INFLAMMATION OF HEART

INTRODUCTION

Among the most common infections of the heart are infective endocarditis, myocarditis, and
pericarditis. The ideal managementis prevention.

Definition
Myocarditis is an inflammatory disease of the heart muscle (myocardium) that can result from a
variety of causes. While most cases are produced by a viral infection, an inflammation of the heart
muscle may also be instigated by toxins, drugs, and hypersensitive immune reactions. Myocarditis is a
rare but serious condition that affects both males and females of any age.

myocarditis
An inflammatory condition of the myocardium due to fungal, viral, or bacterial infection. It can also be
related to a collagen disease, serum sickness, chemical agent or rheumatic fever.
( Jonas: Mosby's Dictionary of Complementary and Alternative Medicine. (c) 2005, Elsevier)

TYPE OF MYOCARDITIS

primary myocarditis
usually the result of a primary viral or protozoal infection of the myocardium.

secondary myocarditis
associated with an infectious or noninfectious systemic disease or associated with another
cardiovascular disorder

acute isolated myocarditis  a frequently fatal, idiopathic, acute myocarditis affecting chiefly the
interstitial fibrous tissue.
Fiedler's myocarditis  acute isolated myocarditis

giant cell myocarditis  a subtype of acute isolated myocarditis characterized by the presence of
multinucleate giant cells and other inflammatory cells, and by ventricular dilatation, mural thrombi,
and wide areas of necrosis.

granulomatous myocarditis  giant cell myocarditis, including also granuloma formation.

hypersensitivity myocarditis  that due to allergic reactions caused by hypersensitivity to various

agents, particularly sulfonamides, penicillins, and methyldopa.

interstitial myocarditis  that affecting chiefly the interstitial fibrous tissue

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ETIOLOGY

While there are several contributing factors that may lead to myocarditis, the primary cause is viral.
Myocarditis usually results from the Coxsackie B virus, and may also result from measles, influenza,
chicken pox, hepatitis virus, or the adenovirus in children.

Additional causes of myocarditis include:

 Bacterial infections, such as tetanus, gonorrhea, or tuberculosis
 Parasite infections, such as Chagas' disease (which is caused by an insect-borne protozoan
most commonly seen in Central and South America)
 Rheumatic fever
 Surgery on the heart
 Radiation therapy for cancer that is localized in the chest, such as breast or lung cancer
 Certain medications.

illegal drugs and toxic substances may also produce acute or chronic injury to the myocardium. These
studies also indicate an increase in the incidence of toxic results from the use of cocaine. This illegal
drug causes coronary artery spasm, myocardial infarction (heart attack), and arrhythmias, as well as
myocarditis. malnutrition encourages the Coxsackie B virus to flourish, leading to the potential
development of myocarditis. Human immunodeficiency virus (HIV) is also now recognized as a cause
of myocarditis, though its prevalence is not known

INCIDENCE
The incidence of myocarditis isestimated to be 1 to 10 cases per 100,000 persons. The rate may
be higher because the variety of clinical presentations may causeunderreporting Mortality varies with
the severity ofsymptoms. Most patients with mild symptoms recover completely.Other patients may
develop cardiomyopathy and heartfailure. Patients with symptomatic heart failure and an
ejectionfraction of less than 45% had a 1-year mortality rate of 20% anda 4-year mortality rate of 56%.

PATHOPHYSIOLOGY

Myocarditis usually results from a viral, bacterial, mycotic, parasitic,protozoal, or spirochetal

infection. It also may occur in patientsafter acute systemic infections such as rheumatic fever, inthose
receiving immunosuppressive therapy, or in those with infective endocarditis. Myocarditis may result
from an allergic reactionto pharmacologic agents used in the treatment of other diseases. It may begin
in one small area and then spread throughoutthe myocardium. The degree of myocardial involvement
determines the degree of hemodynamic effect and resulting signs and symptoms. It is theorized that
dilated cardiomyopathy is a latentmanifestation of myocarditis.

CLINICAL MANIFESTATIONS

The symptoms of acute myocarditis depend on the type of infection,the degree of myocardial damage,
and the capacity of the myocardium to recover. The patient may be asymptomatic, and the infection
resolves on its own. The patient may develop mildto moderate symptoms and seek medical attention.
The patient may also sustain sudden cardiac death or quickly develop severecongestive heart failure.

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 The patient with mild to moderate symptoms often complains of fatigue and dyspnea, palpitations,and
occasional discomfort in the chest and upper abdomen.

ASSESSMENT AND DIAGNOSTIC FINDINGS

Assessment of the patient may reveal no abnormalities; as a result,the entire illness goes unrecognized.
The patient may complain of chest pain (with a subsequent cardiac catheterization
demonstratingnormal coronary arteries). The patient without any abnormal heart structure (at least
initially) may suddenly develop dysrhythmias. If the patient has developed structural abnormalities
(eg, systolic dysfunction), the clinical assessment may disclosecardiac enlargement, faint heart sounds,
gallop rhythm, and a systolicmurmur.

TREATMENT
While myocarditis is a serious condition, there is no medical treatment necessary if it results from a
general viral infection. The only steps to recovery include rest and avoidance of physical exertion.
Adequate rest becomes more important to recovery if the case is severe myocarditis with signs of
dilated cardiomyopathy (disease of the heart muscles). In this case, medical treatment for congestive
heart failure may include the following medications: angiotensin converting enzyme (ACE) inhibitors,
diuretics to reduce fluid retention, digitalis to stimulate a stronger heartbeat, and low-dose beta-
blockers.
If myocarditis is caused by a bacterial infection, the disease is treated with antibiotics to fight the
infection. If severe rhythm disturbances are involved, cardiac assist devices, an "artificial heart," or
heart transplantation may be the only option for complete recovery.

