RHD- Rheumatic Heart Disease - Valvular Disease Nursing management , nursing care

1. RHEUMATIC HEART
DISEASE AND VALULAR
HEART DISEASES
MATHEW VARGHESE V
MSN(RAK),FHNP (CMC Vellore), CSTPN,CCEPC
Nursing officer
AIIMS Delhi

2. INTRODUCTION:
 Structural, infectious and inflammatory disorders
of the heart present many challenges for the
patient, and health care team.
 Two AV valves (mitral and tricuspid) and two
semi lunar valves (aortic and pulmonic) control
blood flow through the heart.
 Valvular heart disease is defined by the valves
affected and the type of dysfunction: stenosis or
regurgitation.

3. RHEUMATIC FEVER
AND
RHEUMATIC HEART DISEASE
 Rheumatic fever is a systemic inflammatory disease
caused by an abnormal immune response to an infection
by a group of A beta-hemolytic streptococci (GAS) in the
tonsilo-pharyngeal area.
 Rheumatic Heart Disease is the permanent heart valve
damage resulting from one or more attacks of ARF. It is
thought that 40-60% of patients with ARF will go on to
developing RHD. The commonest valves affecting are
the mitral and aortic, in that order. However all four
valves can be affected

4. EPIDEMIOLOGY:
 In 2017, there were 3,046 deaths due to Rheumatic
Valvular Heart Disease and 24,811 deaths due to non-
rheumatic valvular heart disease in the United States.
 Worldwide 319400 death due to rhd in 2015,cases were
33.4 million and DALY BECAUSE OF RHD WERE 10.5
MILLION
 in india Daly rate 270/one lakh,death rate 7.86per one
lakh(global burden of disease 2017)
 Prevalence is 0.5/1000 children aged 5-15 years
 More than 3.6 million patients of rhd(2011 census),44000
added every year
 Mortality rate is 1.5-3.3 percent per year

5. RISK FACTORS:
 Children between the age of 5 - 15 years.
 Poor economic conditions
 People living in crowded conditions and
substandard housing
 People in close contact with school age children.
 In malnourished and immuno compromised
population especially in developing countries

6. PHASES OF RHEUMATIC HEART
DISEASE:
 Acute phase:
 Acute rheumatic pancarditis (Inflammation of
endocardium, myocardium and pericardium)
 Myocarditis: the heart muscle itself gets
inflamed.
 Pericarditis: the pericardial, or exterior, heart
surface.
 Endocarditis: endocardia, or interior, heart
surface.

7. CHRONIC PHASE
Acute changes may progress to scarring and development
of chronic Valvular deformities
Chronic scarring of the valves constitutes the most important
long-term problem of rheumatic fever, and usually becomes
clinically manifest decades after the acute process.
Other cardiac complications:
 Bacterial endocarditis.
 Arrhythmia.
 Chronic heart failure.
 Rheumatic Scarring of heart valve.

8. PATHOPHYSIOLOGY:

10. CLINICAL MANIFESTATIONS:
 major manifestations:
 Acute rheumatic carditis: (present with dysnoea
,palpitation ,chest pain, murmer(carey-coomb’s))
 Polyarthritis:
 Rheumatic chorea (sydenham’s chorea)
 Erythema marginatum:
 Subcutaneous nodules:
 minor manifestations:
 Fever, with a temperature of 38 degree c (100.40 f).
 Weakness, malaise, weight loss and anorexia.

11. JONES CRITERIA FOR DIAGNOSIS
“JONES CAFE PAL”

13. DIAGNOSTIC FINDINGS IN RHD
DIAGNOSTIC FINDINGS IN RHEUMATIC HEART DISEASE:
 WBC count and ESR is elevated
 C- reactive protein is positive.
 Cardiac enzymes levels may increase in severe carditis.
 Anti streptolysin- O titre is elevated 95% of patients within 2
months onset.
 Throat cultures continue to find presence of GABS; however
they usually occur in small numbers. Isolating them is
difficult.
 ECG reveals no diagnostic changes, but 20% of patient
show a prolonged PR interval.

