1) The document discusses various infective diseases of the heart, focusing on pericarditis. It defines pericarditis as inflammation of the pericardium, and describes different types including acute and chronic forms. 2) Causes of pericarditis include viral, bacterial, parasitic and fungal infections, drug reactions, collagen diseases, myocardial injury, radiation, and neoplasms. Common symptoms are chest pain, palpitations, fever and dyspnea. Diagnosis involves EKG, echocardiogram, cardiac enzymes and sometimes pericardiocentesis. 3) Treatment involves NSAIDs, colchicines, or corticosteroids depending on severity. Some

1. INFECTIVE DISEASES
OF HEART
MS. MINU SHARMA
MSc Nursing 2nd yr.
Himalayan College of Nursing, Dehradun

3. INFECTIVE DISEASES OF
HEART
The infections are named for the layer
of heart most involved in the infectious
process:
 Pericarditis (pericardium)
 Myocarditis (myocardium)
 Endocarditis (endocardium)

7. PERICARDITIS
 Pericarditis refers to the inflammation
of the pericardium, the membraneous
sac enveloping the heart.

8. Incidence
 Incidence varies with the cause.
 Pericarditis occurs after
pericardectomy in 5 % - 30% patients.
 1% - 3 % of cases develop after 10
days to 2 months after acute
myocardial infarction.
 Pericarditis may be acute or chronic.

9. Pericarditis
Acute
Pericarditis
Chronic
Pericarditis

10. Acute
pericarditis
Serous
pericarditis
Fiberous
pericarditis
Purulent
pericarditis
Hemorrhagic
pericarditis
Chronic
pericarditis
Adhesive
mediastino
pericarditis
Constrictive
pericarditis

11. Acute pericarditis
 Serous pericarditis is usually caused
by noninfectious inflammation such as
occurs in rheumatoid arthritis and
systemic lupus erythematosus .

12.  Fibrous and serofibrinous
pericarditis represent the same basic
process and are the most frequent
type of pericarditis. Common causes
include acute myocardial infarction
(MI), postinfarction (including Dressler
syndrome), uremia, radiation and
trauma

13.  Purulent or suppurative pericarditis
due to causative organisms may arise
from direct extension, hematogenous
seeding, or lymphatic extension, or by
direct introduction during cardiotomy.
Immunosuppression facilitates this
condition.
Clinical features include fever, chills, and
spiking temperatures.
Constrictive pericarditis is a serious
potential complication.

14.  Hemorrhagic pericarditis involves
blood mixed with a fibrinous or
suppurative effusion, and it is most
commonly caused by tuberculosis or
direct neoplastic invasion.
This condition can also occur in severe
bacterial infections.
Hemorrhagic pericarditis is common after
cardiac surgery and may cause
tamponade.
The clinical significance is similar to
suppurative pericarditis

15. Chronic pericarditis
Adhesive mediastino pericarditis is
a reaction that usually follows
suppurative or caseous pericarditis,
cardiac surgery, or irradiation.
 This condition is rarely caused by a
simple fibrinous exudate.
 The pericardial potential space is
obliterated, and adhesion of the
external surface of the parietal layer to
surrounding structures occurs.

16.  Clinically, systolic contraction of the
ribcage and diaphragm and pulsus
paradoxus may be observed.
 The increased workload may cause
massive cardiac hypertrophy and
dilatation, which can mimic an
idiopathic cardiomyopathy.

17.  Constrictive pericarditis is usually
caused by suppurative, caseous, or
hemorrhagic pericarditis.
The heart may become encased in a
0.5-cm–thick to 1-cm–thick layer of
scar or calcification, resembling a
plaster mold.

18. Etiology
 INFECTION
Viral infection :
 Accounts for 1-10% of cases.
 The disease is usually a short self-limited
disease that lasts 1-3 weeks and can occur
as seasonal epidemics, especially
coxsackievirus B and influenza.

19.  Causative viruses include
coxsackievirus B, echovirus,
adenoviruses, influenza A and B viruses,
enterovirus, mumps virus, Epstein-Barr
virus, human immunodeficiency virus
(HIV), herpes simplex virus (HSV) type
1, varicella-zoster virus (VZV), measles
virus, parainfluenza virus (PIV) type 2,
and respiratory syncytial virus (RSV),
cytomegalovirus (CMV), and hepatitis
viruses A, B, and C (HAV, HBV, HCV).

