RHEUMATIC HEART DISEASE

MODERATOR PRESENTED BY
Dr Pragya Pathak Shubham Gaur
Associate Professor Msc (N) 1st Year
CON, AIIMS CON,AIIMS
Objectives :
• To define RHD and RF.
• To describes the incidence of RHD .
• To discuss etiopathogenesis of RHD
• To explain the pathophysiology of RHD.

• To tell about Clinical Manifestations (Major and Minor criteria) and Diagnostic
Evaluation of RHD.

• To tell Complication of RHD.

• To explain about the Medical, Surgical and Nursing Management of RHD.

• To tell the prevention prophylaxis of RHD.

• To tell Patient Education and Health Maintenance

• Rheumatic heart disease (RHD) is a life-threatening heart
condition which results from damage to heart valves caused by
one or several episodes of rheumatic fever, an autoimmune
inflammatory reaction to infection with streptococcal bacteria
(streptococcal pharyngitis or strep throat).

• The bacterium Streptococcus pyogenes (group A

streptococcus) can pass easily from person to person in the
same way as other upper respiratory tract infections. These
infections are most common in childhood.
• RHD is a chronic condition resulting from RF that is
characterised by scarring and deformity of the heart valves.
• Rheumatic heart disease is a condition which affects 39 million
people worldwide.

• RHD most commonly occurs in childhood and can lead to death

or life-long disability.
• In some cases, repeated strep infections can lead to rheumatic
fever, which occurs when the immune system reacts against
the tissues of the body, including inflaming and scarring the
heart valves.

• Rheumatic heart disease is caused by damage to the heart

valves and heart muscle from the inflammation and scarring
caused by rheumatic fever.
What is ARF?
• Acute rheumatic fever (ARF) is a sequela of streptococcal
infection—typically following 2 to 3 weeks after group A
streptococcal pharyngitis

• ARF is caused by an autoimmune reaction to the bacterial

infection.
• The chronic stage of RF involves all the layers of the heart
(pancarditis) causing major cardiac sequalae referred to as
rheumatic heart disease.

• In spite of its name suggesting an acute arthritis migrating from

joint to joint, it is well known that it is heart rather than joints
which is first and major organ affected.
• Decades ago, William Boyd gave the dictum ‘rheumatism licks
the joint, but bites the whole heart’.
RF – not a communicable disease but results from communicable
disease (streptococcal pharyngitis)

RF RHD (rheumatic heart disease); a crippling disease.

The clinical course of rheumatic fever involves a childhood

infection with complications in adulthood (cardiac defect).
Group A Streptococcus

• May cause sore throat, tonsillitis or skin infection.

• Spread when an infected person talks, coughs or

sneezes small droplets containing infectious agents into
the air.

• Direct contact with infected wounds or skin sores.

• There is a period of about 3 weeks between the initial

infection with group A Streptococcus and ARF symptoms.
Incidence
• The disease appears most commonly in children between the
age of 5 to 15 years
• Both the sexes are affected equally, though slight female
preponderance.
• In a multicentric survey in school going children by the ICMR,
an incidence of 1 to 5.5 per 1000 children has been reported.
• In India , RF is still endemic and remains one of the major
causes of acquired heart diseases, accounting for 25% to 45%.
Etiopathogenesis
A.ENVIRONMENTAL FACTOR –

