Heart sounds

Heart Sounds
Presenter
Praveen Gupta
18/04/2017
Moderator
Dr Raja Selvaraj
Department of cardiology
JIPMER
Pondicherry
INDIA
605006
1

Heart sound
 Two types
 High-frequency, abrupt terminal checking
of valves,closing or opening
 Mitral and tricuspid closing sounds (M1,
T1), nonejection sounds, opening snaps,
aortic and pulmonic closure sounds (A2,
P2) and early valvular ejection sounds
 Low-frequency, S3 and S3 gallop ,S4
gallop
2
Hurst J, Fuster V, Walsh RA. Hurst's the Heart. McGraw-Hill Medical; 2011.

Heart Sound S1
Two components
 Audible at left lower sternal border
 Louder M1 followed by T1
 Deceleration of blood setting cardiohemic
into vibration
3

Spltting of S1
Normal wide splitting,normal (M1, T1)
 Right bundle-branch block
 LV pacing
 Ectopic beats
 Idioventricular rhythms from LV
Reversed splitting (T1, M1)
 Pacing from the RV
 Ectopic beats and idioventricular
rhythms from RV
4

Factors determining intensity of S1
 Integrity of valve closure
 Mobility of the valve
 Velocity of valve closure
 Status of ventricular contraction
 Transmission characteristics of the
thoracic cavity and chest wall
 Physical characteristics of the
vibrating structures
5

Integrity of Valve Closure
 In severe MR, inadequate coaptation of
the mitral leaflets to a degree that valve
closure is not effective, S1 markedly
attenuated
6

Mobility of the Valve
 Severe calcific fixation of the
mitral valve with severe MS
 complete immobilization,
attenuated M1
7Hurst J, Fuster V, Walsh RA. Hurst's the Heart. McGraw-Hill Medical; 2011.

Velocity of Valve Closure
Relation of S1 with PR interval
 PR decreases from 130 to 30 ms increase
in the intensity of M1
 Mitral leaflets are maximally separated
 At longer PR intervals, there is less
separation of the mitral valve leaflets
 Variable S1
 Complete AV block with AV dissociation
 Mobitz type I AV block
 Ventricular tachycardia with AV
dissociation
 Atrial fibrillation
8

Status of Ventricular Contraction
 Exercise and catecholamine infusion increase the amplitude of S1
 β-blocking agents decreases
 S1 is increased in anemia, arteriovenous fistulas, pregnancy, anxiety, and fever.
 Loud T1 in an ASD
 decrease in the intensity of S1 myxedema, cardiomyopathy, and acute MI
9

Transmission Characteristics of the Thoracic Cavity and
Chest Wall
 Obesity
 Emphysema
 Large pleural
 Pericardial effusions
Decrease the intensity of all auscultatory events,
 Thin body habitus increase the intensity
Physical Characteristics of the Vibrating Structures
 MI and ischemia induced by pacing decrease the intensity of S1
10

S1 in Mitral Stenosis
 A loud M1
 Loud OS,
 Calcific fixation of the stenotic MV occurs, M1 is soft, and the OS is absent
11

S1 in Mitral Valve Prolapse
 Loud M1 heard over apex with nonrheumatic MR; indicate holosystolic MVP
 Increased amplitude of leaflet excursion with prolapse beyond the line of closure
explains the loud M1 associated with holosystolic prolapse
 Middle to late systolic prolapse have a normal S1
 Soft or absent S1 indicate a flail mitral leaflet
12

S1 in LBBB
M1 decreased in intensity and delayed, reversal S1 sequence
LBBB (Delay in onset of LV contraction,LV dysfunction)
 Acute AR attenuation or absence of M1 (Increase in the LVEDP, premature closure
of the mitral valve)
13

Systolic Ejection Sounds
 Originate from left or right of the heart
 Valvular from deformed aortic or
pulmonic valves
 Vascular or root, rapid, forceful ejection
of blood into the great vessels
 Root ejection sounds indicate
abnormalities of great vessels with or
without systemic or PHT
 Definine level of outflow tract obstruction
14

Aortic Valvular Ejection Sounds
 Nonstenotic congenital bicuspid
valves (Mild to severe stenosis )
 With ejection murmur of AS
 Widely transmitted
 Heard best at the apex
 20 to 40 ms after pressure rise onset
in aorta
Ejection click associated with aortic stenosis due to a congenitally bicuspid
valve. Note the high-frequency, high-amplitude sound that follows S1 and is
coincident with the onset of ejection into the aorta. The aortic ejection sound is
formed by sudden cessation of the opening motion of the abnormal valve leaflets
(doming). Note also the delayed carotid upstroke and long systolic
murmur. (From Abrams J: Synopsis of Cardiac Physical Diagnosis. 2nd ed.
Boston, Butterworth Heinemann, 2001, p 135.)

