Heart sounds –origin,normal& abnormal

Dolly mathew

• Brief discrete auditory vibrations charecterized by intensity(loudness),frequency(pitch),& quality

• high frequency sounds – related to opening :OS, ES Closure sounds-S1,S2• Low frequency sounds - early & late diastolic

filling events of the ventricle

S1 – 4 sequential components (phono)

• Small frequency vibrations, coincides with the beginning of LV contraction- felt to be muscular origin

• High frequency M1• High frequency T1• Small frequency vibrations coincides with

acceleration of blood into the great vessel

First heart sound - M1T1• Sudden tensing of MV leaflet after closure of

mitral valve, which sets the surrounding cardiac structures including the blood into vibrations

• Complete coaptation of valve leaflets& final tensing are not simultaneous

• Final tensing responsible for M1

Factors affecting s11. structural integrity of valve : • inadequate coaptation of mitral valve - soft S1 (severe MR )• Loss of leaflet tissue – soft S1 (IE)• thickness & mobility of the valve In mild- mod MS, the increased LA pressure causes the mobile

portions of the mitral valve leaflets to be more widely separated accentuated M1

The stiff noncompliant leaflets & chordae tendinae appear to resonate with increased amplitude

• Calcified mitral valve( long standing MS) immobilizes the valve- soft S1

2. velocity of the valve closure: determined by the position of mitral valve at the onset of ventricular systole

• Position of mitral valve is altered by relative timing of atrial & ventricular systole( PR interval )

• Long PR longer diastolic filling timeLV pressure gradually increases mitral valve leaflets slowly drift together lesser distance between leaflets

• Short PR mitral leaflets are farther apart at the onset of ventricular systole closes with a high velocity large excursion

• Longer PR(180-500ms)- ventricular contraction accelerate blood towards the AV valve only during the time required to stretch the closed valve to its elastic limit

• the rate of ventricular pressure development is negligible & insignificant VA pressure gradient

• when PR markedly prolonged (>550ms) re opening occurs due to continuing blood inflow from pulmonary arterial to venous bed

• The valve is open at the onset of ventricular systole,s1 loud

• Short PR – valve cusps are in their most divergent position when ventricular contraction begin, ventriculoatrial pressure gradient greater, louder s1

• Very short PR- atrial systole coincides with ventricular systole, diminishing the VA gradient at the time of AV valve closure- s1 soft/ inaudible

3. Status of ventricular contraction• Increased myocardial contractility increases the rate

of LV pressure(dP/dt) – loud S1 ( Exercise, high output state)• Decreased dP/dt – soft S1 (A/c MI, myocarditis)• Loss of isovolumic contraction- decreases dp/dt-

decreased velocity of mitral valve closure - soft S1 MR ,large VSD - S1 may be masked by the murmur - loss of isovolumic contraction decreased dp/dt

4. Heart rate • Tachycardia- loud s1• Reasons – short PR interval - wide opened valves due to short

diastole - increased myocardial contractility

5. Transmission characteristics of thoracic cavity & chestwall

-Obesity, emphysema,pericardial effusion decrease the intensity of all auscultatory events

-Thin chest wall increases the intensity

conditions causing Loud S1 (M1) • MS-thickened mobile leaflets, high LA pressure• Interval from LV-LA pressure crossover to mitral valve closure is

same as in normal state, rate of ventricular pressure development (dp/dt) during this period is higher

• MVP ( non rheumatic MR): holosystolic prolapse – S1 loud- due to delay in checking action of mitral valve caused by increased valve displacement

• increased amplitude of leaflet excursion, • summation of normal M1& nonejection click • Exercise – tachycardia induced short PR -Increased LV contractility - increased flow across the valve

Loud T1

• TS• ASD - increased tricuspid flow

• Anomalous pulmonary venous connection - increased tricuspid flow

Soft S1

• MR- decreased mobility, poor coaptation, loss of isovolumic contraction

• Some of the energy of ventricular contraction may be spent developing kinetic energy responsible for the regurgitant flow, diminishing the rate of rise of intraventricular pressure

