Heart murmurs & Dynamic Auscultation

Dr Nithin P G

Outlay of Seminar

• Definition

• What to look for/ how to describe a murmur

• Classification of murmurs

• Types of murmurs

• Dynamic Auscultation

Definition of murmur

• “Relatively prolonged series of audible vibrations”

• Characterized by the timing in

cardiac cycle, intensity (loudness),

frequency (pitch), quality,

configuration, duration and direction

of radiation.

How is a murmur produced and heard?

How is a murmur produced?

Sound is produced by vibration

Turbulence generated in the blood column vibrations set up in the vessel wall & cardiac structures murmurs

How is a murmur produced?

L = linear dimension (internal diameter In pipes)

V = mean fluid velocity Q = volumetric flow rateA = pipe cross-sectional

area m = dynamic viscosity of the fluid

n = kinematic viscosity [ / mr]

r = density of the fluid

Q = V1*A1= V2*A2

Q = P/R

[Re >4000 turbulent flow]

Re => Turbulence => murmur

Auscultation of murmur

Other factors affecting auscultation of murmur

• Distance from chest wall, position of patient

• Underlying soft tissue, lung, fluid

• Quality of apparatus

Auscultation of murmur

Upper 3rd L St-C Jn

4th L cos. cart. in L St. border4th RICS

How to describe a murmur?

Description of a Murmur

• Position in the cardiac cycle

• Site of murmur [max. intensity]

• Intensity

• Quality & Pitch

• Conduction

• Dynamic changes

Position in the cardiac cycle

early systolic mid systolic• Systolic murmur late systolic pan/holo systolic early diastolic• Diastolic murmur mid diastolic pre systolic

• Continuous murmur

Site of murmur

Systolic Diastolic Continuous

Apex MR MS, Flow mur.

LLSB TR, VSD TS, Flow mur.

RSOV to RV, RLSB- RSOV to RA, Cor AVF

ULSB PS PR, AR PDA- 1 & 2 LICS,APW- 3 LICS

URSB AS

Others

Intensity- Grading

FREEMAN & LEVINE GRADINGGRADE 1- faintest murmur which can

be heard only with special effort.

GRADE 2- soft but readily audibleGRADE 3- loud without thrillGRADE 4- loud with thrill

GRADE 5- heard with steth partially off the chest

GRADE 6- heard with steth held off the chest wall.

Quality & Pitch

• Depends on two factors1. Pressure difference or gradient- Gr

pitch2. Amount of Flow- Flow pitch

PITCH Hz Flow

Pr Gr

QUALITY

E.g.:

LOW 25-125

rumbling

MDM-MS

MEDIUM

125-300

harsh AS

HIGH >300 blowing MR,AR

Conduction of murmur

Site to which conducted aids in diagnosis

• MS localized to apex

• MR conducted to axilla and back; LLSB in MVP-MR

• AS conducted to Carotids

Classification & types of murmurs

Classification & types of murmurs

early systolic mid systolic• Systolic murmur late systolic pan/holo systolic early diastolic• Diastolic murmur mid diastolic pre systolic

• Continuous murmur

Systolic Murmurs

Midsystolic murmur

• Most common murmur heard in everyday practice.

• Starts at an interval after S1 and ends before S2.

• It could be PATHOLOGICAL INNOCENT/PHYSIOLOGICAL • 5 settings

1. Ventricular outflow obstruction2. Dilation of aorta and pulmonary trunk3. Accelerated systolic flow into aorta or

pulmonary trunk4. Innocent midsystolic murmur( including those

due to morphological changes of valve with no obstruction)

5. Some forms of MR

Ventricular outflow obstruction

Phasic flow across left and right outflow tract

• Isovolumic contraction (b) • Maximal ejection (c) • Start of relaxation and

reduced ejection (d) • Isovolumic relaxation (e)• LV filling, rapid phase (f) • Slow LV filling (diastasis)

(g) • Atrial systole or booster

(a)

AS

• IVC S1 ventricular pressure increases opening of Aorta and pulmonary valve ejection commences and murmur begins

• Ejection increases murmur becomes crescendo• Ejection declines murmur in decrescendo• Murmur ends before ventricular pressure drops

below aortic pressure at which aortic valve and pulmonary valve closes generating a2 and p2