Prognosis
The outlook for a diagnosed case of myocarditis caused by a viral infection is excellent, with many
cases healing themselves spontaneously. Severe or acute myocarditis may be controlled with
medication to prevent heart failure. Because this disease may be mild or may be extreme and cause
serious arrhythmias, the prognosis varies. Cases of myocarditis may vary from complete healing (with
or without significant scarring), to severe congestive heart failure leading to death or requiring a heart
transplant.
Inflammation of the myocardium may also cause acute pericarditis (inflammation of the outer lining of
the heart). Due to the potential effects of the disease, including sudden death, it is imperative that
proper medical attention is obtained.

Prevention
Although myocarditis is an unpredictable disease, the following measures may help prevent its onset.
Individuals should:
 Take extra measures to avoid infections, and obtain appropriate treatment for infections.
 Limit alcohol consumption to no more than one or two drinks a day, if any.
 Maintain current immunizations against diphtheria, tetanus, measles, rubella, and polio.
 Avoid anything that may cause the abnormal heart to work too hard, including salt and
vigorous exercise.

antibiotic prohylasix is recommended for high risk patient before ,immediately or sometime after the
surgical procedure .

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ENDOCARDITIS
DEFINITION

Bacterial endocarditis is an infection of the inner surface of the heart or the heart valves caused by
bacteria usually found in the mouth, intestinal tract or urinary tract. This infection results in a serious
illness which requires prolonged treatment and on occasion produces injury to the heart or even death

CLASSIFICATION

Endocarditis can be classified as either infective or non-infective, depending on whether a foreign

organism is causing the problem. As the valves of the heart do not actually receive any blood supply of
their own, which may be surprising given their location, defense mechanisms (such as white blood
cells) cannot enter. So if an organism (such as bacteria) establish hold on the valves, the body cannot
get rid of them.

Infective endocarditis may also be classified as culture-positive or culture-negative. Culture-

negative endocarditis is due to micro-organisms that require a longer period of time to be identified in
the laboratory. Such organisms are said to be fastidious because they have demanding growth
requirements. Some pathogens responsible for culture-negative endocarditis include Aspergillus
species, Brucella species, Coxiella burnettii, Chlamydia species, and HACEK bacteria. Finally, the
distinction between native-valve endocarditis and prosthetic-valve endocarditis is clinically important.

ETIOLOGY

Bacterial endocarditis occurs when bacteria in the bloodstream (bacteremia) lodge on abnormal heart
valves or other damaged heart tissue. Certain bacteria normally live on parts of your body, such as the
mouth and upper respiratory system, the intestinal and urinary tracts, and the skin. Some surgical and
dental procedures cause a brief bacteremia. Bacteremia is
common after many invasive procedures, but only certain bacteria commonly cause endocarditis.

.Alpha-haemolytic streptococci, that are present in the mouth will often be the organism isolated if a
dental procedure caused the bacteraemia. If the bacteraemia was introduced through the skin, such as
contamination in surgery, during catheterisation, or in an IV drug user, Staphylococcus aureus is
common.

A third important cause of endocarditis is Enterococcus species. These bacteria enter the bloodstream
as a consequence of abnormalities in the gastrointestinal or urinary tracts. Enterococcus species are
increasingly recognized as causes of nosocomial or hospital-acquired endocarditis. This contrasts with
alpha-haemolytic streptococci and Staphylococcus aureus which are causes of community-acquired
endocarditis.Candida albicans, a yeast, is associated with IV drug users and the immunocompromised.
Pseudomonas species, which are very resilient organisms that thrive in water, are may contaminate
street drugs that have been contaminated with drinking water.

RISK FACTORS

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 HIGH RISK

prosthetic cardiac valves

history of bacterial endocarditis (even without heart disease)
complex cyanotic congenital malformations
surgically constructed systemic or pulmonary shunts or conduits
moderate risk
mitral valve prolapse with valvular regurgitation or thickened
leaflets
hypertrophic cardiomyopathy
acquired valvular dysfunction
most congenital cardiac malformations (other than those listed
above and surgical repair of atrial and ventricular septal defect,
or patent ductus arteriosus)

PATHOPHYSIOLOGY

Although uncertain, it is believed that cardiac valves and other endocardial surfaces become infected
after exposure to microemboli from bacteria or fungi circulating in the bloodstream. Dextran-
producing bacteria, such as Streptococcus mutans, have a virulence factor that promotes adherence to
endovascular surfaces. Coagulase-negative staphylococci may produce a biofilm on prosthetic
surfaces, which also promotes adherence. Beta-hemolytic streptococci and enteric gram-negative
bacteria lack recognized adherence factors, and appear less likely to cause endocarditis. Endocardial
surfaces previously damaged from valvular heart disease, endocarditis, surgery, or pacemaker wires
provide a favorable environment for thrombus formation. Over time, microorganisms proliferate in the
thrombus, resulting in a classic vegetation. Microorganisms are released into the circulation, usually on
a continuous basis, which often results in interesting findings.

SIGNS AND SYMPTOMS OF INFECTIVE ENDOCARDITIS

Bacterial endocarditis can produce many different symptoms, including fever, weakness,
breathlessness and rashes. These may be present for weeks before the cause becomes clear.
Endocarditis is usually diagnosed when bacteria is found in the blood. The signs and symptoms of
infective endocarditis depend on the causative organism. Symptoms may include fever, fatigue, weight
loss, new rashes (either painful or painless), headaches, backaches, joint pains, and Confusion

Clinical manifestation related to embolization can occur at any part of the body.
they are:
Stroke , traisent ischemic attacks ,aphasia/ataxia.
Loss of vision from embolization to the brain /retinal artery.
Petechiae on the neck,conjunctiva,chest ,abodem,and mouth.
Roth’s spot-a white /yellowcenter surrounded by bright –red ,irregular halo seenby opthalamoscope.
MI which may result of coronary artery embolism.
Pulmonary embolism
Splintter hemorrages,which look like a tinysplinters under the nail.

