Rheumatic Fever

Ardian Rizal
Department of Cardiology and Vascular Medicine
Faculty of Medicine University of Brawijaya
Objectives
Etiology
Epidemiology
Pathogenesis
Pathologic lesions
Clinical manifestations & Laboratory
findings
Diagnosis & Differential diagnosis
Treatment & Prevention
Prognosis
References
2
Etiology

Acute rheumatic fever is a systemic disease of

childhood,often recurrent that follows group A
beta hemolytic streptococcal infection
It is a delayed non-suppurative sequelae to
URTI with GABH streptococci.
It is a diffuse inflammatory disease of
connective tissue,primarily involving heart,blood
vessels,joints, subcut.tissue and CNS

3
Epidemiology
Ages 5-15 yrs are most susceptible
Rare <3 yrs
Girls>boys
Common in 3rd world countries
Environmental factors over crowding, poor
sanitation, poverty,
Incidence more during fall ,winter & early
spring

4
Pathogenesis

Delayed immune response to infection

with group.A beta hemolytic
streptococci.
After a latent period of 1-3 weeks,
antibody induced immunological
damage occur to heart valves,joints,
subcutaneous tissue & basal ganglia of
brain

5
Group A Beta Hemolytic Streptococcus

Strains that produces rheumatic fever - M types l, 3, 5,

6,18 & 24

Pharyngitis produced by GABHS can lead to  acute

rheumatic fever, rheumatic heart disease & post strept.
Glomerulonepritis

Skin infection- produced by GABHS leads to post

streptococcal glomerulo nephritis only. It will not result in
Rh.Fever or carditis as skin lipid cholesterol inhibit
antigenicity
6
Diagrammatic structure of the group A
beta hemolytic streptococcus
Capsule Antigen of outer
protein cell wall
Cell wall of GABHS
induces antibody
Protein antigens response in
victim which
Group carbohydrate result in
autoimmune
Peptidoglycan damage to heart
valves,
Cyto.membrane
sub cutaneous
tissue,tendons,
Cytoplasm joints & basal
ganglia of brain
……………………………………………
……...
7
Pathologic Lesions
Fibrinoid degeneration of connective
tissue,inflammatory edema, inflammatory cell infiltration
& proliferation of specific cells resulting in formation of
Ashcoff nodules, resulting in-
-Pancarditis in the heart
-Arthritis in the joints
-Ashcoff nodules in the subcutaneous tissue
-Basal gangliar lesions resulting in chorea

8
Clinical Features
1.Arthritis
Flitting & fleeting migratory polyarthritis, involving major
joints
Commonly involved joints-knee,ankle,elbow & wrist
Occur in 80%, involved joints are exquisitely tender
In children below 5 yrs arthritis usually mild but carditis
more prominent
Arthritis do not progress to chronic disease

9
2.Carditis

Manifest as pancarditis(endocarditis, myocarditis and

pericarditis),occur in 40-50% of cases
Carditis is the only manifestation of rheumatic fever
that leaves a sequelae & permanent damage to the
organ
Valvulitis occur in acute phase
Chronic phase  fibrosis,calcification & stenosis of
heart valves(fishmouth valves)

10
Rheumatic
heart
disease.
Abnormal
mitral
valve.
Thick,
fused
chordae

11
Another view of
thick and fused
mitral valves in
Rheumatic
heart disease

12
3.Sydenham Chorea

Occur in 5-10% of cases

Mainly in girls of 1-15 yrs age
May appear even 6/12 after the attack of rheumatic
fever
Clinically manifest as-clumsiness, deterioration of
handwriting,emotional lability or grimacing of face
Clinical signs- pronator sign, jack in the box sign ,
milking sign of hands

13
4.Erythema Marginatum

Occur in <5%.
Unique,transient,serpiginous-looking lesions
of 1-2 inches in size
Pale center with red irregular margin
More on trunks & limbs & non-itchy
Worsens with application of heat
Often associated with chronic carditis
15
5.Subcutaneous nodules