20. Bacterial infections
 Accounts for 1-8% of pericarditis
cases
Result from direct pulmonary
extension, hematogenous spread,
myocardial abscess or endocarditis,
penetrating injury to chest wall from
either trauma or surgery, or a
subdiaphragmatic suppurative lesion.

21. Parasitic : Parasitic organisms include
Entamoeba, Echinococcus, and
Toxoplasma.
Fungal : Fungal organisms that may
cause acute pericarditis include
Histoplasma, Blastomyces,
Coccidioides, Aspergillus, and
Candida. Myocardial injury

22. Cont...
 Myocardial injury
Myocardial infarction
Cardiac trauma
Post cardiac surgery
Hypersensitivity

23. Cont...
 Collagen diseases
Rheumatic fever: Pericarditis in those
with rheumatic fever occurs more
commonly in lower socioeconomic
groups and in children, often
accompanying endocarditis and
myocarditis, with a worse prognosis.
Consider rheumatic fever as an
etiology in any child with pericarditis.

24. Scleroderma :Scleroderma refers to a
group of rare chronic autoimmune
diseases in which the skin and
connective tissues tighten and harden; it
is a progressive disease. Inflammation of
the lining around the heart (the
pericardium)develops pericarditis ;
causes chest pain and fluid build-up
around the heart (pericardial effusion).
Systemic lupus erythematosus
Rheumatoid arthritis

25.  Drug reaction
Procainamide : Pericarditis can also
develop from a drug-induced lupus
syndrome caused by medications
including procainamide, hydralazine,
methyldopa, isoniazid, mesalazine, and
reserpine.
Doxorubicin: The anthracycline
antineoplastic agents, such as doxorubicin
and cyclophosphamide, have direct
cardiac toxicity and can cause acute
pericarditis
Penicillin : Penicillin and cromolyn sodium,
induce pericarditis through a
hypersensitivity reaction

26.  Methysergide: Methysergide
antimigraine drug belongs to the group
of medicines known as ergot alkaloids.
It causes constrictive pericarditis
through mediastinal fibrosis

27.  Smallpox vaccination infrequently
leads to myocarditis. IN A REVIEW of
a large vaccination program in the US
military, approximately 12 per 100,000
vaccinated troops developed
myopericarditis within 14 days of
vaccination. Whether this was due to a
direct viral cytopathic effect or an
immune-mediated phenomenon is
unclear.

28. Cont...
 Radiation therapy
 Cobalt therapy
 Metabolic disorders
Uremia
Myedema
 Chronic anemia
 Neoplasm
 Aortic dissection

30. Acute pericarditis. fibers covering
surface of heart.

31. Clinical Manifestations
 PHYSICAL EXAMINATION FINDING
Dyspnea/tachypnea, particularly in patients with
sizable effusions
Pericardial friction rub : Pericardial friction rubs
are triphasic :
(1) An atrial systolic rub that precedes S1
(2) A ventricular systolic rub occurs between S1
and S2 and is coincident with the peak
carotid pulse
(3) An early diastolic rub occurs after S2
(usually the faintest). Diaphragm at LL sternal,
lean forward, listen at inspiration

32. • Ewart sign: Ewart's sign is a set of findings on
physical examination in people with large
collections of fluid around their heart (pericardial
effusions).Dullness to percussion ("woody" in
quality), egophony, and bronchial breath sounds
may be appreciated at the inferior angle of the left
scapula when the effusion is large enough to
compress the left lower lobe of the lung
• Fever usually low grade but occasionally reach
104°F [40°C]
• Varying degrees of consciousness may also be
present

33. ◦ Tachycardia and cardiac arrhythmias, such
as premature atrial and ventricular
contractions, are occasionally present
◦ Pulsus paradoxus occurs in 70-80% of
patients with pericardial tamponade and is
measured by careful auscultation with a
blood pressure cuff. The first
sphygmomanometer reading is recorded at
the point when the beats are audible during
expiration and disappear with inspiration.
The second reading is taken when each
beat is audible during the respiratory cycle.