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Oler ‘s node –painful ,erthamatous ,pea-size nodules on the tips of the finger&toes resulting from
inflammation around a small,infected embolus.
Finger clubbing .
Janeway’s lesion-flat ,small,nontender red spots on the plam of the hands& soles of the feet.
Evidence of an immunologic reaction to infection ,including arthragia,proteinuria,casts,& acidosis.

ON PHYSICAL EXAMINATION

A new heart murmur as well as new skin, fingernail, and retinal lesions are typical physical findings in
endocarditis. echocardiogram that shows evidence of endocarditis in the heart. In many cases the
infection develops quite slowly. This is sometimes called 'sub-acute bacterial endocarditis' or 'SBE'.
Symptoms can develop gradually, over weeks or months, and can be vague at first. Heart murmurs
tend to develop and can be heard. Murmurs are caused by abnormal flow of blood through faulty or
damaged valves.

DIAGNOSIS

endocarditis may be suggested by the patient's symptoms and by physical examination. Unfortunately,
the symptoms are often nonspecific and may only suggest the condition. In most cases, patients with
endocarditis experience fever. During physical examination, the physician often discovers a new heart
murmur.

Bacteria in the bloodstream are highly suggestive of endocarditis and if endocarditis is suspected,
multiple sets of blood cultures

Additional evidence for the diagnosis will come from your physical examination, a heart murmur,
which indicates possible heart valve damage. Additional testing includes:

Blood cultures - In these tests, several blood samples will be drawn over a 24-hour period.. Results of
this sensitivity testing will guide the doctor in selecting the specific antibiotic that will be most
effective in treating the endocarditis.

Echocardiography -By using echocardiography, check for vegetations (abnormal growths that
contain infecting organisms) on the heart valves or elsewhere inside the heart look for abscesses inside
the heart and for signs of damage to natural or artificial heart valves. The best type of
echocardiography for evaluating heart valves is transesophageal echocardiography, in which a tube is
inserted through your mouth, allowing images of the heart to be obtained from just behind it. This test
may be recommended if the diagnosis remains uncertain after conventional echocardiography.
Transesophageal echocardiography is also a much better test for evaluating artificial heart valves.

Serological tests - These are blood tests that look for evidence of icreased immune system activity,
which is a sign of infection. Serological tests may be helpful in the small percentage

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TREATMENT

High dose antibiotics are administered by the intravenous route to maximize diffusion of antibiotic
molecules into vegetation(s) from the blood filling the chambers of the heart. This is necessary because
neither the heart valves nor the vegetations adherent to them are supplied by blood vessels. Antibiotics
are continued for a long time, typically two to six weeks. The type of antibiotic and the length of
therapy depend on the results of the blood cultures, which identify the species of infecting bacteria and
its sensitivity to specific antibiotics. PENCILIN is the drug of choice,even though many antimicrobial
agent is also used.In fungal endocarditis ,an antifungal agent ,such as amphotericin B (Abelest
,amphocin,Fungizone) is the usual treatment.

SURGICAL MANAGEMENT

Surgical removal of the valve is necessary in patients who fail to clear micro-organisms from their
blood in response to antibiotic therapy, or in patients who develop cardiac failure resulting from
destruction of a valve by infection. A removed valve is usually replaced with an artificial valve which
may either be mechanical (metallic) or obtained from an animal such as a pig; the latter are termed
bioprosthetic valves. Infective endocarditis is assocaited with a 25% mortality.

Aortic or mitral valve excision and replacement are requried for the patient who develop congestive
heart failure

PERICARDITIS
Pericarditis refers to an inflammation of the pericardium, themembranous sac enveloping the heart. It
may be a primary illness,or it may develop in the course of a variety of medical andsurgical disorders.

INCIDENCES
The incidence of pericarditis varies with thecause. For example, pericarditis occurs after
pericardectomy(opening of the pericardium) in 5% to 30% of patients after cardiac
surgery .Pericarditis that occurs within10 days to 2 months after acute myocardial infarction
(Dressler’ssyndrome) causes 1% to 3% of all cases of pericarditis
Pericarditis may be acute or chronic. It may be classifiedby the layers of the pericardium becoming
attached to each other(adhesive) or by what accumulates in the pericardial sac: serum(serous), pus
(purulent), calcium deposits (calcific), clotting proteins(fibrinous), or blood (sanguinous).

ETIOLOGY

The following are some of the causes underlying or associatedwith pericarditis:

• Idiopathic or nonspecific causes
• Infection: usually viral (eg, Coxsackie, influenza); rarely
bacterial (eg, streptococci, staphylococci, meningococci,
gonococci); and mycotic (fungal)
• Disorders of connective tissue: systemic lupus erythematosus,
rheumatic fever, rheumatoid arthritis, polyarteritis
• Hypersensitivity states: immune reactions, medication reactions,

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serum sickness
• Disorders of adjacent structures: myocardial infarction,
dissecting aneurysm, pleural and pulmonary disease
(pneumonia)
• Neoplastic disease: caused by metastasis from lung cancer
or breast cancer, leukemia, and primary (mesothelioma)
neoplasms
• Radiation therapy
• Trauma: chest injury, cardiac surgery, cardiac catheterization,
pacemaker implantation
• Renal failure and uremia
• Tuberculosis
PATHOPHYSIOLOGY

Pericarditis can lead to an accumulation of fluid in the pericardialsac (pericardial effusion) and
increased pressure on theheart, leading to cardiac tamponade. Frequent or
prolonged episodes of pericarditis may also lead to thickening anddecreased elasticity that restrict the
heart’s ability to fill properlywith blood (constrictive pericarditis). The pericardium may become
calcified, further restricting ventricular expansion duringventricular filling (diastole). With less filling,
the ventricles pumpout less blood, leading to decreased cardiac output and signs andsymptoms of heart
failure. Restricted diastolic filling may resultin increased systemic venous pressure, causingperipheral
edemaand hepatic failure.