• History of the infection of the pharynx, upper respiratory tract

with this microorganism about 2-3 weeks prior to attack of RF.
• Subsequent or on going attacks of streptococcal infection
Outbreak or epidemic
• Socioeconomic factors like poverty, poor nutrition, density of
population, overcrowding
Geographic distribution of the disease
• Climate- higher in subtropical and tropical regions with cold,
damp climate near river and waterways
B. HOST SUSCEPTIBILITY –
• Identical twins
• Clustering of disease in families
• Individuals with HLA Class II alleles
• First degree relatives- D8-17 on B cells
C. IMMUNOLOGIC EVIDENCES –
• Cell wall polysaccharide of GAS forms antibodies which are
reactive against cardiac valves
• Hyaluronate capsule of GAS is identical to human hyaluronate
present in joints
• Membrane antigens of GAS reacts with –
• Sarcolemma of smooth and cardiac muscle
• Dermal fibroblasts
• Neurons of caudate nucleus
 Cardiac Lesions and Valve Deformities - About 40% of RF
episodes are marked by carditis, meaning that all layers of the
heart (endocardium, myocardium, and pericardium) are
involved. This gives rise to the term Rheumatic Pancarditis.

 Extracardiac Lesions - The lesions of RF are systemic and

involve the skin, joints, and CNS. Painless subcutaneous
nodules, arthralgias or arthritis, and chorea may develop.
Clinical manifestation

As per revised WHO criteria (2004) based on revised Jones’

criteria (first described by TD Jones in 1994, and last revised in
1992), following some major and minor criteria

Jones criteria for the diagnosis of acute rheumatic fever 2 major

criteria or 1 major & 2 minor criteria along with the absolute
requirement

JONES CAFEPALE
MAJOR CRITERIA :

1.Carditis – It is the most important manifestation of RF and

results in three signs :

• a heart murmur or murmurs of mitral or aortic regurgitation, or

mitral stenosis;

• cardiac enlargement and HF secondary to myocarditis; and

• pericarditis resulting in muffled heart sounds, chest pain,

pericardial friction rub, or signs of effusion.
Cardiomegaly
2. Monoarthritis or polyarthritis :
• It is the most common finding in RF.
• The inflammatory process affects the synovial membranes of
the joints, causing swelling, heat, redness, tenderness, and
limitation of motion.
• The larger joints, particularly the knees, ankles, elbows, and
wrists, are most frequently affected.
3. Erythema marginatum-
• less common feature of RF.
• Transient bright pink,
nonpruritic meshlike macular
rash occurs mainly on the
trunk and proximal parts of
the extremities and may be
exacerbated by heat (e.g.,
warm bath).
4. Subcutaneous nodules- usually associated with severe
carditis.
• These nodules are small (0.5 to 2 cm in diameter), spherical or
ovoid, firm hard and painless swelling.
• They are attached to deeper structures and often remain
unnoticed by patient.
• Characteristics location are extensor surfaces of the wrists,
elbows, ankles and knees.
5. Chorea (Sydenham’s syndrome or Saint Vitus’ dance)

• occurs as a result of the involvement of central nervous system.

• This is characterised by disordered and involuntary jerky

movements especially of the face and limbs, trunk; muscle
weakness; disturbances of speech and gait and the extremities
accompanied by some degree of emotion instability.
 
MINOR CRITERIA

• Fever
• Arthralgia
• Previous history of rheumatic fever
• Lab findings of elevated ESR >15mm/hr in men,
> 20mm/hr in women
• Raised C reactive protein, and leucocytosis
• ECG findings of prolonged PR interval
DIAGNOSIS
SUPPORTING EVIDENCE OF
MAJOR
MINOR MANIFESTATIONS ANTECEDENT GROUP A
MANIFESTATIONS
STREPTOCOCCAL INFECTION******

Carditis Clinical features: -Elevated or increasing

Arthralgia streptococcal antibody titer
Fever
Polyarthritis
Erythema
marginatum History of (<45 days)
-Positive throat culture or rapid
Laboratory features: streptococcal antigen test or
Subcutaneous Elevated acute phase
nodules streptococcal sore throat or scarlet
reactants: ESR, C-reactive fever)
protein
Chorea
Prolonged PR interval
ESSENTIAL CRITERIA

An absolute requirement for the diagnosis of acute rheumatic

fever is supporting evidence of a recent GABHS infection
Recent Group A Streptococcus infection
Hallmarks of GAS sore throat:

