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Auscultation of the Heart

I. Auscultatory Valve Area

• 1. MV: apex, fifth left intercostal


space, medial to the
midclavicular line
• 2. PV: second left intercostal space
• 3. AV: second right intercostal space
• 4. AV2: left third intercostal space
• 5. TV: lower part of sternal
• 6. Other part
II. Auscultatory order
• Apex→PV →AV →AV2 →TV
III. Content of auscultation
• 1. Heart rate
• 2. Heart rhythm
• 3. Heart sound
• 4. Heart murmurs
• 5. Pericardial friction sound
1. HR
• Varies with age, sex. Physical activity and
emotional status
• Normal adult: 60-100/min
• Sinus tachycardia: >100/min
• Sinus bradycardia: ≤60/min
2. Heart rhythm
• 1) Sinus arrhythmia
• 2) Premature beat:
A sudden extrasystole of the heart
in the basic of normal heart rhythm
S1↑; S2↓
Pulse absent
Ectopic point at atrial, AV node, ventricle
Premature beat
• 3) Atrial fibrillation:
Mechanism: a very high frequency impulse
coming from the atrial ectopic
point, in multi-reentry
Three inconsistence: ventricular rhythm
S1 intensity
Heart rate>pulse
(Pulse deficit)
Atrial fibrillation
3. Heart sound: S1, S2, S3, S4
• S1: S1 indicates the beginning of the ventricular
contraction
1) Vibration of the closure of
A-V(atrioventricular) valve
2) Opening of the semilunar valve
3) Acceleration of the blood in arteries
• S1: Character of auscultation
1) Area: apex
2) Pitch↓
3) Lasting time:longer 0.1s
4) Together with apex impulse
• S2: Vibration of the closure of AV, PV,
during the beginning of ventricular
diastole,
Indicates the beginning of ventricular
diastole
• S2: Character of auscultation
1) Area: loudest at the basic
2) Pitch ↑
3) Lasting time↓ 0.08s
• The differentiate between S1~S2
1) S1 apex , pitch ↓, lasting time ↑
S2 basic, pitch ↑ lasting time ↓
__ __
2) Duration: S S ↓, S2 S1 ↑
1 2

3) Apical pulse:S1
• S3: Mechanism:
In early diastole filling blood moves from

atrium to ventricle, Produces the


vibration
of ventricle wall
• Character: at apex or superinternal of apex
0.12~0.18'' after S2
frequency ↓ intensity↓
• S4: Occur late in diastole, with effective
4. Abnormal of heart sound
• Change in loudness
Both S1 and S2
↑: Thinner chest wall
Activity of the heart increased
↓: Fat, edema,
Pericardial effusion, heart failure
• Change in S1:
S1 depends on: myocardial contraction
filling degree of ventricle
elastic and position of the valve
S1↑: 1) MS
2) Tachycardia: in high fever, the
diastolic period was shortened
S1↓: 1) Infarction
2) MI
• Change of S2:
S2 depends on (1) the pressure within the
great vessel
(2) the situation of semiluner
valves
A2↑: hypertension
P2 ↑: pulmonary hypertension in MS, MI
A2↓: AS ,AI
P2 ↓: PS, PI
• Change in quality of heart sound
When the myocardial muscle is damaged
severely, S1 is similar to S2. The heart
sound like a pendular—pendular
rhythm.Usuallyaccompany with
tachycardia—embryocardia.
• Splitting of heart sounds
Splitting of S1: it is due to closure of MV
and TV asynchronously loudest over the
apex in RBBB
• Splitting of S2:
1) In normal person, physiologic splitting
– due to the closure of AV and PV
asynchronously in inspiration
2) In pathological situation
– delay of emptying time of one side of the heart
such as ASD,MS.
3) The influence of respiration
in inspiration: the pressure within the
thorax↓, venous return to RV↑, so
empty time to be delayed, PV closure
more later.
4) Paradoxical splitting of S2
– the abnormal is within the left heart,(AS),
the emptying time of LV is delayed, the
order of valve closure is reversed. In
inspiration, the two components then
more closer together or may be single.
5)Fixed splitting 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.
5. Extra sounds In diastolic period

