Download - Heart Vulvular diseases and heart sounds
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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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