 High fever, tender anterior cervical lymph nodes

 Close contact with infected person
 Strawberry tongue, petechiae on palate
 Excoriated nares( crusted lesions) in infants
 Tonsillar exudates in older children
 Abdominal pain

GOLD STANDARD: POSITIVE THROAT CULTURE

ASO titre:

• well standardized
• elevated in 80% of patients with ARF
• ASO titre of 333 Todd unit in children & 250 Todd unit in
adults are considered elevated
Slide agglutination test (Streptozyme):

• Detect antibodies against 5 different GABHS antigens

• Rapidly, relatively simple to perform & widely available
• Less standardized & less reproducible than other tests and
should not be used as a diagnostic test for evidence of an
antecedent GAS infection
HISTOLOGICAL FINDINGS
• Pathological examination of the insufficient valves may reveal
verrucous lesions at the line of closure.

• Aschoff bodies (perivascular foci of eosinophilic collagen

surrounded by lymphocytes, plasma cells, and macrophages)
are found in the pericardium, perivascular region of the
myocardium, and endocardium.

• Anitschkow cells are plump macrophages within aschoff bodies

•
• In the pericardium, fibrinous and serofibrinous exudates may
produce an appearance of “bread and butter” pericarditis
TREATMENT
Bed rest

Antibiotic Therapy:

10 days of orally administered penicillin or erythromycin or a

single intramuscular injection of benzathine penicillin to
eradicate GABHS from the upper respiratory tract

Afterwards, the patient should be started on long-term antibiotic

prophylaxis
TREATMENT
Anti-inflammatory Therapy:

Anti-inflammatory agents (salicylates, corticosteroids) should

be withheld if arthralgia or atypical arthritis is the only clinical
manifestation of presumed acute rheumatic fever
Acetaminophen can be used

Patients with typical migratory polyarthritis & with carditis

without cardiomegaly or congestive heart failure:
treatment with oral salicylates, 100 mg/kg/day in 4 divided
doses PO for 3-5 days, followed by 75 mg/kg/day in 4 divided
doses PO for 4-8 wk
TREATMENT

Patients with carditis & cardiomegaly or congestive heart

failure:
treatment with corticosteroids
Prednisone 2 mg/kg/day in 4 divided doses for 2-6 wk followed
by a tapering of the dose that reduces the dose by 5 mg/24 hr
every 2-3 days. At the beginning of the tapering of the
prednisone dose, aspirin should be started at 75 mg/kg/day in 4
divided doses to complete 12 wk of therapy
TREATMENT
Sydenham Chorea

• Occurs after the resolution of the acute phase of the disease

• Anti-inflammatory agents are usually not indicated
• Sedatives: phenobarbital (16-32 mg every 6-8 hr PO) is the
drug of choice
• If phenobarbital is ineffective, then haloperidol
(0.01-0.03 mg/kg/24 hr divided bid PO) or chlorpromazine
(0.5 mg/kg every 4-6 hr PO) should be initiated
• Long-term antibiotic prophylaxis
What is RHD? Natural history of disease if adequate
secondary prevention is not given
Example age timeline (years)
5 10 13 15 16

Heart
medications
Heart failure are needed.
starts to Eventually,
develop. The valve surgery
Leaking valves: patient may
heart chambers may be
develop needed.
get stretched. symptoms
Blocked valves: including
The valve is
heart muscle breathlessness.
left damaged
struggles hard
and scarred.
to move blood
May cause
forwards
ARF leakage then
episodes later,
make blockage, or
valve(s) both.
inflamed.
Does ARF always led to RHD?
• No, RHD is more likely if:
– Heart is affected in ARF (carditis)
– ARF is severe
– ARF occurs at a young age
– Recurrent ARF episodes occur
• However, you can’t accurately predict who will go on to
develop recurrent ARF and RHD
– hence EVERYONE who has had ARF, even if there was
no carditis, needs secondary prophylaxis with long-term
penicillin.
Which valves are affected?
Mitral valve is affected in over 90% of cases of RHD
Mitral regurgitation most commonly found in children & adolescents
Mitral stenosis represents longer term chronic disease, commonly in adults
Most common complication of mitral stenosis is atrial fibrillation

