faculty of medicine universitas brawijaya
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Rheumatic Fever. Faculty of Medicine Universitas Brawijaya. Objectives. Etiology Epidemiology Pathogenesis Pathologic lesions Clinical manifestations & Laboratory findings Diagnosis & Differential diagnosis Treatment & Prevention Prognosis References. Etiology. - PowerPoint PPT PresentationTRANSCRIPT
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Faculty of Faculty of MedicineMedicine
Universitas Universitas BrawijayaBrawijaya
Faculty of Faculty of MedicineMedicine
Universitas Universitas BrawijayaBrawijaya
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ObjectivesObjectivesEtiologyEtiology
EpidemiologyEpidemiology
PathogenesisPathogenesis
Pathologic lesionsPathologic lesions
Clinical manifestations & Laboratory Clinical manifestations & Laboratory findingsfindings
Diagnosis & Differential diagnosisDiagnosis & Differential diagnosis
Treatment & PreventionTreatment & Prevention
PrognosisPrognosis
ReferencesReferences
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EtiologyEtiologyAcute rheumatic fever is a systemic Acute rheumatic fever is a systemic disease of childhood,often recurrent that disease of childhood,often recurrent that follows follows group A beta hemolytic group A beta hemolytic streptococcal infectionstreptococcal infection
It is a delayed non-suppurative sequelae It is a delayed non-suppurative sequelae to URTI with to URTI with GABH streptococci.GABH streptococci.
It is a diffuse inflammatory disease of It is a diffuse inflammatory disease of connective tissue,primarily involving connective tissue,primarily involving heart,blood vessels,joints, subcut.tissue heart,blood vessels,joints, subcut.tissue and CNSand CNS
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EpidemiologyEpidemiology
Ages Ages 5-15 yrs 5-15 yrs are most susceptibleare most susceptible
Rare Rare <3 yrs<3 yrs
Girls>boysGirls>boys
Common in Common in 3rd world countries3rd world countries
Environmental factors--Environmental factors-- over crowding, over crowding, poor sanitation, poverty,poor sanitation, poverty,
Incidence more during Incidence more during fall ,winter & fall ,winter & early springearly spring
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PathogenesisPathogenesis
Delayed immune response to infection Delayed immune response to infection with with group.A beta hemolytic group.A beta hemolytic streptococci.streptococci.
After a latent period of After a latent period of 1-3 weeks, 1-3 weeks, antibody induced immunological antibody induced immunological damage occur todamage occur to heart valves,joints, heart valves,joints, subcutaneous tissue & basal subcutaneous tissue & basal ganglia of brainganglia of brain
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Strains that produces rheumatic fever - Strains that produces rheumatic fever - M types l, 3, 5, 6,18 & 24M types l, 3, 5, 6,18 & 24
PharyngitisPharyngitis- - produced by GABHS can produced by GABHS can lead to- lead to- acute rheumatic fever ,acute rheumatic fever ,
rheumatic heart disease & rheumatic heart disease & post strept. Glomerulonepritis post strept. Glomerulonepritis
Skin infection-Skin infection- produced by GABHS leads produced by GABHS leads to to post streptococcal glomerulo nephritispost streptococcal glomerulo nephritis only. It will not result in Rh.Fever or only. It will not result in Rh.Fever or carditis as skin lipid cholesterol inhibit carditis as skin lipid cholesterol inhibit antigenicityantigenicity
Group A Beta Hemolytic Streptococcus
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Diagrammatic structure of the group A beta hemolytic streptococcus
Capsule
Cell wall
Protein antigens
Group carbohydrate
Peptidoglycan
Cyto.membrane
Cytoplasm
…………………………………………………...
Antigen of outer protein cell wall of GABHS induces antibody response in victim which result in autoimmune damage to heart valves, sub cutaneous tissue,tendons, joints & basal ganglia of brain
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Pathologic LesionsPathologic LesionsFibrinoid degeneration of connective Fibrinoid degeneration of connective tissue,inflammatory edema, inflammatory cell tissue,inflammatory edema, inflammatory cell infiltration & proliferation of specific cells infiltration & proliferation of specific cells resulting in formation of resulting in formation of AAshcoff nodulesshcoff nodules, , resulting in-resulting in-
--PancarditisPancarditis in the heart in the heart
--Arthritis Arthritis in thein the joints joints
--Ashcoff nodulesAshcoff nodules inin the subcutaneous the subcutaneous tissue tissue
-Basal gangliar lesions resulting in -Basal gangliar lesions resulting in choreachorea
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Rheumatic Carditis Histology (40X)Rheumatic Carditis Histology (40X)
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Histology of Myocardium in Rheumatic Carditis Histology of Myocardium in Rheumatic Carditis ((200X)200X)
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Clinical FeaturesClinical Features
Flitting & fleeting migratory polyarthritis, Flitting & fleeting migratory polyarthritis, involving major jointsinvolving major joints
Commonly involved joints-Commonly involved joints-knee,ankle,elbow & wristknee,ankle,elbow & wrist
Occur in 80%,involved joints are Occur in 80%,involved joints are exquisitely tenderexquisitely tender
In children below 5 yrs arthritis usually In children below 5 yrs arthritis usually mild but carditis more prominentmild but carditis more prominent
Arthritis do not progress to chronic diseaseArthritis do not progress to chronic disease
1.Arthritis
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Clinical Features (Contd)Clinical Features (Contd)
Manifest as Manifest as pancarditispancarditis(endocarditis, (endocarditis, myocarditis and pericarditis),occur in 40-myocarditis and pericarditis),occur in 40-50% of cases50% of cases
Carditis is the only manifestation of Carditis is the only manifestation of rheumatic fever that leaves a sequelae & rheumatic fever that leaves a sequelae & permanent damage to the organpermanent damage to the organ
Valvulitis occur in acute phaseValvulitis occur in acute phase
Chronic phase- fibrosis,calcification & Chronic phase- fibrosis,calcification & stenosis of heart valvesstenosis of heart valves(fishmouth valves)(fishmouth valves)
2.Carditis
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Rheumatic heart disease. Abnormal mitral valve. Thick, fused chordae
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Another view of thick and fused mitral valves in Rheumatic heart disease
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Clinical Features (Contd)Clinical Features (Contd)
Occur in 5-10% of casesOccur in 5-10% of cases
Mainly in girls of 1-15 yrs ageMainly in girls of 1-15 yrs age
May appear even 6/12 after the attack of May appear even 6/12 after the attack of rheumatic feverrheumatic fever
Clinically manifest as-clumsiness, Clinically manifest as-clumsiness, deterioration of handwriting,emotional deterioration of handwriting,emotional lability or grimacing of facelability or grimacing of face
Clinical signs- Clinical signs- pronator sign, jack in the pronator sign, jack in the box sign , milking sign of handsbox sign , milking sign of hands
3.Sydenham Chorea
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Clinical Features (Contd)Clinical Features (Contd)
Occur in <5%.Occur in <5%.