CLINICAL MANIFESTATIONS

The most characteristic symptom of pericarditis is chest pain, althoughpain also may be located
beneath the clavicle, in the neck,or in the left scapula region. The pain or discomfort usually
remainsfairly constant, but it may worsen with deep inspirationand when lying down or turning. It may
be relieved with a forwardleaningor sitting position. The most characteristic sign of pericarditisis a
friction rub. Other signs may include mild fever, increased white blood cell count, and increased
erythrocyte sedimentationrate (ESR). Dyspnea and other signs and symptoms ofheart failure may
occur as the result of pericardial compressiondue to constrictive pericarditis or cardiac tamponade.

ASSESSMENT AND DIAGNOSTIC FINDINGS

Diagnosis is most often made on the basis of the patient’s history,signs, and symptoms. An
echocardiogram may detect inflammationand fluid build-up, as well as indications of heart failure, and
help to confirm the diagnosis. Because the pericardial sac surroundsthe heart, a 12-lead ECG detects
ST changes in many, ifnot all, leads.

MEDICAL MANAGEMENT
The objectives of management are to determine the cause, administertherapy, and be alert for cardiac
tamponade. When cardiacoutput is impaired, the patient is placed on bed rest until the
fever, chest pain, and friction rub have subsided.Analgesics and NSAIDs such as aspirin or ibuprofen
may beprescribed for pain relief during the acute phase. They alsohasten the reabsorption of fluid in
the patient with rheumaticpericarditis. Corticosteroids (eg, prednisone) may be prescribedif the

8
pericarditis is severe or if the patient does not respondto NSAIDs. Colchicine may also be used as an
alternativemedication.
Pericardiocentesis, a procedure in which some of the pericardialfluid is removed, may be performed to
assist in the identificationof the causative agent. It may also relieve symptoms,especially if there are
signs and symptoms of heart failure. A pericardialwindow, a small opening made in the pericardium,
maybe performed to allow continuous drainage into the chest cavity.Surgical removal of the tough
encasing pericardium (pericardiectomy)may be necessary to release both ventricles from
theconstrictive and restrictive inflammation.

PERICARDIOCENTESIS

Pericardiocentesis, a procedure where a thin needle is inserted through the chest wall into the
pericardial sac, may be considered if too much fluid is present (see cardiac tamponade below), or to
aid in establishing the cause of the pericarditis (for example, infection, cancer, etc.) by analyzing the
fluid that is removed. Pericardotomy (cutting a hole in the pericardial sac) or pericardectomy
(removing the sac completely) may be needed for recurrent pericarditis of scarring within the
pericardial sac.

Except in emergencies (eg, cardiac tamponade), pericardiocentesis, a potentially lethal procedure,

should be done using echocardiographic guidance in a cardiac catheterization laboratory and should be
supervised by a cardiologist or thoracic surgeon if possible. Resuscitation equipment must be at hand.
IV sedation (eg, MORPHINE)

COMPLICATIONS OF PERICARDITIS

Cardiac tamponade

If there is enough fluid in the pericardia sac, there may be enough pressure on the outside of the heart
to prevent it from beating adequately to push blood to the body and lungs. The pressure within the sac
itself needs to be higher than the pressure within the heart chambers, but symptoms gradually progress
as the heart function is compromised. This can be a true medical emergency.

9
The symptoms tend to be nonspecific but can include shortness of breath and difficulty with exercise
or doing daily activities. Additional complaints may be due to the illness or disease that caused the
effusion to accumulate in the first place.

Upon physical examination the following signs may be present:

← blood pressure may be low;veins in the neck can dilate (jugular venous distention);

← fluid can accumulate in parts of the body that are below the heart due to gravity (edema);
← heart sounds can be muffled because the fluid in the pericardial sac blocks normal heart sounds
from being heard with a stethoscope;
← lung examination may reveal fluid back up as well.

Testing likely will include an urgent EKG, chest x-ray and echocardiogram.

Cardiac tamponade may be a true emergency that is treated by pericardiocentesis, a procedure where a
long needle is inserted through the chest wall into the pericardial sac and fluid is removed. This
relieves the pressure within the sac and temporarily resolves the acute emergency. A plastic tube or
catheter may be left in the chest until the underlying illness that cause the tamponade is addressed and
further accumulation of fluid in the pericardium is prevented. Admission to the hospital is usually
required.

Constrictive pericarditis

If the heart or the pericardial sac is damaged because of trauma, or disease invades the space, then
there can be scarring of the space. This scarring can prevent the heart from expanding to collect blood
from the body. This limits the ability of the heart to function because it cannot collect blood and pump
it to the lungs and then back to the body. The heart is constricted and cannot dilate normally. There
may or may not be fluid detectable around the heart.

Bleeding into the pericardium from trauma or from a heart operation is the most common cause of
constrictive pericarditis, but tumors, or infections like tuberculosis or fungus can also be the cause.

The constriction occurs slowly over time and will cause shortness of breath on exertion and decreased
ability to exercise. Swelling in the legs and the abdomen may exist because it is difficult for blood to
return to the heart and fluid leaks out into the tissues.

Diagnosis is made again by history, physical examination, EKG, echocardiography and sometimes
computerized tomography (CT) of the chest.

