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Topics :Diseases of the heart valves, Heart sounds

Presented by :

Dr Barkam NAGARAJU

MD(General Medicine)

Diseases of the heart valves

Valve regurgitation Congenital Acute rheumatic carditis Chronic rheumatic

carditis Infective endocarditis Syphilitic aortitis Valve ring dilatation

Valve stenosis Congenital rheumatic carditis Senile degeneration

Causes of valve disease

Rheumatic Heart Disease Acute rheumatic fever Chronic rheumatic heart disease

Pathogenesis

Immune-mediated delayed response to infection with specific strain of group A streptococci that possess antigen which cross-react with cardiac myosin & sarcolemmal membrane protein

Ab against the streptococcal Ag mediate inflammation in endocardium,myocardium,pericardium,joint & skin

Fibrinoid degeneration in the collagen of connective tissues

Aschoff nodules –only in the heart

Clinical features

Streptococcal pharyngitis Fever,anorexia,lethargy,joint pain 2-3 wks after initial attack of pharyngitis Arthritis Rashes Carditis Neurological changes

Jones criteria for the diagnosis of acute Rheumatic fever

Major manifestations

Carditis Erythema marginatum

Polyarthritis Subcutaneous nodules

Chorea Minor manifestations

Fever Raised ESR or CRP

Arthralgia Leucocytosis

Previous rheumatic fever First degree AV block

Plus

Supporting evidence of streptococcal infection;recent scarlet fever, raised ASO or other streptococcal antibody titre, positive throat swab culture

Investigations

Positive blood culture Raised antistreptolysin O(ASO)

without evidence of recent streptococcal infection Isolated chorea pancarditis

Carditis

Pancarditis Declines with increasing age (90% at 3yrs-30% in adolescent) Breathlessness Palpitation Chest pain Tachycardia Cardiac enlargement New or changed cardiac murmur

Carditis

Soft MDM(Carey coombs murmur) AR 90% TV & PV rarely involved Pericarditis Cardiac failure ECG –conduction defect,ST-T changes

Arthritis

Early feature Acute,painful,asymmetric and migratory joint

inflammation of the large joints Red, tender & swollen b/t a day & upto 4 wks Characteristically response to aspirin

Skin lesions

Erythema marginatum <5% Red macules which

fade in the centre Remain red at the

edges Trunk & proximities

but not the face May coalesce or

overlap

Subcutaneous nodules 5-7% 0.5-2 cm Firm & painless Extensor surface of

bone or tendon 3 wks after onset of

other menifestations

Sydenham’s chorea(st Vitusdance)

Late neurological manifestation 3/12 after episode of ARF 1/3 of cases More common in females Emotional lability Purposeless choreiform movements of the hands,feet or

face Explosive & halting speech Spontaneous recovery within a few months 1/4 of pts with Sydenham’s chorea –chronic rheumatic ht

disease

Investigations

Evidence of a systemic illness(non-specific)

Raised WBC,ESR,CRP Evidence of preceding streptococcal infection(specific)

Throat swab culture(pt& family contact)

( + ) in 10-25% of cases

ASO titre >200(adults) ,>300(children)

1/5 of cases & most cases of chorea

Investigations

Evidence of carditis

CXR

cardiomegaly,pulmonary congestion

ECG

Features of pericarditis,1st & 2nd Degree ht block, low QRS voltage

Echo;

Cardiac dilatation,Valve abnormalities,

Pericardial effusion

Chronic rheumatic heart disease Mitral valve – more than 90 % Aortic valve Tricuspid valve Pulmonary valve Isolated mitral stenosis-25% Mixed mitral stenosis & regurgitation

Pathology

Progressive fibrosis Predominantly involved heart valves Involvement of pericardium & myocardium

m/contribute to heart failure & conduction disorder Fusion of the mitral valve commissures &

shortening of the cordae tendinae –mitral stenosis+/- mitral regurgitation

Similar changes in other valves

Mitral valve disease

Mitral stenosis

causes Almost always rheumatic in origin Heavy calcification in elderly Congenital

Pathophysiology

In rheumatic MSprogressive calcification of fusion of cups fibrosis the valve leaflet & subvalvular

apparatus

Mitralvalve orifice

restricted flow from LA to LV

pulmonary venous congestion(enlarged LA & LV filling mainly on LA contraction)

