HEART SOUNDSS1, S2

PRANEETH.SPG IN GENERAL MEDICINE

AMC

Cardiac cycle

• The cardiac events that occur from beginning of one heart beat to the beginning of the next are called the cardiac cycle.

• the temporal sequence of events in the cardiac cycle.

• The three basic events are LV contraction, LV relaxation, and LV filling…

Atrial systole• Duration 0.1 sec • During ventricular relaxation

blood flows from atria to ventricles.

• When both atria contracts almost simultaneously and pumps remaining 25% of blood flows in respective ventricles .

• Contraction of atria increases pressure inside atria to 4-6 mmHg in right atrium and abt 7-8mmHg in left atrium.

LEFT VENTRICULAR CONTRACTION.• LV pressure starts to build up when the arrival of

calcium ions at the contractile proteins starts to trigger actin-myosin interaction.

• Soon after, LV pressure in the early contraction phase builds up and exceeds that in the left atrium (normally 10 to 15 mm Hg), followed about 20 milliseconds later by M1.

• The exact relation of M1 to mitral valve closure is open to dispute.

• Although mitral valve closure is often thought to coincide with the crossover point at which the LV pressure starts to exceed the left atrial pressure, in reality mitral valve closure is delayed because the valve is kept open by the inertia of the blood flow.

Isovolumetric contraction• Duration 0.05 sec

• At beginning of this phase AV valve are closed but semilunar valves are not yet opened.

• Volume of blood inside both ventricles remains the same hence this phase is called as isovolumic phase of contraction.

• When pressure in left ventricle is slightly above 80 mmHg and right ventricular pressure slightly above 8 mmHg then the ventricular pressures push the semilunar valves open.

Rapid ejection phase• The duration of this phase is abt

0.11 sec.

• Abt.2/3rd of stroke volume is ejected in this rapid ejection phase.

• The pressure inside the left ventricle rises to 120mmHg during this phase.

• The end of rapid ejection phase occurs at abt the peak of ventricular pressure

• The right ventricle ejection begins before that of left and continues even after the left ventricular ejection is complete.

Reduced ejection phase• Duration 0.14 sec.• Rest one third stroke volume is ejected.

• As the cytosolic ca2+ ion concentration starts to decline because of uptake of calcium into the SR more and more myofibers enter the state of relaxation, and the rate of ejection of blood from the left ventricle into the aorta falls.

• During this phase, blood flow from the left ventricle to the aorta rapidly diminishes but is maintained by aortic recoil, the Windkessel effect. The pressure in the aorta exceeds the falling pressure in the left ventricle.

Protodiastole• At the end of ventricular systole ventricles start

relaxing allowing rapid fall in the intraventricular pressure.

• This is the period of protodiastole which lasts for 0.04 sec.

• At the end of this phase elevated pressure in distended arteries (Aorta and Pulmonart artery) immediately pushes the blood back toward the ventricles which snaps the aortic and pulmonary semilunar valves .

• It also causes dicrotic notch in the down slope of aortic pressure called Incisura.

• Incisura indicates end of systole and the onset of diastole.

Isovolumetric relaxation phase

• The ventricles continue to relax as closed chambers as semilunar valves are closed and AV valves are not yet open.

• This causes rapid fall of pressure inside ventricles (from 80mmHg to abt 2 to 3 mmHg in left ventricle)

• This phase lasts for 0.06 sec.• Because the ventricular volume

remains constant this phase is called isovolumic relaxation phase.

Rapid filling phase• As LV pressure drops below that in the left atrium, just after mitral valve opening, the phase of rapid or early filling occurs to account for most of ventricular filling.• Active diastolic relaxation of the ventricle may also contribute to early filling .• Such rapid filling may cause the physiologic third heart sound (S3), particularly when there is a hyperkinetic circulation.

Reduced filling phase

• After the rapid filling phase,pressure in ventricles rises slowly,

• As pressures in the atrium and ventricle equalize, LV filling virtually stops (diastasis, separation).

