SECOND HEART SOUND

Dr SHAJUDEEN .K DM Cardiology

Resident Calicut Medical

college

History• “S2 is the key to auscultation” : Aubrey

Leathem

• Respiratory variation first described by

Potain (1866)

• Term “Hangout interval” coined by shaver

laboratory.

Genesis of S2

• During systole blood flow from LV to Aorta

& RV to PA. Once pressure in the great

vessels becomes more than corresponding

ventricle and hang out interval is over,

blood flow reverses , this retrograde flow

is stopped suddenly by semilunar valves

when the elastic limits of the tensed

leaflets are met during closure of valves

• This causes vibrations in the

cardiohemic system. High frequency

generated from this vibration is the

Second heart sound.

Timing Of S2

Hang out interval

• It is the time interval from the crossover

of the pressure between RV and PA or LV

and Aorta during the ejection phase of

systole to the actual closure of the

Pulmonary or Aortic valve respectively.

Cardiac cycle recorded by high fidelity catheter tipped manometer

Normal values of Hangout intervals

• Pulmonary circulation: 43-86 msec

• Systemic circulation :< 15msec

• ie Pulmonary hangout interval >Systemic

Factors influencing the duration of Hangout interval

• Pressure in the arteries

• Vascular resistance

• Compliance of Vessels

• Aorta is a higher pressure and less

compliant vessel so hangout interval of

aortic is less than the pulmonary side

• Pulmonary circulation is Low pressure ,low

resistance, high capacitance

circulation .So hang out interval more

Features of S2

Frequency Higher than S1(S1 25-45Hz , S2 50HZ)

Duration 0.11 sec( Shorter than S1 0.14 Sec)

Components of S2 Aortic component (A2) & Pulmonary component (P2)

Timing of A2 coincides Incisura of Aortic pressure trace

Timing of P2 coincides Incisura of pulmonary artery pressure trace

Normally A2 – P2 interval : During inspiration During expiration

40-50 msec<30msec

Normally A2 is earlier and Louder than P2

Normally A2 heard in Aortic area, Pulmonary area , and Apex

Normally P2 heard at pulmonary area only (P2 heard at apex only if PHN Present or If the apex is formed by RV (eg ASD))

Reasons for Higher frequency S2 compared to S1

• The tautness of the semilunar valves more

compared to A-V valves.

• The Greater elastic coefficient of the taut

arterial walls that provide the principal

vibrating chambers for the second sound,in

comparison with the much looser, less

elastic ventricular chambers that provide the

vibrating system for the first heart sound.

Why S2 duration shorter than S1?

• Normally duration of S1 is 0.14 second

and S2 is 0.11 second .

• The reason is that, semilunar valves

are more taut than the A-V valves, so

they vibrate for a shorter time than do

the A-V valves.

Normal S2

EXPIRATION(Split < 30msec)

INSPIRATION(Split > 30msec)

Why P2 Delayed?

• RV systolic ejection last longer than LV

ejection even though RV and LV

Mechanical systole has same duration

• This occurs due to prolonged hangout

interval of pulmonary circulation.

Why A2 is earlier and louder than P2

• Due to High Diastolic pressure gradient acoss the

aortic valve

• When compared to pulmonary circulation,

LV ejection time is small as aortic hangout

interval is less

Clinical Examination Of s2

• At 2nd to 3rd Left ICS preferably with

Diaphram of the stethescope.

• Spliting best apreciated at second

Left intercostal space.

Clinical examination of S2

Two important Points to observe whileexamining for S2 are.

• Splitting of S2

• Intensity of each component of S2

Splitting Of S2

Normal Splitting of S2

EXPIRATION(Split < 30msec)

INSPIRATION(Split > 30msec)

Normal splitting of S2

Normal A2 P2 interval

During expiration : < 30

msec

During inspiration : 40-50 ms

Splitting occurs because of delayed P2

(73%)

and early A2 (27%).