14. MEDICAL MANAGEMENT:
 The goals of medical management include:
 Eradicate infection
 Maximizing cardiac output
 Promoting comfort
 Bed rest
 Salicylates
 Corticosteroids
 ANTIBIOTICS-BENZATHANE PENICILLIN,PROCAINE
PENICILLIN,ERYTHROMYCIN,SULPHONAMIDES

15. NURSING MANAGEMENT
 Assessment:
 Obtain baseline vital signs
 Assess the heart for pleural friction rub and the
lungs for crackles
 Palpate peripheral pulses
 Assess baseline ECG
 Assess the nutritional status and hydration status
 Assess the psychosocial data

16. NURSING DIAGNOSIS
1. Activity intolerance related to reduced
cardiac reserve and reduced cardiac out
put
2. Chronic pain related to the inflammatory
response in joints.
3. Imbalance Nutrition less than body
requirement, related to fever,
inflammation, anorexia, and fatigue.
4. Risk for ineffective therapeutic regimen
management related to a need for
lifelong therapy.

17. ACTIVITY INTOLERANCE RELATED TO REDUCED
CARDIAC RESERVE AND REDUCED CARDIAC
OUT PUT
 Goal :TO IMPROVE ACTIVITY TOLERANCE
 Interventions
 Provide adequate bed rest,
 salicylates as ordered
 Check vital signs
 Assess clients stamina and response to
exercise
 Reduce or discontinue activity if chest
pain,confusion,drop in b p

18. CHRONIC PAIN RELATED TO THE
INFLAMMATORY RESPONSE IN JOINTS
 Goal :The client will experience increase comfort as
evidence by (I) reports of reduced discomfort
(II)expression of joint pain reduction (III) reduced use of
pain medication (IV) a relaxed body posture and ability
to sleep.
 Interventions:
 Obtain a clear description of the pain or discomfort.
 Identify the source of greatest discomfort as a focus for
intervention.
 Administer analgesics as needed.
 Use salicylates round the clock as prescribed.
 Balance rest and activity according to the degree of pain
and activity tolerance.

19. The client will maintain or restore adequate nutritional
balance.
Interventions:
Administer high protein, high-carbohydrate diet.
Administer vitamin and mineral supplements as advice.
Give oral hygiene every 4 hours.
Weight daily.
Provide small, attractive and frequent serving.
Provide adequate fluids to prevent dehydration from
fever.
Restrict sodium, if the client shows signs of severe
Carditis or heart failure
IMBALANCE NUTRITION LESS THAN BODY
REQUIREMENT, RELATED TO FEVER,
INFLAMMATION, ANOREXIA, AND FATIGUE

20. RISK FOR INEFFECTIVE THERAPEUTIC REGIMEN
MANAGEMENT RELATED TO A NEED FOR
LIFELONG THERAPY.
 Expected outcome:
 The client and the client family will demonstrate adequate
knowledge of rheumatic fever.
 Interventions:
 Explain the need for lifelong therapy.
 Take good care of the teeth and gums. Obtain prompt dental
care for cavities and gingivitis. Prophylactic medication maybe
needed before any invasive dental procedures.
 Avoid people who have upper respiratory tract infection or
who have had a recent streptococcal infection.
 Notify the physician if any manifestations of streptococcal sore
throat develop.
 Advice client who have had rheumatic fever that they must
guard against infections for the rest of their lives to avoid
development of heart disease.


21. VALVULAR HEART DISEASE:
 The valves of the heart control the flow of blood through the
heart into the pulmonary artery and aorta by opening and
closing in response to the blood pressure changes.
 Maintain one-way blood flow through your heart.
 The four heart valves make sure that blood always flows
freely in a forward direction and that there is no backward
leakage.

23. PARTS OF VALVE

24. TYPES OF VALVE DISEASE:

25. VALVULAR STENOSIS:
The valve opening narrows
 The valve leaflets may become fused or thickened that the
valve cannot open freely.
 Obstructs the normal flow of blood.
 Effects:
 The chamber behind the stenotic valve is subject to
greater stress must generate more pressure (work
hard) to force blood through the narrowed opening.
 Initially, the heart compensates for the additional
workload by gradual hypertrophy and dilation of the
myocardium, and then further leads to heart failure.