Occur in 10%
Painless,pea-sized,palpable nodules
Mainly over extensor surfaces of
joints,spine,scapulae & scalp
Associated with strong seropositivity
Always associated with severe carditis

16
Other features (Minor features)

Fever-(up to 101 degree F)

Arthralgia
Pallor
Anorexia
Loss of weight

17
Laboratory Findings

High ESR / LED

Anemia, leucocytosis
Elevated C-reactive protien
ASO titre >200 Todd units.
(Peak value attained at 3 weeks,then
comes down to normal by 6 weeks)
Anti-DNAse B test
Throat culture-GABHstreptococci

18
ECG- prolonged PR interval, 2nd or 3rd degree
blocks,ST depression, T inversion

2D Echo cardiography- valve edema,mitral

regurgitation, LA & LV dilatation,pericardial
effusion,decreased contractility

19
Diagnosis

Rheumatic fever is mainly a clinical diagnosis

No single diagnostic sign or specific laboratory
test available for diagnosis
Diagnosis based on MODIFIED JONES
CRITERIA

20
 Jones Criteria (Revised) for Guidance in the
Diagnosis of Rheumatic Fever*
Major Manifestation Minor Supporting Evidence
Manifestations of Streptococal Infection
Carditis Clinical Laboratory
Polyarthritis Previous Acute phase
Chorea rheumatic reactants: Increased Titer of Anti-
Erythema Marginatum fever or Erythrocyte Streptococcal Antibodies ASO
Subcutaneous Nodules rheumatic sedimentation (anti-streptolysin O),
heart disease rate, others
Arthralgia C-reactive Positive Throat Culture
Fever protein, for Group A Streptococcus
leukocytosis Recent Scarlet Fever
Prolonged P-
R interval

*The presence of two major criteria, or of one major and two minor criteria,
indicates a high probability of acute rheumatic fever, if supported by evidence of
Group A streptococcal nfection.

Recommendations of the American Heart Association

21
Exceptions to Jones Criteria

 Chorea alone, if other causes have been

excluded
 Insidious or late-onset carditis with no other
explanation
 Patients with documented RHD or prior
rheumatic fever,one major criterion,or of
fever,arthralgia or high CRP suggests
recurrence

22
Differential Diagnosis

Juvenile rheumatiod arthritis

Septic arthritis
Sickle-cell arthropathy
Kawasaki disease
Myocarditis
Scarlet fever
Leukemia

23
 Treatment
Step I - primary prevention
(eradication of streptococci)
Step II - anti inflammatory treatment
(aspirin,steroids)
Step III- supportive management &
management of complications
Step IV- secondary prevention
(prevention of recurrent attacks)
24
STEP I: Primary Prevention of Rheumatic Fever
(Treatment of Streptococcal Tonsillopharyngitis)
Agent Dose Mode Duration
Benzathine penicillin G 600 000 U for patients Intramuscular Once
27 kg (60 lb)
1 200 000 U for patients >27 kg
or
Penicillin V Children: 250 mg 2-3 times daily Oral 10 d
(phenoxymethyl penicillin) Adolescents and adults:
500 mg 2-3 times daily
For individuals allergic to penicillin
Erythromycin: 20-40 mg/kg/d 2-4 times daily Oral 10 d
Estolate (maximum 1 g/d)

or
Ethylsuccinate 40 mg/kg/d 2-4 times daily Oral 10 d
(maximum 1 g/d)
Recommendations of American Heart Association
05/05/1999 Dr.Said Alavi 25
Step II: Anti inflammatory treatment
Clinical condition Drugs
Arthritis only Aspirin 75-100
mg/kg/day,give as 4
divided doses for 6
weeks
(Attain a blood level 20-
30 mg/dl)
Carditis Prednisolone 2-2.5
mg/kg/day, give as two
divided doses for 2
weeks
Taper over 2 weeks &
while tapering add
Aspirin 75 mg/kg/day
for 2 weeks.
Continue aspirin alone
100 mg/kg/day for
another 4 weeks