34.  A difference of more than 10 mm Hg
defines pulsus paradoxus. This
decrease is important in patients with
more slowly developing tamponade,
because they may lack findings of the
Beck triad. If an associated
hemorrhage is outside pericardial sac,
hypotension and tachycardia without
elevated jugular venous distension
may be found.

35. In Constrictive Pericarditis : -
 Pedal edema
 Hepatomegaly
 Ascites
 JVD
 Kussmaul’s sign
 Pericardial knock (early diastolic
sound) heard at the apex
 Usually - no friction rub

36.  CLINICAL FINDING
 Palpitations may be the presenting
complaint, but chest pain is the
cardinal symptom of pericarditis
 Common associated signs and
symptoms include low-grade
intermittent fever, dyspnea/tachypnea

37. In uremic patients, heart rates may be
deceptively slow with tamponade, fever,
and hypotension due to autonomic
impairment.
Patients with cardiac tamponade may
present subacutely with symptoms of
anxiety, dyspnea, fatigue, or altered mental
status. They may have a history of medical
illnesses associated with pericardial
involvement, particularly end-stage renal

38. Complications of Pericarditis
 Pericardial Effusion
 Cardiac Tamponade

39. Pericardial Effusion
 Can occur rapidly or slowly
 Pulmonary compression-cough,
dyspnea, and tachypnea
 Phrenic nerve art sounds distant,
muffled
 Slow build-up; no immediate effects
 If rapid  compression of heart
 tamponade!

41. Cardiac Tamponade
 Compression of heart
 Occur acutely (trauma) or sub-acutely
(malignancy)
 Symptoms- chest pain, confusion,
anxious, ^ CVP, restless, muffled heart
sounds
 Later- tachypnea, tachycardia, and dec.
CO, NVD and pulsus paradoxus
 With slow onset dyspnea may be only
symptom

42. PERICARDIUMCARDIAC TAMPONADE
Original heart size
Excess pericardial fluid

43. Cardiac tamponade
Physiology- Paradoxical pulse is a pulse that markedly
decreases in amplitude during inspiration. On inspiration,
more blood is pooled in the lungs and so decreases the return
to the left side of the heart; this affects the consequent stroke
volume.
Definition- a decrease in
systolic BP with inspirations
that is exaggerated in cardiac
tamponade

45. Collaborative Care
-Pericarditis, Pericardial Effusion,
Cardiac Tamponde
 Diagnostic Tests
 Medications
 Surgical/Therapeutic Interventions
 Nursing Diagnosis/Interventions

46. Diagnostic Tests- to R/O
 CBC-inc. WBC, ESR, and CRP
 Cardiac Enzymes- inc. but not as much as with MI
 EKG- diffuse St elevation *important to different
from MI changes (acute pericarditis)
 Echo- for wall movement
 CXR; Doppler imaging
 CT or MRI- for pericardial effusion
 Pericardiocentesis fluid- determine cause; treat
cardiac tamponade

47. Medications-
 ASA or tylenol Acetaminophen
decreases fever and pain , but does not
help inflammation.Adult dosing is 2
regular strength (325 mg) every 4 hours
or 2 extra-strength (500 mg) every 6
hours. Maximum dose is 4,000 mg per
day.
 NSAIDS : Drug-induced pericarditis
treatment includes stopping the
administration of the offending agent and
anti-inflammatory therapy as needed.
Treatment is with aspirin or NSAIDs

48.  NSAID regimens — The 2004 European
Society of Cardiology guidelines
recommended the use of an NSAID for
the treatment of acute pericarditis.
Commonly used NSAID regimens include
:
 Ibuprofen — Depending on the severity of
the pericarditis and individual medication
response, a dose of 400 to 800 mg of
ibuprofen three times daily is usually
adequate for symptom relief. Ibuprofen
can be the preferred NSAID because of
its rare side effects, favorable impact on
coronary artery blood flow, and large

49.  Indomethacin — Indomethacin can be
administered at a dose of 50 mg three
times daily for one to two weeks
followed by slow tapering.
 Aspirin — Aspirin can be given at a
dose of 750 to 1000 mg every six to
eight hours followed by gradual
tapering every week for a treatment
period of three to four weeks.