2nd RAPID FILLING PHASE• Renewed filling requires that the

pressure gradient from the atrium to the ventricle increase. This is achieved by atrial systole (or the left atrial booster),

• which is especially important when a high cardiac output is required, as during exercise, or when the left ventricle fails to relax normally, as in LV hypertrophy.

PHASES OF CARDIAC CYCLE PHASE DURATION

Atrial systole 0.1 sec

Isovolumic contraction 0.05 sec

Maximal ejection 0.11 sec.

Reduced ejection 0.14 sec.

Protodiastole 0.04sec

Isovolumetric relaxation 0.06sec

Rapid filling phase 0.11sec

Reduce filling phase,diastasis 0.19sec

2nd Rapid filling phase 0.1sec

PHYSIOLOGIC SYSTOLE CARDIOLOGIC SYSTOLE

Isovolumic contraction From M1 to A2, including:

Maximal ejection Major part of isovolumic contraction*

Maximal ejection

Reduced ejection

PHYSIOLOGIC DIASTOLE CARDIOLOGIC DIASTOLE

Reduced ejection A2-M1 interval (filling phases included

Isovolumic relaxation

Filling phases

•cardiologic systole, demarcated by heart sounds rather than by physiologic events, • starts fractionally later than physiologic systole and ends significantly later.

FIRST HEART SOUND

S1

Cause of S1 --theories

• 2 THEORIES• LUISADA et.al• Onset of isovolumetric contraction results in

prominent tensing of LV walls,septum,mitral valve apparatus which produces transient sound

• 2nd audible component due to ejection component coincident with opening of aortic valve

• CRAIGE,LEATHAM et.al• First component reflects sudden tensing of

closed mitral leaflets ,which sets the surrounding cardiac structures and blood into vibration.

• Second component produced due to tricuspid valve

HOW TO LISTEN TO S1• TIMING• Just precedes carotid upstroke• S1 will appear to initiate the outward LV thrust of

apex beat.• CHARACTERISTICS• Medium to high frequency but lower pitch than S2• Q-M1 60ms• Q-T1 90ms• M1-T1 30ms• Splitt s1 can be appreciated in tricuspid area• Loud M1 at apex may mask T1

Split S1

• Tricuspid area• Localised• Low frequency• Not palpable• Best during inspiration

DD of split S1Normal split

S4-S1

S1- ejection clickS1- NEC

S4 Vs Split S1

• Low pitched generally,with bell,localised• Often palpable

• LV S4 is audible at apex in left lateral position,on expiration,isometric hand grip increases

• RV S4 audible at tricuspid area,during inspiration,straight leg raising

When apparent splitting of S1 heard at base we should suspect presence of an ejection sound or early midsysolic click.

• Aortic click• Discrete, snappy • Occur later S1• BEST at aortic area • Heard all over chest• LVH features• Systolic thrill at aortic

area

• Pulmonary click• Better heard in

expiration• Localised to pul area• RVH• Systolic thrill at

pulmonary area

NEC

• Best at apex• Widely audible• High frequency• Not palpable• Loud and earlier on standing

• Intensity normal accentuated diminished variability

• Split

FIRST HEART SOUND Intensity determined by• Structural integrity of mitral valve• Postion of AV valves at time of ventricular

contraction• Integrity of isovolumetric systole • Heart rate• P-R interval • Myocardial contractility

Mitral valve apparatus

ELEMENTS OF MITRAL VALVE APPARATUS

Left atrial myocardium

Annulus Leaflets Subvalvar

apparatus• Chordae tendinae• Papillary muscles LV myocardium

The mitral annulus

• The mitral annulus is a fibrous ring that connects with the leaflets.

• appears to be more D-shaped, rather than circular as prosthetic valves

• The annulus functions as a sphincter that contracts and reduces the surface area of the valve during systole to ensure complete closure of the leaflets. Thus, annular dilatation of the mitral valve causes poor leaflet apposition, which results in mitral regurgitation.

