Sinus of Valsalva aneurysm
 Aortic root or myocardial abscesses
 Arterial emboli, infarcts, mycotic aneurysms
 Arthritis, myositis
 Glomerulonephritis, acute renal failure
 Stroke syndromes
 Mesenteric or splenic abscess or infarct
COLLABORATIVE MANAGEMENT:
 The penicillin, often in combination with gentamicin, remain the cornerstones of
therapy for endocarditis caused by penicillin-susceptible streptococci.
 For penicillin-allergic patients, vancomycin is substituted.
 IV ceftriaxone (Rocephin), given once daily for 4 weeks, is another option, and even a
2-week course in combination with gentamicin has proven successful.

Antibiotic Dosage Regimen Duration (wk)

Penicillin G 12-18 MU IV q24hr 4

Ceftiaxone 2 g IV q24hr 4

Ceftriaxone plus gentamicin 2 g IV q24hr 2

1 mg/kg IV q8hr

Vancomycin 1 g IV q12hr 4

 For relatively penicillin-insensitive streptococci, the penicillin dosage is higher and

duration of therapy is 2 weeks.
 Gentamicin is given for the first 2 weeks; treatment for endocarditis caused by
enterococci is longer; both penicillin and gentamicin are given for 6 weeks
 Patients who are penicillin-allergic, should receive vancomycin, provided the isolate
is susceptible.
 For vancomycin-resistant enterococci (VRE), anecdotal success has been reported
using streptogramin quinupristin-dalfopristin (Synercid) either alone or in
combination with doxycycline and rifampin. A newer antimicrobial agent, linezolid
(Zyvox), has in vitro activity against VRE, and has been reported successful in the
treatment of a small series of cases. Daptomycin may also be a promising antibiotic
for VRE endocarditis, but has not yet been field tested.

Antibiotic Dosage Regimen Duration (wk)†

Penicillin G or ceftriaxone plus gentamicin 4 MU IV q4hr 4-6

2 g IV q24hr 4-6

1 mg/kg IV/IM q8hr 2

Vancomycin 1 g IV q12hr 4-6

Treatment of Endocarditis Caused by Enterococci

Isolate Dosage Regimen Duration (wk)

Penicillin-Susceptible

All organisms 4-6

Ampicillin 2 g IV q4hr + gentamicin* l mg/kg IV q8hr or vancomycin 1 g IV q12hr
Penicillin-Resistant

Beta-lactamase†

Ampicillin-sulbactam 3 g IV q6hr + gentamicin* l mg/kg IV q8hr 6

Intrinsically resistant 6

Vancomycin 1 g IV q12hr + gentamicin* 1 mg/kg q8hr

Penicillin- and Vancomycin-Resistant

Enterococcus faecium

Linezolid 600 mg IV or PO q12hr or quinupristin-dalfopristin 7 mg/kg q8hr

≥8

Enterococcus faecalis

Imipenem-celastatin 500 mg 7 mg/kg q6hr + ampicillin, 2 g IV q4hr or ceftriaxone 2 g IV q24hr +

ampicillin 2 g IV q4hr

≥8

 The preferred treatment for native valve endocarditis (NVE) caused by methicillin-
susceptible staphylococci is oxacillin or cefazolin for 4 to 6 weeks. If the organism is
methicillin-resistant, vancomycin is used. Gentamicin may be added for the first 3 to
5 days. This will shorten the duration of the bacteremia; however, if continued
longer, it does not improve the cure rate and may cause renal toxicity.

 Antibiotic therapy for staphylococcal PVE must be more aggressive because of the
greater likelihood of treatment failure or relapse. When the isolate is methicillin-
susceptible, oxacillin plus rifampin is given for 6 weeks and gentamicin for the first 2
weeks. When the isolate is methicillin-resistant, vancomycin is substituted for
oxacillin.

