Clicks & pericardial rub

CLICKS &

PERICARDIAL RUB

Dr. A.Meghana 2nd year P.G

CLICKS Normally AV valves & semilunar valves open

noiselessly. When these valves open noisely clicks occur. Clicks

Ejection Clicks Non ejection Clicks Opening Snaps

(Early systole) (Mid/late systole) (Diastole)

EJECTION CLICKS Sharp, high pitched, early systolic sounds

coincide with carotid upstroke Clicks are arise from : -- Movement of valve cusps -- Dilatation of ascending aorta/main

pulmonary artery -- Normal valve May be aortic or pulmonary in origin. Present in elderly people & is of no significance.

A click is of value in determining whether the obstruction to ventricular outflow is at valvular level,though it may be absent due to rigidity of the cusps.

1.Valvular ejection clicks.a.Aorticb.Pulmonary.2. Vascular ejection clicks.a.Aorticb.Pulmonary.

TYPES OF EJECTION CLICKS

Mechanism: Stenosis or deformity of either semilunar valve

Abrupt doming motion of the valve coming to an abrupt halt at the onset of ejection.

The doming & halting motion seen on echocardiogram coincides with clinically audible click

Valvular Ejection clicks.

Causes of Valvular ejection clicks

Aortic valve• Valvular aortic stenosis

• Congenital bicuspid aortic valve• Congenital quadricuspid aortic valve

as in truncus arteriosus

Pulmonary valve• Valvular pulmonary

stenosis

VASCULAR EJECTION CLICKS

Due to sudden distention of vessel beyond the valve along with the opening movement of the valve.

MECHANISM & SIGNIFICANCE OF VASCULAR CLICKS

MECHANISM SIGNIFICANCE• increased pressure beyond the

valve • Systemic Hypertension  • Pulmonary Hypertension• increased flow across the valve • Hyperkinetic Circulatory States

 • Left to right shunts for

pulmonary side

 • Regurgitation of Semilunar

valves• Dilatation of the vessel beyond

the valve• Dilatation of aneurysm of

ascending aorta

 • Dilatation of pulmonary artery

due to   Increased Flow  Increased pressure  Idiopathic dilation

CAUSES OF VASCULAR CLICKS

AORTIC VASCULAR CLICKS PULMONARY VASCULAR CLICKS

• Systemic Hypertension • Pulmonary Hypertension• Aneurysm of ascending

aorta• Idiopathic dilatation of pulmonary

artery• Aortic regurgitation • Left to right shunts• Tetralogy of fallot • Anemia• Anemia  • Thyrotoxicosis • Thyrotoxicosis

VASCULAR VERSUS VALVULAR CLICKS

FEATURE VASCULAR CLICKS VALVULAR CLICKSecond Heart Sound         

• Intensity • Loud• Diminished or

Normal     

• Split • Normal (Or) Close Split• Abnormal Wide split

or Reversed  (Or) Single S2  • Palpable artery

beyond valve• Often Palpable particularly

pulmonary artery • Impalpable

Commonest congenital anomaly occuring in 2% of the live births.

Its Importance lies in its predisposition to IE & potential development of AS/AR/ both

Click is due to – one cusp being larger than other & mildly incompetent.

EJECTION CLICK OF CONGENITAL BICUSPID AORTIC VALVE

A Loud aortic ejection click may be the only manifestation in the absence of AS/AR.

Best heard with diaphragm of stethoscope. Absence of AS/AR

Click/loud first heart sound

First heart sound louder at base > apex

Ejection click All patients present with fever look for this sign to rule

out IE early.

EJECTION CLICKS OF AORTIC STENOSIS

Classically heard in aortic stenosis of bicuspid valve Intensity correlates with pliability of valve Ejection click occurs earlier as severity of AS

increases & it corresponds to anacrotic wave.

SIGNIFICANCE Best audible at aortic area but it is widely audible Constant, does not vary with respiration Localises the obstruction to the valve. May be absent when the valve is clacified or

immobile Its often mistaken for loud S1. EC- Best heard at base S1- Best heard at apex Premature opening of aortic valve never occurs

(LVEDP > Aortic DP).

