Without echocardiography is like traveling on a horseback ... · Without echocardiography is like...
Transcript of Without echocardiography is like traveling on a horseback ... · Without echocardiography is like...
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Diagnosis of valvular heartdisease
Without echocardiography is
like traveling on a horseback or at
best on a steam train
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Echocardiography
2D
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Diagnosis of valvular heart desease
�Aortic valve disease
–Aortic stenosis
� congenital (bicuspid) (50% <70years)� rheumatic (commissural fusion)� degenerative (calcification) (50% >70 years)
–creates resistance to ejection� the normal orifice=2-3 cm2, reduction leads to systolic pressure drop "gradient" between the LV and aorta:LV pressure load
concentric hypertrophy, compliance
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Clinical symptoms (AS)Fenyvesi
�1.Chest pain ,angina pectoris�2.Effort syncope :"graying out" or loss of con -
sciousness. At times a few minutes after the patient stops the exercise.
�3.heart failure, eventual depression of contractility ,dilatation of LV
�4.Sudden death (SCD) , arrhythmia
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Physical examination(AS) �Auscultation
–diamond shaped ejection murmur ending before S2,P.max in the aortic area� transmitted to the carotid, thrill may be
palpable� may be musical at the apex� differenciate from pansystolic:shape and S2
–Ejection click : "blah" ,"butter"� after the onset of S1 0,03-0,06 s, valvular upward tensing of a mobile cusp, rare after the third decade of life
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S2 soft the "absent A2" is only an illu-sion ,caused by the very loud murmurprolonged LV systole may causeparadox splitting of S2
S4 very common caused by LV hyper-trophy
S3 only in heart failurePulse parvus et tardus, a concomitant
AR can "normalize" itBlood pressure : narrowed pulse
pressure
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Apex impulse :presystolic apical simul-taneously with S4
not dysplaced, not hyperkinetic , a pro-longed outward thrust in 2/3 of systole
Physical signs of AS not reliable for seve-rity-even with chest Rtg and ECG
Echocardiography :LV thicknessvalve areaDoppler gradient
Catheterization, difficulties,peak-to-peakversus maximal gradient!
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Calculating pressure gradients across stenotic valves
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AS natural courseAS natural course
Ross, Braunwald Circ. 1968.
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AS Aortic valve area< 1cm2
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Aortic regurgitation
�Valve incompetence : diastolic flow of bloodfrom the aorta into the left ventricle
�Major causes:� in the past :rheumatic fever, syphilis (!)� recently :connective tissue diseases� ankylosing spondylitis� rheumatoid arthritis� the Marfan -syndrome� acute form:bacterial endocarditis�Pathology :disease of the aorta or of the valve
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Pathopysiology: volume load, LVdilatation if not accompanied byincrease in wall thickness it leadsto increased wall stress
extreme increase in stoke volumeClinical symptoms:
asymptomatic for many years symptoms of LV failure : fatigue,
dyspnea,oedema more specific : palpitation, pulsation in
the neck, dizziness
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Physical signs in AR i
�The peripheral circulation–Pulse :celer et altus (Corrigan's pulse)–Duroziez' murmur :a biphasic bruit over any
larger arteryTraube sign : booming syst and diast sound
–capillary pulsation (Quincke)–uvula pulsation (Müller's sign)–Musset's sign :bobbing of the head with each
pulsation–Hill's sign :an exaggerated difference between
popliteal and brachial blood pressure> 60 mmHg
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Blood pressure
Extreme widening of the pulse pressurediastolic approaching zero
Apex impulsedisplaced down and to the left , hyperdynamic,a prolonged diastolic
filling wave
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Auscultation of AR
�Murmurs :–protodiastolic ,high pitched,p.max left sternal � border,"safety belt radiation",the patient
must stop breathing-sitting leaning foreward–systolic ejection murmur --increased stroke
volume–diastolic rumble :the Austin Flint murmur–S1 normal, possible systolic click–S3 is a rule in A.R.