Pathophysiology

Increase in heart rate

shortens diastole

Further rise in LA pressure

Demand an increase in cardiac output

Further increase in left atrial pressure

Pathophysiology

MV orifice 5cm2

1cm2 or less in severe MS Remain asymptomatic until MV orifice 2cm2

At first,symptoms occur only on exercise Severe stenosis ; breathlessness at rest Reduced lung compliance due to chronic

pulmonary congestion Low cardiac output ;fatigue

Pathophysiology

Progressive dilatation of the LA

Atrial fibrillation

Tachycardia Loss of atrial contraction

Marked Haemodynamic deterioration with rapid rise in LA pressure

Pulmonary oedema

Pathophysiology

More gradual rise in LA pressure

An increase pulmonary vascular resistance

Pulmonary hypertension

Right ventricular hypertropy & dilation

Tricuspid regurgitation

Rt heart failure

Pathophysiology

In sinus rhythm < 20% Small LA Severe pulmonary hypertension

All pts with MS particularly in those with AF

LA thrombosis

systemic thromboembolism

Clinical features

Symptoms Breathlessness Fatigue Oedema Ascites Palpitation Haemoptysis Cough Chest pain Symptoms of

thromboembolic complications

Signs AF Mitral facies Auscultation;

loud 1st heart soundopening snapMid-diastolic murmur

Signs of raised pulmonary capillary pressurecrepitations,pulmonary oedema,effusions

Signs of pulmonary hypertension

RV heave,loud P2

Investigations

ECG LAH(If not in AF) RVH

CXR Enlarged LA Signs of pulmonary venous

congestion

Echo Thickened immobile cusps Reduced valve area Reduced rate of diastolic

filling of LV

Doppler Pressure gradient across

the mitral valve Pulmonary arterial

pressure LV function

Cardiac catherization Assessment of

coexisting coronary artery disease

&mitral regurgitation

Management

Medical treatment Pts with minor symptoms

Definitive treatment Pts remain symptomatic with medical treatment Balloon valvuloplasty Mitral valvotomy Mitral valve replacement

Medical treatment

Atrial fibrillation Anticoagulant Digoxin B blockers Rate limiting calcium antagonist

Heart failure Diuretics

Prophylaxis of infective endocarditis Antibiotics

Specific management

Mitral balloon valvuloplasty Treatment of choice

Criteria significant symptomsisolated MSno or trivial MRmobile non-calcified valve/subvalve apparatus on echoLA free of thrombus

Specific management

Closed or open mitral valvotomy No facilities or expertise for balloon valvuloplasty s/receive prophylactic antibiotics for IE Follow up 1-2 yrly

Mitral valve replacement

substantial mitral reflux

rigid or calcified

Mitral regurgitation

Causes Rheumatic disease Mitral valve prolapse After mitral valvotomy or valvuloplasty Dilation of LV and mitral valve ring Damage to valve cusps and cordae Damage to papillary muscle Myocardial infarction

Pathophysiology

Chronic Mitral regurgitation

Gradual dilation of the LA

with little in pressure gradual LV diastolic

pressure& LA pressure

No symptoms Breathlessness & pulmonary oedema

Pathophysiology

Acute mitral regurgitation

Rapid rise in LA pressure

Marked symptomatic deterioration

Mitral valve prolapse

Floppy mitral valve Congenital Degenerative myxoematous changes A features of connective tissue disorders

Pathophysiology (MVP)

Mildest form Regurgitation haemodynamically

significant

Competent valve

during systole Infective

endocarditis

Bulge back to LA

Mid-systolic click click followed by Antibiotics

( no murmur) late systolic murmur

Clinical features

Symptoms Breathlessness Fatigue Palpitation Oedema Ascites

Signs AF/flutter/cardiomegaly Auscultation;

apical pansystolic murmur±thrillsoft S1,apical S3

Signs of raised pulmonary venous congestion

(crepitations,pulmonary oedema,effusions)

Signs of pulmonary hypertension & RHF

RV heave,loud P2

Investigations

ECG LAH(If not in AF) LVHCXR Enlarged LA Enlarged LV Signs of pulmonary

venous congestion Pulmonary oedema

Echo Thickened immobile cusps Reduced valve area Reduced rate of diastolic

filling of LVDoppler Detects & quantifies

regurgitationCardiac catheterization Dilated LA,LV,MR Pulmonary hypertension Assessment of coexisting

coronary artery disease

Treatment

Medical treatment Moderate severity

Definitive treatment Pts remain symptomatic with medical treatment Progressive radiological cardiac enlargement or

echo cardiac evidence of deteriorating LV function Mitral valve replacement/repair