50.  Corticosteroids
 Anti-anxiety medication proton pump
inhibitors

51. Surgical/invasive Interventions
(remove fluid-treat tamponade)
 Pericardiocentesis
◦ Hook needle to V lead- guided by EKG and
echo
◦ Look for ST elevation
◦ Withdraw fluid
◦ Afterward watch for cardiac tamponade (PP),
dysrhythmias, pneumothorax
 Pericardial window
 Percutaneous balloon pericardiotomy
 Sclerosing agent- tetracycline (Bonds layers
together)

52. Pericardiocentesis

53. Procedure in which opening is made in pericardium to drain fluid
that has accumulated around heart-ericardial window can be made
via a small incision below end of the breastbone (sternum) or via a
small incision between the ribs on the left side of chest.
Pericardial
Window

54. Nursing Diagnosis for
Pericarditis
 Acute pain related to tissue ischemia
secondary to arterial occlusion, tissue
inflammation as evidenced by patient facial
expression .
 Ineffective Breathing Pattern related to
inflammatory process as evidenced by
dyspnea
 Risk for Decreased Cardiac Output related
to structural abnormalities of the heart
 Activity Intolerance related to imbalance
between oxygen supply and metabolic

55. Nursing Management
 Collaboration of oxygen and delivery
of analgesic drugs and drug side
effects observed.
 Observation of vital signs.
 Perform 12 lead ECG, 24 lead if
necessary
 Recognize complications
 Bed rest with Fowler position / semi-
Fowler position client with pillows.
 Positioning/sit up/lean forward

56.  Instruct client to deep breathe or use
incentive spirometer every 1 - 2 hours
 Space activities
 Prevent complications of immobility
 Psychological support
 Appropriate medication selection

57. Research study
 A systematic review was performed in
Europe to assess the efficacy and safety
of colchicine for pericarditis prevention.
Randomised clinical trials on
pharmacological prevention of
pericarditis were included. study found
that colchicine 0.5-1.0 mg daily was safe
and efficacious for the primary and
secondary prevention of pericarditis and
should be considered as first line therapy
for pericarditis prevention.

58. Myocarditis
Myocarditis-uncommon inflammation of
heart muscle

59. Etiology
 Virus
 Bacterial infection
 HIV infection
 Lyme’s disease
 Giant cell
 Chagas’ disease

60.  Other agents are also able to provoke
myocarditis, such as alcohol,
radiation, chemicals, and drugs

61.  A recent study also showed that severe
emotional stress could produce heart
failure that starts abruptly, with evidence
of inflammation of heart muscle as well.

62. Myocarditis- infection in muscles of heart; most commonly caused by Coxsackie B virus that
follows a respiratory or viral illness, bacteria and other infectious agents

63. Risk factor-myocarditis
 Treatment of URI
 Toxic or chemical effects
 Autoimmune disorders
 Post pericarditis
 Metabolic-lupus
 Heat stroke or hypothermia

64. PATHOPHYSIOLOGY
Viral, bacterial,
mycotic, parasitic,
protozoal, or
spirochetal infection.
Myocarditis

65.  It also may occur in patient after acute
systemic infection such as rheumatic
fever, in those receiving
immunosuppressive therapy, or in
those with infective endocarditis

66. Clinical Findings
 Systemic signs/symptoms
 Chest pain due to coexisting
pericarditis
 Pericardial friction rub
 In severe cases - symptoms of
progressive heart failure like CHF,
pulmonary rales, pedal edema
 Frequent manifestation are fatigue,
dyspnea, palpitation and chest pain

67.  Tachycardia, dysrhytmia
 Fatigue
 Joint pain or swelling
 Leg swelling
 Shortness of breath

68.  Pericarditis frequently occurs with
myocarditis- check friction rub
 Congestive heart failure
 Pulmonary involvement
 Sudden death

69. Diagnostic Tests
A physical examination may show no
abnormalities, or may reveal the
following:
 Abnormal heartbeat
 Fever
 Tachycardia
 Edema in the legs

70.  An Electrocardiogram : T wave
inversions; saddle-shaped ST-
segment elevations may be present.
 A Chest X-Ray

72.  Echocardiogram
 Magnetic resonance imaging (MRI)
scan
 Heart biopsy
 Elevated C-reactive protein (CRP)
and/or Erythrocyte sedimentation rate
(ESR)