In children ejection click always heard in

valvular aortic stenosis

ejection click absent with aortic stenosis obstruction at sub valvular or supra valvular

Adults ejection click absent calcified valves

Calcification of aortic valve is a rule in AS beyond age 40 .

Persistence of aortic valvular ejection click with AS -- milder obstruction

EJECTION CLICK OF VALVULAR PULMONARY STENOSIS

• Best heard at pulmonary area & usually localized to that area only.

• It is decreased in intensity with inspiration - only right sided cardiac event behave in this manner.

• With normal inspiration - PADP decreased and RVDP may remain unchanged as VR increases or may fall due to transmission of negative intra pleural pressure.

• In pul. val. stenosis in inspiration increased VR Right ventricle(RVH) increased RVEDP>PADP Pre mature opening of pulmonary valve in diastole itself Decreased intensity of ejection click

Mild PS - -RVEDP normal -Premature opening of pulmonary valve not

possible -Click may not vary. Moderate to severe PS - -varies with respiration. -better heard only during expiration. -decreased or absent during inspiration. Extremely severe PS - -click may be heard only during expiration or may be absent all together.

Features Aortic click Pulmonary clickSite of best audibility

Conduction

Relation with respiration

Accompanying features

Aortic area

Widely audible

Constant

LVH

•Slow rising carotid pulse•Systolic thrill at aortic area, neck•Reverse split, diminished or absent A2

Pulmonary area

Localized to pul. Area

Variable, better – expiration

RVH

•Prominent a wave in JVP•Systolic thrill at pulmonary area•Wide split S2, with diminished P2

NON EJECTION CLICKS• These are systolic sounds occuring at the AV valves in

prolapse of mitral or tricuspid valves due to myxomatous degeneration of valve.

CAUSES CARDIAC• Mitral valve prolapse

syndrome• Tricuspid valve

prolapse syndrome• Aneurysm of

membranous ventricular septum with VSD

• Ebstein’s anomaly• Severe AR

EXTRA CARDIAC• Left sided pneumothorax• Pleuro pericardial

adhesions• Spontaneous mediastinal

emphysema• Emphysematous bleb or

bullae close to heart• Funnel chest• Sounds produced by

cardiac pacemakers• Artificial valve sounds

FEATURES OF NON EJECTION CLICK

Sharp, high frequency clicky sounds Confined to apex, transmitted widely on

precordium Occurs in middle to late systole Shows respiratory or positional variation or even

in timing from beat to beat Usually single, but multiple clicks also

MITRAL VALVE PROLAPSE SYNDROME

• It’s common clinical syndrome due to diverse pathogenic mechanisms affecting leaflets,chordae tendinae,papillary muscle,annulus.

• Also known as Systolic click syn./Barlows syn./Billowing mitral cusp syn./Redundant cusp syn./Floppy valve syn./Myxomatous mitral valve.

NORMAL MECHANISM• During ventricular systole

left.ven.pres>left.atr.pres

mitral leaflet prolapse into lt.atr

two cusps of leaflets prevents prolapse

Chordae tendinae& papillary muscles

IN MVP• Myxomatous degeneration & elongation of

mitral leaflets(posterior l.let/chordae tendinae)

• mitral valve closes with onset of ventricular systole, further upward movement of valve leaflet into left atrium.

• Sudden halt of the prolapsed leaflets & tensing of the slack & elongated tendinae

• click

DETERMINANTS OF S1-NON EJECTION CLICK

• Based on degree of abnormality of valve, prolapse occur at a particular end diastolic volume of the ventricle - click volume.

• Click volume for individual patients is constant unless the lesion progress

• Determinants 1.left ventricular end diastolic volume

2.rate of left ventricular ejection

• All the maneuvers - VEDV-- degree of prolapse -click occurs late & dec. in intensity

• VEDV - Increase prolapse - click earlier &louder

RELATIONSHIP OF VENTRICULAR SIZE TO DEGREE OF VALVE PROLAPSE

FEATURES• High frequency• Single or multiple• Best heard at apex• Best heard with diaphragm of stethoscope• Click occurs in mid systole & may be followed

by late systolic murmur, characteristically changes in length with posture.