26
3.Step III: Supportive management &
management of complications

Bed rest
Treatment of congestive cardiac failure:
-digitalis,diuretics
Treatment of chorea:
-diazepam or haloperidol
Rest to joints & supportive splinting

27
STEP IV : Secondary Prevention of Rheumatic Fever
(Prevention of Recurrent Attacks)
Agent Dose Mode

Benzathine penicillin G 1 200 000 U every 4 weeks* Intramuscular

or
Penicillin V 250 mg twice daily Oral

or
Sulfadiazine 0.5 g once daily for patients 27 kg (60 lb Oral
1.0 g once daily for patients >27 kg (60 lb)

For individuals allergic to penicillin and sulfadiazine

Erythromycin 250 mg twice daily Oral

*In high-risk situations, administration every 3 weeks is justified and

recommended
Recommendations of American Heart Association
Dr.Said Alavi 28
Duration of Secondary Rheumatic Fever
Prophylaxis
Category
Rheumatic fever with carditis and
residual heart disease
(persistent valvar disease*)
Duration
At least 10 y since last
episode and at least until
age 40 y, sometimes lifelong
prophylaxis

Rheumatic fever with carditis 10 y or well into adulthood,

but no residual heart disease whichever is longer
(no valvar disease*)

Rheumatic fever without carditis 5 y or until age 21 y,

whichever is longer
Recommendations of American Heart Association

*Clinical or echocardiographic evidence.

29
Prognosis
Rheumatic fever can recur whenever the
individual experience new GABH streptococcal
infection,if not on prophylactic medicines

Good prognosis for older age group & if no

carditis during the initial attack

Bad prognosis for younger children & those with

carditis with valvar lesions

30
31
 Valvular Heart Disease

MITRAL STENOSIS
 ETIOLOGY
RHEUMATIC VALVULAR DISEASE

MOST COMMON CAUSE OF MITRAL

STENOSIS
– Pure mitral stenosis 25%
– Pure mitral regurgitation 35%
– Combined MS and MR 40%
15 TO 20 YEAR LATENCY PERIOD
 ETIOLOGY
OTHER CAUSES

CONGENITAL
MALIGNANT CARCINOID
SLE OR RHEUMATOID ARTHRITIS
AMYLOID
METHYLSERGIDE THERAPY
 PATHOLOGY
SYMPTOMATIC MITRAL STENOSIS

THICKENED MITRAL CUSPS

– +/- CALCIFIC DEPOSITS
FUSION OF VALVE COMMISSURES
SHORTENING OF CHORDAE WITH FUSION
“FISH MOUTH” OR FUNNEL ORIFICE
 HISTORY

PRINCIPLE SYMPTOM IS DYSPNEA

– Reduces compliance of the lung
PULMONARY EDEMA
– Effort, emotional stress, infection, fever,
pregnancy
ATRIAL FIBRILLATION
– Increased rate causes increased LA to LV
gradient
 HISTORY

CHEST PAIN
– 15% DUE TO RV HTN, EMBOLIZATION
THROMBOEMBOLISM
– 20% HISTORICALLY INVOLVED
– CORRELATES INVERSELY WITH CARDIAC
OUTPUT
– CORRELATES DIRECTLY WITH LA SIZE
AND AGE OF PATIENT
 PHYSICAL EXAMINATION

ARTERIAL PULSE NORMAL OR DIMINISHED

JUGULAR PRESSURE PROMINENT a WAVE

PALPATION
– INCONSPICUOUS LV, RV HEAVE IN
PULMONARY HTN
 PHYSICAL EXAMINATION
AUSCULTATION

ACCENTUATED S1

OPENING SNAP
– SUDDEN TENSING OF VALVE LEAFLETS
– A2-OS INTERVAL SHORTENS WITH
SEVERITY

DIASTOLIC MURMUR
 PATHOPHYSIOLOGY

NORMAL VALVE AREA 4 TO 6cm2

NORMAL MEAN LA TO LV PRESSURE
GRADIENT 2 TO 4mmHg
MILD MITRAL STENOSIS 2cm2
CRITICAL MITRAL STENOSIS 1cm2 or less
– 20MMhg GRADIENT REQUIRED FOR FLOW
 MANAGEMENT
NATURAL HISTORY