COMMISURES• the mitral valve as a continuous veil inserted

around the circumference of the mitral orifice.• The free edges of the leaflets have several

indentations.• Two of these indentations, the anterolateral

and posteromedial commissures, divide the leaflets into anterior and posterior.

• These commissures can be accurately identified by the insertions of the commissural chordae tendineae into the leaflets

MITRAL LEAFLETS

ANTERIOR LEAFLET• The anterior leaflet is located posterior to the aortic root• large and semicircular in shape. • free edge with few or no indentations.• The 2 zones on the anterior leaflet are referred to as rough and clear

zones, according to the chordae tendineae insertion. • 2 zones are separated by a prominent ridge on the atrial surface of

the leaflet, which is the line of the leaflet closure. • The prominent ridge is located approximately 1 cm from the free

edge of the anterior leaflet.• Distal to the ridge is a rough zone that has a crescentic shape.• During systole or mitral valve closure, the rough zone of the anterior

leaflet will appose to the rough zone of the posterior leaflet.• The rough zone is thick and has chordae tendineae insertions on the

ventricular surface.

POSTERIOR LEAFLET• The posterior leaflet is the section of the mitral valve that is

located posterior to the 2 commissural areas• It has a wider attachment to the annulus than the anterior leaflet. • It is divided into 3 scallops by 2 indentations or clefts. • The middle scallop is larger than the other two. • The 3 zones on the posterior leaflets are referred to as rough,

clear, and basal zones, according to the chordae tendineae insertion.

• The rough zone is distal to the ridge of the line of the leaflet closure.

• Like that of the anterior leaflet, the clear zone has no chordae tendineae insertion. It is located in the middle part of the posterior leaflet, between the rough zone and the basal zone.

• The basal zone is located between the clear zone and the mitral valve annulus.

chordae tendineae• Small fibrous strings that originate either from

the apical portion of the papillary muscles or directly from the ventricular wall and insert into the valve leaflets or the muscle.

• 2 types• Commisural chordae• Leaflet chordae

• Commissural chordae• Commissural chordae are the chordae that

insert into the commissures• Two types of commissural chordae exist.

Posteromedial commissural chordae insert into the posteromedial commissural area; anterolateral commissural chordae insert into the anterolateral commissural area.

leaflet chordae

• the chordae that insert into the anterior or posterior leaflets.

• Two types of chordae tendineae are connected to the anterior leaflet.

• The first is rough zone chordae, which insert into the distal portion of the anterior leaflet known as the rough zone.

• The second is strut chordae, which are the chordae that branch before inserting into the anterior leaflet.

• .

• The posterior leaflet has 3 types of chordae tendineae.

• The first is rough zone chordae, which are the same as that of the anterior leaflet.

• The second is basal chordae, insert into the basal zone of the posterior leaflet.

• The third type of chordae is cleft chordae, these insert into the clefts or indentations of the posterior leaflet, which divide the posterior leaflet into 3 scallops

• Unlike the anterior leaflet, the posterior leaflet does not have strut chordae.

Papillary muscle

• arise from the apex and middle third of the left ventricular wall.• The anterolateral papillary muscle is normally larger than the

posteromedial papillary muscle and is supplied by the left anterior descending artery or the left circumflex artery.

• The posteromedial papillary muscle is supplied by the right coronary artery.

• Extreme fusion of papillary muscle can result into mitral stenosis.

• rupture of a papillary muscle, usually the complication of acute myocardial infarction, will result in acute mitral regurgitation

• Chronically, rheumatic fever leads to commissural fusion, valve thickening, and calcification. The appearance of the mitral valve with shortened, fused chordae and scarred commissures has been likened to the mouth of a catfish (fish-mouth deformity).

S1 in mitral stenosis• Loud snapping s1 is one of the hallmark of MS• Loud s1 is due to

•LA,LV pressure cross over occurs after LV pressure has begun to rise.

