Percussion and

Auscultation of the
Heart
Xinyang Hu
2nd Affiliated Hospital, ZUMS
 Percussion
Relative cardiac outline
 Preparation

I A quite environment
II Fully expose the chest area
III Gentle indirect percussion with finger tips.
IV Cardiac dullness indicates cardiac outline.
 Methodology
Basic anatomic terms:
• Anterior median line: a vertical median line of
the sternum.
• Mid-clavicular line: a vertical line passing the
1/2 joint of the clavicle (sternal end to
scapular end).
 Methodology
I Finger position: in parallel with intercostal space when in supine position.
II Direction: from exterior to interior,
from inferior to superior, from left to right.

III Left border: start from 2-3cm exterior to

apex impulse.
Right border: identify superior border of liver dullness first, and start one
intercostal space above it.
IV Border indication: from resonance to dullness.
 Cardiac dullness
 Standard description of normal relative
cardiac dullness:
right (cm) intercostal space left (cm)
----------------------------------------------------------------------
2-3 II 2-3
2-3 III 3.5-4.5
3-4 IV 5-6
V 7-9
----------------------------------------------------------------------
The distance between anterior median line and left
mid-clavicular line (8-10cm)
 Normal cardiac outline:
a) Left border: cardiac waist (3rd intercostal
space) is about 1/2 of the maximum width.
b) Apex : interior to left mid-clavicular line.
c) Right border: <3cm in 2nd an 3rd
intercostal space ， <4cm in 4th
intercostal space.
 Abnormal cardiac outline:
a) Boot-shaped heart: indicates enlargement of left
ventricle. i.e. aortic type, AR, hypertensive
heart disease
b) Pear- shape heart: indicates enlargement of left
atrium and pulmonary artery. i.e. mitral type, MS
c) Spherical heart: i.e. general type, indicates
cardiomyopathy/ pericardial effusion
Boot-shaped heart Pear- shape heart
Auscultation
 Choice of chest pieces
• Diaphragm side: for sounds/murmurs with
high pitch, press tightly on the chest.
• Bell: for sounds/murmurs with low pitch,
touch gently on the chest.
 Patient’s position
• Supine

• Left-lateral decubitus

• Sitting
The areas best for auscultation do not exactly correlate
with the anatomical location of the valves.
 Auscultatory Valve
Area
a) Mitral valve area: apical region
b) Pulmonary valve area: near left sternal border,
2nd intercostal space.
c) Aortic valve area: near right sternal border, 2nd
intercostal space.
d) Secondary aortic valve area: near left sternal
border, 3rd and 4th intercostal space.
Erb’s point
b) Tricuspid valve area ： left region near inferior
border of sternum.
 Aortic valve area Pulmonary valve area

Secondary aortic valve area

Tricuspid valve area

Mitral valve area
 Auscultatory order

• Apex PV AV AV2  TV counterclockwise

• Apex AV /AV2  PV  TV 8

• PV AV AV2  ApexTV trans Z

• Diaphragm  Bell
 Contents of auscultation
• 1. Heart rate
• 2. Heart rhythm
• 3. Heart sound
• 4. Extra cardiac sound
• 5. Cardiac murmur
• 6. Pericardial friction sound
Heart Rate
• Varies with age, physical activity and
emotional status
• Normal adult: 60-100 beats/min
• Sinus tachycardia: >100 beats/min
• Sinus bradycardia: <60 beats/min
Heart rhythm
• Regular
• Irregular
Sinus irregularity
Premature beat
Atrial fibrillation:
1 ） Rhythm: irregularly irregular

2 ） S1 intensity: variable

3 ） Heart rate vs. pulse rate: pulse deficit

 Heart sounds
Two basic heart sounds:
•The first heart sound ( S1)
• The second heart sound ( S2 )
 S1
• Generated by the closure of mitral and tricuspid
valves and the vibrations associated with the
tensing of the chordae tendineae and the
ventricular walls

• Indicates the beginning of the ventricular systole.

