heart sounds and murmur

Heart Sounds & Murmurs

Dr.Vitrag Shah

First year resident,MD Medicine

April-2012

GMC,Surat

www.medicalgeek.com

Dr.Vitrag Shah - www.medicalgeek.com

Different areas for auscultation of 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 intercostalspace(Neoaortic/Erb’s area)

5. TV: lower part of left sternal border

6. Other part


Auscultatory order

ApexPV AV AV2 TV

Or

ApexTV AV2PV AV

Content of auscultation1. Heart rate

2. Heart rhythm

3. Heart sound

4. Heart murmurs


Function of the valves Valves prevent the back flow of blood.

The papillary muscles will not close the valves,they will maintain the closure of the valves.

The importance of chordea tendinei attached to the papillary muscles is because during ventricular contraction the ventricle size decreases and the papillary muscle must contract to shorten the chordea tendinei to prevent the leakage of valves


Heart sounds

The bell and diaphragm of the stethoscope accentuate sounds of different pitches. The bell emphasizes low-pitched sounds such as normal heart sounds and the diastolic murmur of mitral stenosis. The diaphragm filters these sounds and helps to identify high-pitched sounds such as the early diastolic murmur of aortic regurgitation or a pericardial friction rub.

Normal heart valves make a sound when they close but not when they open. The classic 'lub-dub' sounds are caused by closure of the atrioventricular (mitral and tricuspid) valves followed by the outlet (aortic and pulmonary) valves.

the first and second heart sounds

extra heart sounds (third and fourth, heard in diastole)

additional sounds, e.g. clicks and snaps

pericardial rubs

murmurs in systole and/or diastole.


Cause of the heart sounds

Slapping of the valves leaflets is not enough to generate a heart sound.

The causes of the 1st heart sound:

During systole the AV valves are closed & blood tries to flow back to the atrium back bulging the AV valves. But the taut chordaetendinae stop the back bulging and causes the blood to flow forward.

This will cause vibration of the valves, blood & the walls of the ventricles which is presented as the 1st heart sound.


The causes of the 2nd heart

sound:

During diastole, blood in the blood vessels

tries to flow back to the ventricles cause the

semilunar valves to bulge. But the elastic

recoil of the arteries cause the blood to

bounce forward which will vibrate the blood

the valves and the ventricle walls.

This is presented as the 2nd heart sound.


Difference between the 1st and

2nd heart sounds

The 1st sound lasts longer because the AV valves are less taut than the semilunar valves which will enable them to vibrate for longer time.

The 2nd heart sound had higher frequency due to

The semilunar valves are more taut

The great elastic coefficient of the taut arteries which provides the principle vibrations of the 2nd heart sound


First heart sound

The first heart sound (S1), 'lub', is caused by closure of the mitral and tricuspid valves at onset of ventricular systole and is best heard at the apex.

Components of S1

Mitral Valve Closure Best Heard: Apex

Tricuspid Valve Closure Best heard: Lower Left Sternal Boarder


Abnormalities of intensity of the

first heart soundQuiet

Low cardiac output

Poor left ventricular function

Long P-R interval (first-degree heart block)

Rheumatic mitral regurgitation , Calcified MS

Loud

Increased cardiac output

Large stroke volume

Mitral stenosis

Short P-R interval

Atrial myxoma (rare)

Variable

Atrial fibrillation

Extrasystoles

Complete heart block Dr.Vitrag Shah - www.medicalgeek.com

S1

Wide Splitting

RBBB

PVC from Left Ventricle

Single Sound

Normal

LBBB

PVC from Right Ventricle

Paced Beats


Second Heart Sound The second heart sound (S2), 'dub', is caused by closure of

the pulmonary and aortic valves at the end of ventricular systole and is best heard at the left sternal edge.

It is louder and higher-pitched than the first sound, and the aortic component is normally louder than the pulmonary one.

Physiological splitting of the second heart sound occurs because left ventricular contraction slightly precedes that of the right ventricle so that the aortic valve closes before the pulmonary valve.