If there is significant scarring of the pericardial sac, pericardotomy, an operation to split open the
pericardium to free up the constriction around the heart may be required to improve function.

NURSING ASSESSMENT

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  Assess for fatigue, palpitations, fever, dyspnea, and chest pain.
 Auscultate heart sounds.
 Evaluate history for precipitating factors.

NURSING DIAGNOSES
 Hyperthermia related to inflammatory/infectious process
 Decreased Cardiac Output related to decreased cardiac contractility and dysrhythmias
 Activity Intolerance related to impaired cardiac performance and febrile illness

Nursing Interventions
Reducing Fever
 Administer antipyretics as directed.
 Check temperature every 4 hours.
 Administer antibiotics as directed.

Maintaining Cardiac Output

 Evaluate for clinical evidence that disease is subsiding—monitor pulse, auscultate for
abnormal heart sounds (murmur or change in existing murmur), check temperature, auscultate
lung fields, monitor respirations.
 Record daily intake and output.
 Record daily weight.

Check for peripheral edema.

 Elevate head of bed, if necessary, to enhance respiration.

 Treat the symptoms of heart failure as prescribed (see pages 412 and 413).
 Evaluate patient's pulse and apical rate for signs of tachycardia and gallop
rhythm—indications that heart failure is recurring.
 Evaluate for evidence of dysrhythmias—patients with myocarditis are prone to develop
dysrhythmias.
o Institute continuous cardiac monitoring if evidence of a dysrhythmia develops.
o Have equipment for resuscitation, defibrillation, and cardiac pacing available in the
event of life-threatening dysrhythmia.

Reducing Fatigue
 Ensure bed rest to reduce heart rate, stroke volume, BP, and heart contractility; also helps to
decrease residual damage and complications of myocarditis, and promotes healing.
o Prolonged bed rest may be required until there is reduction in heart size and
improvement of function.
 Provide diversional activities for patient.
 Allow patient to use bedside commode rather than bedpan (reduces cardiovascular workload).
 Discuss with patient activities that can be continued after discharge.
o Discuss the need to modify activities in the immediate future.
o Explore with patient lifestyle modifications and discuss adequacy of self-concept.

Patient Education and Health Maintenance

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Instruct patient as follows:
 There is usually some residual heart enlargement; physical activity may be slowly increased;
begin with chair rest for increasing periods; follow with walking in the room and then outdoors.
 Report any symptom involving rapidly beating heart.
 Avoid competitive sports, alcohol, and other myocardial toxins (doxorubicin [Adriamycin]).
 Pregnancy is not advisable for women with cardiomyopathies associated with myocarditis.
 Prevent infectious diseases with appropriate immunizations.
 Encourage family to support patient and learn about the illness.

Evaluation: Expected Outcomes

 Afebrile
 BP and heart rate stable; no dysrhythmias noted
 Maintains bed rest

INFECTION OF HEART
RHEUMATIC HEART DISEASE
Rheumatic heart disease is a complication of rheumatic fever. Rheumatic fever, which results from an
untreated strep throat, can damage the heart valves, causing them to fail to close properly or not open
enough. When a valve fails to close properly, it allows blood to leak backward. When a valve does not
open enough, the heart must pump harder to force blood through the narrowed opening. When damage
to the heart is permanent, the condition is called rheumatic heart disease. Rheumatic fever is an acute
infectious disease that occurs primarily in children and young adults .

Rheumatic heart disease is a condition in which permanent damage to heart valves is caused by
rheumatic fever. The heart valve is damaged by a disease process that generally begins with a strep
throat caused by streptococcus A bacteria, that may eventually cause rheumatic fever.

DEFINITON
Rheumatic fever is an inflammatory disease that may develop two to three weeks after a Group A
streptococcal infection (such as strep throat or scarlet fever). It is believed to be caused by antibody
cross-reactivity and can involve the heart, joints, skin, and brainAcute rheumatic fever commonly
appears in children between ages 5 and 15, with only 20% of first time attacks occurring in adults

PATHOPHYSIOLOGY

Can occur after an untreated Group A Beta hemolytic streptococcal pharyngeal infection. It is believed
to be caused by antibody cross-reactivity. This cross-reactivity is a Type II hypersensitivity reaction
and is termed molecular mimicry. Usually, self reactive B cells remain anergic in the periphery without
T cell co-stimulation. During a Strep. infection, mature antigen presenting cells such as B cells present
the bacterial antigen to CD4-T cells which differentiate into helper T 2 cells. Helper T2 cells

12
subsequently activate the B cells to become plasma cells and induce the production of antibodies
against the cell wall of Streptococcus. However the antibodies may also react against the myocardium
and joints[11], producing the symptoms of rheumatic fever.

Group A streptococcus pyogenes has a cell wall composed of branched polymers which sometimes
contain "M proteins" that are highly antigenic. The antibodies which the immune system generates
against the "M proteins" may cross react with cardiac myofiber protein myosin[12],heart muscle
glycogen and smooth muscle cells of arteries, inducing cytokine release and tissue destruction.
However, the only proven cross reaction is with perivascular connective tissue. This inflammation
occurs through direct attachment of complement and Fc receptor-mediated recruitment of neutrophils
and macrophages. Characteristic Aschoff bodies, composed of swollen eosinophilic collagen
surrounded by lymphocytes and macrophages can be seen on light microscopy. The larger
macrophages may become Aschoff giant cells. Acute rheumatic valvular lesions may also involve a
cell-mediated immunity reaction as these lesions predominantly contain T-helper cells and
macrophages.