73.  Markers of myocardial damage
 Biopsy

74. Medications
 In the acute phase, supportive therapy
 For symptomatic patients, digoxin and
diuretics.
 For patients with moderate to severe
dysfunction, cardiac function can be
supported use of :
 Antibiotics
 Oral therapy with ACE inhibitors (Captopril,
Lisinopril)

75.  Inotropes
 Antiviral with interferon-a
 Corticosteroids or immunosuppressents
 HF drugs-
 Diuretic
 Beta blockers
 Antiarrhythmics
 Anticoagulants
 Heart transplantation

76. COMPLICATION
 Atrial fibrillation
 Ventricular tachyarrhythmias
 Dilated cardiomyopathy
 Sudden cardiac death
 Multisystem organ failure

77. ARTICLE REVIEW
 Myocarditis is an uncommon cause of cardiac
disease that can result in arrhythmia,
congestive heart failure, and death. Myocardial
injury in myocarditis is due in part to activated
cellular and humoral immune components
directed toward normal cardiac tissue. Although
numerous therapies for myocarditis, including
corticosteroids and immunosuppressive agents,
have been applied in animal experiments and in
human studies, none have demonstrated
survival benefit over untreated controls. In
many patients, myocarditis may spontaneously
resolve. Information about myocarditis
pathogenesis, manifestations, and treatment

78. Endocarditis
 Endocarditis is an inflammation of
the inner layer of the heart , the
endocardium.

80. Types of Endocarditis
 Sub acute bacterial endocarditis
 Acute bacterial endocarditis
 Native wall endocarditis
 Prosthetic wall endocarditis

82.  Nonbacterial thrombotic endocarditis
 Rheumatic endocarditis
 Infective endocarditis

84. RHEUMATIC ENDOCARDITIS
 Acute rheumatic fever, which occurs
most often in school age children, may
develop after an episode of group A
beta haemolytic streptococcal
pharyngitis. Patients with rheumatic
fever may develop rheumatic heart
disease.

85. Pathophysiology
Tissue are not invaded and directly damaged by destructive
organism
Leukocytes accumulate in affected tissue and nodule
Myocardium involve in inflammatory process
Rheumatic myocarditis develops
Rheumatic endocarditis,result in permanent side effect

86. CLINICAL MANIFESTATION
 Tiny vegitations or growth
 Pin head sized beads arranged in a
row along valve flap
 Valvular regurgitation
 Rheumatic fever
 Heart murmur

87. ASSESSMENT AND
DIAGNOSTIC FINDING
 Shortness of breath
 lung cracles and wheezes in lung
 Systemic symptoms
 Lung : Pneumonia, Pulmonary
abscess

88.  Kidney : Hematuria,Renal failure
 Spleen : Left upper quadrant pain
 Heart : Myocardial infraction
 Brain : Stroke

89. PREVENTION
 Early adequate treatment of
streptococcal infection familiar with sign
and symptom of streptococcal
pharyngitis
Fever
Chills
Sore throat
Diffuse redness of throat with exudates on
oropharynx

90. MEDICAL MANAGEMENT
 Long term antibiotic therapy is
recommended treatment and penicillin
administration.

91. INFECTIVE ENDOCARDITIS
 Infective endocarditis is an infection of
valves and endothelial surface of the
heart.
 Endocarditis usually develops in
people with cardiac structural defects

92.  High Risk-
◦ Mechanical prosthetic heart valve
◦ Natural prosthetic heart valve
◦ Prior infective endocardititis
◦ Valve repair with prosthetic material
◦ Most congenital heart diseases

93.  Moderate Risk-
◦ Valve repair without prosthetic material
◦ Hypertrophic cardiomyopathy
◦ Mitral valve prolapse with regurgitation
◦ Acquired valvular dysfunction

94.  Low Risk-
◦ Heart murmurs
◦ Mitral valve prolapse without regurgitation
◦ Coronary artery disease
◦ People with pacemakers/ defibrillators

95. Clinical manifestation
 Stroke ,aphasia or ataxia
 Loss of vision from embolization to the
brain or retinal artery
 Petechiae
 Splinter hemorrhages
 Osler nodes