ALTERATIONS IN S1- NEC INTERVAL,EFFECT OF MANUVERS

MANEUVERSDECREASING IN VEN. SIZEa.Standingb.Valsalva phage 2c.Squattingd.Nitroglygerinee.AmylnitrateINCREASING IN VEN.SIZESUPINEEXPIRATIONVALSALVA PHASE4PHENYLEPHRINEPROMPT SQUATTING

S1-NEC S1-MDecreased Decreased

Increased Increased

SITUATIONS - MVP COULD OCCUR

• Young patient with chest pain• Unexplained st-t changes in inferolateral

leads with/without chest pain• Recurrent palpitations/unexplained

atr/ven. arrhythmias• Any patient with fever/syncope• Young patient with stroke• All patients with MR/ASD/MARFANS

SYNDROME/Chest deformity

Systolic / not

Ejection click

Non ejection click

Any associated MR

aortic pulmonary

vascularvalvular

mild moderate severe

valvularvascular

Approach to patient with clicks in systole

FINDING INTERFERENCE

• Changes with posture• NEC• No change with posture• Best heard at aortic

area, widely audible at LSB & APEX

• If aortic, A2 is normal or accenuated,S2 normally split

• If aortic,A2 is diminished,S2 - reversible split

• Non ejection click• MR?• Ejection click,

aortic/pulmonary• Aortic eje. click

• Aortic vascular click

• Aortic valvular ejection click

FINDING INTERFERENCEBest heard at pulmonary area, not widely audible

Loud p2,palpable pul.ar

•Wide split S2,diminished p2,impalpable pul.ar.,systolic thrill at pul.area•Better heard during expiration in standing posture

Pulmonary vascular/valvular click

•Pul. vascular click

•Pul.val .click mild/moderate/severe

•Moderate/severe pul.stenosis

EXTRA CARDIAC SYSTOLIC SOUNDS

o Due to movement of heart in relation to other mediastinal structures.

o Causes• Lt sided pneumothorax - usually evanescent,

particular in later stages of resolving Lt. Pneumothorax; affected by respiration & changes with posture

• Pleuro pericardial adhesions• Spontaneous mediastinal emphysema - peculiar

crunching sounds synchronous with the heart• Emphysematous bleb or bullae

• Funnel chest - sub sternal crunching sounds, arising in joint of 7th costal cartilage with sternum

• Cardiac pace makers - contraction of skeletal muscle

• Artificial valve sounds - vary with type - artificial/prosthetic

DIASTOLIC SOUNDS Opening snap Peri cardial knock Tumour flop Third&Fourth heart sounds

OPENING SNAP• Normally thin AV valves open noiselessly• In diseased ,opening produce clicking

noises -opening snap1.OS due to; AV Stenosis with mobile valve2.OS due to AV abnormality without stenosis• Clinically audible opening snap almost

always means mitral stenosis.

OPENING SNAP OF MITRAL VALVE• MECHANISM• Fibrous thickening & often calcification of margins

of large anterior leaflet, commissures are also fused by fibrosis/calcium.

• Thickening of mitral valve

• High pressure in left atrium (atr > ven) at onset of diastole

• Abrupt doming motion of valve towards left ventricle

• Opening snap

MISSING OS IN MITRAL STENOSIS

Severely calcified mitral valve - lack of mobility of cusps

Significant mitral regurgitation - lack of movement of valve, sec. to impingement on it of regurgitant stream of blood

Severe aortic regurgitation - duration of preceding diastole is long allows high LA pressure to fall

Severe aortic stenosis CAD with LVD

• Any condition associated with LVF• Very close S2-OS (<30ms)• Auscultatory incompetence• Fusion of matting of chordae tendinae & papillary

muscles of LV• OS heard but mistaken for wide split S2

CHACTERSTICS OF OS

• Sharp, high frequency, snappy, clicking character• Site of maximum intensity along left sternal edge

at 4 ICS midway between pulmonary &apical area• Transmitted over wide area i.e basal &

suprasternal notch• Best heard with diaphragm• Accentuated by exercise• in standing position shows wider separation than

usual from S2

• Not change significantly with respiration• Persistence despite presence of AF• Persistence, after mitral valvotomy, in

both calcified & uncalcified stenosis (sub valvular fusion)

• Accentuated S1

BEST WAY TO LISTENING OS

• In classical MS with easily audible OS, auscultate for 20-30 min until you get an audible feel of it.