•Rapidly increasing LV pressure in early systole contribute to loud s1

•Persistent LA,LV gradient in late diastole keeps the leaflets wide open.

•Increased distance the cusps must travel during their closing motion contributes to loud s1

•Thickened leaflets and chordae may resonate with high amplitude than normal valve.

MS with soft s1

• Extensive mitral valve calcification• Congestive heart failure • Large right ventricle, • Severe pulmonary hypertension• Very mild mitral stenosis• MS plus MR with dominant MR• MS with AR

Integrity of isovolumetric contraction

Rate of rise of LV pressure falls steeply resulting in decreased velocity of closure of mitral valve.

Severe MR Severe ARLarge VSDLV aneurysm

Loud S1 in MR

• Associated MS• MR of MVP • Rheumatic MR with well preserved AML• Severe TR for MS mistaken as MR• Loud ejection click of AS

Myocardial contractility

• INCREASED• Exercise• Hypoglycemia• Thyrotoxicosis• Pheochromocytoma• Drugs—

sympathomimetics,beta2 stimulants

• DECREASED• Myocardial infarction• Myocarditis• Cardiomyopathy• Ventricular dysfunction• Drugs—beta

blockers,CCB’s

Soft S1

• Bradycardia• Prolonged PR interval

• MR• AR – premature closure of MV

• LBBB delayed contraction of LV

Variable S1

• Atrial fibrillation• CHB• Ventricular tachycardia• atrial flutter with varying block• atrial tachycardia with varying block• multi focal atrial tachycardia • Ventricular ectopics

Splitting of S1

• Ebsteins anomaly T1 delayed• ASD• RBBB• LV paced beats

SECOND HEART SOUND

S2

Produced by –

• Sudden deceralation of retrograde flow of blood column in aorta and pulmonary artery when the elastic limits of tensed leaflets are met –create vibration in cardiohemic system.

• MEDIUM TO HIGH PITCHED• 2 components aortic and pulmonary

• A2 P2 Each coincide with incisura of great arterial pressures i.e peak deacceleration of blood mass followed by rebound pressure.

• The time interval from crossover of pressures to actual occurrence of sounds is called

hang out interval.• As aorta has high resistance and low

complaince , recoil from ejected blood is early so less hangout period.

• PA hangout period is 2-5 times more than that of aorta

• PA- 80ms, A-30ms• This difference produces normal split of S2.

• Normal S2 split in inspiration and single sound in expiration

• Split heard in 2-3 left ICS• Frequency both components same• Amplitude A2 > P2• P2 only heard at II left ICS• A2 is heard at Rt II nd ICS,Lt parasternal space,

apex

Normal splitting

Splitting during inspiration

•Decrease in intrathoracic pressure,incresed blood flow to RV,increased RV ejection time

1/3 of split

•Decreased pulmonary venous return , decreased Q-A2 interval

•Decreased pulmonary vascular resistance ,increased hangout period ,increased Q-P2 interval

2/3 of split

Abnormal splitting• Wide &variable splitting• Wide & fixed splitting• Narrow fixed splitting• Reversed / paradoxial splitting• Persistantly single

Wide variable splitting

• Persistant expiratory audible split in upright posture

• Increased Q-P2 interval• Decreased Q-A2 interval

Increased Q-P2 interval

• Pulmonary stenosis• Massive pulmonary embolus• Pulmonary hypertension with RVF• Idiopathic dilatation of pulmonary artery• Pulmonary regurgitation• Late pregnancy, advanced renal failure• Complete RBBB, PVC of LV origin, LV epicardial

pacing, WPW syndrome

Decreased Q-A2 interval

• Severe MR• VSD• Pericardial tamponade• Left atrial myxoma• Pulmonary hypertension with pulmonary

embolism• Minor interventricular conduction defects• Pectus excavatum, straight back syndrome