Unique,transient,serpiginous-looking Unique,transient,serpiginous-looking lesions of 1-2 inches in sizelesions of 1-2 inches in size
Pale center with red irregular marginPale center with red irregular margin
More on trunks & limbs & non-itchyMore on trunks & limbs & non-itchy
Worsens with application of heatWorsens with application of heat
Often associated with chronic carditisOften associated with chronic carditis
4.Erythema Marginatum
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Clinical Features (Contd)Clinical Features (Contd)
Occur in 10%Occur in 10%
Painless,pea-sized,palpable nodulesPainless,pea-sized,palpable nodules
Mainly over extensor surfaces of Mainly over extensor surfaces of joints,spine,scapulae & scalpjoints,spine,scapulae & scalp
Associated with strong seropositivityAssociated with strong seropositivity
Always associated with severe carditisAlways associated with severe carditis
5.Subcutaneous nodules
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Clinical Features (Contd)Clinical Features (Contd)
Other features (Minor features)
Fever-(up to 101 degree F)Fever-(up to 101 degree F)
ArthralgiaArthralgia
PallorPallor
AnorexiaAnorexia
Loss of weightLoss of weight
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Laboratory FindingsLaboratory Findings
High ESRHigh ESR
Anemia, leucocytosisAnemia, leucocytosis
Elevated C-reactive protienElevated C-reactive protien
ASO titre >200 Todd units.ASO titre >200 Todd units.(Peak value attained at 3 (Peak value attained at 3
weeks,then weeks,then comes down to normal by comes down to normal by 6 weeks)6 weeks)
Anti-DNAse B testAnti-DNAse B test
Throat culture-GABHstreptococciThroat culture-GABHstreptococci
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Laboratory Findings (Contd)Laboratory Findings (Contd)ECG-ECG- prolonged PR interval, 2nd or 3rd prolonged PR interval, 2nd or 3rd degree blocks,ST depression, degree blocks,ST depression, T T inversioninversion
2D Echo cardiography-2D Echo cardiography- valve edema,mitral valve edema,mitral regurgitation, LA & LV dilatation,pericardial regurgitation, LA & LV dilatation,pericardial effusion,decreased contractilityeffusion,decreased contractility
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DiagnosisDiagnosisRheumatic fever is mainly a clinical Rheumatic fever is mainly a clinical diagnosisdiagnosis
No single diagnostic sign or specific No single diagnostic sign or specific laboratory test available for diagnosislaboratory test available for diagnosis
Diagnosis based on Diagnosis based on MODIFIED JONES MODIFIED JONES CRITERIACRITERIA
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Jones Criteria (Revised) for Guidance in theDiagnosis of Rheumatic Fever*
Major Manifestation MinorManifestations
Supporting Evidence of Streptococal Infection
Clinical LaboratoryCarditisPolyarthritis
ChoreaErythema Marginatum
Subcutaneous Nodules
Previousrheumaticfever orrheumaticheart diseaseArthralgiaFever
Acute phasereactants:Erythrocytesedimentationrate, C-reactiveprotein,leukocytosis Prolonged P-R interval
Increased Titer of Anti-Streptococcal Antibodies ASO (anti-streptolysin O),othersPositive Throat Culture for Group A StreptococcusRecent 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 ofGroup A streptococcal nfection.
Recommendations of the American Heart Association
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Exceptions to Jones CriteriaExceptions to Jones Criteria
Chorea alone, if other causes have been Chorea alone, if other causes have been excludedexcluded
Insidious or late-onset carditis with no Insidious or late-onset carditis with no other explanationother explanation
Patients with documented RHD or prior Patients with documented RHD or prior rheumatic fever,one major criterion,or of rheumatic fever,one major criterion,or of fever,arthralgia or high CRP suggests fever,arthralgia or high CRP suggests recurrencerecurrence
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Differential DiagnosisDifferential Diagnosis
Juvenile rheumatiod arthritisJuvenile rheumatiod arthritis
Septic arthritisSeptic arthritis
Sickle-cell arthropathySickle-cell arthropathy
Kawasaki diseaseKawasaki disease
MyocarditisMyocarditis