• Then move away from site of best audibility to site of least audibility when it becomes fainter.

• This is the type sound one hears in a difficult patient with MS - silent MS

TIME INTERVALS OF SOUNDS

• S2 split –inspiration• S2single –expiration• S2 wide split• S2-OS interval• S2-Peri cardial knock• S2-S3 pathological

interval • S2-S3normal -children

• 0.04-0.05 sec• <0.03 sec• 0.06-0.12 sec• 0.04-0.12 sec• 0.10-0.12 sec• 0.12-0.16 sec

• 0.12-0.20 sec

RELATION BETWEEN S2 -OS & SEVERITY OF MS

• Interval between the onset of S2 – OS• The time at which the OS occurs is a function of left atrial

pressures• Left atrial pressure is higher with increasing severity of

MS• Crossover point of pressures, i.e where LA pressure

exceeds LV pressure, occur earlier, closer to A2• S2-OS interval has an inverse relation with severity of

MS in most situations

S2-OS INTERVAL IN VARIOUS DEGREES OF MS

DEGREE OF MS S2-OS LA Pre. MVAcm2 (sec) (mm Hg)• Mild 0.12 15 1.5-2.5• Moderate 0.08 20 1.0-1.5• Severe 0.04 25 <1.5

CONDITIONS WHERE S2-OS IS UNREALIABLE

CONDITION MECHANISM SHORT/WIDENED

• Tachycardia shortening of diastole shortened• Bradycardia prolonged diastole prolonged• Hypertension early aortic closure widened• Aortic regurgitation early aortic closure widen/shortened• Aortic stenosis delayed aortic closure shorten/widened• Low cardiac output lower lt. atr. pressure widened severe RVF severe TR severe PAH• Increased LVEDP obliteration of trans mitral widened CAD gradient cardiomyopathy with sys./dia. dys.

MECHANISMS ALTERING S2-OS INTERVAL

• Alteration in heart rate• Alteration in left atrial pressure• Alteration in LVEDP• Alteration in aortic pressure• Conditions affecting velocity of mitral valve

opening• Aortic regurgitation• Decreased left ventricular compliance• Mitral valve calcification

SOUNDS AROUND S2 MISTAKEN FOR OS

DIFFERENTIAL DIAGNOSIS OF OS Split S2 - loud at apex & lt. sternal border - second component is softer on inspiration - OS - widely split S2 on inspiration, becomes wider on inspiration - OS - standing increases S2-OS interval - S2-soft/muffled -2nd component is not OS, its P2

• Triple heart sound at left sternal border - OS

• Peri cardial knock in constrictive peri carditis

• Tumour flap of left atrial myxoma

• Rarely mitral valve vegetation that moves rapidly from LA to LV ,strikes at base of ventricular septum

OTHER CAUSES OF OS• MR with thickened posterior rigid, normal anterior

leaflet• Primary sub endocardial fibro elastosis, stiffness

& fibrosis of mitral valve• LA myxoma - markedly raised LA pressure• Excessive blood flow through the mitral orifice—

VSD/PDA/TA/TOF—after blalock taussig shunt• Prolapse of mitral valve with click/click & systolic

murmur• Massive ascitis - heart striking against diaphragm• Gargoylism - with involvement of heart• Congenital MS - Abnormal leaflets-no pliable bellies

OPENING SNAP OF TRICUSPID VALVE

• Rare• Best heard at lower end of sternum/along

its right border • Seen in - TS with MS & Mitral snap - ASD with left to right shunt - Chronic constrictive pericarditis

OS—AV ABNORMALITY WITHOUT STENOSIS

MITRAL OPENING SNAP• MR• MVP• VSD• PDA• 2&3 degree heart block• TA• TOF after shunt• Thyrotoxicosis• HOCM(valve thickening)