AS

• Harsh, crescendo-decrescendo MSM

• Early sys peak short duration vs. Late systolic peak long duration

• Always Symmetrical [vs. PS]

• ES absent in calcific valves, sub and supra valvular AS

• Length and loudness do not necessarily corresponds to severity but length more suggestive of severity than other murmurs

S4

Reverse splitting S2

AS

• Gallaverdin phenomenon/ hourglass phenomenon

Lower n (aortic) vs. Higher n (mitral) periodic vibrations of stiffened non calcific aortic valve

• Differentiating from MRMR AS [ Gallaverdin]

Apical mid sys/ Holosystolic

Apical mid sys

A2 buried in late sys vibrations

Clear S2 heard

P/PVC unchanged P/PVC mur =

End of Long cycles in AF unchanged

End of Long cycles in AF =

AS

Postextrasystolic enhancement results from the variable interaction of three factors:

1) Increase in the contractile state (inotropism) of the ventricular muscle which is more evident if there is hypertrophy and/or depressed ventricular function.

2) The pause provides longer filling time for the ventricle, which is more consequential in hypertrophic ventricles (e.g., aortic stenosis) than in ventricular volume overload states (e.g., mitral regurgitation).

3) Lastly, there is more time for arterial runoff, and in the case of aortic regurgitation, more backflow into the ventricle. This effect lowers the arterial diastolic pressure and the impedance to forward flow (afterload) in the beat following the pause.

AS

Valvular AS

Supra valvular

Sub valvular

BP difference

nil RUL > LUL Nil

Thrill Max 2 RICS; Supra sternal & carotids

Max Right carotid

Mid LSB

Ejection sound

Present Absent Absent

Murmur Maximum

2 RICS 1 RICS Mid LSB

Assoc AR +/- rare +/-

HOCM• Dynamic LVOT obstruction• Factors increasing

gradient– LV Contractility

• Exercise• Cathecolamines• Digitalis

– Ventricular Volume • Valsalva• Standing• Nitroglycerine/ Amyl

nitrate• Tachycardia

– Aortic impedance and pressure• Sustained Handgrip• Passive Leg Raise

PS• Murmur brought on by

a phasic ejection click; radiates up & left

• As severity increases length increases and P2 becomes soft (abruptness of closure reduced), S2 split widens, S4

• Loses symmetry becomes kite shaped

• May engulf A2 and P2 may be inaudible; may be confused with VSD

PS

Other causes of MSM

Dilation of Aorta & Pulmonary trunk• Short soft midsystolic murmur• Left sided murmurs in marfan’s syndrome,

syphilis• Right sided murmurs in idiopathic dilation

of pulmonary artery, pulmonary hypertension

MSM of Hyperdynamic circulation• Normal aorta or pulmonary trunk but

increased flow• Anaemia, pregnancy, fever, thyrotoxicosis

Other causes of MSM

OS-ASD• Rapid flow across pulmonary valve to

dilated pulmonary trunk

Pure AR• Due to Accelerated LV ejection

Physiological causes

Innocent systolic murmur

• Still’s murmur

• Pulmonary mid systolic murmur

• Peripheral pulmonary systolic murmur

• Supraclavicular or brachiocephalic systolic murmur

• Aortic sclerosis

• Systolic mammary soufflé

Physiological murmurs

Still’s murmur

• Short buzzing murmur ‘twanging of a rubber band’

• Pure medium frequency by periodic vibrations of pulmonic leaflets at their attachment

Physiological murmurs

Pulmonary mid systolic murmur & Peripheral pulmonary systolic murmur

• Angulation and disparity between pulmonary trunk and its branches turbulent flow

• Normally disappears with maturity of pulmonary bed

Physiological murmurs

Supraclavicular or brachiocephalic systolic murmur

• Aortic origins of major normal brachiocephalic arteries

• Crescendo-decrescendo, abrupt onset, short, sometimes radiating below clavicle

• vs. supra valvular AS – these murmur are softer below clavicle and decreases with shoulder abduction

Physiological murmurs

Mammary Soufflé

• Late Pregnancy or puerperium

• Sometimes continuous louder in systole, distinct gap from S1 [ time for ejected blood to reach mammary arteries]