Scarlet feverScarlet fever
LeukemiaLeukemia
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TreatmentTreatmentStep IStep I - primary prevention - primary prevention
(eradication of streptococci)(eradication of streptococci)
Step IIStep II - anti inflammatory treatment - anti inflammatory treatment (aspirin,steroids)(aspirin,steroids)
Step IIIStep III- supportive management & - supportive management & management of complications management of complications
Step IVStep IV- secondary prevention - secondary prevention (prevention of recurrent (prevention of recurrent
attacks)attacks)
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05/05/199905/05/1999 Dr.Said AlaviDr.Said Alavi 2626
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
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Arthritis only Aspirin 75-100mg/kg/day,give as 4divided doses for 6weeks(Attain a blood level 20-30 mg/dl)
Carditis Prednisolone 2-2.5mg/kg/day, give as twodivided doses for 2weeksTaper over 2 weeks &while tapering addAspirin 75 mg/kg/dayfor 2 weeks.Continue aspirin alone100 mg/kg/day foranother 4 weeks
Step II: Anti inflammatory treatmentClinical condition Drugs
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Bed rest Bed rest
Treatment of congestive cardiac failure: Treatment of congestive cardiac failure: --digitalis,diureticsdigitalis,diuretics
Treatment of chorea:Treatment of chorea: - -diazepam or haloperidoldiazepam or haloperidol
Rest to joints & supportive splintingRest to joints & supportive splinting
3.Step III: Supportive management & management of complications
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Dr.Said AlaviDr.Said Alavi 2929
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
orPenicillin V 250 mg twice daily Oral
orSulfadiazine 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
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Duration of Secondary Rheumatic Fever Prophylaxis
Category Duration
Rheumatic fever with carditis and At least 10 y since last residual heart disease episode and at least until (persistent valvar disease*) 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
*Clinical or echocardiographic evidence.Recommendations of American Heart Association
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PrognosisPrognosis
Rheumatic fever can recur whenever the Rheumatic fever can recur whenever the individual experience new GABH individual experience new GABH streptococcal infection,if not on streptococcal infection,if not on prophylactic medicinesprophylactic medicines
Good prognosis for older age group & if no Good prognosis for older age group & if no carditis during the initial attackcarditis during the initial attack
Bad prognosis for younger children & Bad prognosis for younger children & those with carditis with valvar lesionsthose with carditis with valvar lesions
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VALVULAR HEART VALVULAR HEART DISEASEDISEASE
MITRAL STENOSISMITRAL STENOSIS
GG
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ETIOLOGYETIOLOGYRHEUMATIC VALVULAR DISEASERHEUMATIC VALVULAR DISEASE
MOST COMMON CAUSE OF M ITRAL MOST COMMON CAUSE OF M ITRAL STENOSISSTENOSIS– Pure mitral stenosis 25%Pure mitral stenosis 25%– Pure mitral regurgitation 35%Pure mitral regurgitation 35%– Combined MS and MR 40%Combined MS and MR 40%
15 TO 20 YEAR LATENCY PERIOD15 TO 20 YEAR LATENCY PERIOD
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ETIOLOGYETIOLOGYOTHER CAUSESOTHER CAUSES
CONGENITALCONGENITAL
MALIGNANT CARCINOIDMALIGNANT CARCINOID
SLE OR RHEUMATOID ARTHRITISSLE OR RHEUMATOID ARTHRITIS
AMYLOIDAMYLOID
METHYLSERGIDE THERAPYMETHYLSERGIDE THERAPY
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PATHOLOGYPATHOLOGYSYMPTOMATIC MITRAL STENOSISSYMPTOMATIC MITRAL STENOSIS
THICKENED MITRAL CUSPSTHICKENED MITRAL CUSPS– +/- CALCIFIC DEPOSITS+/- CALCIFIC DEPOSITS
FUSION OF VALVE COMMISSURESFUSION OF VALVE COMMISSURES
SHORTENING OF CHORDAE WITH SHORTENING OF CHORDAE WITH FUSIONFUSION
““FISH MOUTH” OR FUNNEL ORIFICEFISH MOUTH” OR FUNNEL ORIFICE
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HISTORYHISTORY
PRINCIPLE SYMPTOM IS DYSPNEAPRINCIPLE SYMPTOM IS DYSPNEA