TRICUSPID OPENING SNAP• ASD• TR

CONFUSION AROUND S1&S2

SOUNDS AROUND S1

SOUNDS AROUND S2

PERI CARDIAL KNOCK Sharp, high pitched sound Heard in early diastole Occurs 0.10 - 0.12 sec. after S2 Best heard with diaphragm at lower left sternal border Seen in constrictive pericarditis Corresponds to abrupt cessation of ventricular expansion after AV valve opening & prominent y - descent in JVP

TUMOUR FLOP• Seen in atrial myxomas• Arise from diastolic prolapse of tumour across the

mitral valve• Loud and low frequency• Only heard in certain positions• Mostly myxomas cause no sounds• MITRAL VALVE VEGETATION• Physical movement of veg. across mitral valve

apparatus• Heard with diaphragm of stethoscope in left lateral position

Pericardial Rub• Hallmark of the pericardial inflammation • Mechanism - Parietal and visceral surfaces of pericardium

moving against each other.

Importance

• Valuable diagnostic sign in acute pericarditis.

• If loud it may mask underlying important murmurs.

• When confined to one phase of cardiac cycle, confused with cardiac murmurs.

Characterstics

• Quality - extremly variable even in same case

i.e., varying from a soft, blowing, murmur like sound to extremely harsh, loud, rubbing, leathery, scracthy sound. “ like two pieces of sand paper rubbing against each other”.

• Timing - Although synchronous with heart beat, does not

coincide strictly with the systole or diastole. It is Uni/bi/tri phasic in timing . 3 components when heard , they are related to

the movement of heart during Ventricular Systole.Atrial Systole.Rapid ventricular filling phase.

Frequency order: most audible component Ventricular Systole > Atrial Systole > Rapid

ventricular filling phase.

• To and fro rub is the most common and it is due to ventricular systolic and Atrial systolic components.

• The three component rub is audible in less than half of the cases.

• Single component rub is very rare and it is seen In setting of Atrial Fibrillation or resolving stage of pericarditis.

• Site of maximum intensity – best heard over 2nd and 3rd left interspaces over

bare area of the heart.• Transmission – seldom transmitted remaining localized to a small area. “ if loud, heard in back and neck “• Constancy -

Inconstancy is a striking feature .The intensity, character, site of audibility , and duration of Rub may vary from day to day. It is usually transitory or evanescent, persisting for a few days of hour only.

• Relation to posture - it is louder in upright than recumbant position. increased by bending or stooping forward. palpable fremitus or rub on palpation i.e., felt

as well as heard. Intensity and clarity of sound increases with

pressure of Auscultatory chestpiece, in childern and thin chested individuals, best heard with diaphragm• Relation to respiration -

variable, usually better heard with held inspiration.

When to check for pericardial rub

Significance of pericardial friction rub after acute MI

• It indicates transmural MI• Contra indication to anti coagulant

therapy.• Cause of persistant pain following MI.• May be the cause for post MI fever.• Prompt relief with steroids.

Differences between Pleural friction and Pericardial

friction RubPleural friction • Independent of

cardiac rhythm• It conforms to the

respiratory movements.

• Grossly affected by respiration and cessation of breathing.

Pericardial friction• Related to cardiac

rhythm.• Not conforms to

respiratory movement.• Not affected.

Pleural rub

Pericardial rub

Difference between pericardial rub and

murmur.

• Pleuro pericardial friction - when Pleural friction in dry pleurisy affects the anterior margin of the lung, adjacent to the heart, pleural friction sounds may conform to the cardiac rhythm instead of the respiratory movements.

The sounds occur with the beating of the heart, they disappear on deep inspiration, expiration or holding the breath.

Differential diagnosis of pericardial rub

• Systolic Murmur (single component rub)• To and fro murmur (biphasic rub)• Early diastolic murmur of aortic regurgitation.• Continuous murmur• Artifact• Hammans sign (mediastinal Emphysema)• Ebstein anomly of tricuspid valve.• Tricuspid stenosis • Right atrial tumor producing RV inflow

abstruction.• Means – Lermann scratch in thyrotoxicosis.