• 2 or 3 RICS/ LICS• Light Pressure

augments murmur becomes continuous; firm Pr abolishes murmur

Pan Systolic/ Holo Systolic Murmur

Flow from a chamber or vessel whose pressure or resistance throughout systole is higher than pressure or resistance of the chamber receiving the flow

• Mitral Regurgitation• Tricuspid Regurgitation• Ventricular Septal Defect• Aorto Pulmonary Window• Patent Ductus Arteriosus with PAH

Mitral Regurgitation

• S1 to S2 provided MV remains incompetent and gradient remains

HolosystolicEarly systolicLate systolicSometimes MSM

• Radiates to axilla and back becos jet directed posterolaterally in LA

LLSB when jet directed against atrial septum near base of aorta

Tricuspid Regurgitation

• LLSB- RA• Rivero Carvallo’s sign- Increased VR, increased RV

volume Increased SV velocity of regurgitant flow Sometimes TR heard only during inspiration Carvallo’s sign disappears in RV failure• Diff from organic TR

– PSM vs. ESM– High n vs. Medium n– Features of PAH present

Ventricular Septal Defect

Depends on site, size and gradient

• Very restrictive VSD- ESM decrescendo pattern

• Mod and NR VSD- PSM• Sub arterial VSD- 1 or 2 LICS

similar to PS murmur• Septal aneurysms- click with

LSM or PSM with late Sys Accentuation

• Large shunt – MDM• NR VSD with PAH- ESM • PSM absent in Eissenmenger

Syndrome

Other PSM

• Aorto Pulmonary Window with PAH– Otherwise continuous murmur– Diastolic component reduced with increasing PAH

• PDA with PAH– Similar mechanism

ESM

Acute Mitral Regurgitation

• Decrescendo murmur

• Non distensible LA , large v wave approaching LV pressure in late systole

• Maximum flow early systole and minimum to nil flow in late systole

Other ESM

• Normal pressure TR, Organic TRTall RA v waves reach the level of normal RV

pressure in late systole, so lower rate of regurgitant flow

Moderate to low frequency as compared to high frequency in high pressure TR

• VSD with PVR or small muscular VSD-Equalization of pressures in cases of PAH-Small VSD closes in late systole

LSMMVP• Leaflets remains competent

during early ventricular contraction but overshoot in late systole [critical V. dimensions]

• One or more mid systolic clicks precede murmur [sudden deceleration of the column of blood against the prolapsed leaflet or scallops]

• Longer and softer– Prompt standing after

squatting– Valsalva II

• Short & louder– squatting– Sustained hand grip– Amyl nitrate

Other LSM- papillary muscle dysfunction

Post Pap Muscle . Late systolic cresendo to S2

Barlow’s syndrome refers to the spectrum of symptoms caused by MVP [click or murmur alone to palpitations, chest pain, or syncope]

Diastolic Murmurs

Early diastolic murmur

• AR murmur

-Soft high frequency early diastolic murmur with pt sitting & leaning forward in full held expiration

-3 LICS [ 2 & 3 RICS in root dil]

-musical quality in eversion

-Austin Flint murmur

-Cole- Cecil murmur- AR murmur in left axilla due to higher position of apex

AR

• Difference between acute and chronic AR

• Austin Flint Murmur to be discussed

A/C AR C/C AR

Short mur. -early equalization of diastolic pressures

Long mur.

Medium n –velocity less rapid and pressure gradient lower

High n

Associated S4

High Pressure PR

• High pitched soft blowing decrescendo murmur usually lasts throughout diastole heard in the left upper sternal border