 Characteristics of S1
• Pitch
• Loudest at apex
• Dull
• Lasting time: 0.1s
 S2

• Generated by the vibration of the closure of AV, PV

• Indicates the end of ventricular systole
 Characteristics of S2
• Pitch 
• Louder than S1 at the heart base
• Loudest at base
• Lasting time: 0.08s
 Phonocardiogram ( PCG)
• Graphically representing heart sounds
 Two components of S2

• Aortic component (A2)

• Pulmonic component (P2)

Normally, the aortic valve closes slightly

ahead of the pulmonic valve.
 Intensity: P2 vs. A2
• P2 > A2: children and adolescent

• P2 = A2: adult

• P2 < A2: elder

 Difference between S1 & S2
------------------------------------------------------------------------------------
S1 S2
Mechanism closure of A-V valves closure of the semilunar valves
Phase beginning of systole end of systole
Pitch blunt and loud sharp and soft
Duration long short
Timing S1-S2 SHORTER than S2-S1
Auscultation area apical region cardiac base
------------------------------------------------------------------------------------
 S3 and S4
• The third heart sound (S3)
• The fourth heart sound(S4)
 S3
• Generated by the vibration of ventricle wall
in early diastole while blood filling from
atrium to ventricle

• Can be heard in children and adolescent

 Characteristics of S3
• Early-diastole
• Low pitch &intensity ， dull and blunt
• Short duration
• at apex or higher
 S4
• By the end of diastole, atrial contraction
further stretches the ventricles. The
filling and stretching generated S4.
• Prior to S1
• Very low
• Usually not heard
 Heart sound abnormality

• Intensity changes

• Characteristics changes

• Abnormal split
 Factors affect loudness of heart sound

• Filling level of ventricle

Position of the valve
• Elasticity and integrity of the valve
• Ventricular contractility
• Thickness of the chest wall
• The distance between the chest wall and
the heart
 S1

• Mitral stenosis: mitral valve low location

• Short P-R interval: not full filling of LV

• Tachycardia and hyperactivity of

myocardium
 S1
• Mitral insufficiency

• Longer P-R interval

• Ventricle over-filling: aortic regurgitation

• Myocardial hypo-contraction: MI, Cardiomyopathy,

HF
 Variable S1
• Frequent VPB
• Atrial fibrillation
• III AVB
 Intensity changes of S2
Related with
• The pressure within the great vessel

• The situation of semilunar valves

intactness and elasticity
 Intensity changes of S2

• A2: hypertension, Atherosclerosis

• A2: Aortic stenosis, Aortic regurgitation

• P2 : pulmonary hypertension in MS, MR

• P2 : Pulmonary stenosis , Pulmonary
regurgitation
 Change of intensity
----------------------------------------------------------------------------------------------------------------
Status Pathophysiology Diseases
S1 increased less ventricular filling, increased mitral stenosis
myocardial contractility fever, hyperthyroidism
decreased incomplete valve intactness mitral/aortic regurgitation

decreased myocardial contractility cardiomyopathy,

myocardial infarction,
heart failure
irregular atrial fibrillation ，
complete atrioventricular block
S2 increased increased aortic/ pulmonary hypertension
artery pressure atherosclerosis
pneumocardial disease
congenital heart disease
decreased incomplete valve intactness aortic/ pulmonary artery stenosis
hypotension
------------------------------------------------------------------------------------------------------------------
Change in quality of heart sounds

• Monophony: S1≈S2
Usually accompany with tachycardia
Pendular rhythm （ embryocardia ）
May indicate severe myocardial
damage, e.g. AMI, severe myocarditis.
 Split of heart sounds
• Asynchronization of valves

• Closure of TV later than MV: 0.02-0.03s

• Closure of PV later than AV: 0.03s

• Audible >0.035s
 Split of S1

• Electrical activity delay: RBBB

• Mechanical activity delay: PAH
 Split of S2
• Due to delay of ejection time of one side
of the ventricle

• Physiologic splitting
– Due to the closure of AV and PV
asynchronously in inspiration, especially in
the younger
 Influence of respiration

In inspiration: the pressure within the

thorax, venous return to RV, so RV
ejection time prolongs and PV closure
delayed.
 Abnormal split of S2
• General splitting: Prolonged RV ejection time
CRBBB, PS, MS
• Paradoxical splitting: Prolonged LV ejection

CLBBB, AS, HTN

• Fixed splitting: ASD
Paradoxical S2 split
– When the ejection time of LV is
delayed , the order of valve closure is
reversed.
Fixed split of S2:
– in ASD, S2 is widely split over the PV
area with little or no change in the
degree of splitting in either phase of
respiration.
 Extra cardiac sounds
• Extra sounds In systolic period
– Early systolic ejection click
– Middle and late systolic click
• Extra sounds In diastolic period
– Gallop rhythm
– Opening snap
– Pericardial knock
– Tumor plop
• Iatrogenic extra cardiac sound
 Gallop rhythm

• In diastole, the blood into ventricle with poor wall

tension from atrium produces vibration, cause S3
or S4.