Aortic Valvular Ejection Sounds
 With sharp anacrotic notch on the
upstroke of the aortic pressure curve
 With maximal excursion of the
domed valve when elastic limits are
met
 Intensity of sound correlates directly
with mobility of valve
 No correlation between intensity and
severity of the obstruction
Ejection click associated with aortic stenosis due to a congenitally bicuspid
valve. Note the high-frequency, high-amplitude sound that follows S1 and is
coincident with the onset of ejection into the aorta. The aortic ejection sound is
formed by sudden cessation of the opening motion of the abnormal valve leaflets
(doming). Note also the delayed carotid upstroke and long systolic
murmur. (From Abrams J: Synopsis of Cardiac Physical Diagnosis. 2nd ed.
Boston, Butterworth Heinemann, 2001, p 135.)

Pulmonic Valvular Ejection Sounds
 Occurs at maximal excursion of the
stenotic pulmonic valve
 Pulmonic ejection click decreases with
inspiration in mild to moderate PS
17

Vascular Ejection Sounds
 Originating from aortic root
 Common in HTN with tortuous sclerotic aortic root
 Coincident with the upstroke of central aortic pressure
 Sound occurs at the moment of complete opening of the aortic valve
 Tend to be poorly transmitted from the aortic area and are not heard well at the apex
 Interpreted as an exaggeration of the ejection component of the normal S1
18

Pulmonary Vascular Ejection Sounds
 From pulmonary artery & due to dilatation of the pulmonary artery
 Dilatation can be idiopathic or secondary to severe PH
 Louder during expiration
 Louder in 2ND and 3RD left intercostal spaces
 Occurring during upstroke of pulmonary artery pressure recording
19

Nonejection Sounds
 Midsystolic click
 Prolapse of the mitral or tricuspid
valve
 With a systolic regurgitant
murmur
20

Nonejection Sounds
 Sharp
 High-frequency
 Clicking quality
 Confined to the apex
 Transmitted widely on the precordium
 Can isolated finding
 In middle to late systole
 Can be multiple clicks
21

Nonejection Sounds
 Occurs at time of maximal prolapse
 Upright posture, click moves earlier
 Squatting, click toward S2
 Differentiating nonejection click
from early ejection sounds, a split S2,
or an S3

Heart sound (S2)
 High-frequency
 Two component, A2 and P2
 Produced by the sudden deceleration of
retrograde flow of the blood column in the
aorta and pulmonary artery
 Increased intensity of A2 and P2 in
systemic and PH
23

Normal Physiologic Splitting
 In expiration, A2 & P2 separated by <30
ms
 Heard by the clinician as a single sound
 During inspiration, both components
audible ,caused by a delayed P2
 P2 softer than A2 and rarely audible at apex
 When P2 is heard at the apex significant
PH is present
 Single S2 during both phases of respiration
normal in subjects older than 40 years of
age
24

Abnormal Splitting of S2
 Exists by presence of audible expiratory
splitting (>30 ms)
 Must be present in both the supine and
upright
 There are three causes of audible expiratory
splitting
 (1) wide physiologic splitting primarily
caused by delayed P2,
 (2) Reversed splitting primarily caused by
delayed A2
 (3) narrow physiologic splitting as seen in
PH, where A2 and P2 are heard as two distinct
sounds during expiration at a narrow splitting
interval.
25

Wide physiologic splitting of S2
 Right bundle-branch block
 Severe PH and PS
 ASD
 Acute MR
 Idiopathic dilatation of the pulmonary artery
 Mild PS with aneurysmal dilatation of the pulmonary artery
26

Reversed splitting of S2
 Caused by a delay in A2
 P2 preceding A2.
 Paradoxical movement of A2 and P2
with respiration
 During inspiration, P2 moves toward
A2, and the splitting interval narrows
 During expiration, the two
components separate, and audible
expiratory splitting is present
 Indicates cardiovascular disease
27

Reversed splitting of S2
 RV ectopic and paced beats
 Complete LBBB
 Hypertrophic cardiomyopathy
 Valvular AS,
 Hypertensive cardiovascular diseas ( rare)
 Ischemic heart disease
 Episodes of angina pectoris
 Poststenotic dilatation of the aorta
 Chronic AR
 Patent ductus arteriosus
 Type B Wolff-Parkinson-White syndrome
28

Narrow Physiologic Splitting
 Common finding in severe PH
 In contrast to the normal situation, where only a single sound is heard during expiration, both
A2 and P2 are easily heard, even though the splitting interval is less than 30 ms because of the
increased intensity and high-frequency composition of P2
 Wide, persistent splitting sign of abnormal RV performance in patients with primary PH
 Fixed splitting of S2 occasionally has been documented in severe RV failure secondary to PH.
29

Single S2
 Delay A2 produce when splitting interval
<30 ms
 One component of S2 is either absent or
inaudible
 Eisenmenger VSD
 Inability to hear the fainter of the two
components of the sound (usually P2)
because of emphysema, obesity, or
respiratory noise
 Seen in older than 50 years of age
30

Opening Snaps
 Opening of AV valve silent event
 With thickening and deformity of the
leaflets sound is generated in early diastole
 High-frequency
 Early diastolic sound
 Absent in thickened and immobile valves
31