26. VALVULAR REGURGITATION:
 Leakage or Backflow of Blood Results from incomplete
Closure of the Valve
Due to:
 Scarring and retraction of valve leaflets
OR
 Weakening of supporting structures
Effects:
 Causes the heart to pump the same blood twice (as the
blood comes back into the chamber).

28. MITRAL STENOSIS:
Almost always
rheumatic in
origin.
Older people:
 by heavy
calcification of
mitral valve
congestion.
Congenital (rare)

29. PATHOPHYSIOLOGY

30. CLINICAL FEATURES:
SYMPTOMS
 Dyspnea on exertion(pulmonary venous hypertension)
 Fatigue and decreased exercise tolerance(low cardiac output)
 Dry cough, wheezing
 Hemoptysis, palpitations
 Orthopneoa,Paroxysmal nocturnal dyspnea
 Repeated respiratory infections
 Dysrhythmias

31. CLINICAL FEATURES:
 SIGNS:
 Atrial fibrillation
 Mitral facies
 Auscultation - Loud first heart
sound, opening snap
 Crepitation’s, pulmonary edema,
effusions
 RV heave, loud P2 (pulmonary
hypertension).

32. INVESTIGATIONS:
 ECG: - Right ventricular hypertrophy tall R waves
 Chest X-ray: - enlarged LA & appendage
 ECHO: - thickened immobile cusps
 Reduced valve area.
 Enlarged la.
 Reduced rate of diastolic filling of LV.
 Doppler: - pressure gradient across mitral valve.
 Cardiac catheterization: - pressure gradient between
LA and LV

33. MANAGEMENT:
MEDICALLY SURGICALLY
Balloon mitral Valvuloplasty
Anticoagulant
To reduce the risk of systemic
embolism
Mitral Balloon
Valvuloplasty
Digoxin, beta blockers, or rate
limiting calcium antagonists.
To control ventricular rate
in atrial fibrillation
Mitral Valvotomy
Diuretic
To control pulmonary
congestion
Valve Replacement

34. MITRAL REGURGITATION:

35. ETIOLOGY:
 Congenital:
 Cleft mitral valve or parachute mitral valve
 Acquired
 Rheumatic heart disease
 Endocarditis
 Mitral valve prolapse
 Connective tissue disorders like Marfan’s syndrome
 Trauma
 Chordae Tendineae rupture
 Calcification of mitral valve
 Dilated Cardiomyopthy
 Idiopathic

36. CLINICAL FEATURES
 SYMPTOMS
 Dyspnea,
 Fatigue,
 Weakness,
 Symptoms of acute
pulmonary edema,
 Puffiness of face
 SIGNS
 Pulse most probably
normal irregular if AF
present.
 Widened pulse
pressure,
 Raised jugular venous
pressure

37. DIAGNOSIS
 ECG
 Echocardiography ,and
 Color Doppler

38. MEDICAL MANAGEMENT
 Salt restricted diet
 Diuretics
 Vasodilators.
 Digoxin
 Anticoagulants and
 Long term antibiotic prophylaxis by benzathane
penicillin
 SURGICAL MANAGEMENT
 Valve replacement

39. MITRAL VALVE PROLAPSE
 Synonyms; ‘floppy’ mitral valve, click –murmur
syndrome or barlows syndrome
 One of the most common cause of mild mitral
regurgitation

40. CAUSED BY
 Congenital anomalies
 Degenerative myxomatous changes feature of
connective tissue
 Disorders like Marfan’s syndrome.

41. MARFAN SYNDROME
 Marfan syndrome is an inherited disorder that
affects connective tissue — the fibers that support
and anchor your organs and other structures in
your body.
 Marfan syndrome most commonly affects the heart,
eyes, blood vessels and skeleton.
 MFS is caused by a mutation in FBN1, one of the
genes that makes fibrillin, resulting in aortic
dilatation, aneurysm formation, aortic dissection,
aortic regurgitation and mitral valve prolapse.