Treatment

Atrial fibrillation Anticoagulant Digoxin

Heart failure Diuretics Vasodilators e.g ACEI

Prophylaxis of infective endocarditis Antibiotics

Treatment

Mitral valve repair MVP More advantage > MV replacement Prevent irreversible LV damage Those with CAD-CABG + MV repair by inserting

annuloplasty ring to overcome annular dilation & to bring the valve leaflets closer together

Aortic valve disease

2nd most frequently affected by rheumatic fever Commonly both mitral & aortic valves are affected In elderly structurally normal TV; similar process of

arthrosclerosis in arterial wall Haemodynamically significant AS develops slowly Age 30-60 rheumatic fever

50-60 bicuspid AV

70-90 degenerative AS

Aortic stenosis

Aortic stenosis(AS)

CausesInfants,children,adolscents Congenital AS Congenital subvalvular AS Congenital supravalvular ASYoung adults and middle-aged Calcifications and fibrosis congenital bicuspid aortic valve Rheumatic ASMiddle-aged to elderly Senile degenerative aortic stenosis Calcifications of bicuspid aortic valve Rheumatic AS

Pathophysiology

Steadily increase pressure gradient across the AV

LV increasingly hypertrophied

Inadequate coronary blood flow

Angina

Pathophysiology

Fixed outflow obstruction

limit the increase in CO required by exercise

Effort related hypotension

Syncope

LV can no longer overcome outflow obstruction

Pulmonary oedema

Clinical features

SymptomsMild to moderate-

asymptomatic Exertional dyspnoea Angina Exertional syncope Sudden death Episodes of acute

pulmonary oedema

Signs Slow rising carotid pulse Narrow pulse pressure Thrusting apex beat(LV

overload) Harsh ejection systolic

murmur Soft S2 Signs of pulmonary

venous congestion(crepitations,pulmonary oedema)

Investigations

ECG LVH LBBBCXR Normal Enlarged LV Dilated ascending aorta(PA ) Calcified valve(lateral)Echo calcified valve with restricted

opening Hypertrophied LV

Doppler Severity of stenosis Detection of associated

aortic regurgitationCardiac catheterization Assessment of coexisting

coronary artery disease Pressure gradient b/t LV &

aortaCT/MRI Degree of valve calcification &

stenosis

Management

Asymptomatic Under review

Symptomatic –prompt surgery Moderately severe/ severe stenosis yearly doppler

echo Pts remain symptomatic with medical treatment

Elderly –relatively benign prognosis-medical treatment

Management

AV replacement Severe stenosis with symptoms Asymptomatic - careful exercise test;symptoms on moderate

exertion

Valloon valvuloplasty congenital AS no long term value in elderly pts with calcified AS

Anticoagulants AF Coexisting mitral valve disease Valve replacement with mechnical prosthesis

Aortic stenosis in old patients

Most common form

Syncope,angina,heart failure

Low pulse pressure

Surgery –successful in those aged 80 without co-morbid condition

higher operative mortality

Prognosis without surgery is poor if pt has symptoms

Valve replacement –bioprosthetic valve

Aortic regurgitation

Aetiology Congenital Bicuspid or disproportionate cusps

Acquired Rheumatic disease Infective endocarditis Trauma Aortic dilatation(marfan’s

syndrome,aneurysm,dissectionsyphillis,ankylosing spondylitis

Clinical features

Symptoms

Mild- moderate AR Often asymptomatic Awareness of heart beat

Severe AR Breathlessness Angina

Clinical features

Signs Pulse Large or collapsing pulse Low diastolic pressure&

pulse pressure ,Bounding peripheral pulses

Capillary pulsations in nail beds

Femoral bruit(pistol shot)-duroziez’s sign

Head nodding with pulse De Musset ‘s sign

Murmur Early diastolic murmur Systolic murmur(stroke

volume) Austin flint murmur(soft

mid-diastolic murmurOther signs

Displaced,heaving apex beatpre-systolic impulse4th heart sound pulmonary venous congestion