• When HR>100bpm, hearts sounds audibly

resemble the gallop of a horse

• Indicating that the ventricular function decreased.

 S3 gallop

S1 + S2 + pathologic S3
Characteristics of S3 gallop

– Lower in pitch
– After S2
– Best heard at apex
S4 gallop: late diastolic gallop

S1 + S2 + pathologic S4
 S4 gallop

Late diastolic gallop

– atrium gallop
• At late diastole, related to atrial
contraction
• Precede S1, far from S2
• low-pitch; best heard at apex
• Indicating ventricle overload, eg. HCM
decreased LV function
• Quadruple rhythm:
S1 + S2 + S3 + S4
• Summation gallop
– Overlapping of S3 Gallop and S4 Gallop
while heart rate increases
– Heart failure with tachycardia
 Opening snap
– In Mitral Stenosis
– In early diastole of LV, the blood from
LALV, the opening MV suddenly stopped
make itself vibration
 Opening snap
– After S2.
– Brief in duration.
– High in pitch. Indicate a flexible valve
 Pericardial knock
– In constrictive pericarditis after
inflammation, pericardial constricted,
limit the diastole of ventricle, produce
the vibration of ventricular wall.
– 0.1s after S2,
– Loudest at apex.
 Tumor plop
• LA myxoma
• Apex or L3-4
• 0.08-0.12s after S2
• Later than OS
• Change with posture
 Extra sound in systolic
period:
• Early systolic ejection sound
– Caused by the opening of stenotic aortic
or pulmonic valve
– After S1, high in pitch.
– PV area: PS, ASD, PDA inspiration, expiration 
– AV area: AS, AI, HTN
Middle and late systolic clicks

– Caused by Mitral Valve Prolapse

– Click: after S1, close to S2
best heard at apex
lower in pitch
Mitral Valve prolapse syndrome:
Middle and late systolic clicks +
murmur
 Heart murmurs
• Murmur is abnormal sound
• Produced by vibration result from
turbulent blood
 Mechanism of murmur
– Blood velocity
– Valve Stenosis
– Valve Regurgitation
– Abnormal connection
– Vibration of loose structure
– vessel stenosis or dilation
eg. Aortic coarctation, aneurysm
 Features of murmur
• Location: best heard
• Phase
• Intensity/Loudness
• Character/Quality
• Radiation
• Posture, inspiration and movement
 Phase of murmur
systolic murmurs
diastolic murmurs
continuous murmurs
biphasic murmurs
early,middle,late,whole
all diastolic murmurs and continuous murmurs are
pathologic
 Quality
– Depend on: frequency and intensity of
sound wave
– Related to: pathology and
hemodynamic changes of the heart
– Soft, harsh, musical.
– SM: blowing, musical (seagull)
– DM: blowing, sigh-like, rumbling.
– CM: machine-like, hum
 Radiation
• transmitted direction
– With the bloodstream by which they
are produced or propagated from
their point of origin in many directions
– AS: neck, suprasternal fossa
– MR: left subaxillary or subscapular
– MS: limited
 Intensity
Related to :
• The severity of abnormality
• The velocity of blood flow
• The pressure gradient of valve
• The myocardial contraction
 Levine’s grading system