Opening snap
 Crisp
 Sharp sound
 Heard in the midprecordial location
 Best in the area from the left sternal
border to just inside the apex
 Often heard well at the base of the heart
 Diastolic rumble follows opening snap
 No variation in the intensity or timing of
the mitral opening snap with respiration
32

Opening snap
 Intensity correlates with valve
mobility
 Loud in mobile stenotic valves
 Absent with severe calcific valve
 Intensity of M1 parallels the intensity
of the opening snap
 The opening snap occurs at the
maximal mitral valve opening shortly
after LV–left atrial pressure
crossovers.
33

Factors that influence the timing of the opening snap
relative to A2
 Rate of LV pressure decline
 Level of the LV pressure at the time of A2
 Level of the left atrial pressure
 Increasing severity of MS,shortening of
the A2–opening snap interval
 Imperfect correlation between A2–
opening snap interval and mitral area
 A2–opening snap interval in atrial
fibrillation vary with cycle length
34

Differential diagnosis of opening snap
Differentiated from other early diastolic sounds S3, the pulmonary component of a widely split S2
35

Third and Fourth Heart Sounds
 Low-frequency
 Related to early and late diastolic
filling of the ventricles
 Disease states called gallop sounds
 Gives information of ventricular
function and compliance
36

Third heart sound (S3)
 Physiologic S3 benign finding
 Commonly in children, adolescents,
and young adults
 Rarely after 40 years of age, when
present associated with a thin,
asthenic body
 Low-frequency sound that
 Follows A2 by 120 to 200 ms
37

Third heart sound (S3)
 Occurs during rapid filling of the ventricle
 Best heard at the apex
 In left lateral position
 Stethoscope's bell pressed lightly against
skin
 Differentiated from the pathologic S3
primarily by the "company it keeps."
38
 RV S3 heard at the lower left sternal edge
and increase in intensity with inspiration
 LV systolic dysfunction
 Diuresis, S3 decreases
 S3 with cardiomyopathy/Myocardial
infacrtion ominous sign

Third heart sound(S3)
 Chronic AR
 Acute AR
 AV valve regurgitation
 Large left-to-right shunts
 VSD
 Patent ductus arteriosus
 ASD
 Restrictive cardiomyopathy
39

Fourth Heart Sound (S4)
 Best heard at the apex
 In left lateral position
 Varies with respiration
 Heard best during expiration
 S4 just prior to S1
 Also termed atrial diastolic gallop or the
presysolic gallop
 Atrial contraction must be present for S4
 Absent in atrial fibrillation
40

Fourth Heart Sound (S4)
 Audibility depends on its intensity and frequency, separation from S1
 Degree of separation is determined primarily by PR interval
 A loud S1 also can mask the audibility of a preceding softer S4
 Left-sided S4 and S3 augmented post-tussively and sustained handgrip exercise
 Maneuvers that increase venous return increase the audibility by increasing the intensity of
the sound and by causing it to occur earlier, thereby separating it further from S1.
 Decreased venous return does the opposite
 Accompanied by a palpable presystolic apical impulse
 S4 generated by right atrial contraction heard best at the lower left sternal border
 Accentuated with inspiration
41

Fourth Heart Sound(S4)
 Systemic hypertension
 Severe valvular AS
42

Prosthetic valves sound
 Type of valve,
 its position,
 whether it is functioning normally
 Mechanical valves produce opening and closing clicks
 Are easily audible
 Can be heard even without a stethoscope.
 Ball-in-cage valves produce the loudest and most distinctive opening and closing clicks
 The metallic ball of the Starr-Edwards valve also produces multiple early systolic clicks
 Absence or decrease in intensity of clicks occur with valve obstruction or LV dysfunction.
 A decrease in the intensity of the opening and closing clicks, and the absence of the opening
click are also indications of valve malfunction.

Extracardiac Sounds
Pacemaker Sounds
 High-frequency sounds of brief duration with transvenous pacemakers located in
the RV apex
 Extracardiac in origin
 within 6-10 ms with the pacemaker spike
 caused by stimulation of intercostal nerves adjacent to endocardial electrodes
 Should suggest myocardial perforation by the endocardial lead
45

Pericardial Friction Rub
 Inflammation of the pericardial sac with or without fluid
 Very high pitched
 Leathery
 Scratchy in nature
 Seem close to the ear
 Auscultated best with the patient leaning forward or knee–chest position
 Holding his or her breath after forced expiration
46

Pericardial Friction Rub
Three components
 Atrial systole,
 Ventricular contraction
 Rapid early diastolic filling
 Uremic pericarditis
 Acute phase of transmural MI
47

Mediastinal Crunch: Hamman Sign
 When air is present in the mediastinum
 Scratchy sounds (Hamman sign) occur
 Related indirectly to both heartbeat and
respiratory excursion
 Occur most frequently during ventricular
systole
 Caused by air in the mediastinum
 Common after cardiac surgery
48

Approach with cardiac sound
49

Reference
 Hurst J, Fuster V, Walsh RA. Hurst's the Heart. McGraw-Hill
Medical; 2011.
 Google Images
50

Heart sounds

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