20 TO 25 YEAR ASYMPTOMATIC PERIOD

5 YEARS FOR PROGRESSION CLASS II-IV
SURVIVAL
– CLASS III 62% 5 YR SURVIVAL
– CLASS IV 15% 5 YR SURVIVAL
ASYMPTOMATIC CLASS 1 40% WORSENED
OR DIED IN 10 YEARS
 MANAGEMENT
MEDICAL TREATMENT

RHD PCN AND SBE PROPHYLAXIS

SYMPTOMATIC PATIENTS
– ORAL DIURETICS AND ACTIVITY
RESTRICTION
– BETA BLOCKERS AND LOW HEART RATE
– DIGOXIN IN AF AND WITH PULM HTN
ANTICOAGULATION FOR LA SIZE >5.5cm,
EMBOLISM OR ATRIAL FIBRILLATION
 MANAGEMENT
SURGICAL TREATMENT

OPERATE FOR SEVERE SYMPTOMS

– CLASS III OR GREATER (SYMPTOMS WITH
LESS THAN USUAL ACTIVITY)
– PULMONARY HTN DEMANDS OPERATION
ROUTINE CATHETERIZATION MEN>45
MILDY SYMPTOMATIC PATIENTS
– CONSIDER SIZE OF MV ORIFICE,
LIFESTYLE AND HISTORY OF
COMPLICATIONS
 MANAGEMENT
BALLOON VALVULOPLASTY

PROCEDURE OF CHOICE IN RIGHT PT

– TRANSESOPHAGEAL ECHO HELPFUL IN
SORTING OUT WHICH PATIENT
– ECHO SCALE OF PREDICTORS RELATES TO
THICKENING AND CALCIFICATION OF VALVE

RESULTS COMPARABLE TO SURGERY

MORTALITY 2-3%, MORBIDITY 8-12%

 Valvular Heart Disease

MITRAL Insufficiency
 ETIOLOGY
ACUTE VS CHRONIC

INFLAMMATORY
DEGENERATIVE
INFECTIVE
STRUCTURAL
CONGENITAL
 ETIOLOGY
DEGENERATIVE

MYXOMATOUS DEGENERATION OF
LEAFLETS
– MITRAL VALVE PROLAPSE
– MOST COMMON CAUSE OF ACUTE MR IN
US ADULTS
MARFAN SYNDROME
CALCIFICATION OF MV ANNULUS
 ETIOLOGY
INFLAMMATORY

RHEUMATIC HEART DISEASE

– ACUTE RHEUMATIC FEVER VS
CHRONIC
SYSTEMIC LUPUS ERYTHEMATOSUS
SCLERODERMA
 ETIOLOGY
STRUCTURAL

RUPTURED CHORDAE TENDINAE

RUPTURE OR DYSFUNCTION OF PAPILLARY
MUSCLES
DILATATION OF MITRAL VALVE ANNULUS
PARAVALVULAR PROSTHETIC LEAK
ANATOMY OF MITRAL VALVE

VALVE LEAFLETS
– ANTERIOR AND POSTERIOR
MITRAL ANNULUS
– DILATATION
CHORDAE TENDINAE
PAPILLARY MUSCLES
 PATHOPHYSIOLOGY
VOLUME OVERLOAD

IMPEDENCE TO VENTRICULAR
EMPTYING IS REDUCED
– LV DECOMPRESSES INTO LA
VOLUME OF REGURGITANT FLOW
– DEPENDENT ON SIZE OF REGURGITANT
ORIFICE
AND LV TO LA PRESSURE GRADIENT
 PATHOPHYSIOLOGY
HEMODYNAMICS

