Yusra Pintaningrum

SMF Kardiologi dan Kedokteran Vaskular

FK Universitas Mataram –RSUP NTB
 Valvular
 Rheumatic : almost all cases
 Congenital : isolated lesion or associated with ASD
(Lutembacher syndrome)
 Mucopolysaccharidoses
 Endocardial fibroelastosis
 Prosthetic valve
 Malignant carcinoid
 Inflow obstruction
 Left atrial myoma
 Left atrial ball valve thrombus
 Hypertrophic obstructive cardiomyopathy
 Cor triatriatum
 THICKENED MITRAL CUSPS
 +/- CALCIFIC DEPOSITS
 FUSION OF VALVE COMMISSURES
 SHORTENING OF CHORDAE WITH FUSION
 “FISH MOUTH” OR FUNNEL ORIFICE
1. Dyspnoea on effort
 Reduces compliance of the lung, rising left atrial
pressure is transmitted to pulmonary veins.
 PULMONARY EDEMA
 Effort, emotional stress, infection, fever, pregnancy

2. Fatigue  low cardiac output

3. Haemoptysis  ec. Bronchial vein rupture, alveolar
capillary rupture (pink frothy sputum), pulmonary
infection
4. Systemic emboli
5. Chronic bronchitis  ec. Oedematous bronchial mucosa
6. Chest pain  RV hypertrophy secondary to
pulmonary hypertension; coronary embolism
7. Palpitation : AF
8. Symptoms of right heart failure
9. Symptoms of LA enlargement compressing
10. Infective endocarditis
 ACCENTUATED S1