This splitting increases at end-inspiration because the increased venous filling of the right ventricle further delays pulmonary valve closure.

This separation disappears on expiration.Splitting of the second sound is best heard at the left sternal edge.

On auscultation, you hear 'lub d/dub' (inspiration) 'lub-dub' (expiration).


Abnormalities of the second heart sound Quiet

Low cardiac output

Calcific aortic stenosis

Aortic regurgitation

Loud

Systemic hypertension (aortic component)

Pulmonary hypertension (pulmonary component)

Split Widens in inspiration (enhanced physiological splitting):

Right bundle branch block

Pulmonary stenosis

Pulmonary hypertension

Ventricular septal defect

Fixed splitting (unaffected by respiration):

Atrial septal defect

Widens in expiration (reversed splitting):

Aortic stenosis

Hypertrophic cardiomyopathy

Left bundle branch block

Ventricular pacing


Physiological splitting of S2


Fixed splitting of S2


Reversed splitting of S2


Third heart sound

A third heart sound (S3) is a low-pitched early diastolic sound best heard with the bell at the apex. It coincides with rapid ventricular filling immediately after opening of the atrioventricular valves and is therefore heard after the second as 'lub-dub-dum'.

0.12~0.18'' after S2, frequency intensity.

A third heart sound is a normal finding in children, in young adults and during pregnancy.

A third heart sound is usually pathological after the age of 40 years.

The most common causes are left ventricular failure, when it is an early sign, and mitral regurgitation. In heart failure S3 occurs with a tachycardia and S1 and S2 are quiet (lub-da-dub).


Causes of a third heart sound

Physiological

Healthy young adults

Athletes

Pregnancy

Fever

Pathological

Large, poorly contracting left ventricle

Mitral regurgitation


Fourth heart sound A fourth heart sound (S4) is less common. It is

soft and low-pitched, best heard with the bell of the stethoscope at the apex. It occurs just before the first sound (da-lub-dub). 0.11'' prior to S1

It is always pathological and is caused by forceful atrial contraction against a non-compliant or stiff ventricle.

A fourth heart sound is most often heard with left ventricular hypertrophy (due to hypertension, aortic stenosis or hypertrophic obstructive cardiomyopathy). It cannot occur when there is atrial fibrillation.

Both a third and a fourth heart sound cause a 'triple' or 'gallop' rhythm.


Added Sounds


Pericardial Friction Rub Three Phases

○ Mid Systolic, Mid Diastolic, Pre Systolic

Scratchy, Leathery

Best Heard

○ With Diaphragm of Stethoscope

○ Left Sternal Boarder Leaning over at End Expiration

Apposition of Abnormal Visceral and Parietal Pericardium

Confused with Hamman’s Sign in Post Open Heart Surgery

(Crunch Sound from Mediastinal Air)

It may be audible over any part of the precordium but is often

localized. It is most often heard in acute viral pericarditis and

sometimes 24-72 hours after myocardial infarction. Pericardial rubs

vary in intensity over time, and with the position of the patient.

A pleuro-pericardial rub is a similar sound that occurs in time with the

cardiac cycle but is also influenced by respiration and is pleural in

origin. Occasionally a 'crunching' noise can be heard caused by air in

the pericardium (pneumopericardium). Dr.Vitrag Shah - www.medicalgeek.com

Early Systolic Sounds

Ejection Sound- Usually High Frequency

Aortic Valve- Aortic Stenosis, Bicuspid Aortic

Valve

Pulmonary Valve-Pulmonic Stenosis Vary with

Respirations

Prosthetic Valves- Mechanical, Not

Bioprosthetic


Mid-Late Systolic Sounds

Click

High Frequency Sound Found in Mitral Valve

Prolapse

Occurs Earlier with Valsalva Maneuver or

Squatting to Standing


Early Diastolic Sounds

Opening Snap of Mitral Stenosis (MS)

○ High pitched-Left Lateral Decubitus Position, Apex.