FORWARD CARDIAC OUTPUT USUALLY

DEPRESSED
– TOTAL LV OUTPUT (FORWARD AND
BACKWARD) INCREASED
NORMAL LA COMPLIANCE (ACUTE MR)
– LITTLE ENLARGEMENT OF LA, HIGH LA
PRESSURE
LOW LA COMPLIANCE (CHRONIC MR)
– ENLARGED LA, MINIMALLY INCREASED LA
PRESSURE
CLINICAL MANIFESTATIONS
NATURAL HISTORY

VARIABLE AND DEPENDS ON MR VOLUME

MILD MR STABLE IN MAJORITY FOR YEARS
– MINORITY DEVELOP SEVERE MR
MORE RAPIDLY WITH DEGENERATIVE
DISEASE THAN RHEUMATIC
CLINICAL MANIFESTATIONS
SYMPTOMS USUALLY NOT UNTIL LV
STARTS TO FAIL

LONGER TIME INTERVAL IN MR THAN

MITRAL STENOSIS

RIGHT HEART FAILURE IN END STAGE

MR
 PHYSICAL EXAMINATION
CAROTID UPSTROKE SHARP, RAPID
FALLOFF
S1 USUALLY SOFT, WIDELY SPLIT S2
HOLOSYSTOLIC MURMUR
– APEX TO AXILLA
SYSTOLIC EJECTION MURMUR
– ISCHEMIC MR
 PHYSICAL EXAMINATION
MITRAL VALVE PROLAPSE
– MID TO LATE SYSTOLIC EJECTION
MURMUR
– MID SYSTOLIC NON-EJECTION CLICk
LABORATORY EXAMINATION

CHEST XRAY
– CARDIOMEGALY (ECCENTRIC
HYPERTROPHY)
– LEFT ATRIAL ENLARGEMENT
REGURGITANT VOLUME
– MILD 25%, MODERATE 40%, SEVERE
75%
 ECHOCARDIOGRAPHY
GOOD ANATOMICAL DETAIL
LA SIZE, THROMBUS, LV FUNCTION
UNDERLYING ETIOLOGY OF MR
INFECTIVE ENDOCARDITIS
DOPPLER
– SEVERITY OF MR, SIZE OF MR JET
 MANAGEMENT
MEDICAL MANAGEMENT
AFTERLOAD REDUCTION
– REDUCES IMPEDENCE TO EJECTION IN
AORTA
– ACE INHIBITORS AND HYDRALAZINE
ACUTE MR
– IV NITROPRUSSIDE CAN BE LIFESAVING
DIGOXIN, DIURETICS IN CHRONIC MR
FOLLOW LV SIZE AND FUNCTION
 SURGICAL TREATMENT
OPERATE FOR SYMPTOMS

ENLARGING LEFT VENTRICULAR SYSTOLIC

DIMENSION (>5.5CM), EJECTION FRACTION
<55% ARE PREDICTORS OF BAD OUTCOME

OPERATIVE MORTALITY 2 TO 7% IN CLASS II

TO III PATIENTS

RECONSTRUCTION IS BETTER THAN

REPLACEMENT IF POSSIBLE
Valvular Heart Disease

AORTIC STENOSIS
 ETIOLOGY
OBSTRUCTION TO LV OUTFLOW

HYPERTROPHIC CARDIOMYOPATHY
SUPRAVALVULAR
SUBVALVULAR
CONGENITAL
ACQUIRED
 ETIOLOGY
CONGENITAL AORTIC STENOSIS
UNICUSPID
– SEVERE AND DEADLY IN INFANCY
BICUSPID
– MANIFESTED LATER IN LIFE
– MOST COMMON CONGENITAL CARDIAC
ANOMALY IN LIVE BIRTHS (1%)
TRICUSPID
– CUSPS OF UNEQUAL SIZE
 ETIOLOGY
ACQUIRED AORTIC STENOSIS

RHEUMATIC HEART DISEASE

DEGENERATIVE
ATHEROSCLEROTIC
CALCIFIC DUE TO PAGET’S DISEASE
RHEUMATOID
 ETIOLOGY
DEGENERATIVE CALCIFIC AORTIC STENOSIS

PRIMARY CAUSE OF ADULT AORTIC

STENOSIS
YEARS OF MECHANICAL STRESS
DEPOSITION OF CALCIUM AT CUPAL BASE
PRESERVED COMMISSURES
RISK FACTORS
– DIABETES AND HYPERLIPIDEMIA
 ETIOLOGY
RHEUMATIC AORTIC STENOSIS