• 1) Gallop:
Three or four sounds are spaced to audibly
resemble the center of a horse, the extra
sounds occurs after S2.
• Protodiastolic gallop rhythm
• S3 gallop, ventricular gallop rhythm.
• S1 + S2 + pathologic S3
– In early diastole, the blood through into
ventricle from atrium in failing
myocardium, the ventricular wall tension
is poor, produce vibration. Reflex that the
ventricular function↓
• Auscultation character of S3 gallop:
– lower in pitch
– After S2
– Best hear at apex
– Loudest at the end of expiration.
• S3 gallop: differ from normal S3
– Occur in severe organic heart disease
– HR>100 bpm
– The interval time between S1 and S2 are
almost equal, mimicking quality, normal
S3 is nearer from S2
– Normal S3 will disappear in standing or
sitting position
• Late diastolic gallop
– S4 gallop, atrium gallop
• At late diastole, related to atrial contraction.
In LVEDP ↑ compliance↓ Artial contraction↑
occur precede S1, far from S2
low-pitch; best heard at apex
• Tensity: end of expiration↑(from LA)
end of inspiration ↑(from RA)
• Occur in pressure overload,→LVH, in
myocardial damaged , LV compliance ↓,
such as BP↑, IHSS, CHD.
• Summation gallop
– Overlapping of S3G and S4G while HR↑
• 2) Opening snap
– In MS
– In early diastole of LV, the blood from LA→
LV, the opening MV suddenly stopped make
itself vibration
– After S2. Brief in duration.
– High in pitch. Indicate a flexible valve
• 3) Pericardial knock
– In constrictive pericarditis after
inflamation, pericardial constricted, limit
the diastole of ventricle was limited,
produce the vibration of ventrcular wall.
– 0.1 ″ after S2,
– Loudest at apex.
6. Extra sound in systolic period:
• 1) Early systolic ejection sound
– Dilated great vessel, hypertention with in it.
– After S1, high in pitch.
– PV area: PS , PH inspiration↓, expiration ↑
– AV area: BP ↑,AS
• 2) Middle and late systolic clicks
– In MVP
– Valve, tandae chordea redudent, floppy
– Click: after S1, close to S2
best heard at apex
lower in pitch
Heart murmur
• H M is abnormal sound
• Produce by vibration
• Within the heart or large arteries.
• Mechanism
– Blood velocity↑
– Blood vascosity↓
– Valve: narrowed or incompetent; organic
or relative
– Abnormal connection
– Vibration of loose structure
– Diameter of vessel ↑or ↓
• Character of murmur
• Location:
– Murmur of valvular origin are usually
best heard over their respective valve
area
• Timing:
– Murmurs are timed according to the
phase of cardiac cycle during which they
occur.
– SM, DM , CM.
– Early, middle, late
• Quality
– Depend on: frequency and intensity of
sound wave
– Related to: pathology and hemodynamic
changes of the heart
– Soft, harsh, musical.
– SM: blowing, harsh, 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
– MR
– MS
• Intensity:
– Related to :
• The severity of abnormal
• The velocity of blood flow
• The pressure gradient of valve
• The myocardial contraction
• Six-point scale of for grading the intensity of
heart murmur
– Grade Ⅰ: basely audible