0.04-0.12 sec after A2 (S3 occurs 0.12 sec after A2)

○ Occurs after S2, before S3

○ MS More Severe with Short A2-OS Interval & softer

OS or absent OS

Paricardial Knock

○ Chronic Constrictive Pericarditis

○ Mitral Regurgitation

○ Atrial Myxoma

○ Older Model Prosthetic Mitral Valve


Mechanism of OS

Stenotic anterior mitral valve leaflet suddently bulging download into the left ventricular cavity like a dome, with a snapping sound when the mitral valve is rapidly opened during diastole. So OS is heard only if AML of mitral valve is mobile.

OS occurs when movement of AMV suddenly stops, at point when LVP drops below that of LAP.


OS S2 S3

Area Just inside

apex/entire

chest wall

2nd & 3rd left ICS Only Apex

Relation to

posture

A2-OS interval

wides on

standing

A2-P2 interval

narrows on

standing

Disappear of

sitting

Intensity on

standing

Remain

same/intensified

Decreases -

Relation to

respiration

A2-OS interval

constant

throught

respiration

Split increase

on respiration

None

Intensity on

respiration

Same - RVS3 Load

during

inspiration

A2-OS/A2-

P2/A2-S3

interval

- A2-P2 interval

shorter than A2-

OS interval

A2-S3 interval is

longer than A2-

OS interval

Pitch High(Best heard

with diaphtagm)

High Low (With Bell)


Auscultation-

Timing of A2 to OS Interval

Say Timing

seconds

Severity

of MS

Other

HS’s

Prrr 0.06 Severe

Pada .07-.08 Mod-

severe

Pata .08-.09 Mod

Papa 0.10 Mild PK 0.1-0.110

Tu-

huh .12 A2-S3

0.12-0.18


Gallop:

1)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


Mid Diastolic Sounds

S3

Occurs During Rapid Filling of Left Ventricle (LV) related to LV Volume

Low Frequency Best Heard

○ At the Apex w/Bell

○ Pt in Left Lateral Decubitus Position

Can Be Normal to Age 40???

Can be Pathognomonic for Congestive Heart Failure


Late Diastolic Sounds

S4

During Atrial Phase of LV Filling

○ Consequence of Ventricular Stiffness

Absent in Atrial Fibrillation or Ventricular

Pacing

Low Frequency Sound Best Heart

○ At the Apex

○ Pt in Left Lateral Decubitus Position

HTN, Aortic Stenosis, Ischemic Heart Disease


Diastolic Sounds

Right Sided S3, S4

Left Lower Sternal Boarder

Intensity Varies with Respiration due to Right

Heart Filling (Carvallo’s Sign)

Summation Gallop

Occurrence of an Over Lapping S3 and S4 due

to Tachycardia


Murmurs (Latin word) Sudden deceleration of blood produces

heart sounds while Heart murmurs are produced by turbulent flow (Raynold’snumber >2000) across an abnormal valve, septal defect or outflow obstruction, or by increased volume or velocity of flow through a normal valve.

Murmurs may occur in a healthy heart. These 'innocent' murmurs occur when stroke volume is increased, e.g. during pregnancy, and in athletes with resting bradycardia or children with fever.


Mechanism

Blood velocity

Blood vascosity

Valve: narrowed or incompetent;

organic or relative

Abnormal connection

Vibration of loose structure

Diameter of vessel or


Points to be examined in murmur

Timing

Shape

Intensity

Duration

Location of maximum intensity

Character

Pitch

Radiation

Variation with respiration

Variation with position

Variation with other maneuvers

Best heard with bell or diaphram


Common Murmurs and

Timing

Systolic Murmurs

Aortic stenosis

Mitral insufficiency

Mitral valve prolapse

Tricuspid insufficiency

Diastolic Murmurs

Aortic insufficiency

Mitral stenosis

S1 S2 S1


Describing a heart murmur

1. Timing

murmurs are longer than heart sounds

HS can distinguished by simultaneous palpation of the

carotid arterial pulse

systolic, diastolic, continuous

2. Shape

crescendo (grows louder), decrescendo, crescendo-

decrescendo, plateau

3. Location of maximum intensity

is determined by the site where the murmur originates

e.g. A, P, T, M listening areas


Describing a heart murmur con’t:

4. Radiation

reflects the intensity of the murmur and the direction

of blood flow

5. Intensity

graded on a 6 point scale

○ Grade 1 = very faint

○ Grade 2 = quiet but heard immediately

○ Grade 3 = moderately loud

○ Grade 4 = loud

○ Grade 5 = heard with stethoscope partly off the chest

○ Grade 6 = no stethoscope needed

*Note: Thrills are assoc. with murmurs of grades 4 - 6


Describing a heart murmur con’t:

6. Pitch

high, medium, low depending upto high/medium/low

velosity jet

7. Quality

blowing, harsh, rumbling, and musical

8. Others:

i. Variation with respiration

○ Right sided murmurs change more than left sided

ii. Variation with position of the patient

iii. Variation with special maneuvers

○ Valsalva/Standing => Murmurs decrease in length and intensity

EXCEPT: Hypertrophic cardiomyopathy and Mitral valve prolapse


Grades of intensity of murmur

Grade 1 Heard by an expert in optimum conditions

Grade 2 Heard by a non-expert in optimum conditions

Grade 3 Easily heard; no thrill

Grade 4 A loud murmur, with a thrill

Grade 5 Very loud, often heard over wide area, with thrill

Grade 6 Extremely loud, heard without stethoscope

Levine & Freeman’s Grading


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 makemurmur

of TI, TS ,PI

- Expiration:

- Valsalva maneuver: thorax pressure

venous return M of IHSS


3) Exercise:

- HR

- Blood volume

- Blood velocitymake the murmur of MS

Left sided murmurs increases on expiration

while right sided murmur increased on

Inspiration.

Basal (Aortic & Pulmonary) murmurs increases

on sitting and leaning forward while apical (Mitral &

Tricuspid) murmurs increases on left lateral position.


Systolic Murmurs

Derived from increased turbulence associated

with:

1. Increased flow across normal SL valve or into a

dilated great vessel

2. Flow across an abnormal SL valve or narrowed

ventricular outflow tract - e.g. aortic stenosis

3. Flow across an incompetent AV valve - e.g. mitral

regurg.

4. Flow across the interventricular septum


Holosystolic vs Pansystolic

murmur

A holosystolic murmur is one which lasts from the end of S1 to the beginning of S2.

A pansystolic murmur is one which lasts from the beginning S1 to the end of S2, and therefore obscures these heart sounds.

The difference between them is academic in terms of the diagnosis. Pansystolicmurmurs are often louder and more significant.


Diastolic Murmurs

Almost always indicate heart disease

Two basic types:

The term early diastolic murmur is misleading because the murmur usually

lasts throughout diastole, but it is loudest in early diastole.

1. Early decrescendo diastolic murmurs

signify regurgitant flow through an imcompetent semilunar valve

○ e.g. aortic regurgitation

2. Rumbling diastolic murmurs in mid- or late diastole

suggest stenosis of an AV valve

○ e.g. mitral stenosis


Classification and causes of diastolic murmur


Continuous Murmurs

Begin in systole, peak near s2, and continue into all or

part of diastole.