• Associated with loud P2 and other features of PAH

• PR vs. AR– Loud P2, murmur begins after

P2– Normal pulse pressure– Clinical setting– Squatting and sustained

hand grip increases AR

High Pressure vs. Normal Pressure

High Pressure

Normal pressure

Decrescendo Crescendo decrescendo

High frequency

Medium to low pitched

Onset immediately with p2

Delayed in onset

Usu extends throughout diastole

Short duration

Features of PAH present

Usually absent

Mid Diastolic Murmur

-Begin At Clear Interval After S2

I Rapid Filling Phase Av valve obstruction Stenotic AV valves, tumors

Functional obstructionAbnormal patterns of AV flow increased flow

volume

increased flow

velocity II Incompetent Pulmonary Valve [PR with

normal PA Pressure]III Atherosclerotic extramural coronary

arteries

Mid Diastolic MurmurRV- TS

LV- MS- Austin Flint murmur

- Carey-Comb's

OTHERS-Atrial Myxoma

- TR

- ASD

- VSD- PDA- MR

MS

• Low n rough rumbling [sound of distant thunder] MDM

• Localized to apex, better heard in left lateral position with bell

• Length a severity• Long murmurs up to S1 even in long cycles of AF-

severe MS• Late diastolic or Pre systolic accentuation usually

seen in pliable valves and in NSR [ sometimes in AF]

TS

• Similar to MS

• Murmur usually seen associated with AF

• Diff. from MS– Increases during inspiration [Augmentation of

RV volume, RV Diastolic Pr., Flow rate and gradient

across valve] – LLSB

PR with normal PA pressures

• PR assoc with Cong PS, PV IE, repair of RVOT

• Negligible gradient at the start of diastole, gradient increases especially during the IVR phase of RV when murmur reaches maximum intensity.

• 2 & 3 LICS• Medium to low

pitched• Delayed in onset • Short duration• Ending before S1

Austin Flint Murmur• Severe AR regurgitant jet directed toward

the AML prevent the latter from opening well during diastole generating turbulent flow

• Low n MDM or late diastolic, best heard at the apex.

• To differentiate from MS– No OS– Amyl nitrate inhalation AR, Austin flint murmur

Other Mid Diastolic Murmur

• Carey Coomb’s murmurs

– Acute rheumatic fever, mitral valve structures acutely inflamed with some thickening and edema turbulence of flow during the rapid filling phase.

+ moderate MR [increased mitral inflow in diastole]

– Low pitched short MDM.

– good evidence of active carditis

Flow Murmurs

• Increased AV flow

• TR, ASD, MR, VSD, PDA, hyperdynamic circulation

• To differentiate from MS & TS– Short MDM– Medium Pitch- increased flow– Preceded by S3

– Absence of Opening Snap– Thrill less common

Late Diastolic/ Pre-systolic Murmurs

MS• Higher frequency than MDM• Sometimes only PSA heard- mild MS• Generally absent in calcified valves and

most of AF [ may be present during short cycle lengths in AF]

• Cause-– Increased flow during atrial contraction in

late systole– Increased dp/dt of LV contraction

increases turbulence [ esp. in AF short cycles]

Other diastolic murmurs

• Cabot– Locke Murmur- [Diastolic Flow murmur] – The Cabot–Locke murmur is a diastolic murmur that

sounds similar to aortic insufficiency but does not have a decrescendo; it is heard best at the left sternal border. [High flow thru coronary vessels, LMCA, LAD]

– The murmur resolves with treatment of anaemia.

• Dock’s murmur – diastolic crescendo-decrescendo, with late

accentuation, [consistent with blood flow through the coronary] in a sharply localized area, 4 cm left of the sternum in the 3LICS, detectable only when the patient was sitting upright.

– Due to stenosis of LAD

Other diastolic murmurs

• Key–Hodgkin murmur – EDM of AR; it has a raspy quality, [sound of a saw

cutting through wood]. Hodgkin correlated the murmur with retroversion of the aortic valve leaflets in syphilitic disease.

• Rytand’s murmur in complete heart block– MDM or Late diastolic murmur– Atrial contraction coincides with the phase of rapid

diastolic filling increased flow short MDM [intermittent].

– Another theory- Delayed V. contraction following A. contraction may lead to diastolic MR & TR, because AV valve closure does not occur [unless V. systole supervenes]. When higher V than A pressure during atrial relaxation, an incompletely closed AV valve may lead to a reverse gradient with a considerable regurgitation volume.