DD

• S2-OS• S2-Late systolic click• S2-pericardial knock• S2-S3

• S2- OS• Internal to apex• Widely audible • High pitched• Not palpable• No variation with

respiration

• S2—S3

• LVS3 or RVS3• Localised• Low pitch• Palpable

Wide & fixed splitting

•

Failure to increase RV

stroke volume with inspiration

• RVF,• Acute and

chronic pulmonary embolism

• Sev. PAH

RV systole substantially

prolonged

• RBBB with CHF

Simultaneous increase in RV

& LV filling

• ASD

ASD

• Marked increase in pulmonary capacitance prolongs hang out interval to its limit

• RV stroke volume is not influenced by respiratory variation

• Phasic changes in systemic venous return during respiration is associated with reciprocal changes in L -> R shunt

REVERSED OR PARADOXICAL SPLIT• Maximum split in expiration that narrows or

disappears on inspiration.• From base to apex there will be softening of p2• Valsalva maneuver

3 types OF REVERSED SPLIT

Expiratory P2-A2

InspiratoryS2

ExpiratoryP2-A2

InspiratoryA2-P2

ExpiratoryP2-A2

InspiratoryP2-A2

CAUSES OF REVERSED SPLITT

• Left bundle branch block

• Right ventricular pacing

• PVCs of right ventricular origin

• WPW syndrome

• Severe AS• Severe systemic hypertension• Acute MI• Cardiomyopathy• During episode of angina• Severe AR• large PDA• Aneurysm of ascending aorta• Post stenotic dilatation in AS

Pseudo paradoxical split

• Actually s2 split in expiration and inspiration. • But during inspiration COPD patient lung will

muffle P2, • So that single S2 will be heard in inspiration

Narrow splitting

• Ageing• Artifactual muffling of P2• Severe PAH - Hang out interval is encroached

by loss of pulmonary capacitance• Murmur obscuration

Single S2

• Pulmonary atresia• Severe TOF• Tricuspid atresia• TGA• Eisenmenger VSD

with single ventricle

• severe calcified AS• Severe pulmonary

stenosis• Truncus arteriosus

INTENSITY

Intensity is influenced by 1. Pressure beyond the valve2. Flow across the valve3. Size of vessel beyond the valve4. Stenosis of the valve5. Regurgitation of the valve• In AR due to aortic root disease ( syphilis, ankylosing

spondylitis )A2 is accentuated.• In AR due to aortic valve disease ( rheumatic) A2 is

diminished or absent

Causes of loud A2

• Systemic hypertension • Aneurysm of ascending aorta• Aortic regurgitation• Congenital bicuspid aortic valve

Causes of loud P2

• Normal in infants & children• Adults with chest deformity or thin chests• Pulmonary arterial hypertension• Left to right shunts• Hyperkinetic circulatory states

Causes of diminished & absent P2

Diminished P2

• Normal in elderly• Thick chested adults• Pulmonary stenosis• Dysplastic valve

Absent P2

• Tetrology of fallot• Transposition of great

arteries• Truncus arteriosus• Pulmonary atresia• Absent pulmonary valve

• The pulmonic sound is considered accentuated if it is equal to aortic sound in the pulmonary area

• The pulmonic sound is localised to the pulmonary area and the aortic component is widely audible

• Even in the pulmonary area A2 is louder than P2.• Accentuation of pulmonic sound is graded as

mild(+), moderate(++) , severe(+++)

Grading of pulmonic sound intensityGrading of pulmonic sound

basis Correlation to PA pressure

normal Pulmonic sound less than A2

normal PA pressureSystolic < 30Mean 20

Mild or + Pulmonic sound equal to A2

Mild PAH Systolic 30 – 35Mean 20-30

Moderate or ++ Louder than A2 Moderate PAH Systolic 40 – 75Mean 30-50

Severe or +++ Very loud / banging Severe PAH Systolic > 75Mean>50

REFERENCES

• SOMA RAJU CLINICAL METHODS IN CARDIOLOGY

• ABRAMS ESSENTIALS OF CARDIAC PHYSICAL DIAGNOSIS

• EMEDICINE.COM• BRAUNWALD 9TH EDITION

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