Investigations

ECG Initially normal Later LVH T wave inversion

CXR Cardiac dilation Features of left heart

failure

Echo Dilated LV Hyperdynamic LV Fluttering anterior mitral

leaflet

Doppler detects reflux

Cardiac catheterization Dilated LV Aortic regurgitation Dilated aortic root Presence of coexisting

CAD

Management

Treat the underlying conditions Aortic valve replacement ±

aortic root replacement & CABGsymptomatic

Chronic AR without symptoms s/report if symptoms are developed Annually f/up with echocardiogram

AVR if evidence of increasing ventricular size If systolic dimension ≥55mmLV dilation

Control BP Nefidipine/ACEI

Tricuspid valve Disease

Rheumatic in origin <5% Always association with mitral & aortic valve disease Isolated TV stenosis very rare TS & TR features of carcinoid syndrome

Tricuspid stenosis

Clinical features and investigations

Symptoms of associated mitral & aortic valve disease Symptoms of right heart failure Raised JVP with a prominent a wave A slow y descent due to loss of normal rapid RV filling A mid-diastolic murmur at LLSE or RLSE High pitch > murmur of MS Increased by inspiration Hepatomegaly Presystolic pulsation (large a wave) Peripheral oedema Echo & Doppler ;similar appearance of mitral stenosis

Tricuspid regurgitation

Causes

Primary Rheumatic heart disease Endocarditis Ebstein’s congenital anomaly

Secondary

Rv dilatation( chronic LHF

RV infarction

Pulmonary hypertension( corpulmonale)

Clinical features

Non-specific symptoms Tiredness Venous congestion A large systolic phase in JVP A cv wave replace normal x descent PSM at LSE Systolic pulsation of the liver

Investigations

Echocardiogram Dilation of the RV Thickened valve Vegetations in endocarditis Ebstein’s anomaly TV displaced towards the RV

apex

with consequent enlargement of the RA

associated with TR

Management

Correct RV overload Normal pulmonary artery tolerate tricuspid

reflux well valve damage dut to IE not always needs valve

replacement repair of the valve with annuloplasty to bring the

leaflets together in patients undergoing MVR those with rheumatic damage m/require Tricuspid

valve replacement

Pulmonary valve Disease

Causes Carcinoid syndrome Usually congenital Isolated or associated with other abnormalities e.g TOF

Pulmonary stenosis

Clinical features

ESM at left upper sternum Radiation to left shoulder Thrill Preceded ejection click Wide split S2 Loud harsh murmur inaudible P2 RV heave Prominent a wave in JVP

Investigations

ECG RVH

CXR Post-stenotic dilation in the pulmonary artery

Doppler echo

Management

Mild to moderate isolated pulmonary stenosis Not usually progress Not required treatment Low risk for IE Severe Pulmonary stenosis ( resting gradient >50mmHg with normal CO) Percutaneous pulmonary balloon valvuloplasty Not available;surgical valvotomy Long term results very good Post operative pulmonary regurgitation is common Benign

Pulmonary regurgitation

Rarely an isolated phenomenon Usually associated with pulmonary artery dilatation due to

pulmonary hypertension EDM at LSE in MS( Graham steel murmur) Pulmonary hypertension

2 to other disease of left heart

primary pulmonary vascular disease

Eisenmenger’s syndrome Trivial PR frequent doppler finding in normal individuals

Heart sounds

Heart sounds are the noises generated by the beating heart and the resultant flow of blood through it. Specifically, the sounds reflect the turbulence created when the heart valves snap shut. In cardiac auscultation, an examiner may use a stethoscope to listen for these unique and distinct sounds that provide important auditory data regarding the condition of the heart.

In healthy adults, there are two normal heart sounds often described as a lub and a dub (or dup), that occur in sequence with each heartbeat. These are the first heart sound (S1) and second heart sound (S2), produced by the closing of the AV valves and semilunar valves, respectively. In addition to these normal sounds, a variety of other sounds may be present including heart murmurs, adventitious sounds, and gallop rhythms S3 and S4.

first heart tone S1[ The first heart tone, or S1, forms the "lub" of "lub-dub" and is

composed of components M1 and T1. Normally M1 precedes T1 slightly. It is caused by the sudden block of reverse blood flow due to closure of the atrioventricular valves, i.e. tricuspid and mitral (bicuspid), at the beginning of ventricular contraction, or systole. When the ventricles begin to contract, so do the papillary muscles in each ventricle. The papillary muscles are attached to the tricuspid and mitral valves via chordae tendineae, which bring the cusps or leaflets of the valve closed; the chordae tendineae also prevent the valves from blowing into the atria as ventricular pressure rises due to contraction. The closing of the inlet valves prevents regurgitation of blood from the ventricles back into the atria. The S1 sound results from reverberation within the blood associated with the sudden block of flow reversal by the valves.[1] If M1 occurs slightly after T1, then the patient likely has a dysfunction of conduction of the left side of the heart such as a left bundle branch block.