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protodiast
Compare With AS
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severe AIsevere AI
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Chest X -ray dilatation of the LV, elongation ofthe apex inferiorly and posteriorlydilatation of the ascending aorta
Echocardiographyanatomical information on the valveLV chamber dimensionsflow-regurgitation Doppler measure-
mentnon-invasive haemodynamics
Cardiac catheterizationinvasive haemodynamics coronary arteries
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Calculating pressure gradients across stenotic valves
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Mitral stenosis
�Resistance to flow through the mitral apparatus during diastolic filling of the left ventricleMajor causes :� recurrent rheumatic
endocarditis� congenital� calcification(valvular or annulus)� thrombus� myxoma
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Mitral stenosis
Pathology :� commissural adhesions and fusion � chordal scarring and contraction � resulting in a funnel shaped structure
the orifice area is reduced from the normal 4-6 cm2 to < 1,5
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Pathophysiology
A pressure gradient is created between the left atrium and LV LA pressure
pulmonary veins capillaries PAright heart (disproportionate pulmonary hypertension) RV
hypertrophy
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Clinical symptoms :
dyspnoe(paroxysmal) ,fatigue,palpitation(due to atrial fibrillation) systemic or cerebral embolismchronic RV failure,haemoptoechest pain
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Physical examination(MS)
No specific general signs"mitral facies„
• Inspection of the face:
„For by his face straight shall you know his heart”
Shakespeare, King Richard III
Act III, scene IV-53
PalpationApex impulse:usually normal,RV hyper-
trophy may cause sustained parasternal lift in systole
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Physical examination(MS)
Auscultation : one of the most fascinating sound-murmur combinations
1.Accentuation of S1: the M1 is late (Q-S1)because of increased LA pressure
The sudden halting of the valve at itsupward motion happens at a higherrate of LV pressure rise
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2.Opening snap (OS)at the maximal excursion of the anterior
mitral leaflet.The higher the atrial pressurethe shorter the A2 -OS
P.max; lower sternal areaglossary of time intervals:
"blah" 0.03 s"butter" 0.06"d -t" 0.08"pa -pa" 0.12
3.Diastolic rumblep.max apex , lying on the left side or
just turninglow pitched
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opening snap
Mitral stenosis auscult
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4.Presystolic accentuation of the diastolic murmur. Atrial systole is the most acceptedexplanation: no if AF ?!or a high velocity antegrade flow thru a progressively narrowing mitral orifice during early ventricular systole
5.in some cases pulmonaryregurgitant murmur caused by thepulmonary hypertension:
Graham Steell murmur
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ECG dr.Fenyvesi
"mitral " P wave, n otched P in II and a negative deflection in V1AF is common
Chest Roentgenogramleft atrial enlargement with LA appen-dage straightening of the leftcardiac border on the p-a chest filmpulmonary venous alterationsprominent pulm arteryright ventricular enlargement
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LA bulginginto the eso-phagus
a convexleft atrialborder
LA appendage
Chr interstitpulm edema
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EchocardiographyThe most reliable diagnostic techniqueanatomical diagnosis:
leaflet movementorifice size and area
noninvasive haemodynamics: Dopplerestimate of diastolic gradientLV function
Catheterization"standard" technique, now notnecessary, except over age of 4o-45?to exclude coronary artery diseasebefore surgery
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Mitral regurgitation
� occurs when contraction of the left ventricle ejects blood into the left atrium as a result of abnormalities of the mitral apparatus
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Mitral regurgitation
Major causes :�rheumatic fever�coronary heart disease: myocardial
infarctionLV dilatation,papillary muscle dysfunction
�mitral valve prolapse : the most common cause
�bacterial endocarditis :rupture,penetration
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Pathopysiology
Volume overload on the LV and LAsystolic elevation of
LA, PV and P capillary pressuredilatation of LV to accomodate stroke volume
( the diastolic filling volume of LV:1.syst output of RV +2.amount of previous regurgitant
volume)
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In early rapid filling S3! "diastolic gallop"
LV wall thickeningIn coronary heart disease impairedmuscle function and LV shape m.r.