In acute RF, these lesions can be found in any layer of the heart and is hence called pancarditis. The
inflammation may cause a serofibrinous pericardial exudates described as “bread-and-butter”
pericarditis, which usually resolves without sequelae. Involvement of the endocardium typically results
in fibrinoid necrosis and verrucae formation along the lines of closure of the left-sided heart valves.
Warty projections arise from the deposition, while subendothelial lesions may induce irregular
thickenings called MacCallum plaques.

Chronic rheumatic heart disease is characterized by repeated inflammation with fibrinous resolution.
The cardinal anatomic changes of the valve include leaflet thickening, commissural fusion and
shortening and thickening of the tendinous cords

CLINICAL FEATURE

Diagnosis: modified Jones criteria

According to revised Jones criteria, the diagnosis of rheumatic fever can be made when two of the
major criteria, or one major criterion plus two minor criteria, are present along with evidence of
streptococcal infection.

Major criteria

 Migratory polyarthritis: a temporary migrating inflammation of the large joints, usually starting
in the legs and migrating upwards.
 Carditis: inflammation of the heart muscle which can manifest as congestive heart failure with
shortness of breath, pericarditis with a rub, or a new heart murmur.
 Subcutaneous nodules: painless, firm collections of collagen fibers over bones or tendons. They
commonly appear on the back of the wrist, the outside elbow, and the front of the knees.
 Erythema marginatum: a long lasting rash that begins on the trunk or arms as macules and
spreads outward to form a snake like ring while clearing in the middle. This rash never starts on
the face and it is made worse with heat.

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  Sydenham's chorea (St. Vitus' dance): a characteristic series of rapid movements without
purpose of the face and arms. This can occur very late in the disease.

Minor criteria

 Fever
 Arthralgia: Joint pain without swelling
 Raised Erythrocyte sedimentation rate or C reactive protein
 Leukocytosis
 ECG showing features of heart block, such as a prolonged PR interval
 Supporting evidence of Streptococcal infection: elevated or rising Antistreptolysin O titre or
DNAase.
 Previous episode of rheumatic fever or inactive heart disease

Other signs and symptoms

 Abdominal pain
 Nose bleeds

Physical
Physical findings in a patient with rheumatic heart disease include cardiac and noncardiac
manifestations of acute rheumatic fever. Some patients develop cardiac manifestations of chronic
rheumatic heart disease.

 Cardiac manifestations of acute rheumatic fever

 Pancarditis is the most serious and second most common complication of rheumatic fever
(50%). In advanced cases, patients may complain of dyspnea, mild-to-moderate chest
discomfort, pleuritic chest pain, edema, cough, or orthopnea.
 Upon physical examination, carditis is most commonly detected by a new murmur and
tachycardia out of proportion to fever. New or changing murmurs are considered necessary for
a diagnosis of rheumatic valvulitis.

Some cardiologists have proposed that echo-Doppler evidence of mitral insufficiency, particularly in
association with aortic insufficiency, may be sufficient for a diagnosis of carditis (even in the absence
of accompanying auscultatory findings); however, given the sensitivity of modern Doppler devices,
this remains controversial.

o Other cardiac manifestations include congestive heart failure and pericarditis.

o Patients in whom the diagnosis of acute rheumatic fever is made should be frequently
examined because of the progressive nature of the disease.
 New or changing murmurs
o The murmurs of acute rheumatic fever are typically due to valve insufficiency.
o The following murmurs are most commonly observed during acute rheumatic fever:
 Apical pansystolic murmur is a high-pitched, blowing-quality murmur of mitral
regurgitation that radiates to the left axilla. The murmur is unaffected by respiration

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 or position. Intensity varies but is grade 2/6 or greater. The mitral insufficiency is
related to dysfunction of the valve, chordae, and papillary muscles.
 Apical diastolic murmur (also known as a Carey-Coombs murmur) is heard with
active carditis and accompanies severe mitral insufficiency. It is related to relative
mitral stenosis, as the large volume of regurgitant flow recrosses the mitral valve
during ventricular filling. It is heard best with the bell of the stethoscope, while the
patient is in the left lateral position and the breath held in expiration. This murmur is
low pitched, rumbling, and resembles the roll of a distant drum.
 Basal diastolic murmur is an early diastolic murmur of aortic regurgitation and is
high-pitched, blowing, decrescendo, and heard best along the right upper sternal
border after deep expiration while the patient is leaning forward.
 Congestive heart failure
o Heart failure may develop secondary to severe valve insufficiency or myocarditis.
o The physical findings associated with heart failure include tachypnea, orthopnea,
jugular venous distention, rales, hepatomegaly, a gallop rhythm, and peripheral swelling
and edema.
 Pericarditis
o A pericardial friction rub indicates that pericarditis is present.
o Increased cardiac dullness to percussion and muffled heart sounds are consistent with
pericardial effusion.
o A paradoxical pulse (drop in systolic blood pressure with inspiration) with decreased
systemic pressure and perfusion and evidence of diastolic indentation of the right
ventricle on echocardiogram reflect impending pericardial tamponade. In this clinical
emergency, pericardial effusion should be treated by pericardiocentesis.
 Noncardiac manifestations
o Common noncardiac (and diagnostic) manifestations of acute rheumatic fever include
polyarthritis, chorea, erythema marginatum, and subcutaneous nodules.
o Other clinical, noncardiac manifestations include abdominal pain, arthralgias, epistaxis,
fever, and rheumatic pneumonia.
 Polyarthritis is the most common symptom and is frequently the earliest
manifestation of acute rheumatic fever (70-75%). Characteristically, the arthritis begins in the large
joints of the lower extremities (knees and ankles) and migrates to other large joints in the lower or
upper extremities (elbows and wrists). Affected joints are painful, swollen, warm, erythematous, and
limited in their range of motion. The pain is out of proportion to clinical findings. The arthritis
reaches maximum severity in 12-24 hours, persists for 2-6 days (rarely more than 3 wk) at each site,
and rapidly responds to aspirin. Aspirin improves symptoms in affected joints and prevents further
migration of the arthritis. Polyarthritis is more common and more severe in teenagers and young
adults than in younger children.