Aortic valve next most commonly affected

Often occurs with disease of the mitral valve.
Stenosis tends to develop as a long term complication of aortic
regurgitation

Tricuspid and pulmonary valves are much less commonly affected

Usually affected in very severe RHD when all valves are affected
GABHS infection particularly the valves, with
swelling and erosion of the valve leaflets.
Vegetation forms from deposits of fibrin and
blood cells in areas of erosion
Valve leaflets may cause stenosis and
regurgitation. The mitral and aortic valves are
most commonly affected.

Nodules, called Aschoff’s bodies, are

formed by a reaction to inflammation with
swelling and destruction of collagen fibers.
As the Aschoff’s bodies age, they
become more fibrous, and scar tissue
forms in the myocardium.
Valvular lesions in RHD

• Mitral regurgitation
• Mitral stenosis
• Aortic regurgitation
• Aortic stenosis
• Tricuspid regurgitation
• Tricuspid stenosis
MITRAL INSUFFICIENCY

Backflow of blood from the LV to the LA during systole

MITRAL INSUFFICIENCY
Pathophysiology:

• Loss of valvular substance & shortening & thickening of the

chordae tendineae
• Because of the high volume load & inflammatory process, the
left ventricle becomes enlarged
• The left atrium dilates as blood regurgitates into this chamber
• Increased left atrial pressure results in pulmonary
congestion & symptoms of left-sided heart failure
MITRAL INSUFFICIENCY

Clinical manifestations:

• Exertion Dyspnea ( exercise intolerance), fatigue

• Mild disease : NO signs of heart failure
• Severe mitral insufficiency: signs of left sided heart failure
• The heart is enlarged, with a forcible & hyperkinetic apical
left ventricular impulse & often an apical systolic thrill
• Soft S1
 MITRAL INSUFFICIENCY

Clinical manifestations:

• The 2nd heart sound may be accentuated if pulmonary

hypertension is present
• A 3rd heart sound is generally prominent
• A holosystolic murmur is heard at the apex with radiation to
the axilla
• A short mid-diastolic rumbling murmur is caused by
increased blood flow across the mitral valve as a result of
the insufficiency
MITRAL INSUFFICIENCY

Imaging studies:

• ECG: prominent bifid P waves, signs of left ventricular

hypertrophy & associated right ventricular hypertrophy if
pulmonary hypertension is present
• X-rays: prominence of the left atrium & ventricle; congestion of
perihilar vessels, a sign of pulmonary venous hypertension
• 2 D ECHO: enlargement of the left atrium & ventricle &
Doppler studies demonstrate the severity of the mitral
regurgitation
MITRAL INSUFFICIENCY

Complications:

• cardiac failure
• chronic mitral insufficiency -right ventricular failure
• atrial and ventricular arrhythmias
MITRAL INSUFFICIENCY

Management:

Medical:
• Prophylaxis against recurrences of rheumatic fever
• Treatment of heart failure, arrhythmias and infective
endocarditis
• Afterload-reducing agents (ACE inhibitors or angiotensin
receptor blockers):
• reduce the regurgitant volume & preserve left ventricular
function
MITRAL INSUFFICIENCY

Management:

Surgical:
• For patients who despite adequate medical therapy have
persistent heart failure, dyspnea with moderate activity &
progressive cardiomegaly, often with pulmonary hypertension
• Valve repair surgery preferred over valve replacement
MITRAL STENOSIS

Obstruction of LV inflow that prevents proper filling during

diastole

Normal MV Area: 4-6 cm2

MITRAL STENOSIS

Pathophysiology:

• From fibrosis of the mitral ring, commissural adhesions &

contracture of the valve leaflets, chordae & papillary muscles

• It takes 10 years or more for the lesion to become fully

established
MITRAL STENOSIS
Clinical manifestations:

• Correlation between symptoms & the severity of obstruction

• Patients with mild lesions: asymptomatic
• More severe degrees of obstruction: exercise intolerance &
dyspnea
• Critical lesions: orthopnea, paroxysmal nocturnal dyspnea, &
overt pulmonary edema, as well as atrial arrhythmias
MITRAL STENOSIS

Clinical manifestations:

• Pulmonary hypertension: right ventricular dilatation-functional

tricuspid insufficiency, hepatomegaly, ascites & edema

• Hemoptysis: rupture of bronchial or pleurohilar veins or by

pulmonary infarction
MITRAL STENOSIS
Clinical manifestations:

• Jugular venous pressure is increased in severe disease with

heart failure
• prominent "a" wave in jugular venous pulsations: Due to
pulmonary hypertension & right ventricular hypertrophy
• Mild disease: heart size is normal, tapping apex
• Severe mitral stenosis: moderate cardiomegaly
• Cardiac enlargement massive: atrial fibrillation & heart failure
• A parasternal right ventricular lift is palpable when pulmonary
pressure is high
MITRAL STENOSIS
Clinical manifestations:

Auscultatory findings:
• Loud 1st heart sound,
• An opening snap of the mitral valve, and
• A long, low-pitched, rumbling mitral diastolic murmur with
presystolic accentuation at the apex
• Murmur absent in patients with significant heart failure
MITRAL STENOSIS
Imaging studies:

• ECG: prominent & notched P waves & varying degrees of right

ventricular hypertrophy, Atrial fibrillation
• X-rays: Left atrial enlargement & prominence of the pulmonary
artery & right-sided heart chambers; calcifications may be
noted in the region of the mitral valve
• Severe obstruction is associated with a redistribution of
pulmonary blood flow so that the apices of the lung have
greater perfusion (the reverse of normal)
MITRAL STENOSIS
Management:

Medical:
• Mild & moderate MS: anticongestive measures (digoxin &
diuretics)
• Atrial fibrillation: digoxin; procainamide for conversion to sinus
rhythm in hemodynamiclly stable patients
• chronic AF warfarin
• IE prophylaxis
• percutaneous mitral balloon valvotomy: failure to thrive with
repeated respiratory infections
MITRAL STENOSIS
Management:

Surgical: indicated in
• patients with clinical signs & hemodynamic evidence of severe
obstruction
• or ANY SYMPTOMATIC Patient with NYHA Class III or IV
Symptoms
• or Asymptomatic moderate or severe MS with a pliable valve
AORTIC INSUFFICIENCY

Leakage of blood into LV during diastole due to ineffective

coaptation of the aortic cusps

Regurgitation of blood leads to volume overload with dilatation &

hypertrophy of the left ventricle
AORTIC INSUFFICIENCY

Pathophysiology:

• Combined pressure AND volume overload

• Compensatory Mechanisms: LV dilation & LV hypertrophy

• Progressive dilation leads to heart failure

AORTIC INSUFFICIENCY
Clinical manifestations:

• Symptoms are unusual except in severe aortic insufficiency

• The large stroke volume & forceful left ventricular contractions
result in palpitations
• Sweating and heat intolerance are related to excessive
vasodilation
• Dyspnea on exertion can progress to orthopnea and pulmonary
edema
• Nocturnal attacks with sweating, tachycardia, chest pain, &
hypertension
AORTIC INSUFFICIENCY
Clinical manifestations:

• Wide pulse pressure with bounding peripheral pulses

• Systolic blood pressure elevated & diastolic pressure is lowered
• Severe aortic insufficiency: enlarged heart with a left ventricular
apical heave
• Diastolic thrill unusual
• Murmur begins immediately with the 2nd heart sound &
continues until late in diastole over the upper & midleft sternal
border with radiation to the apex and upper right sternal border
AORTIC INSUFFICIENCY
Clinical manifestations:

• It has a high-pitched blowing quality & is easily audible in full

expiration with the diaphragm of the stethoscope placed firmly
on the chest & the patient leaning forward
• An aortic systolic ejection murmur is frequent because of the
increased stroke volume
• An apical presystolic murmur (Austin Flint
murmur) resembling MS is sometimes heard (due to the large
regurgitant aortic flow in diastole preventing the mitral valve
from opening fully)
AORTIC INSUFFICIENCY

Imaging studies:

• ECG: signs of left ventricular hypertrophy & strain with

prominent P waves in severe cases

• X-rays: Enlargement of the left ventricle & aorta

AORTIC INSUFFICIENCY
Imaging studies:

• 2 D ECHO: A large left ventricle & diastolic mitral valve flutter

or oscillation caused by regurgitant flow hitting the valve leaflets
• Doppler studies demonstrate the degree of aortic runoff into
the left ventricle
• Magnetic resonance angiography can be useful in
quantitating regurgitant volume
• Cardiac catheterization is necessary only when the
echocardiographic data are equivocal
AORTIC INSUFFICIENCY
Management:

• Mild and moderate lesions are well tolerated. Unlike mitral

insufficiency, aortic insufficiency does not regress

Medical:
• Afterload reducers (ACE inhibitors or angiotensin receptor
blockers)
• Prophylaxis against recurrence of acute rheumatic fever
• IE prophylaxis
AORTIC INSUFFICIENCY
Management:

• Surgical: Definitive Treatment

• Surgical intervention (valve replacement) should be carried out

well in advance of the onset of heart failure, pulmonary edema,
or angina, when signs of decreasing myocardial performance
become evident as manifested by increasing left ventricular
dimensions on the echocardiogram
AORTIC INSUFFICIENCY
Management:

• Surgery is considered when early symptoms are present, ST-T

wave changes are seen on the electrocardiogram, or evidence
of decreasing left ventricular ejection fraction is noted
• ANY Symptoms at rest
• Asymptomatic treatment if: EF drops below 50% or LV becomes
dilated
Complications of RHD
• Atrial fibrillation • Heart failure
– Common in RHD – Symptoms: shortness of
– Causes irregular heart rate breath, swelling in the legs,
/ palpitations, blackouts cough, fatigue, weakness
etc, causes blood clots in
atrium which can then
• Infective endocarditis
cause stroke – bacterial infection of heart
valve – targets damaged
• Stroke valves
– Ischaemic stroke (blood – Bacteria get into blood via
clot) mouth (especially when
• Due to not enough dental hygiene is poor), open
warfarin, when atrial skin etc
fibrillation or metal valve
– People at high risk receive
are present
•
endocarditis prophylaxis
Also can complicate
infective endocarditis prior to surgical procedures
– Hemorrhagic stroke (bleed – Dental health and hygiene
into brain) reduces risk of endocarditis
• Due to too much warfarin
 NURSING
MANAGEMENT
Nursing assessment-
 Subjective data -
i. Important health information - Past health history: Recent streptococcal
infection, previous history of rheumatic fever or rheumatic heart disease
ii. Functional Health Patterns
 Health perception–health management: Family history of rheumatic fever;
malaise
 Nutritional-metabolic : Anorexia, weight loss
 Activity exercise – palpitations; generalised weakness, fatigue and ataxia
 Cognitive perceptual : chest pain; widespread joint pain and tenderness
(especially large joints)
 Objective data –
• General – fever
• Integumentary – subcutaneous nodules and erythema marginatum
• Cardiovascular – tachycardia, pericardial friction rub, muffled heart sounds;
murmurs; edema
• Neurologic – chorea
• Musculoskeletal – signs of monoarthritis or polyarthritis
• Diagnostic findings
1. Decreased CO related to carditis and possible valve
defects or HF
Outcome criteria – Maintain cardiac output
Nursing interventions –
• Assess and monitor cardiac function regularly
• Promote optimal rest to reduce cardiac work load and
diminish the metabolic needs of the body
• Give explanations of treatment, listening to patient’s concerns
as emotional stress increases work load of the heart
• Administer medication as indicated to treat fluid retention and
improve cardiac contractility
• Monitor and replace electrolyte as necessary since electrolyte
imbalance can negatively affect cardiac function
2. Dyspnea related to disease condition as evidenced by
verbalization by patient or SOB.
Nursing intervention –
• Assess the breathing pattern of patient.
• Auscultate for B/L equal air entry.
• Monitor the Spo2 level.
• Observe respiratory rate and depth, chest expansion, use of
accessory muscles,retraction or flaring of nostrils, skin colour
• Monitor the ABG analysis.
• Provide fowler’s position.
• Allow for rest periods.
• Assist with ADL’s as needed and encourage independence
within limits.
• Administer nebulization and chest physiotherapy.
3.Acute pain related to inflammation or arthralgia as
evidenced by Verbaldescription of pain, Warmth, Edema
Redness at affected joints
Nursing interventions-
 Examine affected joints, degree of joint pain, level of
joint movement.
 Elevate involved extremities above heart level. Improves
circulation to the heart to alleviate edema.
 Maintain bed rest during the acute stage of the disease.
 Advise positional changes every 2 hours while maintaining
body alignment it Prevents contractures and promotes
comfort.
 Encourage the use of nonpharmacologic interventions such as
imagery, relaxation, distraction, cutaneous stimulation, heat
application.
 Stress the importance of limited activity or amount of joint
movement allowed.
 Administer salicylates and anti-inflammatory medications as
prescribed, and advise child that the medication will decrease
the pain; administer a sustained- action analgesic before
bedtime or 1 hour before anticipated movement.
4. Hyperthermia related to illness or inflammatory disease
process as evidenced by Increase body temperature
above normal range Hot, flushed skin ChillsTachycardia,
tachypnea
Outcome criteria –
 Client will demonstrate temperature within the normal range
and be free of chills.
Nursing interventions –
 Assess temperature, heart rate, and blood pressure
frequently.
 Provide a tepid sponge bath
 Eliminate excess clothing and covers.
 Modify the client’s environment such as room temperature
 Maintain bed rest especially during the acute febrile phase.
 Discuss the importance of increased fluid intake to
avoid dehydration
 Administer nonsteroidal anti-inflammatory drug (NSAIDs) as
prescribed; Observe for any untoward effects of NSAIDs.
 Administer a course of penicillin therapy or a single
intramuscular dose of benzathine penicillin.
5. Activityintolerance related to arthralgia or arthritis as
manifested by joint pain; related to congestive heart failure
as manifested by malaise, fatigue, weakness, dyspnea,
shortness of breath, confusion, vertigo, increased pulse,
increase or decrease in respiratory rate and blood pressure
Outcome criteria –
 Perform activities of daily living with minimal or no fatigue or
physiologic distress
Nursing interventions –
 Assess patient response to activity determine extent of
problem and plan appropriate interventions.
 Monitor heart rate and rhythm, BP, and respiratory rate
before, during and after activity to determine degree of
cardiac and pulmonary function.
 Maintain bed rest during febrile periods to promote resolution of
inflammatory process and reduce cardiac workload
 Plan rest period between activities to balance demands that
activity places on heart and to promote healing process
 Teach progressive exercise program after anti-inflammatory
therapy is discontinued, noting patient responses to activity so
that activity is increased to patient’s ability
 Treat arthralgia with rest and medication for pain to promote
healing and enable limited activity
6. Ineffective management of therapeutic regimen related
to lack of knowledge concerning the need for long-term
prophylactic antibiotic therapy and possible disease
sequelae, lack of compliance, lac log resources as
manifested by complications of RHD
Outcome criteria –
 Comply with treatment regimen;
 Express confidence in managing disease
 Describe signs and symptoms of valvular heart disease
Nursing interventions –
 Assess patient’s knowledge, confidence, and resources for
self-care to initiate appropriate interventions
 Teach patient the disease process, possible sequelae, and
continued need for prophylactic antibiotics to increase
pateints control of disease and reduce the possibility of
recurrence
 Provide patient with information on whom to contact when
question arise so that long term care is promoted
 Inform patient about the risk of exposure to streptococcal
infections from such high-risk groups as children and military
personnel to reduce possibility of recurrence
 Teach patient the signs of valvular heart disease such as
excessive fatigue, dizziness, palpitations, or dyspnea on
exertion as this is the most serious complication of RF
 Provide educational resources to patient and family to increase
compliance with therapy
7. Risk of injury related to chorea
 Outcome criteria –
Have no injuries as a result of uncontrolled body activity
 Nursing interventions –
• Monitor for the weakness, ataxia, and choreic movement that
is spontaneous rapid and purposeless which tends to
intensify with voluntary activity to initiate appropriate
interventions for injury prevention
• Eliminate or minimize identified hazards in the environment to
reduce risk of injury
• Educate patient’s family regarding need to safe guard home
environment if appropriate to reduce risk of injury at home
 
