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    Heart Sounds S2

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    Vimal Nishad
    The second heart sound has two components - A2 from the aortic valve closing and P2 from the pulmonary valve closing. [1] During normal inspiration, the interval between A2 and P2 widens noticeably as P2 is delayed, causing a split S2 sound. [2] Abnormal splitting patterns of S2 can provide clues about underlying cardiac abnormalities. Wide, fixed splitting suggests an atrial septal defect, while paradoxical or reversed splitting involves abnormalities of ventricular function. [3] The components of S2 provide information about vascular pressures and valve function that is useful for auscultation.

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    Heart Sounds S2

    Uploaded by

    Vimal Nishad
    31 views31 pages
    The second heart sound has two components - A2 from the aortic valve closing and P2 from the pulmonary valve closing. [1] During normal inspiration, the interval between A2 and P2 widens noticeably as P2 is delayed, causing a split S2 sound. [2] Abnormal splitting patterns of S2 can provide clues about underlying cardiac abnormalities. Wide, fixed splitting suggests an atrial septal defect, while paradoxical or reversed splitting involves abnormalities of ventricular function. [3] The components of S2 provide information about vascular pressures and valve function that is useful for auscultation.

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    The second heart sound has two components - A2 from the aortic valve closing and P2 from the pulmonary valve closing. [1] During normal inspiration, the interval between A2 and P2 widens noticeably as P2 is delayed, causing a split S2 sound. [2] Abnormal splitting patterns of S2 can provide clues about underlying cardiac abnormalities. Wide, fixed splitting suggests an atrial septal defect, while paradoxical or reversed splitting involves abnormalities of ventricular function. [3] The components of S2 provide information about vascular pressures and valve function that is useful for auscultation.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    31 views31 pages

    Heart Sounds S2

    Uploaded by

    Vimal Nishad
    The second heart sound has two components - A2 from the aortic valve closing and P2 from the pulmonary valve closing. [1] During normal inspiration, the interval between A2 and P2 widens noticeably as P2 is delayed, causing a split S2 sound. [2] Abnormal splitting patterns of S2 can provide clues about underlying cardiac abnormalities. Wide, fixed splitting suggests an atrial septal defect, while paradoxical or reversed splitting involves abnormalities of ventricular function. [3] The components of S2 provide information about vascular pressures and valve function that is useful for auscultation.

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    of 31

    Second Heart Sound

    Key to Auscultation

    Dr. I. Sathyamurthy MD, DM, FACC


    FRCP (Edin), FRCP (Glas), DSc (Honoris Causa)
    Sr. Interventional Cardiologist
    Apollo Hospitals, Chennai.
    Heart sounds
    S2

    • Has 2 components Aortic (A2) Pulmonary (P2)

    • Each coincides with the incisura of its arterial pressure wave

    • Inspiratory splitting of S2 – Due to delay in P2

    • During inspiration pulmonary arterial incisura moves away from the


    descending limb of RV pressure due to increase in capaciitance of
    pulmonary vascular bed which delays the P2

    • Expiration has the opposite effect.


    S2

    • A2 louder audible at base, LSB and apex

    • P2 softer confined to 2nd LICS

    • During expiration A2 and P2 are separated by < 30 ms and are heard as


    single sound

    • During inspiration the splitting interval widens and A2 & P2 are heard as
    two distinct sounds
    Abnormal splitting of S2
    3 categories

    • Wide split Fixed


    Non fixed

    • Paradoxically split (Reversed)

    • Persistently single
    Wide splitting of the second heart sound
    Delayed Pulmonic closure

    Delayed electrical activation of the right ventricle

    Prolonged right ventricular mechanical systole

    Decreased impedence of the pulmonary vascular bed (increased “hang out”)

    Early Aortic closure


    Shortened LV mechanical systole(LVET)
    Wide splitting of s2
    Causes of audible expiratory splitting of s2
    I. Increased Q - P2 (Prolonged RV systole)
    (a) Hemodynamic causes
    • PS with intact septum ( A2-P2 delay > 100msec indicates an RV-PA gdt
    of 100mmHg when there is no infundibular stenosis )
    • Massive Pulmonary embolism
    • PAH with RV failure
    • Idiopathic dilatation of PA
    • ASD
    (b) Electrical causes
    • Complete RBBB
    • PVC of LV origin
    • LV pacing
    • WPW with LV pre excitation
    (II) Decreased Q - A2 Interval (Shortened LV systole)

    • MR
    • VSD
    • Pericardial tamponade
    • LA Myxoma
    • Constrictive pericarditis
    Wide split s2 in Cyanotic heart disease
    • TAPVC
    • Single atrium
    • Ebsteins anamoly of tricuspid valve
    • ASD Eisenmenger
    • ASD with left to rt shunt ASD
    with PS and right to left shunt at atrial level
    • Primary Pulmonary hypertension

    Miscellaneous
    • Pectus excavatum
    • Occasionally normal children
    • Straight back syndrome
    Fixed S2 split

    Interval between A2 & P2 is wide and persistent and remains


    unchanged during respiratory cycle

    • Hallmark finding of ASD

    • Delay in P2 is due to  Pulmonary vascular bed capacitance – and 


    Hangout interval (  interval between descending limbs of PA and RV
    pressure pulses ) – Split is wide

    • No significant respiratory variations in RV filling due to reciprocal changes in


    volume of left to right shunt – Split is fixed
    What is hangout interval?