FUSION OF COMMISSURES AND CUSPS

RETRACTION OF CUSPAL BORDERS
REDUCE ORIFICE TO TRIANGULAR
OPENING
ASSOCIATED WITH AORTIC INSUFFICENCY
MITRAL DISEASE COMMON
ISOLATED AORTIC STENOSIS RARE
 HISTORY
ANGINA
– MEDIAN SURVIVAL 5 YEARS
SYNCOPE
– MEDIAN SURVIVAL 3 YEARS
CONGESTIVE HEART FAILURE
– MEDIAN SURVIVAL 2 YEARS
 PHYSICAL EXAMINATION
PULSUS PARVUS AND TARDUS
– IN CAROTID PULSE
REDUCED PULSE PRESSURE
SUSTAINED CARDIAC IMPULSE
DELAYED A2 OR DIMINISHED
HARSH SYSTOLIC EJECTION MURMUR
 PATHOPHYSIOLOGY
GRADUAL DEVELOPMENT OF OBSTRUCTION
TO LV OUTFLOW
LV OUTPUT MAINTAINED BY LV HYPERTROPHY
LV HYPERTROPHY MAY SUSTAIN A LARGE
PRESSURE GRADIENT FROM THE LV TO
AORTA OVER YEARS
ATRIAL CONTRACTION IMPORTANT
– ATRIAL FIBRILLATION MAY CAUSE ABRUPT
AND SEVERE SYMPTOMS
 PATHOPHYSIOLOGY
INCREASE IN AFTERLOAD
INCREASED LV WALL STRESS
COMPENSATED BY THE INCREASED
LV HYPERTROPHY
ULTIMATELY LOSS IN CONTRACTILITY
OF LV MASS AND DEVELOPMENT OF
HEART FAILURE
 LABORATORY
EKG
– LEFT VENTRICULAR HYPERTROPHY IS
PROMINENT FINDING
CHEST XRAY
– MAY BE ENTIRELY NORMAL BECAUSE THE
HYPERTROPHY OF LV IS CONCENTRIC
(CENTRAL) NOT ECCENTRIC LIKE MR OR
AORTIC INSUFFICIENCY
– CALCIFICATION OF AORTIC VALVE MAY BE
SEEN
 ECHOCARDIOGRAPHY
CALCIFIED VALVE WITH THICKENED LEAFLETS
OR COMMISSURES
DECREASED OPENING OF AORTIC VALVE
SEEN
LEFT VENTRICULAR HYPERTROPHY
DOPPLER
– VALVE PRESSURE GRADIENT CALCULATED
– VALVE AREA FROM THIS MEASUREMENT
 MEDICAL HISTORY
EDUCATION IN SYMPTOMS AND
REPORTING
OPERATE FOR SYMPTOMS WHEN VALVE IS
SEVERLY NARROWED
– <1CM2 IN AREA
DO NOT OPERATE ON SEVERE NARROWING
IF ASYMPTOMATIC
ENDOCARDITIS PROPHYLAXIS
SURGICAL MANAGEMENT
RESULTS
5 YEAR ACTUARIAL SURVIVAL 85%
REDUCTION IN LV MASS
IF PATIENTS HAVE CONGESTIVE HEART
FAILURE THEN VALVE REPLACEMENT HAS
10-25% MORTALITY
NORMAL 3-5% MORTALITY IN OR
PORCINE VALVE FOR AGE > 70
SURGICAL MANAGEMENT
ASYMPTOMATIC PATIENTS
– MORTALITY WITHOUT OPERATION IS <5%
PER YEAR
– FOLLOW EVERY 6 MONTHS IN OFFICE
– COUNSEL ON DEVELOPMENT OF
SYMPTOMS OF ANGINA, CHF, SYNCOPE
AORTIC STENOSIS IN THE
ELDERLY
OPERATIVE MORTALITY IN THE
ELDERLY
– 1.8% AGE < 50
– 5.1% AGE 50 - 60
– 7.1% AGE 60 – 70
ISOLATED AV REPLACEMENT IN PTS
AGE 80 TO 89
– 94% HAD GOOD RESULTS
– APPROPRIATE SELECTION
 Valvular Heart Disease