 OPENING SNAP
 SUDDEN TENSING OF VALVE LEAFLETS
 A2-OS INTERVAL SHORTENS WITH SEVERITY
 DIASTOLIC MURMUR
 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
 SYMPTOMATIC PATIENTS
 ACTIVITY RESTRICTION
 ORAL DIURETICS
 BETA BLOCKERS
 DIGOXIN IN AF
 ANTICOAGULATION FOR LA SIZE >5.5cm,
EMBOLISM OR ATRIAL FIBRILLATION
 Closed mitral valvotomy
 Open mitral valvotomy
 Mitral valve replacement
MITRAL INSUFFICIENCY
1. INFLAMMATORY
2. DEGENERATIVE
3. INFECTIVE
4. STRUCTURAL
5. CONGENITAL
 RHEUMATIC HEART DISEASE
 ACUTE RHEUMATIC FEVER VS CHRONIC
 SYSTEMIC LUPUS ERYTHEMATOSUS
 SCLERODERMA
 MYXOMATOUS DEGENERATION OF LEAFLETS
 MITRAL VALVE PROLAPSE
 MOST COMMON CAUSE OF ACUTE MR IN US
ADULTS
 MARFAN SYNDROME
 CALCIFICATION OF MV ANNULUS
 RUPTURED CHORDAE TENDINAE
 RUPTURE OR DYSFUNCTION OF PAPILLARY
MUSCLES
 DILATATION OF MITRAL VALVE ANNULUS
 PARAVALVULAR PROSTHETIC LEAK
 VALVE LEAFLETS
 ANTERIOR AND POSTERIOR
 MITRAL ANNULUS
 DILATATION
 CHORDAE TENDINAE
 PAPILLARY MUSCLES
 Mild MR  asymptomatic
 Acute MR  small LA  acute pulmonary oedema
 Chronic MR  large LA
 CAROTID UPSTROKE SHARP, RAPID FALLOFF
 S1 USUALLY SOFT, WIDELY SPLIT S2
 HOLOSYSTOLIC MURMUR
 APEX TO AXILLA
 SYSTOLIC EJECTION MURMUR
 ISCHEMIC MR
 CARDIOMEGALY (ECCENTRIC HYPERTROPHY)
 LEFT ATRIAL ENLARGEMENT
 AFTERLOAD REDUCTION
 REDUCES IMPEDENCE TO EJECTION IN AORTA
 ACE INHIBITORS AND HYDRALAZINE
 ACUTE MR
 IV NITRAT / NITROPRUSSIDE CAN BE LIFESAVING
 DIGOXIN, DIURETICS IN CHRONIC MR
 FOLLOW LV SIZE AND FUNCTION
 OPERATE FOR SYMPTOMS
 ENLARGING LEFT VENTRICULAR SYSTOLIC
DIMENSION , 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
 Aortic valve stenosis
 Hypertrophy cardiomyopathy
 VSD
 Papillary muscle diysfunction
 Tricuspid regurgitation
AORTIC STENOSIS
 HYPERTROPHIC CARDIOMYOPATHY
 SUPRAVALVULAR
 SUBVALVULAR
 CONGENITAL : bicuspid valve
 ACQUIRED : rheumatic, degenerativ e,
atherosclerosis
 ANGINA
 MEDIAN SURVIVAL 5 YEARS
 SYNCOPE
 MEDIAN SURVIVAL 3 YEARS
 CONGESTIVE HEART FAILURE
 MEDIAN SURVIVAL 2 YEARS
Increased demand Decreased supply
 Increased cardiac work  Prolonged systole with
shorter diastole
 Increased muscle mass  Reversed coronary flow in
from hypertrophy systole from the venturi effect
of narrow valve orifice
 Increased wall stress  High intramural pressure in
from high intracavity systole preventing systolic
coronary flow
pressure  Low aortic perfusion pressure
in diastole with high Left
Ventricle End Diastolic
Pressure
 PULSUS PARVUS AND TARDUS
 IN CAROTID PULSE
 REDUCED PULSE PRESSURE
 SUSTAINED CARDIAC IMPULSE
 DELAYED A2 OR DIMINISHED
 HARSH SYSTOLIC EJECTION MURMUR : heard base
left sternal edge, aortic area, carotids
 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
 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
 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
 congenital acquired
 Valve disease  Rheumatic fever
 Infective endocarditis
 Bicuspid valve  Rheumatoid arhtritis
 Supravalvular stenosis  SLE
 Discrete subvalvar  Hurler syndrome and other
mucopolysaccharidoses
fibromuscular ring  Hypertension
 Supracristal VSD with  Cystic medial necrosis eg.
prolapse or right Marfan syndrome
 Osteogenesis imperfecta
coronary cusp
 Giant cell aortitis
 Aortic root disease  syphilis
 Results in an increase in LV end-diastolic volume
(LVEDV) and end-systolic volume (LVESV)
 The stroke volume (SV) is high in compensated cases
 LV mass is raised with LV hypertrophy
 FAMILY HISTORY WITH MARFAN SYNDROME

 ORTHOPNEA, Dyspnoe on effort

 ANGINA
 EDEMA
 INSPECTION
 BOBBING HEAD OR JARRING OF BODY (de musset’s
sign)
 PALPATION
 WIDENED PULSE PRESSURE
 Duroziez’s sign : to-and-fro murmur audible over
femoral arteries
 Quincke’s plse : capillary pulsation in fingertips or
mucous membranes
 Traube’s sign :”pistol-shot” sound audible over femoral
arteries
 MURMURS
 DIASTOLIC HIGH PITCHED BLOW : LSB
 LOUD SYSTOLIC AORTIC EJECTION FLOW MURMUR
 DIASTOLIC RUMBLE AUSTIN FLINT MURMUR
 MISTAKEN FOR MITRAL STENOSIS
 EKG
 LEFT VENTRICULAR HYPERTROPHY
 WITH STRAIN
 ECHOCARDIOGRAM
 FLOW INTO LV FROM AORTIC VALVE
 LV SIZE
 FLUTTERING OF MITRAL LEAFLET
 BLOOD CULTURES IN ENDOCARDITIS
 CONGESTIVE HEART FAILURE TREATMENT
 DIGOXIN,
 DIURETICS,
 AFTERLOAD REDUCTION
 IV NITROPRUSSIDE MAY BE LIFESAVING
 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