    • Semilunar valve is expected to close at point of cross over of


    ventricular and arterial pressure.

    • In reality it is not so

    • Time interval from cross over of pressures to actual occurrence of


    sound is called HANGOUT interval.

    • Just like a rolling ball is stopped by the friction offered by the ground,
    the ejection of blood is stopped by the resistance offered by the
    pulmonary vasculature
    • Since the pulmonary vascular resistance is low compared
    to the systemic vascular resistance, it takes some time for
    the blood flow from the right ventricle to stop

    • This corresponds to the hangout interval.

    • On the left side of the heart because impedance is much


    greater, the hangout interval between the aorta and LV
    pressure curves is negligible

    • Hang out interval may vary from 30 to 120 msec in the


    pulmonary vascular bed.
    • Hangout interval depends on interrelated factors like :

    • pressure beyond the valve

    • dilatation of the artery

    • distensibility of arterial system

    • vascular impedance

    • phase of respiration.
    Reverse Splitting of the second heart sound
    • Delayed Aortic closure
    Delayed electrical activation of the LV
    Complete LBBB (Proximal type)
    RV paced beat
    RV ectopic beats

    Prolonged left ventricular mechanical systole


    Complete LBBB LVOT
    obstruction
    Hypertensive heart disease
    Arteriosclerotic heart disease
    Chronic IHD
    Contd,

    Decreased impedence of the systemic vascular bed (increased “hang out”)


    Post stenotic dilatation of the aorta secondary to AS or AR
    PDA

    Early pulmonic closure


    Early electrical activation of the RV
    WPW syndrome type B
    TYPES OF REVERSE SPLIT

    Type 1: Classical reverse split


    During expiration prolonged LV systole causes A2 to follow P2.with
    inspiration Q-P2 increased normally but Q-A2 is unchanged or shorten
    resulting a single second sound
    Type 2: S2 reversal only in expiration(P2-A2),
    normal in inspiration(A2-P2)
    In lesser degrees of Q-A2 delay ,inspiration may still result in normal A2-P2
    relationship and audible splitting,although s2 reversal occurs in expiration.
    Reversed or parodoxic splitting

    Type 3 paradoxical split :S2 single in both phases of respiration


    (reverse split not detected by human ear as interval is < 20 msec
    both in inspiration and expiration)

    • Pseudo Reverse Split

    Only Type I Paradoxic splitting can be detected bedside. Type II and Type
    III can be diagnosed only by Phonocardiography .
    Aortic Stenosis

    Mild

    Moderate

    Severe
    Single S2
    • Absence of either component of S2 or fusion of A2P2 without
    inspiratory split give rise to single S2

    Absent A2
    • Severe AS
    • Aortic atresia

    Absent P2
    • Truncus arteriosus
    • Severe TOF
    • Severe PS
    • CHD associated with PS or Pulmonary atresia
    contd.,

    Fusion of A2 and P2
    • Eisenmenger VSD
    • Single Ventricle

    Inaudibility of P2
    • Emphysema
    • Obesity
    • Pericardial effusion
    • Posterior location of PA. Eg.TGA
    Pulmonary Stenosis
    Single A2

    • A2 is the louder component in the pulmonary area and is the only


    component heard over the cardiac apex in normal individuals.

    Determinant of intensity of A2

    • Aortic pressure
    • Relative proximity of aorta to chest wall
    • Size of the aortic root
    • Degree of the opposition of the valve leaflets
    • Valve mobility
    Increased intensity of A2

    • Systemic hypertension
    • Coarctation of Aorta
    • Ascending Aortic aneurysm
    • Relative anterior placement of the aorta - TOF,TGA

    Decreased intensity of A2

    • AR(Lack of apposition of leaflets)


    • Valvular & supravalvular AS(Decreased arterial diastolic pressure)
    Single P2
    Increased intensity of P2

    • Normally P2 is not audible at the apex. If P2 is louder than A2 in 2nd


    LICS or if it is audible at the apex- It is termed loud and indicates PAH

    • In ASD P2 may be audible at the apex in the absence of PAH because


    of RV enlargement and RV occupies the apex.

    • If P2 is very loud and banging it correlates to approximate mean PA


    pressure of > 50mmHg
    Single P2

    Determinants of intensity of P2
    • PA pressure especially the diastolic pressure
    • Size of PA
    • Degree of apposition of PV leaflets

    Loud P2
    • Eisenmenger ASD - Wide splitting of S2 with ↑ P2
    • Eisenmenger PDA - Narrow splitting of S2 with ↑ P2
    • Eisenmenger VSD – S2 is generally single

    Soft P2
    • Pulmonary stenosis
    • TOF(Mild form)
    Cyanotic Congenital Heart Disease

    Anomaly P2 ECG
     PBF
    CTGA  RAD, RVH
    TAPVC  RAD, RAE, RVCD
    Common atrium  RVH, RAD / Superior Axis
    Common ventricle  Variable
    Truncus  CVH, RVH / LVH
     PBF : No PAH
    TOF  RAD, RVH
    TOF, Like anomaly  RAD, RVH
    PS, Intact IVS + ASD  RV Strain
    Tricuspid atresia  LAD, LV dominance
    Ebstein’s  RAD, Low Voltage, RVCD
     PBF : PAH
    Eisenmenger’s  RAD, RVH
    Phonocardiography
    • Single Vs Closed split
    • Confirmation P2 or A2
    • Reversed Splitting
    • For teaching purpose
    Thank You

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