AORTIC INSUFFICIENCY
 ETIOLOGY
¾ OF PATIENTS WITH PURE AI ARE
MALES
2/3 OF PATIENTS FROM RHEUMATIC
FEVER
– THICKENING AND DEFORMATION OF
INDIVIDUAL VALVE CUSPS
INFECTIVE ENDOCARDITIS
– VARIOUS PREVIOUSLY DAMAGING
ETIOLOGIES
 ETIOLOGY
PROLAPSE OF AN AORTIC CUSP
CONGENITAL FENESTRATIONS OF
CUSP
TRAUMATIC RUPTURE
ASCENDING THORACIC AORTA
DISSECTION
MARKED AORTIC ROOT DILATATION
SYPHILIS, ANKYLOSING SPONDYLITIS
 PATHOPHYSIOLOGY
MARKED INCREASE IN STROKE
VOLUME OF LEFT VENTRICLE
– EXTRA BLOOD FROM LEAKING BACK
INTO LV TO EJECT
CONTRAST TO MITRAL
INSUFFICIENCY
– AI: EJECTING BLOOD INTO HIGH
AFTERLOAD (AORTA)
– MI: EJECTING BLOOD INTO LOW
AFTERLOAD (LEFT ATRIUM)
 PATHOPHYSIOLOGY
DILATATION OF LEFT VENTRICLE
– TO MAINTAIN ADEQUATE FORWARD
CARDIAC OUTPUT
REVERSE PRESSURE GRADIENT
FROM AORTA TO LV IN DIASTOLE
CAUSES BACK FLOW
ACUTE VS CHRONIC INSUFFICIENCY
 HISTORY
FAMILY HISTORY WITH MARFAN
SYNDROME
INFECTIVE ENDOCARDITIS
SYPHYLIS
AWARENESS OF HEARTBEAT
ORTHOPNEA, DOE
ANGINA
EDEMA
 PHYSICAL FINDINGS
INSPECTION
– BOBBING HEAD OR JARRING OF BODY
PALPATION
– ARTERIAL WATER HAMMER PULSE
– CAPILLARY PULSATIONS
– VARIOUS SIGNS
– WIDENED PULSE PRESSURE
 PHYSICAL FINDINGS
MURMURS
– DIASTOLIC HIGH PITCHED BLOW
– LOUD SYSTOLIC AORTIC EJECTION FLOW
MURMUR
– DIASTOLIC RUMBLE AUSTIN FLINT
MURMUR
MISTAKEN FOR MITRAL STENOSIS
 LABORATORY
EKG
– LEFT VENTRICULAR HYPERTROPHY
WITH STRAIN
– ECHOCARDIOGRAM
FLOW INTO LV FROM AORTIC VALVE
LV SIZE
FLUTTERING OF MITRAL LEAFLET
– BLOOD CULTURES IN ENDOCARDITIS
 TREATMENT
CONGESTIVE HEART FAILURE
TREATMENT
– DIGOXIN, DIURETICS, AFTERLOAD
REDUCTION
IV NITROPRUSSIDE MAY BE LIFESAVING
 TREATMENT
SURGERY
– SYMPTOMATIC PATIENTS SHOULD BE
OPERATED UPON
– ASYMPTOMATIC PATIENTS FOLLOWED
FOR LEFT VENTRICULAR ENLARGEMENT
AND SYSTOLIC DIMENSIONS ON
ECHOCARDIOGRAM
– YEARLY ECHOCARDIOLOGY
– MORTALITY <5% IF GOOD LV
– MORTALITY 5-10% IF POOR LV FUNCTION