– Reduces compliance of the lungReduces compliance of the lung
PULMONARY EDEMAPULMONARY EDEMA
– Effort, emotional stress, infection, fever, Effort, emotional stress, infection, fever, pregnancypregnancy
ATRIAL FIBRILLATIONATRIAL FIBRILLATION
– Increased rate causes increased LA to LV Increased rate causes increased LA to LV gradientgradient
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HISTORYHISTORY
CHEST PAINCHEST PAIN– 15% DUE TO RV HTN, EMBOLIZATION15% DUE TO RV HTN, EMBOLIZATION
THROMBOEMBOLISMTHROMBOEMBOLISM– 20% HISTORICALLY INVOLVED20% HISTORICALLY INVOLVED– CORRELATES INVERSELY WITH CARDIAC CORRELATES INVERSELY WITH CARDIAC
OUTPUTOUTPUT– CORRELATES DIRECTLY WITH LA SIZE CORRELATES DIRECTLY WITH LA SIZE
AND AGE OF PATIENTAND AGE OF PATIENT
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PHYSICAL EXAMINATIONPHYSICAL EXAMINATION
ARTERIAL PULSE NORMAL OR ARTERIAL PULSE NORMAL OR DIMINISHEDDIMINISHED
JUGULAR PRESSURE PROMINENT a JUGULAR PRESSURE PROMINENT a WAVEWAVE
PALPATIONPALPATION– INCONSPICUOUS LV, RV HEAVE IN INCONSPICUOUS LV, RV HEAVE IN
PULMONARY HTNPULMONARY HTN
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PHYSICAL EXAMINATIONPHYSICAL EXAMINATIONAUSCULTATIONAUSCULTATION
ACCENTUATED S1ACCENTUATED S1– PROLONGED Q-S1 INTERVALPROLONGED Q-S1 INTERVAL
OPENING SNAPOPENING SNAP– SUDDEN TENSING OF VALVE LEAFLETSSUDDEN TENSING OF VALVE LEAFLETS– A2-OS INTERVAL SHORTENS WITH A2-OS INTERVAL SHORTENS WITH
SEVERITYSEVERITY
DIASTOLIC MURMURDIASTOLIC MURMUR
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PATHOPHYSIOLOGYPATHOPHYSIOLOGY
NORMAL VALVE AREA 4 TO 6cm2NORMAL VALVE AREA 4 TO 6cm2
NORMAL MEAN LA TO LV PRESSURE NORMAL MEAN LA TO LV PRESSURE GRADIENT 2 TO 4mmHgGRADIENT 2 TO 4mmHg
MILD MITRAL STENOSIS 2cm2MILD MITRAL STENOSIS 2cm2
CRITICAL MITRAL STENOSIS 1cm2 or CRITICAL MITRAL STENOSIS 1cm2 or lessless– 20MMhg GRADIENT REQUIRED FOR FLOW20MMhg GRADIENT REQUIRED FOR FLOW
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MANAGEMENTMANAGEMENTNATURAL HISTORYNATURAL HISTORY
20 TO 25 YEAR ASYMPTOMATIC 20 TO 25 YEAR ASYMPTOMATIC PERIODPERIOD5 YEARS FOR PROGRESSION CLASS 5 YEARS FOR PROGRESSION CLASS II-IVII-IVSURVIVALSURVIVAL– CLASS III 62% 5 YR SURVIVALCLASS III 62% 5 YR SURVIVAL– CLASS IV 15% 5 YR SURVIVALCLASS IV 15% 5 YR SURVIVAL
ASYMPTOMATIC CLASS 1 40% ASYMPTOMATIC CLASS 1 40% WORSENED OR DIED IN 10 YEARSWORSENED OR DIED IN 10 YEARS
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MANAGEMENTMANAGEMENTMEDICAL TREATMENTMEDICAL TREATMENT
RHD PCN AND SBE PROPHYLAXISRHD PCN AND SBE PROPHYLAXIS
SYMPTOMATIC PATIENTSSYMPTOMATIC PATIENTS
– ORAL DIURETICS AND ACTIVITY ORAL DIURETICS AND ACTIVITY RESTRICTIONRESTRICTION
– BETA BLOCKERS AND LOW HEART RATEBETA BLOCKERS AND LOW HEART RATE
– DIGOXIN IN AF AND WITH PULM HTNDIGOXIN IN AF AND WITH PULM HTN
ANTICOAGULATION FOR LA SIZE >5.5cm, ANTICOAGULATION FOR LA SIZE >5.5cm, EMBOLISM OR ATRIAL FIBRILLATIONEMBOLISM OR ATRIAL FIBRILLATION
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MANAGEMENTMANAGEMENTSURGICAL TREATMENTSURGICAL TREATMENT
OPERATE FOR SEVERE SYMPTOMSOPERATE FOR SEVERE SYMPTOMS
– CLASS III OR GREATER (SYMPTOMS WITH CLASS III OR GREATER (SYMPTOMS WITH LESS THAN USUAL ACTIVITY)LESS THAN USUAL ACTIVITY)
– PULMONARY HTN DEMANDS OPERATIONPULMONARY HTN DEMANDS OPERATION
ROUTINE CATHETERIZATION MEN>45ROUTINE CATHETERIZATION MEN>45
MILDY SYMPTOMATIC PATIENTSMILDY SYMPTOMATIC PATIENTS
– CONSIDER SIZE OF MV ORIFICE, CONSIDER SIZE OF MV ORIFICE, LIFESTYLE AND HISTORY OF LIFESTYLE AND HISTORY OF COMPLICATIONSCOMPLICATIONS
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MANAGEMENTMANAGEMENTBALLOON VALVULOPLASTYBALLOON VALVULOPLASTY
PROCEDURE OF CHOICE IN RIGHT PTPROCEDURE OF CHOICE IN RIGHT PT– TRANSESOPHAGEAL ECHO HELPFUL IN TRANSESOPHAGEAL ECHO HELPFUL IN
SORTING OUT WHICH PATIENTSORTING OUT WHICH PATIENT– ECHO SCALE OF PREDICTORS RELATES ECHO SCALE OF PREDICTORS RELATES
TO THICKENING AND CALCIFICATION OF TO THICKENING AND CALCIFICATION OF VALVEVALVE
RESULTS COMPARABLE TO SURGERYRESULTS COMPARABLE TO SURGERYMORTALITY 2-3%, MORBIDITY 8-12%MORTALITY 2-3%, MORBIDITY 8-12%
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VALVULAR HEART VALVULAR HEART DISEASEDISEASE