96.  Janeway lesions
 Roth spots
 Myocardial infraction
 Pulmonary embolous
 Finger clubbing

97. Pathophysiology

98. Diagnostic test
 History
 Laboratory tests
◦ Blood cultures
◦ WBC with differential
 Complete blood count (CBC)
 Electrolytes
 Creatinine

99.  BUN
 Glucose
 Coagulation panel
◦ ESR, CRP
 Echocardiography
 Chest x-ray

100. Treatment
 Prophylactic treatment for patients
◦ Removal or drainage of infected tissue
◦ Renal dialysis
◦ Ventriculoatrial shunts
 Antibiotic administration
◦ Monitor antibiotic serum levels
◦ Subsequent blood cultures
◦ Renal function monitored
 BUN, Creatinine

101.  Antibiotic therapy
 Fever
◦ Comfort with ASA, Ibuprofen etc
 Surgical
◦ Early valve replacement.

102. Complications
 Emboli (50% incidence)
◦ Right side- pulmonary emboli
◦ Left side-brain, spleen, heart, limbs,etc
 CHF-check edema, rales
 Arrhythmias
 Death

103. RESEARCH STUDY
A study was conducted by AHA on prevention of
infective endocarditis concluded the major changes
in the recommendations these are :
(1) Only an extremely small number of cases of
infective endocarditis might be prevented by
antibiotic prophylaxis for dental procedures even if
such prophylactic therapy were 100% effective.
(2) Infective endocarditis prophylaxis for dental
procedures is reasonable only for patients with
underlying cardiac conditions associated with the
highest risk of adverse outcome from infective
endocarditis.
(3) For patients with these underlying cardiac
conditions, prophylaxis is reasonable for all dental
procedures that involve manipulation of gingival
tissue or the periapical region of teeth or perforation
of the oral mucosa

104. (4) Prophylaxis is not recommended based
solely on an increased lifetime risk of
acquisition of infective endocarditis.
(5) Administration of antibiotics solely to
prevent endocarditis is not
recommended for patients who undergo
a genitourinary or gastrointestinal tract
procedure. These changes are intended
to define more clearly when infective
endocarditis prophylaxis is or is not
recommended and to provide more
uniform and consistent global
recommendations.

105. RHEUMATIC HEART DISEASE
 Rheumatic fever is an inflammatory
disease of heart potentially involving
all layers of the heart.
 Rheumatic heart disease is a chronic
condition resulting from rheumatic
fever that is characterized by scarring
and deformity of the heart valves.

106.  Rheumatic fever is an inflammatory
disease that occurs following a
Streptococcus pyogenes infection, such
as streptococcal pharyngitis
 Caused by antibody cross-reactivity that
can involve the heart, joints, skin, and
brain, the illness typically develops two
to three weeks after a streptococcal
infection.
 Acute rheumatic fever commonly
appears in children between the ages of
6 and 15, with only 20% of first-time
attacks occurring in adults

107. CLINICAL MANIFESTATION
 Modified Jones criteria were first
published in 1944 by T. Duckett Jones,
revised by the American Heart
Association in collaboration with other
groups.

108. Major criteria
 Carditis

109.  Subcutaneous
nodules
 Polyarthritis

110.  Sydenham's
chorea
 Erythema
marginatum

111. Minor criteria
 Fever
 Arthralgia
 Raised erythrocyte sedimentation rate
or C reactive protein
 Leukocytosis
 ECG showing features of heart block,
such as a prolonged PR interval
 Previous episode of rheumatic fever or
inactive heart disease

112. Other signs and symptoms
 Abdominal pain
 Nose bleeds
 Preceding streptococcal infection: recent
scarlet fever, raised antistreptolysin O or
other streptococcal antibody titre, or
positive throat culture.
 mitral valve disease

113.  Aortic valve disease
 The mechanical valve problems
 Atrial fibrillation

114. PATHOPHYSIOLOGY

115. DIAGNOSTIC TEST
 Medical history
 Physical examination for signs of
rheumatic fever, including joint pain
and inflammation. Abnormal rhythms
or murmurs that may signify that the
heart has been strained.