Factors affecting normal splitting of S2

• Age :

As age increases split duration decreases. Single

S2 during both phases of respiration is a normal

finding in subjects with age >40yrs• Depth of respiration• Position of body : In recumbent position prominent splitting in both phases of respiration is a normal finding

Mechanism of increased split in inspiration

Recent views regarding inspiratory widening of split

• Complex interplay of dynamic

changes in pulmonary vascular

impedence and changes in

pulmonary and systemic venous

return. Net effect is prolonged RV

ejection and a concomittent decrease

in LV ejection causing widening of

split in inspiration.

Decreased pulmonary venous flow

to the left atrium. So LV ejection time decreases so A2 occurs

early

Inspiration causes more negative intrathoracic

pressure

1) Increased venous

return 2) Increase capacitance

of the pulmonary

vessels

Pulmonary hang out interval

increases & RV ejection time increases

So A2 P2 interval > 30 msec

Abnormal Splitting Of S2

• Abnormal splitting can be either

absent/inaudible split (single S2) or

presence of audible expiratory splitting

both in supine and upright position

Abnormal Splitting of S2 includes

• Persistent physiological split

• Wide fixed split of S2

• Reverse split of S2

• Narrow Physiological split with Loud P2

• No Split : ie Single S2

Expiratory split interval> 30msec

Audible expiratory splits

Wide Persistent physiological split

Wide physiological splitting important mechanism

• Delayed P2 Delayed electrical activation of RV Prolonged RV mechanical systole Increased Pulmonary Hang out

interval

• Early A2 Shortened LV mechanical systole

Delayed electrical activation of RV

• Complete RBBB

• LV ectopic beat

• LV pacing

Prolonged RV mechanical systole

• Moderate to severe PS with intact IVS

• Right heart failure

• Acute Massive pulmonary embolism

• Anomalous venous connection to RA

Increased Hangout interval

• Mild Pulmonary stenosis

• Idiopathic dilatation of pulmonary

artery

• Normo tensive ASD

• Unexplained audible expiratory

splitting in normal subjects

Shortened LV mechanical systole

• Severe Mitral Regurgitation

• Moderate to Large VSD

Wide fixed splitting

Wide fixed splitting

A2 P2 widely split and split remains fixed ie remains unchanged during respiration or valsalva

• Wide : Due to delay in P2 because of

increased pulmonary vascular

capacitance prolonging the hangout

interval and increased RV ejection

time

• Fixed : As little or no change in RV

filling and stroke volume during

inspiration .so little or no inspiratory

delay occurs to P2

Causes of wide fixed split

• Moderate to Large Ostium Secundum ASD

• Severe right heart failure

Reverse or paradoxical splitting of S2

Reverse or paradoxical splitting splitting

• S2 Split>30msec during expiration with

reversal of sequence ie P2-A2

• Presence of reverse splitting always

indicate significant underlying Heart disease

• Almost all cases of reversed split are due to

dalayed A2

Types of Reversed split

• Type 1 or classic : Only this type is

audible clinically

• Type 2 Detected Phonographically• Type 3

Type 1 Reversed split

No split during inspiration. But splitting

during expiration with reverse sequence

due to delay in A2

It occurs due to delayed LV Electro

mechanical systole

Type 2 or Partially Reversed splitting of S2

Normal Inspiratory splitting But Expiratory splitting of S2 with Reverse sequence

• It resemble wide fixed split.But during expiration sequence of sound is P2-A2

Type 3 Reversed splitting of S2

ie similar to type 2 but difference is that

A2 P2 and P2-A2 seperation is ≤30 ms

and so S2 is heard as a single sound in

both phase of respiration

Clinical recognition of Reversed split of S2

• Trace the two components of S2 to the apex.If the

second component of S2 is tracable up to apex , reverse

split present.

• (normally only first component of S2(ie A2) is tracable up

to apex, And second component is heard only at

pulonary area.In reverse split A2 is the second

component.)