• Calcific MS- immobility of mitral valve

• Severe AR- - pre closure of mitral valve as a result of rapid

increase in the LV filling pressureIn a/c AR, aortic pressure markedly reduced, LV

pressure markedly elevated, leading to equilibration of pressure at the onset of LV systole

Since the energy of ventricular contraction is immediately converted into kinetic energy in the form of aortic transvalvular flow, the energy producing the mitral valve displacement is reduced

• LBBB- delay in onset of LV contraction- delayed M1

- decreased LV contractility - concomitant 1st degree AV block - presence of noncompliant LV leading to

preclosure of mitral valve• a/c myocardial infarction- - decreased ventricular contractility, - associated MR, -LBBB

Variable S1• AF - varying cycle length - varying force of ventricular

contraction• S1 intensity & mitral valve closure velocity closely related in

AF (Mills& Craige)• With short ventricular cycle lengths AV valve closure may

begin during the rapid filling phase of the immediately preceding diastole,during which MV leaflets are relatively divergent, leading to loud S1

• If S1 occur after rapid filling phase, intensity is likely to be related to rate of ventricular pressure development

• S1 amplitude & rate of pressure development tend to increase with increase in cycle length until a critical length is reached, little changes thereafter

• So difficult to relate the observed intensity to the cycle length

• CHB- varying PR interval- Intermittent loud S1- cannon sound• VT with AV dissociation - varying position of AV valves at

ventricular systole• Atrial flutter with varying conduction• Pulsus alternance – regular alternation in the intraventricular

pressure development• Electrical alternance- heart is swinging in a pendular arc ,

whose period is twice the heart rate , ventricular systole occur at each end of the pendular arc

• Alternating distance & fluid volume between the source of sound production & chestwall

wide splitting S1• Electrical delay(delayed RV contraction)-RBBB ( with normal sequence) - LV pacing - Ectopics from LV• Mechanical delay -Ebstein’s anomaly (sail sound due to delayed

activation, increased RA pressure) - TS& RA myxoma ( due to increased RA pressure)• Reverse splittingT1M1- RV pacing( delayed LV contr) -RV ectopics(delayed LV contr) -LBBB(delayed LV contr) - MS, LA myxoma(Hemodynamically significant mitral valve obstruction can cause reverse

splitting, mitral valve closure delayed due to increased LA pressure that must be overcome by rising the LV pressure before closure can occur)

Second heart sound • High frequency, 120 – 150Hz• Events associated with closure of aortic & pulmonary

valves• Sudden deceleration of reterograde bloodflow in the

aorta & PA, which sets the entire cardiohemic system into vibrations

• A2 louder (higher pressure in aorta) P2 later to (longer RV ET and more HI)

• Normal split- <30 ms exp, 40-50 ms insp• Inspiratory split- P2 delay accounts for 73% & early A2

accounts for27%

• P2 delay 2/3rd due to increased hangout interval during inspiration, and 1/3rd due to increased RV ejection time

• Expiratory split of S2 must be confirmed in sitting position- P2 occurs earlier and the split disappears

Hangout interval• Semilunar valves expected to close at the

point of cross over of pressures, however these valves closes slightly later

• Hangout interval (30 ms Ao &80ms PA)

• Factors affecting intensity of A2 / P2• Great artery pressure• Elastic recoil of great artery root- determined

primarily by the rate at which stroke volume is ejected

• status of Semilunar valve• Size of vessel• Position of vessel

Loud A2-• Hyperkinetic states( increased flow across normal valve)• Hypertension ( higher pressure in the aorta )• Aortic root dilation(increased flow, dilated vessel)• TGA ( Aorta arises more anteriorly ) Loud P2-• Pulmonary hypertension( dilated pulmonary

trunk,increased PA pressure)• ASD ( dilated pulmonary trunk, increased flow

across the valve)• straight back syndrome( decreased AP diameter)