42. MARFAN SYNDROME
 Marfan syndrome features may include:
 Tall and slender build
 Disproportionately long arms, legs and fingers
 A breastbone that protrudes outward or dips inward
 A high, arched palate and crowded teeth
 Heart murmurs
 Extreme near sightedness
 An abnormally curved spine and flat feet

43. PATHOPHYSIOLOGY

44. CLINICAL MANIFESTATIONS:
 SYMPTOMS:
 Fatigue & weakness –
due to decreased cardiac
output – predominant
complaint.
 Exertional dyspnea &
cough – pulmonary
congestion.
 Palpitations – due to
atrial fibrillation (occur in
75% of pts.).
 Edema, ascites – Right-
sided heart failure.
 SIGNS:
 Atrial fibrillation.
 Cardiomegaly.
 Apical pan systolic
murmur +/- thrill.
 Soft S1, apical S3.
 Signs of pulmonary
venous congestion
(crepitations, pulmonary
edema, effusions).
 Signs of pulmonary
hypertension & right
heart failure.

45. MANAGEMENT:
MEDICALLY SURGICALLY
Vasodilators
(e.g. ACE inhibitors)
betablockers
Mitral Valve Repair
To treat mitral valve
prolapse
Diuretics OR
If atrial fibrillation
presents,
 Anticoagulant
 Digoxin
Mitral Valve
Replacement

46. AORTIC STENOSIS:
 Aortic valve stenosis is narrowing of the orifice
between the left ventricle and the aorta.

47. ETIOLOGY OF AORTIC STENOSIS
INFANTS, CHILDREN AND ADOLESCENTS
 Congenital aortic stenosis
 Congenital sub valvular/supra valvular aortic stenosis
YOUNG ADULTS TO MIDDLE-AGED
 Calcification and fibrosis of congenitally bicuspid aortic
valve
 Rheumatic aortic stenosis
MIDDLE-AGED TO ELDERLY
 Senile degenerative aortic stenosis
 Calcification of bicuspid valve
 Rheumatic aortic stenosis

48. PATHOPHYSIOLOGY:

49. CLINICAL FEATURES:
 Symptoms:
 •Mild or moderate stenosis:
usually asymptomatic
 •CARDINALSYMPTOMS
(CO fails to rise to meet
demand)
 Exertional dyspnea
 Angina (due to demands of
hypertrophied LV)
 Exertional syncope
 Sudden death
 Episodes of acute
pulmonary edema
 Signs:
 Ejection systolic murmur (
systolic crescendo-
decrescendo murmur which
may radiate into the carotid
arteries and to the apex of
the left ventricle).
 Slow-rising carotid pulse
 Thrusting apex beat (LV
pressure overload)
 Narrow pulse pressure
 Signs of pulmonary venous
congestion (e.g.
crepitations)

50. INVESTIGATIONS:
 ECG: - Left ventricular hypertrophy- left bundle branch block.
 Chest X-ray: - May be normal
Enlarged LV & dilated ascending aorta (PA view)
Calcified valve on lateral view
 ECHO: - Calcified valve with restricted opening, hypertrophied
LV
 Doppler: - Measurement of severity of stenosis
Detection of associated aortic regurgitation
 Cardiac catheterization: - To identify coronary artery
disease
May be used to measure gradient between LV and aorta.

51. MANAGEMENT:
Asymptomatic aortic stenosis Kept under review
Moderate/severe stenosis Evaluated every 1-2 years
with Doppler echocardiography (to detect progression in severity)
Symptomatic severe aortic stenosis Valve Replacement
Congenital aortic stenosis Aortic Balloon Valvuloplasty
Atrial fibrillation or post valve replacement with a
Mechanical prosthesis
Anticoagulant

52. AORTIC REGURGITATION
 Aortic regurgitation is the flow of blood back into the
left ventricle from the aorta during diastole.
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53. ETIOLOGY:
Congenital-Bicuspid valve or
disproportionate cusps
Acquired:
Rheumatic disease
Infective endocarditis
Trauma
Aortic dilatation (Marfan’s syndrome, aneurysm,
dissection, syphilis)