116.  Throat culture & blood test
 Chest X-ray
 Electrocardiogram (ECG)
 Echocardiogram,

117. COMPLICATIONS
 Endocarditis
 Heart failure

118. TREATMENT
 Bed rest
 Hospital admission to treat heart
failure
 Antibiotics for infection
 NSAIDS

119.  Corticosteroids
 Salicyclates
 Balloons inserted through a vein to
open up stuck valves
 Heart valve surgery to repair or
replace damaged heart valves.

120. NURSING DIAGNOSIS
1) Decreased Cardiac Output related to: a
disturbance in the closure of the mitral valve
(valve stenosis).
2) Ineffective Peripheral Tissue Perfusion
related to: decreased metabolism primarily
due to vasoconstriction of peripheral blood
vessels.
3) Acute Pain related to: inflammation of the
synovial membrane.

121.  4) Hyperthermia related to: inflammation of the
synovial membrane, and inflammation of the
heart valves.
5) Imbalanced Nutrition, Less Than Body
Requirement related to: an increase in stomach
acid caused by the sympathetic nervous
system compensation.
6) Activity intolerance related to: muscle
weakness, prolonged bed rest or
immobilization.
7) Self-Care Deficit related to: Musculoskeletal
Disorders: polyarthritis / arthralgia and therapy
bed rest.

122. 8) Impaired Skin Integrity related to:
inflammation of the skin and tissue
subcutan.
9) Risk for Impaired Gas Exchange
related to: the accumulation of blood in
the lungs due to increased atrial filling.
10) Risk for Injury related to: involuntary
movements, irregular, rapid and muscle
weakness / chorea

123. NURSING INTERVENTION
 Monitor blood pressure, pulse apical
and peripheral pulse
 Monitor cardiac rhythm and the
frequency
 Sleeping position 45º semifowler
 Instruct the client to do stress
management techniques (quiet
environment, meditation)
 Collaboration and providing
oxygenation therapy

124.  Energy saving clients during the acute
 Maintain a sleep until the results of
laboratory and clinical status improved
 In line with the better situation, monitor the
gradual increase in the level of activity
 Create a schedule of activity and rest
 Teach to participate in activities.
 Teach the children / parents who do not
realize that the movement is connected with
the Korean and temporary.
 In case of chorea, protect from accidents,
bedrest and provide appropriate sedation
program.

125. RESEARCH STUDY
 Two-dimensional echocardiographic
studies were performed in 293 patients
with rheumatic heart disease who
underwent open-heart mitral valve
surgery during an 18-month period.
Diagnostic confirmation of a left atrial
thrombus was based on direct inspection
of the left atrium during surgery and
histopathologic examination. Two-
dimensional echocardiographic
recordings were reviewed. Of the 293

126.  This diagnosis was confirmed at surgery and
histopathologic study in 30 (specificity
98.8%). A thrombus was not found in three
patients. In 21 other patients, left atrial
thrombi were present but were not detected
by two-dimensional echocardiography
(sensitivity 58.8%). Ten of these 21 had
thrombi in the left atrial cavity. In 11 patients,
thrombi were located in the left atrial
appendage, all of which were missed by
two-dimensional echocardiography.
Excluding these 11 left atrial appendage
thrombi, the sensitivity of two-dimensional
echocardiography for detecting left atrial
cavity thrombi was 75.0 %.


127. Reference
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 Suzzane ,Brenda Suddarth’s B ,textbook of
medical surgical nursing 12th ed. Lippincot
Williams and Wilkins; vol:1;2012; 814-21
 Suzzane ,Brenda Suddarth’s B ,textbook of
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Williams and Wilkins; vol:1; 2004; 778-84.
 Chintamani,Levis’s medical surgical nursing
7th ed.Elsevier;2011; 860-71
 Mohan H Patholology quick review 2nd ed.
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128.  Tripathi KD Essentials of medical pharmacology 6th ed.
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overview#showall
 http://www.misanjuandedios.org/files/MIOCARDITIS.pdf
 http://www.mayoclinic.com/health/myocarditis/DS00521/
DSECTION=treatments-and-drugs
 http://en.wikipedia.org/wiki/Myocarditis#Causes
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 http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001234
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 http://www.medicinenet.com/pericarditis/article.htm
 http://www.escardio.org/communities/Working-
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