– Grade Ⅱ: usually readily heard


– Grade Ⅲ: loud
– Grade Ⅳ: quite loud
– Grade Ⅴ: even most pronounced
– Grade Ⅵ: may be heard with the stethoscope
removed from the chest wall.
• PCG
– Crescendo type
– Decrescendo type
– Crescendo-decrescendo type
– Continuous
– Regular
• Physiological maneuver
1) Change the body position
- Left recumbent: MS
- Sitting, leaning forward: AI
- Squatting from standing, supine position,
raising two legs may increase venous
return, SV↑ CO↑
- Murmur of MI, AI↑
- Murmur of IHSS↓
2) Respiration
- Deep inspiration: thorax pressure↓
venous return↑, pulmonary circulation↑
clockwise rotation of heart make
murmur
of TI, TS ,PI↑
- Expiration:
- Valsalva maneuver: thorax pressure↑
venous return↓ M of IHSS↑
3) Exercise:
- HR↑
- Blood volume↑
- Blood velocity↑
make the murmur of MS↑
The clinical value of heart murmur
1. Important in diagnosis
2. Organic M : MS
Relative M: valve , supporting tissues
of the valve abnormal
Functional M: increased flow across
a normal valve
• 1. Systolic murmur
• 1) MV area : produced by MI
– Organic: RHD, MVP
Character: pan systolic
Harsh, Loud >3/6
Radiate to the left axilla
Maneuver insp↓ exp↑
– Relative murmur: Dilated LV
BP↑
Acute rheumatic fever
Severe anemia
Character:
– Functional M: Valve(-) blood flow faster
Fever
Anemia
Hyperthyroidism
Character:
• 2) AV area—AS
– Organic: RHD
Character: Harsh, crescendo-decrescendo,
radiate→neck, Thrill, S2↓
– Relative: Arteriosclerosis, Dilation of aorta,
HP
• 3) PV area
– Most are functional:
– Relative: ASD, PA dilation
– Organic: congenital PS
• 4) TV area—TI
– Most are relative, duo to dilate of RV
character like MI, but increased in
inspiration, organic SM are rare
• 5) Other position
– VSD: harsh and loud
Third-forth intercostal space
Left to the sternal border
Thrill
• 2. Diastolic murmur
1) MV area
– Organic: RHD—MS, Apex
Mid-late diastolic
Rumbling, decrescendo-crescendo
Thrill, S1↑, OS
– Relative:
LVH;
AI; Austin-Flint murmur
2) AV area – AI rheumatic
– decrescendo, sigh-like
– best heard at aortic second area
– radiate to the left side of the lower part of
sternal
3) PV area
– Most are produced by relative PI
4) TV area
– It is rare in clinical
• Continuous murmur
– In patent ductus Arteriosus
– Begins after S1, crescendo, peak intensity
at S2, envelop S2, decreased at early-
middle diastole producing a large
diamond sharp.
– Harsh, mimic the sound of machine
rotating
– Best heart at second intercostal space,
left to sternal artery-vein fistula.
Pericardial friction sound
• It is produced by the rubbing on 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
• Harsh,
• Resemble massage the ear using the finger
• Best heard at 3th-4th in intercostal space
• Left to the sternal border
• Common cause is pericarditis (TB, non-
specific, rheumatic)
• Also can been heard in AMI, uremia, SLE
Major symptom and sign of common
diseases in circulatory system
• Mitral Stenosis (MS)
– Rheumatic
• Commissural thickening, adherent fusion
• Orifice of MV stenosis,blood flow from
LA→ LV was limited.
• LAP↑, LAH, Pulmonary V and capillary
pressure ↑ dilatation, stasis, PAP↑ → RV
over load → RV failure
• LV filling ↓ CO↓
– Symptoms:
• Exertional dyspnea, cough, hemoptysis
• Paroxysmal noctunnal dyspnea
– Signs:
• Mitral face, apical pulse left side
• Diastolic thrill at apex
• Cardiac waist prominence
• Diastolic murmur at apex
• OS S1 ↑ P2 ↑ splitting
Graham-Steel murmur.
• Mitral Insufficiency(MI)
– Etiology: Rheumatic
Non-rheumatic
– Organic
– Relative: duo to the LV enlargement.
in systolic period, blood flow from
LV→LA LA filling degree↑ P↑
In diastolic period, LV accepts
more blood→dilation
CO↓
– Symptom: fatigue , palpitation, dyspnea
– Sign :
• Apical pulse→left, lower
• Apical beat heavy
• Cardiac dullness enlarged→left
• Pausystolic, murmur at apex
• Radiate to left axilla, subscapular
• P2↑ spitting S1↓
• Aortic Stenosis (AS)
– Rheumatic, atherosclerosis, congenital
Narrowed orifice of AV, the resistence of
LV to output the blood↑
LV contractility↑, LVH
Aorta P↓ blood flow in coronary A and
peripheral A↓
– Symptom: palpitation, fatigue, angina,
syncope
– Sign:
• Apical impulse↑, to left
• Systolic thrill in AV area, pulse↓
• Cardiac dullness→left
• Ejection SM in AV area, radiate to neck
• A2↓ splitting paradoxically
• Aortic insufficiency(AI)
– Rheumatic, arteriosclerosis, infective
endocarditis, syphilis,
– In AI, LV receives both blood from LA,
AO→volume overload→LV dilation→
relative MI, relative MS
Diastolic pressure↓, pulse pressure↑
– Symptom: palpitation, angina
– Sign:
• Apical impulse→left, inferiorly
• Cardiac dullness enlarged→left, inferiorly
• Boot-shaped shadow –cardiac waist↓
• DM in AV2 area →apex
• S1↓, A2↓
• Relative MI—SM at apex
• Relative MS—Austin Flint, DM
• Peripheral vascular sign:
pulse pressure↑ water hammer pulse,
carotic pulsation↑, Musset sign(moving
head with each heart beat),capillary
pulsation, pistol shot sound, Duroziez M.
Pericardial Effusion
• Inflammatory (TB, purulent) non inflammatory
(rheumatism, uremia)
• Pericardial cavity P↑, limit the dilation of
heart, blood flow from systemic venous to the
RV↓, RV filling ↓ output ↓
– Symptom:
• Depends on the volume and the
velocity of effusion producing.
• Pericardial compression, dyspnea.
• Infection: fever, fatigue
• Cough, dysphagia
– Sign:
• Cardiac impulse↓
• Apical pulsation↓
• Cardiac dullness enlarged,
coincide with position
• Pericardial friction rub
• Heart sound↓
• In massive effusion: neck vein
engagement, inspiration↑
• Paradoxical pulse, venous pressure↑
• Ewart sign: the lung was pressed by
the effusion,
• in the area of left scapula inferior
angle with dullness, vocal fremitue,
bronchovesicular breath sound
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