Continuous murmur

Continuous murmur

• Begin in systolic and continues without interruption through the timing of S2 into all or part of diastole

• Flow from zone of higher resistance into lower resistance without phasic interruption b/w systole & diastole

1. Connection b/w high pressure chamber/vessel & low pressure chamber/vessel

2. Disturbance in flow patterns in arteries3. Disturbances in flow patterns in veins

Connection b/w high pressure chamber/vessel & low pressure

chamber/vessel1. From the aorta

a. Persistent ductus arteriosusb. Aorto-pulmonary windowc. RSOV

2. From the coronary artery:1. Coronary arteriovenous fistulae draining into RA, RV,

PA2. ALCAPA

3. Other arteriovenous communications1. Broncho-pulmonary collaterals2. Chest wall arteries–pulmonary vessels3. Peripheral A-V Fistula

4. Others1. Lutembacher syndrome with restricted ASD

PDA

• Gibson’s murmur• At 1 or 2 LICS• NR- high frequency soft murmur peaks around S2• Mod R- loud coarse machinery murmur with eddy

sounds

SEVERITY

PDA with no continuous murmur

• Neonates- due to high PVR

• Very small ductus• Very large ductus &

large VSD- due to equalization of pulm and sys Pr

• PAH- first dia component goes, then sys

• AS, CoA- due to low aortic pressure

Continuous murmurs

• APW– 2 or 3 LICS– Usually associated with early devp of eissenmenger

• RSOV– No peaking at S2 seen [peaks in sys or dia.]– To RA- RLSB RV- LLSB RVOT- 3 LICS

• Lutembacher syndrome with restricted ASD– LLSB [body of RA]

Continuous murmurs

• C-AVF– RA- RLSB or RUSB– CS- back b/w spine & Lt scapula– RV inflow- LLSB– RVOT- Upper to Mid LSB [beat to beat change in

murmur may be present, RV systolic compression, valsalva softens murmur]

– PA- ULSB [no eddy sounds]

• ALCAPA– Murmur louder in diastole [LV contr. I/C flow] – Do not peak at S2– Usu LUSB or RUSB

- LA- ULSB rad to Lt ant ax line

- Lt SVC- upper to mid LSB

Disturbance in flow patterns in arteries

• AV Fistula– Murmur heard in the venous side

• Due to rapid blood flow- – cervical venous hum, mammary soufflé,

hyperthyroidism, hemangioma, hyperemia of neoplasm (HCC, RCC, Paget’s disease)

• Stenosed arteries with inadequate distal collaterals– aortic arch vessel occlusions, atherosclerotic carotids,

coarctation of aorta, main pulmonary artery stenosis and periph pulmonary artery stenosis

Disturbances in flow patterns in veins

Venous hum• Healthy children, young healthy adults, pregnancy• Sitting, Bell, medial aspect of Rt SCl fossa, with face

pulled leftwards & upwards disappears when returned to normal position

• Louder in diastole, +/- high pitched whine• Radiation to infra clavicular areas confuse with other

mur. Check by obliteration

Dynamic Auscultation

Dynamic Auscultation

It refers to the technique of altering

circulatory dynamics by a variety of

physiological and pharmacological

maneuvers and determining the effects of

these maneuvers on heart sounds and

murmurs .

Intervention

• Position

• Physical maneuvers

• Pharmacological

Position

A. Lt Lateral DecubitusLV impulse [apical sounds, murmurs better heard]Act of turning increases HR[ MDM & PSA of MS ], induces PVC [AS murmur vs. MR murmur

(n/c)]

B. Sitting leaning forward full held expirationAR & PR EDM

C. Sitting with legs danglingFurther reduces venous returnIf S2 fails to fuse on sitting

D. Elbow Knee PositionPericardial friction rub

Position

E. Standing to squatting and vice versa– Standing[ venous return, BP ]; [opp. in squatting] 1. All murmurs [except HOCM , MVP earlier]

• HOCM [ LV contractility, after load, preload]• MVP [ preload, afterload ]

2. A2- P2 , A2-OS , A2-S3 (n/c)

F. Hyperextension of shoulders supraclavicular Systolic murmurs

G. Stretching of NeckVenous hum

H. Passive elevation of both legsTransiently increases venous return, increase S3

Physical Maneuvers

Inspiration

• Right sided events become more prominent

• S2 split appreciable

• RVs3 RVs4 prominent

• Tricuspid sys & dia Mur increased

• Pulm ejection sound reduced

Expiration

• Left sided events become more prominent

• Diff AR & PR

• Pericardial friction rub [exhalation & supine]