The second heart tone S2

The second heart tone, or S2, forms the "dub" of "lub-dub" and is composed of components A2 and P2. Normally A2 precedes P2 especially during inspiration when a split of S2 can be heard. It is caused by the sudden block of reversing blood flow due to closure of the semilunar valves (theaortic valve and pulmonary valve) at the end of ventricular systole and the beginning of ventricular diastole. As the left ventricle empties, its pressure falls below the pressure in the aorta. Aortic blood flow quickly reverses back toward the left ventricle, catching the pocket-like cusps of the aortic valve, and is stopped by aortic valve closure. Similarly, as the pressure in the right ventricle falls below the pressure in the pulmonary artery, the pulmonary valve closes. The S2 sound results from reverberation within the blood associated with the sudden block of flow reversal.

Splitting of S2, also known as physiological split, normally occurs during inspiration because the decrease in intrathoracic pressure increases the time needed for pulmonary pressure to exceed that of the right ventricular pressure. A widely split S2 can be associated with several different cardiovascular conditions, including right bundle branch block, pulmonary stenosis, and atrial septal defect

Third heart sound S3

 Third heart sound Rarely, there may be a third heart sound also called a protodiastolic

gallop, ventricular gallop, or informally the "Kentucky" gallop as an onomatopoeic reference to the rhythm and stress of S1 followed by S2 and S3 together (S1=Ken; S2=tuck; S3=y).

"lub-dub-ta" or "slosh-ing-in" If new, indicates heart failure or volume overload.

It occurs at the beginning of diastole after S2 and is lower in pitch than S1 or S2 as it is not of valvular origin. The third heart sound is benign in youth, some trained athletes, and sometimes in pregnancy but if it re-emerges later in life it may signal cardiac problems, such as a failing left ventricle as in dilated congestive heart failure (CHF). S3 is thought to be caused by the oscillation of blood back and forth between the walls of the ventricles initiated by blood rushing in from the atria. The reason the third heart sound does not occur until the middle third of diastole is probably that during the early part of diastole, the ventricles are not filled sufficiently to create enough tension for reverberation.

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It may also be a result of tensing of the chordae tendineae during rapid filling and expansion of the ventricle. In other words, an S3 heart sound indicates increased volume of blood within the ventricle. An S3 heart sound is best heard with the bell-side of the stethoscope (used for lower frequency sounds). A left-sided S3 is best heard in the left lateral decubitus position and at the apex of the heart, which is normally located in the 5th left intercostal space at the midclavicular line. A right-sided S3 is best heard at the lower-left sternal border. The way to distinguish between a left and right-sided S3 is to observe whether it increases in intensity with inspiration or expiration. A right-sided S3 will increase on inspiration, while a left-sided S3 will increase on expiration

Fourth heart sound

S4 S4 when audible in an adult is called a presystolic gallop or atrial gallop.

This gallop is produced by the sound of blood being forced into a stiff or hypertrophic ventricle.

"ta-lub-dub" or "a-stiff-wall" It is a sign of a pathologic state, usually a failing or hypertrophic left

ventricle, as in systemic hypertension, severe valvular aortic stenosis, and hypertrophic cardiomyopathy. The sound occurs just after atrial contraction at the end of diastole and immediately before S1, producing a rhythm sometimes referred to as the "Tennessee" gallop where S4 represents the "Ten-" syllable. It is best heard at the cardiac apex with the patient in the left lateral decubitus position and holding his breath. The combined presence of S3 and S4 is a quadruple gallop, also known as the "Hello-Goodbye" gallop. At rapid heart rates, S3 and S4 may merge to produce a summation gallop, sometimes referred to as S7.

Atrial contraction must be present for production of an S4. It is absent in atrial fibrillation and in other rhythms in which atrial contraction does not precede ventricular contraction.

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