54. PATHOPHYSIOLOGY OF AORTIC
REGURGITATION

55. CLINICAL FEATURES:
 Symptoms:
 Mild or moderate aortic regurgitation:
 Usually asymptomatic (because compensatory
ventricular dilatation and hypertrophy occur)
. ‘palpitation
 Severe aortic regurgitation:
 Breathlessness include breathing difficulties (e.g.
orthopnea, paroxysmal nocturnal dyspnea), especially
at night.
 Angina

56. SIGNS:
 Pulse- Large volume or ‘collapsing’ pulse
 Low diastolic and increased pulse pressure
 Bounding peripheral pulse
 Capillary pulsation in nail beds: Quincke’s sign
 Femoral bruit(‘pistol shot’): Duroziez’s sign
 Head nodding with pulse: de Musset’s sign

57.  Murmurs:
 Early diastolic murmur
 Systolic murmur (increased stroke volume)
 Austin Flint murmur (soft mid-diastolic). (Characteristic
murmur is best heard to the left sternum during held
expiration)
 Other signs:
 Displaced, heaving apex beat (volume overload)
 Pre-systolic impulse
 4th heart sound
 Crepitations (pulmonary venous congestion)

58. INVESTIGATIONS:
 ECG: initially normal later left ventricular
hypertrophy & T-wave inversion.
 Chest x-ray: -
 -Features of left heart failure.
 ECHO: -
 dilated LV,
 Hyper dynamic LV
 fluttering anterior mitral leaflet
 Doppler: - detects reflux
 Cardiac catheterization:
 - dilated LV
 -Aortic regurgitation
 -dilated aortic root.

59. MANAGEMENT:
 Treatment may be required for underlying conditions,
such as endocarditis or syphilis.
 Aortic regurgitation with symptoms
 Aortic valve replacement (may be combined with
aortic root replacement and coronary bypass surgery)
 Asymptomatic patients
 Annually follow up with echocardiography for evidence
of increasing ventricular size.
 Systolic BP should be controlled with vasodilating
drugs, such as nifedipine or ACE inhibitors.

60. TRICUSPID STENOSIS:
 Usually occurs together with aortic or mitral
stenosis.
 May be due to rheumatic heart disease (<5%)
 Decreased blood flow from right atrium to right
ventricle leads to decreased right ventricular output
and then decreased left ventricular filling and finally
decreased cardiac output.

61. CLINICAL FEATURES:
 Symptoms of right-
sided Heart failure
 Hepato megaly
 Ascites
 Peripheral edema
 Neck vein
engorgement
 Decreased cardiac
output – fatigue,
hypotension
 Raised JVP
 Mid-diastolic murmur
(best heard at lower left
or right sternal edge).

62. MANAGEMENT:
 Valve replacement
 Valvotomy
 Balloon Valvuloplasty

63. TRICUSPID REGURGITATION:
 Common, and is most
frequently ‘functional’ as
a result of enlargement of
right ventricle
 An insufficient tricuspid
valve allows blood to flow
back into the right atrium
venous congestion &
decrease right ventricular
output decrease blood
flow towards the lungs

64. ETIOLOGY:
 Primary:
 Rheumatic heart
disease
 Endocarditis,
particularly in injection
drug-users.
 Ebstein’s congenital
anomaly
 Secondary:
 Right ventricular
dilatation due to
chronic left heart
failure(‘functional
tricuspid regurgitation’)
 Right ventricular
infarction
 Pulmonary
hypertension

65. CLINICAL FEATURES:
 Usually non-specific
 Tiredness (reduced
forward flow)
 Edema
 Hepatic enlargement
(venous congestion).
 Raised JVP
 Pan systolic murmur
(leftsternal edge)
 Pulsatile liver

66. MANAGEMENT:
 Correction of the cause of right ventricular overload
(if TR is due to right ventricular dilatation)
 Use of diuretic and vasodilator treatment of CCF
 Valve repair
 Valve replacement

67. PULMONARY STENOSIS:
 CLINICAL FEATURES:
 Symptoms:
 Fatigue, dyspnea on exertion, cyanosis.
 Poor weight gain or failure to thrive in infants
 Hepatomegaly, ascites, edema.
 Signs:
 Ejection systolic murmur(loudest at the left upper
sternum & radiating towards the left shoulder)
 Murmur often preceded by an ejection sound (click)
 May be wide splitting of second heart sound (delay in
ventricular ejection)
 May be a thrill (best felt when patient leans forward and
breathes out).