Treatment of Prosthetic Valve Endocarditis Caused by Staphylococci

Isolate Antibiotic Dosage Regimen Duration (wk)

MSSA or MSSE Oxacillin + gentamicin + rifampin 2 g IV q4hr ≥6

1 mg/kg IVor IM q8hr 2

 300 mg PO q8hr ≥6

MRSA or MRSE Vancomycin + gentamicin + rifampin 1 g IV q12hr ≥6

1 mg/kg IV/IM q8hr 2

300 mg PO q8hr ≥6

 CARDIAC VALVE SURGERY:Surgery (debridement, valve repair or replacement) is

frequently required for abscess, persistent infection despite antimicrobial therapy
(ie, persistent positive blood cultures or recurrent emboli), or severe valvular
regurgitation.
Timing of surgery requires experienced clinical judgment. If heart failure caused
by a correctable lesion is worsening (particularly when the organism is S. aureus, a gram-
negative bacillus, or a fungus), surgery may be required after only 24 to 72 h of antimicrobial
therapy. In patients with prosthetic valves, surgery may be required when TEE shows valve
dehiscence on a paravalvular abscess, when valve dysfunction precipitates heart failure,
when recurrent emboli are detected, or when the infection is caused by an antimicrobial-
resistant organism

NURSING MANAGEMENT:
 ASSESSMENT:

Subjective Assessment:
 Important health information:
Past health history: CAD, valvular or congenital heart disease, previous
endocarditis,.nosocomial bacteremia.

 Medications: immunosuppressive therapy.

 Suregery or other treatment: invasive technique like cardiac catheterization,
cystoscopy, intravascular procedures, recent dental or surgical procedures.

Functional Health patterns:

 Health perception and health management.

 Nutritional status.
 Elimination.
  Activity – exercise.
 Sleep – rest.
 Cognitive – perceptual.

ASSESSMENT NURSING GOAL NURSING RATIONALE EXPECTED

DIAGNOSIS INTERVENTION OUTCOME
Subjective Hyperthermia Maintain Assess the client. Helps plan Reduced body
data: related toinfection normal body care. temperature,
Spatient says “ of cardiac tissue as temperature Monitor vital Checks any stable vitals.
sister i am evidenced signs. alteration
feeling hot” bytempeature
elevation, Provide cold or Reduces body
Objective data: diaphoresis, chills tepid sponging. temperature.
Patient looks
weak, flushed, Ensure adequate Prevents
Temperature hydaration dehydration.
above 99F.
tachycardia Remove Promotes heat
extraclothing. loss

Administer anti Reduces body

pyretics. temperature.

Reduce physical Decrease

activity cardiac
workload.
Adminiater Treat the
antibiotics. causative
agent.

Monitor blood Evaluate

cultures and patient’s
WBC count. response to
treatment

Subjective Decreased cardiac To maintain Assess the Helps plan Maintains

data: output related to cardiac patient nursing care. cardiac output.
valvularinsuficiency output.
Patient says as evidenced by Monitor vital Monitor any
that “ sister i increased heart signs, blood change in
am feeling rate, dyspnea, pressure. cardiac
weak and decreased blood function.
having difficulty pressure. Auscultate heart
in breathing” rate.
To monitor
Objective data: Monitor lung respiratory
sounds. function.
Tachycardia,
decreased Monitor intake Monitor renal
blood pressure, output. function and
Shortness of perfusion.
breath.
Increase
Administer contractility
prescribed
medications. Decreases
oxygen
Encourage rest. demand.