1. Cervical venous hum

Audible in kids; can be abolished by compression over the IJV

2. Mammary souffle

Represents augmented arterial flow through engorged breasts

Becomes audible during late 3rd trimester and lactation

3. Patent Ductus Arteriosus

Has a harsh, machinery-like quality

4. Pericardial friction rub

Has scratchy, scraping quality


Non-Audible murmurs at apex

and pulmonary area


Functional Murmur: short and soft SEM

Normal S1 and S2

Normal cardiac impulse

No evidence for hemodynamic

abnormality


Innocent or Normal Murmurs-

Systolic Vibratory Systolic Murmur (Still’s Murmur)

Pulmonic Systolic Murmur (Pulmonary Trunk)* Mammary Soufflé*

Peripheral Pulmonic Systolic Murmur (Pulmonary Branches)

Supraclavicular or Brachiocephalic Systolic Murmur

Aortic Systolic Murmur*common in pregnancy

Still’s Murmur ○ Medium Frequency, Vibratory, Originating from

Leaflets of Pulmonic Valve


Innocent or Normal Murmurs-

Continuous

Venous Hum

Continuous Mammary Soufflé


Changing murmurs

Murmurs which change in character or

intensity from moment to moment.

Carey-coombs’ murmur

Infective endocarditis

Atrial Thrombus

Atrial Myxomas


The Carey Coombs murmur or

Coombs murmur A clinical sign which occurs in patients with

mitral valvulitis due to acute rheumatic fever.

It is described as a short, mid-diastolic rumble best heard at the apex, which disappears as the valvulitis improves.

It is often associated with an S3 gallop rhythm, and can be distinguished from the diastolic murmur of mitral stenosis by the absence of an opening snap before the murmur.

The murmur is caused by increased blood flow across a thickened mitral valve.


Named murmurs Carey Coombs murmur- Mid diastolic murmur, in

rheumatic fever

Austin Flint murmur- mid- late diastolic murmur,inAortic Regurgitation.

Graham- Steel murmur- high pitched, diastolic, inpulmonary regurgitation.

Rytands murmur - mid diastolic atypical murmur, in Complete heart block.

Docks murmur-diastolic murmur, Left Anterior Descending(LAD) artery stenosis.

Mill wheel murmur- due to air in RV cavity following cardiac catheterization.

Stills murmur- inferior aspect of lower left sternalborder, systolic ejection sound,vibratory/musical quality,in subaortic stenosis, small VSD

Gibson’s murmur: continous machinary murmur of PDA


Gallaverdin Phenomenon: The Gallavardin phenomenon is a clinical sign found in

patients with aortic stenosis. It is described as the dissociation between the noisy and musical components of the systolic murmur heard in aortic stenosis.

The harsh noisy component is best heard at the upper right sternal border radiating to the neck due to the high velocity jet in the ascending aorta. The musical high frequency component is best heard at the cardiac apex.

The presence of a murmur at the apex can be misinterpreted as mitral regurgitation. It is presumably due to high frequency vibrations traveling to the apex from the calcific aortic valve.

However, the apical murmur of the Gallavardin phenomenon does not radiate to the left axilla and is accentuated by a slowing of the heart rate (such as a compensatory pause after a premature beat) whereas the mitral regurgitation murmur does not change.

The sign is named after Louis Gallavardin, having been described by Gallavardin and Ravault in 1925.


Dynamic Auscultation

All patients with a new murmur should

undergo dynamic auscultation:

Respiration: right sided murmurs are louder during

inspiration, expiration has the opposite effect

Valsalva manoeuvre:

Postural Changes

Isometric exercise

Squatting:

Vasoactive agents – Amyl Nitrite


Respiration

Expiration :A2,P2 of second Heart sound separated <30ms ;single sound

Inspiration: Splitting interval widens ;A2,P2 heard as 2 distinct sounds

DIASTOLIC & EJECTION SOUNDS:

S3 & S4 from Rt ventricle;augment in inspiration ;diminish during exhalation.

Opening Snap of MV- soft in inspiration;loud in exhalation

Inspiration decreases intensity of ejection sounds in PS , No effect on aortic ejection sounds.

MURMURS

Inspiration: Diastolic murmur of TS,Pulmonaryregurgitation murmur,systolic murmur of TR,pre-systolic murmur of Ebstein anomaly are accentuated

Mid-systolic click, systolic murmur of MVP accentuated.