MITRAL MITRAL INSUFFICIENCTYINSUFFICIENCTY
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ETIOLOGYETIOLOGYACUTE VS CHRONICACUTE VS CHRONIC
INFLAMMATORYINFLAMMATORY
DEGENERATIVEDEGENERATIVE
INFECTIVEINFECTIVE
STRUCTURALSTRUCTURAL
CONGENITALCONGENITAL
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ETIOLOGYETIOLOGYDEGENERATIVEDEGENERATIVE
MYXOMATOUS DEGENERATION OF MYXOMATOUS DEGENERATION OF LEAFLETSLEAFLETS– MITRAL VALVE PROLAPSEMITRAL VALVE PROLAPSE– MOST COMMON CAUSE OF ACUTE MR IN MOST COMMON CAUSE OF ACUTE MR IN
US ADULTSUS ADULTS
MARFAN SYNDROMEMARFAN SYNDROME
CALCIFICATION OF MV ANNULUSCALCIFICATION OF MV ANNULUS
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ETIOLOGYETIOLOGYINFLAMMATORYINFLAMMATORY
RHEUMATIC HEART DISEASERHEUMATIC HEART DISEASE– ACUTE RHEUMATIC FEVER VS ACUTE RHEUMATIC FEVER VS
CHRONICCHRONIC
SYSTEMIC LUPUS SYSTEMIC LUPUS ERYTHEMATOSUSERYTHEMATOSUS
SCLERODERMASCLERODERMA
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ETIOLOGYETIOLOGYSTRUCTURALSTRUCTURAL
RUPTURED CHORDAE TENDINAERUPTURED CHORDAE TENDINAE
RUPTURE OR DYSFUNCTION OF RUPTURE OR DYSFUNCTION OF PAPILLARY MUSCLESPAPILLARY MUSCLES
DILATATION OF MITRAL VALVE DILATATION OF MITRAL VALVE ANNULUSANNULUS
PARAVALVULAR PROSTHETIC LEAKPARAVALVULAR PROSTHETIC LEAK
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ANATOMY OF MITRAL VALVEANATOMY OF MITRAL VALVE
VALVE LEAFLETSVALVE LEAFLETS– ANTERIOR AND POSTERIORANTERIOR AND POSTERIOR
MITRAL ANNULUSMITRAL ANNULUS– DILATATIONDILATATION
CHORDAE TENDINAECHORDAE TENDINAE
PAPILLARY MUSCLESPAPILLARY MUSCLES
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PATHOPHYSIOLOGYPATHOPHYSIOLOGYVOLUME OVERLOADVOLUME OVERLOAD
IMPEDENCE TO VENTRICULAR IMPEDENCE TO VENTRICULAR EMPTYING IS EMPTYING IS REDUCEDREDUCED– LV DECOMPRESSES INTO LALV DECOMPRESSES INTO LA
VOLUME OF REGURGITANT FLOWVOLUME OF REGURGITANT FLOW– DEPENDENT ON SIZE OF REGURGITANT DEPENDENT ON SIZE OF REGURGITANT
ORIFICEORIFICEAND LV TO LA PRESSURE GRADIENTAND LV TO LA PRESSURE GRADIENT
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PATHOPHYSIOLOGYPATHOPHYSIOLOGYHEMODYNAMICSHEMODYNAMICS
FORWARD CARDIAC OUTPUT USUALLY FORWARD CARDIAC OUTPUT USUALLY DEPRESSEDDEPRESSED– TOTAL LV OUTPUT (FORWARD AND TOTAL LV OUTPUT (FORWARD AND
BACKWARD) INCREASEDBACKWARD) INCREASEDNORMAL LA COMPLIANCE (ACUTE MR)NORMAL LA COMPLIANCE (ACUTE MR)– LITTLE ENLARGEMENT OF LA, HIGH LA LITTLE ENLARGEMENT OF LA, HIGH LA
PRESSUREPRESSURELOW LA COMPLIANCE (CHRONIC MR)LOW LA COMPLIANCE (CHRONIC MR)– ENLARGED LA, MINIMALLY INCREASED LA ENLARGED LA, MINIMALLY INCREASED LA
PRESSUREPRESSURE
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CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONSNATURAL HISTORYNATURAL HISTORY
VARIABLE AND DEPENDS ON MR VARIABLE AND DEPENDS ON MR VOLUMEVOLUME
MILD MR STABLE IN MAJORITY FOR MILD MR STABLE IN MAJORITY FOR YEARSYEARS– MINORITY DEVELOP SEVERE MRMINORITY DEVELOP SEVERE MR
MORE RAPIDLY WITH DEGENERATIVE MORE RAPIDLY WITH DEGENERATIVE DISEASE THAN RHEUMATICDISEASE THAN RHEUMATIC
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CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS
SYMPTOMS USUALLY NOT UNTIL LV SYMPTOMS USUALLY NOT UNTIL LV STARTS TO FAILSTARTS TO FAIL
LONGER TIME INTERVAL IN MR THAN LONGER TIME INTERVAL IN MR THAN MITRAL STENOSISMITRAL STENOSIS
RIGHT HEART FAILURE IN END STAGE RIGHT HEART FAILURE IN END STAGE MRMR
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PHYSICAL EXAMINATIONPHYSICAL EXAMINATION
CAROTID UPSTROKE SHARP, RAPID CAROTID UPSTROKE SHARP, RAPID FALLOFFFALLOFF
S1 USUALLY SOFT, WIDELY SPLIT S2S1 USUALLY SOFT, WIDELY SPLIT S2
HOLOSYSTOLIC MURMURHOLOSYSTOLIC MURMUR– APEX TO AXILLAAPEX TO AXILLA
SYSTOLIC EJECTION MURMURSYSTOLIC EJECTION MURMUR– ISCHEMIC MR ISCHEMIC MR
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PHYSICAL EXAMINATIONPHYSICAL EXAMINATION
MITRAL VALVE PROLAPSEMITRAL VALVE PROLAPSE– MID TO LATE SYSTOLIC EJECTION MID TO LATE SYSTOLIC EJECTION
MURMURMURMUR– MID SYSTOLIC NON-EJECTION CLICKMID SYSTOLIC NON-EJECTION CLICK– VALSALVA PROLONGS MURMUR AND VALSALVA PROLONGS MURMUR AND
BRINGS IT TO START CLOSER TO S1BRINGS IT TO START CLOSER TO S1
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LABORATORY EXAMINATIONLABORATORY EXAMINATION
