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 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 INSPIRATION (Split < 30msec) (Split > 30msec) 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 while examining for S2 are. Splitting of S2 Intensity of each component of S2

Splitting Of S2

Normal Splitting of S2 (Split < 30msec) INSPIRATION 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.

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 Decreased pulmonary venous flow to the left atrium. So LV ejection time decreases so A2 occurs early 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 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 S2 In 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 flow across the valve Hyperkinetic States Anteriorly placed Aorta TGA Pulmonary atresia PTA 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

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: Increased flow across the valve 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 and Fixed in MR : MR+ ASD 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