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1 Diagnosis of valvular heart disease Without echocardiography is like traveling on a horseback or at best on a steam train
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Without echocardiography is like traveling on a horseback ... · Without echocardiography is like traveling on a horseback or at best on a steam train. 2 Echocardiography 2D . 3 Diagnosis

May 30, 2020

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Page 1: Without echocardiography is like traveling on a horseback ... · Without echocardiography is like traveling on a horseback or at best on a steam train. 2 Echocardiography 2D . 3 Diagnosis

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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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54

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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68Venous return decreases, hence LV volume also

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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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