• Innocent pulm mid sys murmur becomes more prominent becos of reduced AP diameter

Inspiration followed by forced exhalation against a closed glottis for 10 to 20 seconds

Physician has to keep flat of the hand on the abdomen to provide the patient a force to breathe against

Not attempted in patients with IHD

Normal response has four phases

Valsalva Maneuver

Valsalva Maneuver

• initial pulm VR = SV

• I/T Pr directly transmitted to aorta. I/T Pr = VR =

BP

sympathetic tone HR

Sudden I/T Pr = BP

sudden return of peripherally pooled blood to the vaso-constricted arterialsystem (20 to the increased sympathetic tone)

Phase II – Decrease in systemic venous return , systolic pressure and pulse pressure

• S3 & S4 attenuated

• A2-P2 interval narrows

• All murmurs except MVP / HOCM decrease

Phase III- increased Left murmurs & Phase IV- increased Right murmurs

Valsalva Maneuver

Valsalva Maneuver

I/T Pr = VR = BP

sympathetic tone HR

sudden return of peripherally pooled blood to the vaso-constricted arterialsystem (20 to the increased sympathetic tone)

PHASE II

PHASE IV

MAXIMAL SYMPATHETIC ACTIVATION

FLAT PART OF STARLING’S CURVE

HEART FAILURE

ASD

MS

Isometric Exercise

Calibrated Handgrip device or a handball.Better to carryout bilaterally, sustained for 20-30 secsNot to be done in arrhythmia / Ischemia

Transient but significant increase in SVR, BP, HR , CO , LV filling pressure , Heart size

1. LVS3 & LVS4 increases2. Systolic Murmur of AS reduced – reduced gradient

across aortic valve3. AR , MR , VSD – increased4. MDM of MS – increased 5. Syst Murmur of HOCM reduced6. MVP murmur + click delayed

• Few minutes of brisk walking sufficient

• Must be auscultated quickly before effect wears off

– Increases Ms murmur in low output states

– Wide Split of S2 in RVF further widens after exercise

Isotonic Exercise

Pharmacological Maneuvers

Inhalation of Amyl Nitrate [Crush ampoule in towel, 3-4 deep breaths over 10–15 s]

Lasts 2 minutes

No reduction in stroke volume as seen in NTG

First 30 secs 30 to 60 secs > 60 secs

Decreased Sys Art Pressure

Reflex Tachycardia

Increased CO, HR

Amyl Nitrate inhalation

• AS vs. MR

• TR vs. MR

• PS vs. TOF

• MS vs. Austin F

• PR vs. AR

• HOCM vs. MVP [n/c]

Long cycle length

Long cycle length after PVC or in long cycles of AF

– Increases murmur of AS, HOCM, PS

– Murmurs of MR, TR has no change

Thank you

AnatomyThe pulmonary orifice is situated in the upper angle of the third left sternocostal articulation; the aortic orifice is a little below and medial to this, close to the articulation. The left atrioventricular opening is opposite the fourth costal cartilage, and rather to the left of the midsternal line; the right atrioventricular opening is a little lower, opposite the fourth interspace of the right side. The lines indicating the atrioventricular openings are slightly below and parallel to the line of the coronary sulcus. The coronary sulcus can be indicated by a line from the third left, to the sixth right, sternocostal joint

AR Pressure Tracing

• Femoral artery pr 140/45• LV Pr 118/39• Pp= 100 [ n =40]• End Diastolic Diff between Aorta and lv is 5-6 mm [ n

= 70]

• Wide PP, Rapidly rising slope, elevated LVEDP, near end diastolic equalization of pressures between aorta and LV = AR

Pharmacological Maneuvers

Inhalation of Amyl Nitrate [Crush ampoule in towel, 3-4 deep breaths over 10–15 s]

First 30 secs 30 to 60 secs > 60 secs

Decreased Sys Art Pressure

Reflex Tachycardia

Increased CO, HR

S1 – AugmentedA2 – DiminishedOS – Becomes louderA2-OS interval shortensS3- Either ventricles – augmentedAS , PS , HOCM , TR , Functional murmursAll augmented