68. INVESTIGATIONS:
 ECG: - Right ventricular hypertrophy
 Chest x-ray: - Post-stenotic dilatation in the
pulmonary artery
 Doppler echocardiography is the definitive
investigation

69. MANAGEMENT:
 Mild to moderate isolated pulmonary stenosis is
relatively common and does not usually progress or
require treatment
 Severe pulmonary stenosis percutaneous
pulmonary balloon Valvuloplasty
 OR surgical Valvotomy

70. PULMONARY REGURGITATION:
 A rare condition
 Usually associated with pulmonary hypertension which
may be
 Secondary of the disease of left side of the heart
 Primary pulmonary vascular disease
 Eisenmenger’s syndrome
 Blood flows back into right ventricle leads to right ventricle
and atrium hypertrophy and finally symptoms of right-
sided heart failure.
 Trivial PR is a frequent finding in normal individuals and
has no clinical significance.

71. MANAGEMENT AT GLANCE:
 Medical management:
 Prophylactic antibiotic therapy( rheumatic fever, infective
endocarditis)
 If the patient is having the signs of heart failure it should be
treated first for example by vasodilators, beta blockers and
diuretics.
 Low sodium diet should be prescribed to the patient
 Anticoagulant therapy is used to treat pulmonary
embolization.

72. MANAGEMENT AT GLANCE:
Percutaneous trans-luminal balloon Valvuloplasty:
Splits open the fused commissures
Threading a balloon tipped catheter from the femoral artery
or vein to the stenotic valve so that the balloon may be
inflated in an attempt to separate the valve leaflets.

73. SURGICAL MANAGEMENT:
 VALVULOPLASTY:
 It is the repair of cardiac valve.
• Patient does not require continuous anticoagulant medication.
• Usually require cardiopulmonary bypass machine.

75. VALVULOPLASTY:
 Annuloplasty:
 It is repair of valve annulus (junction
of the valve leaflet and the muscular
heart wall)
 Narrows the diameter of the valve’s
orifice,
 Useful for valvular regurgitation
 Chordoplasty:
 It is repair of chordae tendineae
 Done for mitral valve regurgitation
Caused by stretched or shortened
chordae tendineae
 Valvulotomy ( commissurotomy):
 It is an old surgical method for pure
mitral stenosis.

77. VALVE REPLACEMENT:

79. DIFFERENCE BETWEEN MECHANICAL AND
BIOLOGIC VALVE:

80. NURSING MANAGEMENT:
 Vital signs: HR, BP, RR measured and compared with previous data for
any changes.
 Auscultate heart and lung sounds
 Palpate peripheral pulses.
 Assess sign and symptoms of Heart Failure
 Fatigue,
 dyspnea with exertion,
 increase in coughing,
 hemoptysis,
 multiple respiratory infections,
 Orthopnea, or PND.
 Assess dysrhythmias
 By palpating the patient’s pulse for strength and rhythm (i.e, regular or
irregular) and asks if the patient has experienced palpitations or felt
forceful heartbeats
 Assess for dizziness, syncope, increased weakness, or angina pectoris.

81. NURSING DIAGNOSIS:
 1.Decreased cardiac output related to valvular
incompetence as evidenced by murmurs, dyspnea, and
peripheral edema.
 Expected outcome:
 The cardiac output is restored to maintain organ and tissue
perfusion as evident by normal CVP, arterial pressure,
peripheral pulses and urinary output etc.
 Interventions:
 Monitor cardiovascular status closely
 Assess peripheral pulses.
 Auscultate for heart sounds.
 Monitor ECG pattern for cardiac dysrhythmias.
 Measure urine output 1hrly.
 Observe for cardiac failure.