Clinical recognition of Reversed split of S2

• Valsalva testing

Normally S2 becomes

Reversed split S2 becomes

Strain phase Split narrows widens

Release phase widens Splitt narrows

Differentiation of P2-A2 in reversed Split

• Auscultate from pulmonary area to

apex concentrating on the two

components of S2.

The component which disappears at

apex is the pulmonary component.

Causes of Reversed spliting

• Due to

Delayed A2 Early P2

Causes of Delayed A2

• Delayed Electrical

activation of LV• Complete LBBB

• RV pacing

• RV ectopic beat

• Prolonged LV mechanical

systole• Complete LBBB• Severe AS• Severe HTN (Rarely)• Chronic ischemic heart

d/s• During episode of angina

pectoris(rarely)

Causes of Delayed A2 . . .contiued.

• Decreased Impedance of systemic circulation eg

Post stenotic dilatation

aorta

Chronic severe AR,

PDA.

Early P2

Due to Type B WPW Syndrome

Reversed splitting in LBBB

• In proximal type: Delayed activation of LV

• In peripheral type: There is prolonged

mechanical systole (primarily isovolumic

contraction time increased).

• In most cases of LBBB varying degrees of

both mechanism coexist with one

predominating

Reversed split in angina pectoris

• It occurs rarely• Proposed mechanisms are 1) Prolonged isovolumetric contraction time of ischemic LV

2) Systemic hypertension prolonging LVETime

3) Transient LBBB

Reverse splitting in HTN

• In HTN Loud A2 with normal split is the

common finding

• Reverse split occurs rarely especially in

acute hypertension . Due to increased LV

ejection & isovolumetric contraction time

Single S2

Single S2In this there is absent splitting both in inspiration and expiration

Single S2: Mechanism

• If only one semilunar valve present: eg: Aortic or Pulmonary atresia, Persistent truncus arteriosis

• When P2 inaudible: TGA, TOF, Severe PS, PA

• When Delayed A2 coincides with P2: Severe AS

• When early P2 coincides with A2 : Severe PHTN,

VSD+PHTN

• Any condition producing Paradoxical split with A2-

P2 interval ≤ 30msec

• A2 sound drowned by murmur of AS/MR/VSD

INTENSITY OF S2(A2 P2)

Factors influencing the intensity of S2

• Size of the vessel

• Pressure in the vessel beyond the valve

• Rate of change of Diastolic pressure gradient across the valve.

• Flow across the valve

• Position Of Vessels(Anterior/Posterior)

• Valve anatomy

S2 intensity relation to the rate of change of the diastolic pressure

gradient that develops across the valves

It is the driving forces accelerating the

blood mass retrograde into the base of

the great vessels. This pressure gradient

is the result of the level of diastolic

pressure in the great vessel and the rate

of pressure decline in the ventricle.,

Accentuted A2 Causes

• Increased size of the vessel Ascending aorta aneurysm Root dialatation: Syphilitic AR Ankylosing

Spondylitis Bicuspid Aortic valve with post stenotic dilatation • Incresed pressure in the vessel beyond the valve Systemic Hypertension Coactation of aorta

• Increased flow across the valve

Hyperkinetic States

• Anteriorly placed Aorta

TGA Pulmonary atresia

PTA

Diminished A2

• Occurs due to distortion of aortic leaflet

eg Aortic sclerosis, Calcific AS,

Valvular AR

Aortic atresia(HLHS).

Loud P2• Increased size of

the vessel: Idiopathic

dilatation of pulmonary artery,

ASD • Incresed pressure

in the vessel beyond the valve:

PHTN

• Increased flow across the valve

Hyperkinetic States

ASD • Distance From the

site of origin of sound to the chest wall:

Thin Chest wall Straight Back

syndrome

Grading Of Loud P2

• Grade 1: P2= A2

• Grade 2: P2>A2 Localised to

Pulmonary area

• Grade 3: P2>A2 But heard Beyond the

pulmonary artery

Relation Between P2 intensity and Pulmonary pressure

Pulmonary Systolic pressure

Mean pulmonary pressure

Grade 1 Mild PHTN 30-49 mm of Hg

21-34 mm of Hg

Grade 2 Moderate PHTN

50-75 mm of Hg

35-50mm of Hg

Grade 3 Severe PHTN > 75mm of Hg > 50 mm of Hg

Diminished P2

• Thick chest wall: Obesity • Poor conduction of sound : COPD • Thickened leaflet and diminished valve mobility PS & Dysplastic PV TOF >60 yr old• Decreased Diastolic Gradient pressure in PA: PS,Tricuspid atresia

S2 in different cardiac conditions

Mitral stenosis

• Mild to Moderate MS without PHTN: Normal

A2 & P2

• Severe MS With PHTN : S2 narrow split P2 Loud

Mitral Regurgitation

• Wide variable split : Severe MR• Wide and Fixed in MR : MR+ ASD• Reverse splitting in MR: MR due to HCM

P2 in Mitral regurgitation

• In MR with giant Left atrial

enlargement .P2 is more prominent

even with slight increase in

pulmonary hypertension.It is due to

the enlarged LA displaces the

pulmonary artery anteriorly closer to

the chest wall

Aortic stenosis

• Reverse split : Due to Delayed A2 in Severe AS

• Single S2 : If A2 is Absent/soft or A2 drowned in the

murmur

Aortic regurgitation

• S2 Split normally split/Reverse split

• A2 loud If AR Due to root dilatation • A2 soft if AR due to Valvular disease.

Pulmonary hypertension

• Spectrum of the width of splitting can

happen in PHTN depending on the

selective prolongation of RV systole.

• In PHTN hangout interval will always

be narrow

Spliting of S2 in PHTN

• Narrow physiological split with Loud P2• Wide variable splitting of S2 with Loud P2• Fixed splitting in PHTN due 1) If RV failure: Due to inability of compromised RV to accept the augmented venous return

associated with inspiration• 2) Altered vascular impedence in

pulmonary circulation

S2 in CONGENITAL HEART DISEASE

ASD

• Wide fixed split with loud p2 in absence

of PHTN

is the hallmark of ASD

P2 Loud because Dilated P2 is close to the

chest wall.

Fixed split in ASD Mechanism:

• Fixed : Inspiratory augmentation of

systemic venous return produces less

Left to Right shunt and it causes

delayed A2. And expiratory decrease

in systemic venous return causes

increased Left to right shunt

producing early A2.

VSD

• Small VSD : Normal S2 split with normal intensity P2• Moderate VSD: Normal split with moderate accentuation of P2• Large VSD : Wide variable Split with Loud P2

• VSD with PS physiology :Single Loud S2

PDA

• Small PDA : Normal S2 split and normal intensity P2 but S2 masked by continous murmur

• Large PDA: Normal S2 split with accentuated

P2. Occationally paradoxical splitting can be seen.

Pulmonary stenosis

• Mild PS: Normal S2 Split with decreased intensity P2• Moderate – Severe PS: Wide Variable Split With Diminished

P2• Severe PS : P2 absent

• Dysplastic pulmonary valve : P2 can be normal or inaudible depending severity of stenosis

BISCUSPID AORTIC VALVE

• In the absence of significant AS or

AR S2 normally split with

accentuated A2

• If significant AS: S2 Reversed split

COA

• Normally splitting S2 with

accentuated A2 due to hypertension

• sometimes reverse split can also

happen

S2 in Ebsteins anomaly

• S2 is often single because pulmonary closure is

inaudible due to low pressure in pulmonary trunk

• Wide splitting of S2 can happen if complete RBBB

• Paradoxical split occurs if Type B WPW association

S2 in Anomalous pulmonary venous connection

• If Associated ASD : Wide fixed split

• If Atrial septum intact: S2 normal

split with normal respiratory variation

S2 in Eissenmenger syndrome

• ASD Eissenmenger syndrome: S2 narrow fixed

split

• VSD Eisenmenger syndrome: Single Loud P2

• PDA Eisenmenger syndrome: Closely split S2 with Loud

P2

THANK U