Diminished A2-• Valvular AS ( distorted valve ,diminished mobility)• AR (restricted valve mobility, poor coaptation) Diminished P2• Valvular PS (thickened leaflet, diminished mobility)• Dysplastic valve (distorted valve anatomy&

diminished mobility)

• Inspiration may attenuate P2 due to increased lung interposition

• Massive pulmonary embolism- A2 soft due to decreased cardiac output

P2 loud due to increased PA pressure (may be soft in very large embolus

A2 early, P2 late

Wide physiological splitLate P2-

Electrical causes like RBBB (ET)PS (ET, HI)ASD (HI, ET, RBBB)PH + RVF (ET) IDPA (HI)

Early A2-Severe MR (decreased LV ET- due to loss of isovolumic contraction) VSD (decreased LV ET due to loss of isovolumic contraction) )Pericardial tamponade (ET)

Both-PEVSD

Wide fixed split

• When the RV or LV stroke volume doesnot change with inspiration– RVF– PE

• Simultaneous increase in RV & LV filling- ASD– Delayed P2 due to increased venous return to RV– Delayed A2 due to decreased left to right shunt– No further increase in hi is possible

• Reversed split S2– Types I, II & III (latter two by phono)– inspiration : single S2(P2A2) / Expiration : P2-A2– Typeii - inspiration :A2-P2 / Expiration : P2-A2– Late A2- • Electrical delay- LBBB(delayed activation LV,prolonged

isovolumic contraction time) ,RV pacing, RBBB VPCs, • AS, HOCM(due to large systolic gradient, ?prolonged LV

relaxation)– Early P2-• TR

Single S2• Aging (early P2, delayed A2)• Murmur obscuration (MR, VSD, AS, PS, PDA)• Absent P2 (PS, TOF, PA, TA)• fusionA2-P2 Eisenmenger VSD (same inspiratory delay),

single ventricle• Apparently single S2(inaudible P2)- Emphysema, obesity, pericardial effusion

S3• Mechanism of production• Impact theory - ventricular filling occurs early in the

diastole, if ventricles resist this rapid flow, vibratory activity results which are transmitted to the chest wall

• Ventricular theory - sudden cessation of ventricular filling resulting in distension & vibration of ventricular wall, papillary muscles & chordae

• Valvar theory- sudden limitation of longitudinal expansion of LV wall during early diastole

• Abnormal s3 - altered physical properties of the recipient ventricle &/or increase in the atrioventricular flow during rapid filling phase of ventricle

s3• Follows A2 by 140 to 160 msec (physiological

120-200 msec)• Gallop rhythm - auscultatory phenomenon of

tripling or quadrupling of heart sounds resembles the canter of a horse

Causes of S3

• Normal-– Children and young adults– Hyperkinetic states( diastolic overload with high

atrial pressure)• Diastolic overload states-– MR(earlier, higher frequency), VSD, PDA

• LVF• CCP (earlier, louder, higher pitched, due to

rapid rise of LV pressure)

• Normal S3 disappears in upright position• Abnormal S3 better heard after isotonic

exercise, passive leg raising ( augments the venous return & mid diastolic atrio ventricular flow)

• RV S3- TR , ASD, CCP

S4- atrial gallop- presystolic gallop

• The s4 occurs just after atrial contraction and immediately before S1

• 20 to 30 Hz • caused by stiffening of the walls of the

ventricles (usually the left), which produces abnormally turbulent flow as the atria contract to force blood into the ventricle

• audible in the elderly due to a more rigid ventricle

• LVS4 heard best at the cardiac apex• become more apparent with exercise, with

the patient in left lateral position in expiration• RVS4 most evident LLSB• louder with exercise, inspiration

• Absent in chronic MR (poor LA contractility• Present in acute MR (hyperdynamic atrial

systole)

• Causes- CAD, HT, AS, HCM ( decreased ventricular compliance) acute MR( hyperdynamic atrial systole) a/c AR (Decreased LV compliance) AV blocks (prolonged PR 220-260ms atrial gallop heard in addition to s1)

• CHB - (S4/ summation sound occur randomly in diastole- P&QRS relationship is random)