CHEST XRAYCHEST XRAY– CARDIOMEGALY (ECCENTRIC CARDIOMEGALY (ECCENTRIC
HYPERTROPHY)HYPERTROPHY)– LEFT ATRIAL ENLARGEMENTLEFT ATRIAL ENLARGEMENT
REGURGITANT VOLUMEREGURGITANT VOLUME– MILD 25%, MODERATE 40%, SEVERE MILD 25%, MODERATE 40%, SEVERE
75%75%
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ECHOCARDIOGRAPHYECHOCARDIOGRAPHY
GOOD ANATOMICAL DETAILGOOD ANATOMICAL DETAIL
LA SIZE, THROMBUS, LV FUNCTIONLA SIZE, THROMBUS, LV FUNCTION
UNDERLYING ETIOLOGY OF MRUNDERLYING ETIOLOGY OF MR
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
DOPPLERDOPPLER– SEVERITY OF MR, SIZE OF MR JETSEVERITY OF MR, SIZE OF MR JET
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MANAGEMENTMANAGEMENTMEDICAL MANAGEMENTMEDICAL MANAGEMENT
AFTERLOAD REDUCTIONAFTERLOAD REDUCTION– REDUCES IMPEDENCE TO EJECTION IN REDUCES IMPEDENCE TO EJECTION IN
AORTAAORTA– ACE INHIBITORS AND HYDRALAZINEACE INHIBITORS AND HYDRALAZINE
ACUTE MRACUTE MR– IV NITROPRUSSIDE CAN BE LIFESAVINGIV NITROPRUSSIDE CAN BE LIFESAVING
DIGOXIN, DIURETICS IN CHRONIC MRDIGOXIN, DIURETICS IN CHRONIC MRFOLLOW LV SIZE AND FUNCTIONFOLLOW LV SIZE AND FUNCTION
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SURGICAL TREATMENTSURGICAL TREATMENT
OPERATE FOR SYMPTOMSOPERATE FOR SYMPTOMSENLARGING LEFT VENTRICULAR ENLARGING LEFT VENTRICULAR SYSTOLIC DIMENSION (>5.5CM), SYSTOLIC DIMENSION (>5.5CM), EJECTION FRACTION <55% ARE EJECTION FRACTION <55% ARE PREDICTORS OF BAD OUTCOMEPREDICTORS OF BAD OUTCOMEOPERATIVE MORTALITY 2 TO 7% IN OPERATIVE MORTALITY 2 TO 7% IN CLASS II TO III PATIENTSCLASS II TO III PATIENTSRECONSTRUCTION IS BETTER THAN RECONSTRUCTION IS BETTER THAN REPLACEMENT IF POSSIBLEREPLACEMENT IF POSSIBLE
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VALVULAR HEART VALVULAR HEART DISEASEDISEASE
AORTIC STENOSISAORTIC STENOSIS
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ETIOLOGYETIOLOGYOBSTRUCTION TO LV OUTFLOWOBSTRUCTION TO LV OUTFLOW
HYPERTROPHIC CARDIOMYOPATHYHYPERTROPHIC CARDIOMYOPATHY
SUPRAVALVULARSUPRAVALVULAR
SUBVALVULARSUBVALVULAR
CONGENITALCONGENITAL
ACQUIREDACQUIRED
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ETIOLOGYETIOLOGYCONGENITAL AORTIC STENOSISCONGENITAL AORTIC STENOSIS
UNICUSPIDUNICUSPID– SEVERE AND DEADLY IN INFANCYSEVERE AND DEADLY IN INFANCY
BICUSPIDBICUSPID– MANIFESTED LATER IN LIFEMANIFESTED LATER IN LIFE– MOST COMMON CONGENITAL CARDIAC MOST COMMON CONGENITAL CARDIAC
ANOMALY IN LIVE BIRTHS (1%)ANOMALY IN LIVE BIRTHS (1%)
TRICUSPIDTRICUSPID– CUSPS OF UNEQUAL SIZE CUSPS OF UNEQUAL SIZE
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ETIOLOGYETIOLOGYACQUIRED AORTIC STENOSISACQUIRED AORTIC STENOSIS
RHEUMATIC HEART DISEASERHEUMATIC HEART DISEASE
DEGENERATIVE DEGENERATIVE
ATHEROSCLEROTICATHEROSCLEROTIC
CALCIFIC DUE TO PAGET’S DISEASECALCIFIC DUE TO PAGET’S DISEASE
RHEUMATOIDRHEUMATOID
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ETIOLOGYETIOLOGYDEGENERATIVE CALCIFIC AORTIC STENOSISDEGENERATIVE CALCIFIC AORTIC STENOSIS
PRIMARY CAUSE OF ADULT AORTIC PRIMARY CAUSE OF ADULT AORTIC STENOSISSTENOSIS
YEARS OF MECHANICAL STRESSYEARS OF MECHANICAL STRESS
DEPOSITION OF CALCIUM AT CUPAL DEPOSITION OF CALCIUM AT CUPAL BASE BASE
PRESERVED COMMISSURESPRESERVED COMMISSURES
RISK FACTORSRISK FACTORS– DIABETES AND HYPERLIPIDEMIADIABETES AND HYPERLIPIDEMIA
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ETIOLOGYETIOLOGYRHEUMATIC AORTIC STENOSISRHEUMATIC AORTIC STENOSIS
FUSION OF COMMISSURES AND FUSION OF COMMISSURES AND CUSPSCUSPSRETRACTION OF CUSPAL BORDERSRETRACTION OF CUSPAL BORDERSREDUCE ORIFICE TO TRIANGULAR REDUCE ORIFICE TO TRIANGULAR OPENINGOPENINGASSOCIATED WITH AORTIC ASSOCIATED WITH AORTIC INSUFFICENCYINSUFFICENCYMITRAL DISEASE COMMONMITRAL DISEASE COMMONISOLATED AORTIC STENOSIS RAREISOLATED AORTIC STENOSIS RARE
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HISTORYHISTORY
ANGINAANGINA– MEDIAN SURVIVAL 5 YEARSMEDIAN SURVIVAL 5 YEARS
SYNCOPESYNCOPE– MEDIAN SURVIVAL 3 YEARSMEDIAN SURVIVAL 3 YEARS
CONGESTIVE HEART FAILURECONGESTIVE HEART FAILURE– MEDIAN SURVIVAL 2 YEARSMEDIAN SURVIVAL 2 YEARS
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PHYSICAL EXAMINATIONPHYSICAL EXAMINATION