8. Fatigue related to decreased cardiac function as evidenced by
generalized weakness.
Nursing intervention-
Organize nursing care to allow for rest periods.
• Assist with ADL’s as needed and encourage independence within limits.
• Plan and implement progressive activities .Use active and passive ROM
exercises.
• Provide discharge teaching related to extent of activity to perform.

9. Fear related to surgical procedure, its uncertain outcome, & threat

Nursing intervention-
Encourage patient and family to express fears.
Encourage the patient to describe any concerns related to surgery.
Discuss about patient’s fear about pain & post operative pain management
methods.
Teaching is to be given about post operative exercises.
Measures are to be taken to alleviate undue anxiety
RESEARCH INPUT
Title Outcome in children with newly diagnosed
rheumatic heart disease in Indonesia

PMID PMID: 35067206 , Published in Jan 2022

Background Rheumatic heart disease (RHD) is associated with

high morbidity and mortality, especially in those
with severe RHD or progression of valvular disease
(VD). 

Aim of Study To evaluate outcome and clinical predictors of

valvular progression in children with newly
diagnosed RHD.
RESEARCH INPUT
Methods A retrospective cohort study was conducted in children with newly
diagnosed RHD at Dr Sardjito Hospital, Yogyakarta, Indonesia
during 2013-2020. Clinical and echocardiography data at the time of
diagnosis were collected and patients were followed up for 1 year.
Echocardiography evaluations were undertaken to determine the
progression of VD..
Results A total of 77 patients were recruited, 36 (46.7%) of whom were male,
and the median age (range) was 12.3 years (5.9-17.8). Thirty-three
(42.8%) had progression of VD in the year after diagnosis. By
multivariable analysis, an age at diagnosis of >10 years and high C-
reactive protein (CRP) were independently associated with an
increased risk of valvular progression with an adjusted hazard ratio
(95% CI) of 3.23 (1.09-9.60) and 3.69 (1.45-9.67), respectively.
Conclusion After only 1 year of follow-up, approximately four in 10 children with
newly diagnosed RHD developed progression of VD. An increased
risk of valvular progression was associated with being over 10 years
of age and a high level of CRP.
Take-home messages
• Prevent RHD from occurring
• Prevent existing RHD from getting worse
• Diagnose RHD early, before it starts causing symptoms
• Through repeated education sessions with the patient and
their family, make sure the patient understands that
– RHD is very serious, but
– No matter how severe, there are good treatment options
– Further worsening can be minimised with regular
secondary prophylaxis
– Having a valve replaced doesn’t mean that secondary
prophylaxis can be stopped
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• https://pubmed.ncbi.nlm.nih.gov/35067206/

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