Valsalva Maneuver

Deep inspiration followed by forced exhalation against a closed glottis for 10-20 secs.

Phase 1:transient rise in systemic arterial pressure.

Phase 2:decrease in systemic venous return,systolic pressure & pulse pressure; reflex tachycardia.

Phase 3:abrupt transient decrease in arterial pressure.

Phase 4: overshoot of systemic arterial pressure & reflex bradycardia.


Phase 2:

S3 & S4 attenuated.

A2-P2 interval narrows

Systolic murmurs of AS & PS;MR,TR diminish.

Diastolic murmurs of AR &PR;TS,MS-soften.

Lt ventricular volume decreases;systolic murmur of HOCM amplifies ;click,late systolic murmur of MVP begins earlier.

Phase 3:

Sudden increase in systemic venous return;wide split of S2;augmentation of murmurs & filling sounds Rtside heart.

Phase 4:

Murmurs & filling sounds Lt side return to control & transiently increase.


Postural changes & Exercise:

Lying from standing/passive elevation of both legs :

Widening of S2 split

Augmentation of Rt S3 & S4; Lt S3,S4

Systolic murmurs of PS,AS,MR,TR& VSD augmented

Lt ventricular EDV increased;systolicmurmur of HOCM diminished & mid-systolic click,late systolic murmur of MVP are delayed /attenuated.


Squatting

Increase in venous return & systemic resistance simultaneously;Stroke volume and arterial pressure rise-transient reflex bradycardia.

Augmentation of S3 & S4 (both ventricles)

Systolic murmurs of PS & AS ;diastolic murmurs of TS & MS become louder.(Rt sided preceding Lt)

Elevated arterial pressure;increases blood flow through Rt ventricular outflow tract in TOF

Systolic murmur of VSD increases.

The combtn of increase in arterial pressure and increase in venous return increases Lt ventricular size which decreases obstruction to outflow;intensityof HOCM murmur ;mid-systolic click,late systolic murmur of MVP delayed.


Left Lateral recumbent position

Accentuates S1,S3,S4 from Lt side of the heart.

OS,murmurs of MS,MR;Mid-systolic click and late systolic murmur of MVP.

Isometric Exercise

Increase in systemic vascular resistance,arterialpressure,HR,CO,Lt ventricular filling pressure and heart size.

S3 & S4 on Lt side is accentuated.

Systolic murmur of AS decreases.(reduced pr gradient across aortic valve.)

Diastolic murmur of AR,systolic murmur of MR ,VSD increase in intensity.

Diastolic murmur of MS –louder.

Systolic murmur of HOCM decreases & systolic click, late systolic murmur of MVP is delayed.(increase in LV volume)


Amyl Nitrite

Marked vasodilatation;redtn in systemic arterial

pressure;reflex tachycardia;increase in CO and

HR

S1 augmented;A2 diminished

OS of mitral and tricuspid valve become louder

A2/OS interval shortens

S3 augmented

Systolic murmurs of AS,PS,HOCM,TR and

functional systolic murmurs are accentuated.


Murmur Analysis with Dynamic Auscultation


Back to the Basics

1. When does it occur - systole or diastole

2. Where is it loudest - A, P, T, M

I. Systolic Murmurs:

1. Aortic stenosis - ejection type

2. Mitral regurgitation - holosystolic

3. Mitral valve prolapse - late systole

II. Diastolic Murmurs:

1. Aortic regurgitation - early diastole

2. Mitral stenosis - mid to late diastole


Summary

A. Presystolic murmur

Mitral/Tricuspid stenosis

B. Mitral/Tricuspid regurg.

C. Aortic ejection murmur

D. Pulmonic stenosis (spilling

through S20

E. Aortic/Pulm. diastolic

murmur

F. Mitral stenosis w/ Opening

snap

G. Mid-diastolic inflow murmur

H. Continuous murmur of PDADr.Vitrag Shah - www.medicalgeek.com

THANK YOU


heart sounds and murmur

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