PULSUS PARVUS AND TARDUSPULSUS PARVUS AND TARDUS– IN CAROTID PULSEIN CAROTID PULSE
REDUCED PULSE PRESSUREREDUCED PULSE PRESSURE
SUSTAINED CARDIAC IMPULSESUSTAINED CARDIAC IMPULSE
DELAYED A2 OR DIMINISHEDDELAYED A2 OR DIMINISHED
HARSH SYSTOLIC EJECTION MURMURHARSH SYSTOLIC EJECTION MURMUR
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PATHOPHYSIOLOGYPATHOPHYSIOLOGY
GRADUAL DEVELOPMENT OF OBSTRUCTION GRADUAL DEVELOPMENT OF OBSTRUCTION TO LV OUTFLOWTO LV OUTFLOWLV OUTPUT MAINTAINED BY LV HYPERTROPHYLV OUTPUT MAINTAINED BY LV HYPERTROPHYLV HYPERTROPHY MAY SUSTAIN A LARGE LV HYPERTROPHY MAY SUSTAIN A LARGE PRESSURE GRADIENT FROM THE LV TO PRESSURE GRADIENT FROM THE LV TO AORTA OVER YEARSAORTA OVER YEARSATRIAL CONTRACTION IMPORTANTATRIAL CONTRACTION IMPORTANT– ATRIAL FIBRILLATION MAY CAUSE ABRUPT ATRIAL FIBRILLATION MAY CAUSE ABRUPT
AND SEVERE SYMPTOMSAND SEVERE SYMPTOMS
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PATHOPHYSIOLOGYPATHOPHYSIOLOGY
INCREASE IN AFTERLOADINCREASE IN AFTERLOAD
INCREASED LV WALL STRESS INCREASED LV WALL STRESS COMPENSATED BY THE INCREASED COMPENSATED BY THE INCREASED LV HYPERTROPHYLV HYPERTROPHY
ULTIMATELY LOSS IN CONTRACTILITY ULTIMATELY LOSS IN CONTRACTILITY OF LV MASS AND DEVELOPMENT OF OF LV MASS AND DEVELOPMENT OF HEART FAILUREHEART FAILURE
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LABORATORYLABORATORY
EKGEKG– LEFT VENTRICULAR HYPERTROPHY IS LEFT VENTRICULAR HYPERTROPHY IS
PROMINENT FINDINGPROMINENT FINDINGCHEST XRAYCHEST XRAY– MAY BE ENTIRELY NORMAL BECAUSE THE MAY BE ENTIRELY NORMAL BECAUSE THE
HYPERTROPHY OF LV IS CONCENTRIC HYPERTROPHY OF LV IS CONCENTRIC (CENTRAL) NOT ECCENTRIC LIKE MR OR (CENTRAL) NOT ECCENTRIC LIKE MR OR AORTIC INSUFFICIENCYAORTIC INSUFFICIENCY
– CALCIFICATION OF AORTIC VALVE MAY BE CALCIFICATION OF AORTIC VALVE MAY BE SEENSEEN
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ECHOCARDIOGRAPHYECHOCARDIOGRAPHY
CALCIFIED VALVE WITH THICKENED LEAFLETS CALCIFIED VALVE WITH THICKENED LEAFLETS OR COMMISSURESOR COMMISSURES
DECREASED OPENING OF AORTIC VALVE DECREASED OPENING OF AORTIC VALVE SEENSEEN
LEFT VENTRICULAR HYPERTROPHYLEFT VENTRICULAR HYPERTROPHY
DOPPLERDOPPLER
– VALVE PRESSURE GRADIENT CALCULATEDVALVE PRESSURE GRADIENT CALCULATED
– VALVE AREA FROM THIS MEASUREMENTVALVE AREA FROM THIS MEASUREMENT
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MEDICAL HISTORYMEDICAL HISTORY
EDUCATION IN SYMPTOMS AND EDUCATION IN SYMPTOMS AND REPORTINGREPORTING
OPERATE FOR SYMPTOMS WHEN OPERATE FOR SYMPTOMS WHEN VALVE IS SEVERLY NARROWED VALVE IS SEVERLY NARROWED – <1CM2 IN AREA<1CM2 IN AREA
DO NOT OPERATE ON SEVERE DO NOT OPERATE ON SEVERE NARROWING IF ASYMPTOMATICNARROWING IF ASYMPTOMATIC
ENDOCARDITIS PROPHYLAXISENDOCARDITIS PROPHYLAXIS
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SURGICAL MANAGEMENTSURGICAL MANAGEMENTRESULTSRESULTS
5 YEAR ACTUARIAL SURVIVAL 85%5 YEAR ACTUARIAL SURVIVAL 85%
REDUCTION IN LV MASSREDUCTION IN LV MASS
IF PATIENTS HAVE CONGESTIVE IF PATIENTS HAVE CONGESTIVE HEART FAILURE THEN VALVE HEART FAILURE THEN VALVE REPLACEMENT HAS 10-25% REPLACEMENT HAS 10-25% MORTALITYMORTALITY
NORMAL 3-5% MORTALITY IN ORNORMAL 3-5% MORTALITY IN OR
PORCINE VALVE FOR AGE > 70PORCINE VALVE FOR AGE > 70
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SURGICAL MANAGEMENTSURGICAL MANAGEMENT
ASYMPTOMATIC PATIENTSASYMPTOMATIC PATIENTS– MORTALITY WITHOUT OPERATION IS <5% MORTALITY WITHOUT OPERATION IS <5%
PER YEARPER YEAR– FOLLOW EVERY 6 MONTHS IN OFFICEFOLLOW EVERY 6 MONTHS IN OFFICE– COUNSEL ON DEVELOPMENT OF COUNSEL ON DEVELOPMENT OF
SYMPTOMS OF ANGINA, CHF, SYNCOPESYMPTOMS OF ANGINA, CHF, SYNCOPE
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AORTIC STENOSIS IN THE AORTIC STENOSIS IN THE ELDERLYELDERLY
OPERATIVE MORTALITY IN THE OPERATIVE MORTALITY IN THE ELDERLYELDERLY– 1.8% AGE < 501.8% AGE < 50– 5.1% AGE 50 - 605.1% AGE 50 - 60– 7.1% AGE 60 – 707.1% AGE 60 – 70
ISOLATED AV REPLACEMENT IN PTS ISOLATED AV REPLACEMENT IN PTS AGE 80 TO 89AGE 80 TO 89– 94% HAD GOOD RESULTS94% HAD GOOD RESULTS– APPROPRIATE SELECTIONAPPROPRIATE SELECTION
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AORTIC INSUFFICIENCYAORTIC INSUFFICIENCY
VALVULAR HEART DISEASEVALVULAR HEART DISEASE