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Fenyvesi
Physical examinationLV impulse is displaced downward
and to the left,hyperdynamicParasternal impulse i s caused by
the filling of a large left atriumDiastolic impulse is felt at the apex
simultaneously with the S3
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Auscultation in MI
�Holosystolic murmur : high pitched,radiates to the left axilla
�S1 is usually diminished,the systole is shortearly A2 splitting of S2
�S3 a "protodiastolic gallop" high velocity rapid filling of LV
�In mitral prolapse a midsystolic click late systolic murmur is characteristic
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ECG signs of LA and LV enlargement in CHD signsin prolapse :ST-T changes,QT
prolongation,T negativity in infe-rior leads
Chest Roentgenogramin chronic MR LV and extreme LA enlargement double contour along the right border in prolapse normal
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LA
RA
Straightening of the left heart border
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Echocardiography Fenyvesi
Mitral regurgitationValve anatomy :thickness,calcification
of the mitral apparatus, valve areaValve motion
Noninvasive haemodynamics :assess-ment of regurgitant volumeDoppler techniqueLV function
Prolapse direct evidence:billowing leaf-lets, myxomatous degeneration
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Mitral stenosis and regurgitation
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Cardiac catheterization decreasing significance with new echo techniques
quantitation of mitral regurgitation,left atrial sizeLV functionlarge V wave on "wedged pressure"
curveCoronary anatomy
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Mitral prolapse syndrome
idiopatic(?) or familial autosomal,dominant
The “systolic click-murmur” noticed long ago, but considered of extracardiacoriginP.D. White 19311st descriptionBarlow J.B. 1966detailed analysis ofpathophysiology
„Barlow syndrome”Extrasystolia , syncope
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Clinical symptoms of M R are present
Well tolerated for many yearsfatigue, dyspnea, palpitations, chestdiscomfort, anxiety,"panic syndrome"(?)
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Dynamic: auscultation
Decrease of LV volumemoves prolapse earlier in systole
Increase of LV volumemoves prolapse andclick-murmur later
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TEE echo posterior mitralleaflet prolapse
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Posteriorly oriented MI jetrestricted posterior leaflet Posteriorly oriented MI jetrestricted posterior leaflet
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Mitral valve prolapse
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Mitral prolapse , high grade mitral regurg
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Tricuspid valve disease Tricuspid stenosis
�Rheumatic etiology, never isolated -in 14% of all–rheumatic autopsies,high prevalence in India–usually associated with MS,female !
�Pathophysiology:right atrial-right ventricular � pressure gradient on inspiration
– in sinus rhythm giant atrial "a" wave,–decreased cardiac output
�Clinical symptoms:fatigue,hepatomegaly,ascites, –edema(and patient conspicuously lying flat), –pulsation in the neck(venous)–suspicion of MS, but no pulmonary congestion
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Physical signs:increased venous pulsation in the neck
OS after a mitral OS, p.max left parasternal
harsh presystolic murmurdiastolic murmur and OS inspiration
ECG :right atrial hypertrophy P II and V1greater than 0,25mVoften combined MS wide P II,III,
aVF and +- V1Chest X-ray:enlarged right atrium,widesuperior vena cava, no pulm.engorgement
Echocardiography: direct evidence
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Fenyvesi
Tricuspid regurgitation Usually not a primary valvular disease:
right ventricular dilatationpulmonary hypertension "functional"mitral stenosis TIcor pulmonale
or valvular pathology:Ebstein's anomalyrheumaticmyxomatous degenerationendocarditiscarcinoid syndrome
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Clinical symptoms of TRDecreased cardiac output "right sided
heart failure", usually accompanies mitral disease, thus may alleviate symptoms of left-sided heart failure(as pulmonary congestion,dyspnoe..)
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Physical signsJugular veins dilated, no “x“ descent, +”r„
“v„ and “y„ see figure !!right ventricular impulse
Liver enlarged, pulsatingS3 on inspiration, P2 !Pansystolic murmur,p.max 4th interspace
on inspiration :Carvallo sign
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Prosthetic cardiac valves
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87Medtronic-Hall St.Jude Carbomedics
Starr-Edwards 1960!! Omniscience
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Hancock porcine Carpentier-Edw pericardial
cryopreserved homograft
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A University should be
a place of light
of liberty, and of learning.Benjamin DISRAELI, 1873
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