Sydenham chorea occurs in 10-30% of patients with rheumatic fever. Patients present with difficulty
writing, involuntary grimacing, purposeless (choreiform) movements of the arms and legs, speech
impairment, generalized weakness, and emotional lability. Physical findings include hyperextended
joints, hypotonia, diminished deep tendon reflexes, tongue fasciculations ("bag of worms"), and a
"milk sign" or relapsing grip demonstrated by alternate increases and decreases in tension when the
patient grips the examiner's hand.

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Erythema marginatum, also known as erythema annulare, is a characteristic rash that occurs in 5-
13% of patients with acute rheumatic fever. It begins as 1-3 cm in diameter, pink-to-red nonpruritic
macules or papules located on the trunk and proximal limbs but never on the face. The lesions spread
outward to form a serpiginous ring with erythematous raised margins and central clearing. The rash
may fade and reappear within hours and is exacerbated by heat. Thus, if the lesions are not well
visualized, they can be accentuated by the application of warm towels, a hot bath, or the use of
tangential lighting. The rash occurs early in the course of the disease and remains long past the
resolution of other symptoms. Erythema marginatum also has been reported in association with sepsis,
drug reactions, and glomerulonephritis.

Subcutaneous nodules are currently an infrequent manifestation of rheumatic fever. The frequency
has declined over the past several years to 0-8% of patients with rheumatic fever. When present, the
nodules appear over the extensor surfaces of the elbows, knees, ankles, knuckles, and on the scalp and
spinous processes of the lumbar and thoracic vertebrae where they are attached to the tendon sheath.
They are firm, nontender, and free from attachments to the overlying skin and range in size from a few
mm to 1-2 cm. They vary in number from one to dozens (mean 3-4). Histologically, they contain areas
resembling the Aschoff bodies seen in the heart. Subcutaneous nodules generally occur several weeks
into the disease and resolve within a month. They are strongly associated with severe rheumatic
carditis, and, in the absence of carditis, the diagnosis of subcutaneous nodules should be questioned.

Abdominal pain usually occurs at the onset of acute rheumatic fever. This pain resembles abdominal
pain from other conditions with acute microvascular mesenteric inflammation and may mimic acute
appendicitis. Patients may complain of arthralgias on presentation

Cardiac manifestations of chronic rheumatic heart disease: Valve deformities, thromboembolism,

cardiac hemolytic anemia, and atrial arrhythmias are the most common cardiac manifestations of
chronic rheumatic heart disease.

Valve deformities include the following:

Mitral stenosis occurs in 25% of patients with chronic rheumatic heart disease and in association with
mitral insufficiency in another 40%. Progressive fibrosis (ie, thickening and calcification of the valve)
takes place over time, resulting in enlargement of the left atrium and formation of mural thrombi in
that chamber. The stenotic valve is funnel-shaped, with a "fish mouth" resemblance. Upon
auscultation, S1 is initially accentuated but becomes reduced as the leaflets thicken. P2 becomes
accentuated, and the splitting of S2 decreases as pulmonary hypertension develops. An opening snap of
the mitral valve often is heard at the apex, where a diastolic filling murmur also is heard.

Aortic stenosis from chronic rheumatic heart disease is typically associated with aortic insufficiency.
The valve commissures and cusps become adherent and fused, and the valve orifice becomes small
with a round or triangular shape. Upon auscultation, S 2 may be single because the aortic leaflets are
immobile and do not produce an aortic closure sound. The systolic and diastolic murmurs of aortic
valve stenosis and insufficiency are heard best at the base of the heart

Thromboembolism occurs as a complication of mitral stenosis. It is more likely to occur when the left
atrium is dilated, cardiac output is decreased, and the patient is in atrial fibrillation. The frequency of

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this complication has decreased with the use of anticoagulation and the development of surgical repair
for the valve abnormality.

Cardiac hemolytic anemia is related to disruption of the RBCs by a deformed valve. Increased
destruction and replacement of platelets also may occur

Atrial arrhythmias are typically related to a chronically enlarged left atrium (from a mitral valve
abnormality). Successful cardioversion of atrial fibrillation to sinus rhythm is more likely to be
successful if the left atrium is not markedly enlarged, the mitral stenosis is mild, and the patient has
been in atrial fibrillation for less than 6 months. Patients should be anticoagulated before cardioversion
to decrease the risk of systemic embolization.

TREATMENT

The management of acute rheumatic fever is geared toward the reduction of inflammation with anti-
inflammatory medications such as aspirin or corticosteroids.

Individuals with positive cultures for strep throat should also be treated with antibiotics. Aspirin is the
drug of choice and should be given at high doses of 100 mg/kg/day. One should watch for side effects
like gastritis, salicylate poisoning etc. Steroids are reserved for cases where there is evidence of
involvement of heart. The use of steroids may prevent further scarring of tissue and may prevent
development of sequelae such as Mitral stenosis. Monthly injections of Longacting Penicillin must be
given for a period of 5 years in patients having one attack of Rheumatic fever. If there is evidence of
carditis, the length of Penidure therapy may be up to 40 years. Another important cornerstone in
treating rheumatic fever includes the continual use of low dose antibiotics (such as penicillin,
sulfadiazine, or erythromycin) to prevent recurrence

MAXIZE CARDIAC OUTPUT

Corticosteroid are used for treat carditis ,especially if heart failure is evidened .If the heart failuer
develop ,treatment ,including caradiac glycosides and diuretics is effective.

PROMOTE COMFORT

Client with arthritic manifestation obtained clinical relief with salicylates . bed rest.