Subjective Impaired gas Maintain Assess the Helps to plan Oxygen

data: exchange related proper patient out care. saturation and
Patient says” to increased respiratory respiration
sister im having preload and functioning Helps to within normal
difficulty in mechanical failure Monitor the vital detect limits
breathing” as evidenced by in signs . deterioration .
creased respiratory
Objective data: rate shortness of
breath. To detect any
Tachypnoea, Auscultate abnormal
low oxygen breath sounds. breath sounds.
saturation,
shortness of Promotes
breath. Administer oxygenation of
supplemental the tissue.
oxygen as
prescribed.
Facilitates gas
Position the exchange.
client in
semifowler’s or
fowler’s position Detects
response to
Monitor SPO2 oxygentherapy

Subjective Excess fluid volume Maintain Asses Helps to plan Maintain

data: related to cardiac adequate s the patient. out care. adequate fluid
failureas intake and balance.
Patient says” manifested by output.
sister i feel edena, dyspnea on Monitor weight Helps to check
weak and my exertion weight daily. for fluid
feet are gain accumulation
swollen”
Monitor serum Assess as a
Objective data: and electrolytes. response to
Edema, treatment.
shortness of
breath. Monitor For early
symptoms of recognition of
respiratory pulmonary
difficulty. congestion.

Monitor renal To monitor

function and fluid balance.
intake and
output.

Administer To enhance
diuretics excretion of
fluid.
subjective data: Activity tolerance Promote Assess the Helps to plan Respiratory
Patient says “ related to fatigue comfort patient effective rate within
sister i get tired secondary to nursing care. normal limits
very easily” cardiac during activity.
insufficiency as Helps reduce
Objective data: evidenced by Encourage cardiac
Weakness, dyspnea, shortness alternate rest workload.
shortness of of breath , and activity
breath weakness. period
Determine’s
level of activity
Monitor vitals. tolerance.

Promote
hygiene.
Assist client with
activities of daily
living.

Encourage
relatives to assist
with daily care.
Subjective Disturbed sleep Promote Assess the Helps to Patient gets
data: pattern related to rest and patient’s sleeping estasblish a uninterrupted
nocturnal dyspnea sleep pattern. routine. sleep
Patient says “ as evidenced by
sister i can’t inability to sleep
sleep properly through the night. Adjust the Promotes
at night” environment. sleep.

Objective data:
Adjust Helps support
Patient looks medication patient’s sleep
weak and administration cycle.
drowsy. schedule

Monitor patient’s
sleep pattern and
number of sleep
jours
Subjective Fear and anxiety Relieve fear Assess the level Helps to plan
data: related to and anxiety of fear and nursing care.
Patient says “ perceived threat of anxiety.
im scared bout death secondary to Increase
the disease lack of information Use calm confidence in
outcome” ablout the disease reassuring care giver.
condition, as approach.
Objective data: evidenced by
verbalization Reduces fear
Facial Explain all of unknown.
expression, procedures
verbalization Facilitate
Encourage client coping.
to ventilate

PROGNOSIS:
Untreated, infective endocarditis is always fatal. Even with treatment, death is more likely
and the prognosis is generally poorer for older people and people who have infection with
resistant organisms, an underlying disorder, or a long delay in treatment. The prognosis is
also poorer for people with aortic or multiple valve involvement, large vegetations,
polymicrobial bacteremia, prosthetic valve infections, mycotic aneurysms, valve ring
abscess, and major embolic events. The mortality rate for viridans streptococcal
endocarditis without major complications is < 10% but is virtually 100% for Aspergillus
endocarditis after prosthetic valve surgery.
The prognosis is better with right-sided than left-sided endocarditis because tricuspid valve
dysfunction is tolerated better, systemic emboli are absent, and right-sided S. aureus
endocarditis responds better to antimicrobial therapy.

BIBLIOGRAPHY:
1. Black M. Joyce , Hawks Jane Hokanson, medical surgical nursing; 7th ed: Missouri;
Elsevier;2005.
2. Lewis SM, Heitkemper MM , Medical surgical nursing ; 6th ed: USA : Mosby;2004.
3. Nettina Sandra M, Lippincott manual of nursing practice. 7th ed:
Philadelphia;Lippincott William and Wilkins; 2001.
4. Brunner , suddharth , textbook of medical surgical nursing: 10th ed: Philadelphia ;
Lippincott William and Wilkins; 2004.