• RV S4- PH( increased resistance to ventricular filling) PS, PE ( RV pressure overload)• S3 & S4- non obstructive AV valve• S4- healthy atrium S3 has more inspiratory decrease than S4.• Upright posture- physiological S3 & S4 vanishes

Systolic ejection sounds

• Valvular- arising from deformed valve• vascular or root events - Rapid forceful ejection into great

vessels• Coincident with maximal excursion of domed valve when

its elastic limits are met• Mechanism - Deceleration of oncoming blood column sets

the entire cardiohemic system into vibration• high frequency sound• Intensity of ES correlates directly with mobility of the valve• No correlation with severity of obstruction

Ejection sounds Semilunar valve stenosis-

• Absent in extremely severe stenosis and in calcification.

• Aortic stenosis- common in BAV, less common in acquired valvular AS

• Pulmonic stenosis- – Common in valvular PS– Softens or disappears with inspiration– Absent in very mild PS

Pulmonary valvular ejection soundsOccurs at maximal excursion of stenotic pulmonary valve

Nonejection sounds

• MVP/TVP• a/w systolic regurgitant mr• Caused by tensing of AV valves during systole• Produced by vibrations of the entire

cardiohemic system when the elastic limits of prolapsed valve are suddenly reached

• Standing – click moves earlier, greater degree of prolapse

• Squatting- later prolapse, moves towards s2

diastolic sounds - Opening snap

• Sharp, high pitched brief early diastolic• 60-100ms after A2• Represents the isovolumic relaxation period of the

ventricle, inversely proportional to LA pressure• Sudden stoppage of the opening movements of the

valve(Margolies & Wolferth theory)• Sudden tensing of the valve leaflets by the chordae

tendinae

• AF- shorter A2-OS with short R-R cycles -With Longer preceding R-R, the LA pressure falls,

A2-OS widens

• Stenotic OS-MS,TS• Nonstenotic mitral- MR, ( increased flow,swift opening

of nonstenotic valve); VSD( functional OS)• Nonstenotic tricuspid –TR, ASD(functional opening

snap), ebstein anomaly( increased flow , rapid excursion)

Mild MS A2-OS>120ms mean LAP <5mmHgModerate MS60-80 ; 5-10MmmHg

Severe MS 40-60ms ;>15mmHg

Factors affecting OS

• Heart rate- tachycardia decreases A2-OS ( shortening of diastole)

• Brady increases A2-OS ( prolonged diastole)• Hypertension – A2-OS increased ( LVpressure

takes longer time to descend below LAP& early occurance of A2)

• Increased LVEDP- increased A2-OS (obliteration of transmitral gradient)

Tumour plop;• high frequency heard in atrial myxomas• Abrupt diastolic seating of mobile myxoma

within Rt or Lt AV orifice• Later than OS

Pericardial knock• Diastolic sound caused by loss of pericardial

elasticity that limits ventricular filling• High pitched sound • Louder with inspiration, squatting ( increased

venous return)• Mechanism-structural restriction of diastolic

filling by the restricting pericardial shell• Disappear following pericardiectomy

Prosthetic valve sounds• Mechanical valves • ball-in-cage valve- opening & closing sound• Tilting disc & bileaflet- high pitched metallic closing sound• aortic position: OS analogous to ejection click Closing sound coincides with S2 Clicks occur during the harsh ESM• Mitral position : opening sound analogous to opening snap• closing sound coincides with S1• tilting disc – closing sounds distinctly heard (aortic & mitral position)• Bioprosthetic valves- closing sounds are similar to those of native valves a low frequency early os may be present in mitral position

• Pacemaker sounds• Occuring nearly synchronously with

pacemaker spike• Caused by stimulation of intercostal nerves

adjacent to endocardial electrodes• Results in contraction of intercostal muscles

Pericardial friction rubs

• High pitched, leathery, scratchy sound• Three components

• Mediastinal crunch• Scratchy sounds, due to air in the mediastinum,• Most frequently during ventricular systole & in

a random fashion

Thank you