82.  Activity intolerance related to insufficient oxygenation as
evidenced by weakness, fatigue, shortness of breath, BP
changes.
 Expected outcome:
 The client will have improved tolerance of activity and progress
towards an optimal level of physical activity tolerance.
 Interventions:
 Provide adequate bed rest.
 Administered salicylates as prescribed.
 Check the vital signs.
 If ambulatory, avoid over exertion.
 Assess the client’s stamina and response to exercise to gauge the
degree of gradual activity progression.
 Assess vital signs before and after exercise.
 Reduce or discontinue activity if chest pain, vertigo, dyspnea,
confusion, a drop in BP, an irregular pulse or abnormal heart rate
develops.

83.  Risk for fluid volume and electrolyte imbalance related to
alteration s in blood volume.
 Expected outcome:
 The fluid and electrolyte balance is maintained normal as evident
by normal blood pressure , stable weight and normal serum
electrolyte level.

 Interventions:
 Maintaining intake and output chart.
 Monitor urine output 1hrly.
 Weigh daily at same time by same weighing machine. Notify
physician if weight gain is 2lb or more.
 Monitor ECG for electrolyte imbalance.
 Monitor ABG level.

84.  Deficient knowledge related to lack of experience and exposure
to information about disease and treatment process as
evidenced by verbalization of misconception about measures to
prevent complications.
 Expected outcome:
 The client has improved knowledge about the disease condition and
its treatment process and options.
 Interventions:
 Develop teaching plan for patient and family. Provide specific
instructions for the following:
 Diet and daily weight.
 Activity progression.
 Medication regimen.
 Pulse taking
 Access to emergency medical system.
 Involve family in teaching sessions

85. HEALTH EDUCATION
 Educate client and family about
 Mechanism of action of anticoagulants
 Ask to take drug at 6 pm everyday
 Side effects which need medical attention (bleeding that don’t
stop after 15 mts,blood in urine,black tarry stools,unusual
bleeding from body orifices,severe
headaches,weakness,cold,blue or painful feet)
 Avoid activities that may cause bleeding,avoid alcoholism,
 Wear medic alert bracelet or id card
 Avoid foods rich in vitamin k
 Consult with doctor if any other treatment to be started
 Contact emergency department,if fever ,dyspnoea,bleeding,low
urine output

87. SAFETY ALERT –INR RATIO

88. ANTICOAGULANT THERAPY
 Start oral anticoagulant as soon as they can take orally
 Give a loading dose of 5 mg warfarin
 Titrate dose to achieve the target INR
 INR between 2.5-3.5
 All mechanical MVR
 All mechanical AVR with high risk
 INR between 2-3
 All mechanical AVR with low risk
 All Bio prosthetic valve with high risk
 All bio valves with low risk*3 months
 All patients with prosthetic rings *3months

89. RESEARCH STUDIES
 A qualitative study conducted by Christine M mincham et al in patient
views on the management of rheumatic fever and rheumatic heart
disease in the Kimberley:
 Objective
 To describe, from a patient perspective, factors leading to suboptimal
management of individuals with rheumatic fever (RF) and rheumatic
heart disease (RHD) among members of the Kimberley population.
 Methods
 Qualitative in-depth semi structured and repeated interviews of seven
Kimberley patients, or parents of children, with rheumatic fever and/or
rheumatic heart disease, during 1998.
 Results
 Participants showed variable levels of understanding about RF/RHD,
often relating to the need for secondary prophylaxis. Compliance with
medication was closely linked with positive patient-staff interactions.
From the perspective of health care, living in a remote location was
frequently described as a negative influence. Participants desire more
accessible and culturally appropriate opportunities for learning about
their disease. Participants focused on issues closely related to effective
and ineffective management of RF/RHD. The lessons learned are
indicators for health staff attempting to improve the quality of
management that people receive.

90. National rheumatic heart consortium was established in
india to survey and prevent RF and RHD in india
Govt initiatives for prevention
and control of RHD

91. SUMMARY:
 We have discussed rheumatic heart disease, its
etiology, clinical features, pathophysiology,
diagnostic criteria and its medical and nursing
management. Secondly we discussed valvular
heart disease, its various types, their etiology,
pathophysiology, clinical features, diagnostic
investigations and their medical, surgical and
nursing management.

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1021.
 Sharon L. Lewis, Margaret Mclean Helikemper, Shamom Ruff Dirksen,
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