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• ApexPV AV AV2 TV

III. Content of auscultation

• 1. Heart rate

• 2. Heart rhythm

• 3. Heart sound

• 4. Heart murmurs

1. HR

• Varies with age, sex. Physical activity and emotional status

• Normal adult: 60-80/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

• 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

3. Heart sound: S1, S2, S3, S4

• S1: S1 indicates the beginning of the ventricular

constraction

1) Vibration of the closure of A-V 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:

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

• The differentiate between S1~S2

1) S1 apex pitch , lasting time

S2 basic, pitch lasting time

2) Duration: S1__S2 S2

__S1

3) Apical pulse

• 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

atrial contraction 0.11'' prior to S1

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 asynchronousl

y in inspiration

2) In pathological situation– delay of emptying time of one side of the heart

such as ASD,MS.

3) The influence of respirationin 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

LALV, 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 inflamati

on, 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 phas

e of cardiac cycle during which they occur.

– SM, DM , CM.– Early, middle, late

• Quality– Depend on: frequency and intensity of so

und 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 : basely audible Ⅰ– Grade : usually readily heardⅡ– Grade : loudⅢ– Grade : quite loudⅣ– Grade : even most pronounced Ⅴ– Grade : may be heard with the stethoscopeⅥ 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 murmu

r 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,

radiateneck, 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

LVLA LA filling degree P In diastolic period, LV accepts

more blood→dilation

CO

– Symptom: fatigue , palpitation, dyspnea

– Sign :

• Apical pulseleft, lower

• Apical beat heavy

• Cardiac dullness enlargedleft

• 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 dullnessleft

• 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, AOvolume overloadLV dilationrelative MI, relative MS

Diastolic pressure, pulse pressure– Symptom: palpitation, angina

– Sign:

• Apical impulseleft, inferiorly

• Cardiac dullness enlargedleft, 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 ve

locity 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 engage

ment, inspiration• Paradoxical pulse, venous pressure• Ewart sign: the lung was pressed by th

e effusion,

• in the area of left scapula inferior angle with dullness, vocal fremitue, bronchovesicular breath sound

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