Transcript Infective Endocarditis

Faculty of
Medicine
Universitas
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
Antigen of outer
protein cell wall
of GABHS
Cell wall
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
Capsule
……………………………………………
……...
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
Rheumatic Carditis Histology (40X)
9
Histology of Myocardium in Rheumatic Carditis
(200X)
10
Clinical Features
1.Arthritis
Flitting & fleeting migratory polyarthritis,
involving major joints
Commonly involved jointsknee,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
11
Clinical Features (Contd)
2.Carditis
Manifest as pancarditis(endocarditis,
myocarditis and pericarditis),occur in 4050% 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)
12
Rheumatic
heart
disease.
Abnormal
mitral
valve.
Thick,
fused
chordae
13
Another view of
thick and fused
mitral valves in
Rheumatic
heart disease
14
Clinical Features (Contd)
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
15
Clinical Features (Contd)
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
16
Clinical Features (Contd)
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
17
Clinical Features (Contd)
Other features (Minor features)
Fever-(up to 101 degree F)
Arthralgia
Pallor
Anorexia
Loss of weight
18
Laboratory Findings
High ESR
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
19
Laboratory Findings (Contd)
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
20
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
21
Jones Criteria (Revised) for Guidance in the
Diagnosis of Rheumatic Fever*
Major Manifestation
Carditis
Polyarthritis
Chorea
Erythema Marginatum
Subcutaneous Nodules
Minor
Manifestations
Clinical
Previous
rheumatic
fever or
rheumatic
heart disease
Arthralgia
Fever
Laboratory
Acute phase
reactants:
Erythrocyte
sedimentation
rate,
C-reactive
protein,
leukocytosis
Prolonged PR interval
Supporting Evidence
of Streptococal Infection
Increased Titer of AntiStreptococcal Antibodies ASO
(anti-streptolysin O),
others
Positive Throat Culture
for Group A Streptococcus
Recent Scarlet Fever
*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
22
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

23
Differential Diagnosis
Juvenile rheumatiod arthritis
Septic arthritis
Sickle-cell arthropathy
Kawasaki disease
Myocarditis
Scarlet fever
Leukemia
24
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)
25
STEP I: Primary Prevention of Rheumatic Fever
(Treatment of Streptococcal Tonsillopharyngitis)
Agent
Dose
Benzathine penicillin G
Mode
600 000 U for patients
Intramuscular
27 kg (60 lb)
1 200 000 U for patients >27 kg
Duration
Once
or
Penicillin V
Children: 250 mg 2-3 times daily Oral
(phenoxymethyl penicillin) Adolescents and adults:
500 mg 2-3 times daily
10 d
For individuals allergic to penicillin
Erythromycin:
Estolate
20-40 mg/kg/d 2-4 times daily
(maximum 1 g/d)
Oral
10 d
Oral
10 d
or
Ethylsuccinate
40 mg/kg/d 2-4 times daily
(maximum 1 g/d)
Recommendations of American Heart Association
05/05/1999
Dr.Said Alavi
26
Step II: Anti inflammatory treatment
Clinical condition Drugs
Arthritis only
Carditis
Aspirin 75-100
mg/kg/day,give as 4
divided doses for 6
weeks
(Attain a blood level 2030 mg/dl)
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
27
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
28
STEP IV : Secondary Prevention of Rheumatic Fever
(Prevention of Recurrent Attacks)
Agent
Dose
Benzathine penicillin G
1 200 000 U every 4 weeks*
Mode
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
29
Duration of Secondary Rheumatic Fever
Prophylaxis
Category
Duration
Rheumatic fever with carditis and
residual heart disease
(persistent valvar disease*)
At least 10 y since last
episode and at least until
age 40 y, sometimes lifelong
prophylaxis
Rheumatic fever with carditis
but no residual heart disease
(no valvar disease*)
10 y or well into adulthood,
whichever is longer
Rheumatic fever without carditis
5 y or until age 21 y,
whichever is longer
Recommendations of American Heart Association
*Clinical or echocardiographic evidence.
30
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
31
32
VALVULAR HEART
DISEASE
MITRAL STENOSIS
G
ETIOLOGY
RHEUMATIC VALVULAR DISEASE
MOST COMMON CAUSE OF M ITRAL
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
– PROLONGED Q-S1 INTERVAL
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
INSUFFICIENCTY
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
– VALSALVA PROLONGS MURMUR AND
BRINGS IT TO START CLOSER TO S1
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
AORTIC INSUFFICIENCY
VALVULAR HEART DISEASE
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
– COR BOVINUM
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 LATE OR IN ACUTE
ANGINA
EDEMA
PHYSICAL FINDINGS
INSPECTION
– BOBBING HEAD OR JARRING OF BODY
PALPATION
– ARTERIAL JACK 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