– Grade 1/6: very soft and not heard at first

– Grade 2/6: soft, but can be detected
almost immediate by experienced
auscultator
– Grade 3/6: moderately; there is no thrill
 Levine’s grading system
– Grade 4/6: loud, thrill just palpable
– Grade 5/6: very loud; thrill easily
palpable
– Grade 6/6: very very loud, cab be heard
even without placing the stethoscope
right on the chest wall
Phonocardiogram ( PCG)
– Crescendo type
– Decrescendo type
– Crescendo-decrescendo type
– Continuous
– Plateau-shaped
Physiological maneuver
Change the body position
- Left recumbent: MS
- Sitting, leaning forward: AR
- Squatting from standing, supine
position, raising two legs may increase
venous return, SV CO
Murmur of MR, AR 
Murmur of HOCM 
(hypertrophic obstructive cardiomyopathy)
2) Respiration
- Deep inspiration: thorax pressure
venous return, pulmonary
circulation
clockwise rotation of heart make
murmur of TR, TS ,PR
- Expiration: MR ， MS ， AR ， AS 
- Valsalva maneuver: thorax pressure
venous return Murmur of HOCM
Dynamic auscultation for aortic regurgitation or a pericardial
friction rub; patient in deep expiration
3) Exercise:
- HR
- Blood volume
- Blood velocity
Murmur intensity 
 Innocent Murmurs
Common in asymptomatic adults
Characterized by
– Grade I – II
– Systolic ejection pattern - no  with Valsalva
– Heard in PV and MV
– Blowing, soft
– Short
– No thrill
– Limited radiation
– Can be heard in children or adolescent
 NOT Innocent Murmur
• Loud murmur - grade 3 or above
• Harsh
• Radiation with the blood downstream
• Murmurs associated with a click
• Murmurs associated with other signs or
symptoms e.g. cyanosis
• Associated abnormal S2 – fixed split,
paradoxical split or single S2
• Diastolic murmurs are usually not innocent
 Systolic murmurs
• Ventricular outflow obstruction murmurs
LV outflow obstruction
AS
PS
• Systolic regurgitation murmurs
MR,TR
• VSD murmur
 Systolic murmurs
MV area : produced by MR
– Organic: RHD, MVP
Characteristics: pan systolic
Harsh, Loud >3/6
Radiate to base or left axilla
 Systolic murmurs
– Relative MR: Dilated LV causes
mitral annulus dilatation

– Functional Murmur:
Valve(-) blood flow faster
Fever
Anemia
Hyperthyroidism
 Systolic murmurs
AV area—AS
Characteristics: Harsh,
Crescendo-decrescendo
Radiate  neck
Thrill, S2
A, 正常主动脉瓣 . B, 先天性二叶瓣 C, 风湿性主动脉瓣狭窄 . D, 钙化退变的主动
脉瓣
摘自： Braunwald’s Heart Disease, 9th edition
 Systolic murmurs
PV area
– Most are functional:
– Relative: ASD, MS PH,PA dilation,
relative PS
– Organic: congenital PS
 Systolic murmurs
TV area—TR
– Most are relative, due to dilate of RV.
- character like MR, but increased in
inspiration, organic SM are rare
 Systolic murmurs
– VSD: harsh and loud
Third-forth intercostal space
Left to the sternal border
Thrill
 Diastolic murmurs
• Mitral stenosis (MS)
• Aortic regurgitation (AR)
• Pulmonary regurgitation(PR)
 Diastolic murmurs:
mitral stenosis
– Mid-late diastolic
– Rumbling, decrescendo-crescendo
– Thrill, S1, OS
– At apex, limited
 Diastolic murmurs:
Mitral stenosis

Listening for mitral stenosis at the apex, hear better in the left
lateral position
 Diastolic murmurs
AV area – AR
decrescendo, sigh-like
best heard at second aortic area
 Diastolic murmurs
PV area
– Most are produced by relative PR
TV area
– rare in clinical
 Continuous murmur
Patent Ductus Arteriosus (shunting)
– Begins after S1, crescendo, peak
intensity at S2, envelop S2, decrease
at early-middle diastole
– Harsh, mimic the sound of machine
rotating
– Best heart at left first and second
intercostal space
 Continuous murmur
• Cervical venous hum murmurs
 Some common causes of
Heart Murmurs (1)

LLSB: left lower sternal border; RLSB: right lower sternal border
LUSB: left upper sternal border; RUSB: right upper sternal border
Some common causes of
Heart Murmurs (2)
 Pericardial friction sound
• It is produced by the rubbing of each
other of the parietal and visceral
surfaces of the roughened pericardium.
• During pericarditis
• In both systolic and diastolic
• Systolic component predominates
• Sometime only in systole
 Pericardial friction sound
• Harsh
• Resemble massage the ear using the
finger
• Best heard at 3th-4th intercostal space,
left sternal border
• Common cause is pericarditis
Can been heard in AMI, uremia, SLE
Other auscultatory sounds

Prosthetic valve sounds and murmur

in patients after valve replacements.
Thank you!