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ETIOLOGYETIOLOGY
¾ OF PATIENTS WITH PURE AI ARE ¾ OF PATIENTS WITH PURE AI ARE MALESMALES2/3 OF PATIENTS FROM RHEUMATIC 2/3 OF PATIENTS FROM RHEUMATIC FEVERFEVER– THICKENING AND DEFORMATION OF THICKENING AND DEFORMATION OF
INDIVIDUAL VALVE CUSPSINDIVIDUAL VALVE CUSPS
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS– VARIOUS PREVIOUSLY DAMAGING VARIOUS PREVIOUSLY DAMAGING
ETIOLOGIESETIOLOGIES
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ETIOLOGYETIOLOGY
PROLAPSE OF AN AORTIC CUSPPROLAPSE OF AN AORTIC CUSP
CONGENITAL FENESTRATIONS OF CONGENITAL FENESTRATIONS OF CUSPCUSP
TRAUMATIC RUPTURETRAUMATIC RUPTURE
ASCENDING THORACIC AORTA ASCENDING THORACIC AORTA DISSECTIONDISSECTION
MARKED AORTIC ROOT DILATATIONMARKED AORTIC ROOT DILATATION
SYPHILIS, ANKYLOSING SPONDYLITISSYPHILIS, ANKYLOSING SPONDYLITIS
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PATHOPHYSIOLOGYPATHOPHYSIOLOGY
MARKED INCREASE IN STROKE MARKED INCREASE IN STROKE VOLUME OF LEFT VENTRICLEVOLUME OF LEFT VENTRICLE– EXTRA BLOOD FROM LEAKING BACK EXTRA BLOOD FROM LEAKING BACK
INTO LV TO EJECTINTO LV TO EJECT
CONTRAST TO MITRAL CONTRAST TO MITRAL INSUFFICIENCYINSUFFICIENCY– AI: EJECTING BLOOD INTO HIGH AI: EJECTING BLOOD INTO HIGH
AFTERLOAD (AORTA)AFTERLOAD (AORTA)– MI: EJECTING BLOOD INTO LOW MI: EJECTING BLOOD INTO LOW
AFTERLOAD (LEFT ATRIUM)AFTERLOAD (LEFT ATRIUM)
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PATHOPHYSIOLOGYPATHOPHYSIOLOGY
DILATATION OF LEFT VENTRICLEDILATATION OF LEFT VENTRICLE– TO MAINTAIN ADEQUATE FORWARD TO MAINTAIN ADEQUATE FORWARD
CARDIAC OUTPUTCARDIAC OUTPUT– COR BOVINUMCOR BOVINUM
REVERSE PRESSURE GRADIENT REVERSE PRESSURE GRADIENT FROM AORTA TO LV IN DIASTOLE FROM AORTA TO LV IN DIASTOLE CAUSES BACK FLOWCAUSES BACK FLOW
ACUTE VS CHRONIC INSUFFICIENCYACUTE VS CHRONIC INSUFFICIENCY
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HISTORYHISTORY
FAMILY HISTORY WITH MARFAN FAMILY HISTORY WITH MARFAN SYNDROMESYNDROME
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
SYPHYLISSYPHYLIS
AWARENESS OF HEARTBEATAWARENESS OF HEARTBEAT
ORTHOPNEA, DOE LATE OR IN ACUTEORTHOPNEA, DOE LATE OR IN ACUTE
ANGINAANGINA
EDEMAEDEMA
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PHYSICAL FINDINGSPHYSICAL FINDINGS
INSPECTIONINSPECTION– BOBBING HEAD OR JARRING OF BODYBOBBING HEAD OR JARRING OF BODY
PALPATIONPALPATION– ARTERIAL JACK HAMMER PULSEARTERIAL JACK HAMMER PULSE– CAPILLARY PULSATIONSCAPILLARY PULSATIONS– VARIOUS SIGNS VARIOUS SIGNS – WIDENED PULSE PRESSUREWIDENED PULSE PRESSURE
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PHYSICAL FINDINGSPHYSICAL FINDINGS
MURMURSMURMURS– DIASTOLIC HIGH PITCHED BLOWDIASTOLIC HIGH PITCHED BLOW– LOUD SYSTOLIC AORTIC EJECTION FLOW LOUD SYSTOLIC AORTIC EJECTION FLOW
MURMURMURMUR– DIASTOLIC RUMBLE DIASTOLIC RUMBLE AUSTIN FLINT AUSTIN FLINT
MURMURMURMURMISTAKEN FOR MITRAL STENOSISMISTAKEN FOR MITRAL STENOSIS
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LABORATORYLABORATORY
EKGEKG
– LEFT VENTRICULAR HYPERTROPHYLEFT VENTRICULAR HYPERTROPHY
WITH STRAINWITH STRAIN
– ECHOCARDIOGRAMECHOCARDIOGRAM
FLOW INTO LV FROM AORTIC VALVEFLOW INTO LV FROM AORTIC VALVE
LV SIZE LV SIZE
FLUTTERING OF MITRAL LEAFLETFLUTTERING OF MITRAL LEAFLET
– BLOOD CULTURES IN ENDOCARDITISBLOOD CULTURES IN ENDOCARDITIS
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TREATMENTTREATMENT
CONGESTIVE HEART FAILURE CONGESTIVE HEART FAILURE TREATMENTTREATMENT– DIGOXIN, DIURETICS, AFTERLOAD DIGOXIN, DIURETICS, AFTERLOAD
REDUCTIONREDUCTIONIV NITROPRUSSIDE MAY BE LIFESAVINGIV NITROPRUSSIDE MAY BE LIFESAVING
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TREATMENTTREATMENTSURGERYSURGERY– SYMPTOMATIC PATIENTS SHOULD BE SYMPTOMATIC PATIENTS SHOULD BE
OPERATED UPONOPERATED UPON– ASYMPTOMATIC PATIENTS FOLLOWED ASYMPTOMATIC PATIENTS FOLLOWED
FOR LEFT VENTRICULAR ENLARGEMENT FOR LEFT VENTRICULAR ENLARGEMENT AND SYSTOLIC DIMENSIONS ON AND SYSTOLIC DIMENSIONS ON ECHOCARDIOGRAMECHOCARDIOGRAM
– YEARLY ECHOCARDIOLOGYYEARLY ECHOCARDIOLOGY– MORTALITY <5% IF GOOD LVMORTALITY <5% IF GOOD LV– MORTALITY 5-10% IF POOR LV FUNCTIONMORTALITY 5-10% IF POOR LV FUNCTION
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