Nursing Diagnoses
 Acute Pain related to an imbalance in oxygen supply and demand
 Decreased Cardiac Output related to reduced preload, afterload, contractility, and heart rate
secondary to hemodynamic effects of drug therapy
 Anxiety related to chest pain, uncertain prognosis, and threatening environment

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Nursing Interventions
Relieving Pain
 Determine intensity of patient's angina.
o Ask patient to compare the pain with other pain experienced in the past and, on a scale
of 0 (no pain) to 10 (worst pain), rate current pain.
o Observe for other signs and symptoms, including diaphoresis, shortness of breath,
protective body posture, dusky facial color, and/or changes in level of consciousness
(LOC).
 Position patient for comfort; Fowler's position promotes ventilation.
 Administer oxygen if prescribed.
 Obtain BP, apical heart rate, and respiratory rate.
 Obtain a 12-lead ECG as directed.
 Administer antianginal drug as prescribed.
 Report findings to health care providers.
 Monitor for relief of pain, and note duration of anginal episode.
 Take vital signs every 5 to 10 minutes until angina pain subsides.
 Monitor for progression of stable angina to unstable angina: increase in frequency and intensity
of pain, pain occurring at rest or at low levels of exertion, pain lasting longer than 15 minutes.
 Determine level of activity that precipitated anginal episode.
 Identify specific activities patient may engage in that are below the level at which anginal pain
occurs.
 Reinforce the importance of notifying nursing staff when angina pain is experienced.

Maintaining Cardiac Output

 Carefully monitor the patient's response to drug therapy.
o Take BP and heart rate in a sitting and a lying position on initiation of long-term
therapy (provides baseline data to evaluate for orthostatic hypotension that may occur
with drug therapy).
o Recheck vital signs as indicated by onset of action of drug and at time of drug's peak
effect.
o Note changes in BP of more than 10 mm Hg and changes in heart rate of more than 10
beats/minute.
o Note patient complaints of headache (especially with use of nitrates) and dizziness.
 Administer or teach self-administration of analgesics as directed for headache.
 Encourage supine position to relieve dizziness (usually associated with a
decrease in BP; preload is enhanced by this mechanism, thereby increasing BP).
o Institute continuous ECG monitoring or obtain 12-lead ECG as directed. Interpret
rhythm strip every 4 hours for patients on continuous monitoring (beta-adrenergic
blockers and calcium channel blockers can cause significant bradycardia and varying
degrees of heart block).
o Evaluate for development of heart failure (beta-adrenergic blockers and some calcium
channel blockers decrease contractility, thus increasing the likelihood of heart failure).
 Obtain daily weight and intake and output.
 Auscultate lung fields for crackles.
 Monitor for the presence of edema.
o Monitor laboratory tests as indicated.

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  Be sure to remove previous nitrate patch or paste before applying new paste or patch (prevents
hypotension). To decrease nitrate tolerance transdermal nitroglycerin may be worn only in the
daytime hours and taken off at night when physical exertion is decreased.
 Be alert to adverse reaction related to abrupt discontinuation of beta-adrenergic blocker and
calcium channel blocker therapy. These drugs must be tapered to prevent a “rebound
phenomenon”: tachycardia, increase in chest pain, hypertension.
 Discuss use of chromotherapeutic therapy with health care provider (tailoring of antianginal
drug therapy to the timing of circadian events).
 Report adverse drug effects to health care provider.

Decreasing Anxiety
 Rule out physiologic etiologies for increasing or new onset anxiety before administering as
needed sedatives. Physiologic causes must be identified and treated in a timely fashion to
prevent irreversible adverse or even fatal outcomes; sedatives may mask symptoms delaying
timely identification and diagnosis and treatment.
 Assess patient for signs of hypoperfusion, auscultate heart and lung sounds, obtain a rhythm
strip, and administer oxygen as prescribed. Notify the health care provider immediately.
 Document all assessment findings, health care provider notification and response, and
interventions and response.
 Explain to patient and family reasons for hospitalization, diagnostic tests, and therapies
administered.

 Encourage patient to verbalize fears and concerns about illness through frequent conversations
conveys to patient a willingness to listen.
 Answer patient's questions with concise explanations.
 Administer medications to relieve patient's anxiety as directed. Sedatives and tranquilizers may
be used to prevent attacks precipitated by aggravation, excitement, or tension.
 Explain to patient the importance of anxiety reduction to assist in control of angina. (Anxiety
and fear put an increased stress on the heart, requiring the heart to use more oxygen.) Teach
relaxation techniques.
 Discuss measures to be taken when an anginal episode occurs. (Preparing patient decreases
anxiety and allows patient to accurately describe angina.)
o Review the questions that will be asked during anginal episodes.
O Review the interventions that will be employed to relieve anginal attacks.

CONCLUSION

Rheumatic heart disease is a complication of rheumatic fever. Rheumatic fever, which results from an
untreated strep throat, can damage the heart valves, causing them to fail to close properly or not open
enough.

BIBLIOGRAPY

1. JOYEE.M.BLACK, JANE HOKANSON HAWKS, “MEDICAL SURGICAL NURSING”; 7 TH EDITION,

ELSEVIER PUBLICATIONS.

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2. LEWIS, HEITKEMPER, DIRKSEN, O’ BRIEN, BUCH EX; “MEDICAL – SURGICAL NURSING”; 7 TH
EDITION, ELSERIES PUBLICATIONS.
3. SHAFER’S, “MEDICAL – SURGICAL NURSING”; 7TH EDITION B.I. PUBLICATIONS”.
4 .HTTP://WWW.NLM.NIH.GOV/MEDLINEPLUS/ENCY/ARTICLE/003827.HTM

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