MURMUR AND MURMUR AND Dynamic AuscultationDynamic Auscultation OF Cardiovascular OF Cardiovascular

SystemSystem

ANKUR KAMRA

Defining a heart murmur

A cardiac murmur is defined as a relatively prolonged series of auditory vibrations of

Varying

intensity(loudness), frequency (pitch), quality, configuration, and duration

How is a murmur produced?• Sound is produced by

vibration

• Vibration is generated by turbulence

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

Leatham has attributed the production of

murmurs or turbulence to three main factors: (1) high flow rate through normal or abnormal

orifices, (2) forward flow through a constricted or irregular

orifice or into a dilated vessel or chamber, and (3) backward or regurgitant flow through an

incompetent valve, septal defect, or patent ductus arteriosus. Frequently, a combination of these

factors is operative

CLASSIFICATION• Can be classified into organic, functional and innocent.• Organic refer to structural defect responsible for

murmur• Important is that the term innocent and functional are

not interchangeable.• Functional murmur should subserve a function like

increased flow across aortic valve as in severe AR.• While innocent occur in absence of abnormalities of

heart and circulation, more common in children and on right side.

Description of a Murmur Position in the cardiac cycle

Site of murmur] Shape of murmur

Intensity

Quality & Pitch

Conduction

Dynamic changes

Dynamic Auscultation

Listening to the change in character, behaviour and the intensity of the heart sounds and murmurs to physiological and pharmacological maneuvers…….

“AUSCULTATE WITH ALTERED HEMODYNAMICS”

Conditions and interventions

1. Respiration 2. Postural Change 3. Valsalva maneuver 4. Exercise 5. Change in Cardiac Cycle length 6. Pharmacological agents.

What happen during respiration

• Normal inspiration →1.↑ venous return to right side of the heart due

to fall in intra thoracic pressure → ↑ stroke volume of right side

2.Dilatation of pulmonary vascular system causing decrease in pulmonary impedance there by increasing pulmonary hang out interval(>80 ms)

3.So leads to accentuation of R side murmur

RESPIRATION CONTINUE

• Normal expiration → ↓ lung volume → ↑ pulmonary venous flow– Therefore, left sided murmurs are loudest during

expiration except MR which remain unchanged. While no change is seen 1.When complicated by RVF as due to high RVEDP

no increase in venous return.2.Aortic valvular ES do not vary with respiration3.MR murmur do not vary with respiration

RESPIRATION CONTINUE Assess changes during normal respiration Patient should be in semiupright or sitting posture In RV failure and PHT, no increase in venous return with

inspiration, hence no inspiratory augmentation of right sided murmurs and gallops

Absence of respiratory influence is of no particular diagnostic value.

Effects of inspiration may be accentuated by Muller maneuver.

STANDINGAuscultation is carried out

immediately before and after the change in posture since effects may be quite transient persisting for only 10 – 15 heart beats

If patient is unable to sit upright or stand, rapid application of tourniquets at upper thigh level may reduce venous return reproducing similar response

STANDING

Rapid standing or sitting up from lying position or rapid standing from squatting posture results in

decreased venous return due to venous pooling in legs and splanchnic vessels leads to-

decreased stroke volume decreased mean arterial pressure decrease in heart size followed by reflex increase in heart rate & systemic

resistance

standingAll murmurs decrease except-

ESM of HOCM becomes louder and longer

Click occurs earlier, murmur becomes longer in MVP while loudness shows variable response

Sudden assumption of LYING DOWN POSITIONPASSIVE ELEVATION OF LEGS

Increase in venous return → increase R.V. stroke volume → later after several cardic cycles left ventricle volume also increase .

So Systolic murmur of AS,PS,MR, TR & VSD increase.

MVP & HOCM murmurs decrease due to increase in LVEDV and LV size.

Squatting Sudden change from standing to squatting leads to-• Increases venous return & Stroke Volume • Increase of systemic vascular resistance due to

kinking of iliac artery and reduction of pressure of gravity

• Increase of systemic Arterial pressure with transient bradycardia

Squatting• Increased venous return and CO -

augments most murmurs (AS,PS,MR,AR,VSD) Right heart murmurs do so earlier

• Increased left ventricular volume - decreases murmur of HOCM and delayed murmur and click of MVP

• Ejection murmur of TOF↑ due to increase pulmonary blood flow and decrease in right to left shunt

Other postural changes

Assumption of L Lateral PositionCauses closeness of heart to chest wall and

transient rise of HR. So leads to –

Increased murmur of MS, MR and austin flint murmur of AR

Early appearance of click and systolic murmur of MVP due to increasec HR.

Sitting up and leaning forward

causes more closeness of base of heart to chest wall so AR and PR murmurs more readly audible

PRONE POSITION & KNEE CHEST POSITION

Bring heart close to chest wall making pericardial rub more prominent

Valsalva Maneuver

Relatively deep 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

VALSALVA MANEUVERForced expiration against closed glottis

Manometer method:Patient blows into the mercury manometer

and maintains 40 mmHg for 15 seconds

Valsalva equivalent:Patient pushes back against examiner’s

hand which is pressed downward on mid abdomen.

The maneuver is demonstrated and patient practices the maneuver before assessment of murmur

Caution : Not to be performed in IHD as it will reduce Coronary Blood Flow.

PHASES OF VALSALVA

• PHASE 1-due to increase in intra thoracic pressure there is transient rise in LV output and systemic arterial pressure but there occurs fall in HR

• phase 2(stain phase)- decrease in venous return first to right then to left leads to decrease in systolic, diastolic and pulse pressure and reflex tachycardia

• PHASE 3- cessation of staining result in- sudden increase in systemic venous return but transient decrease in arterial pressure

due to fall in intra-thoracic pressure PHASE 4- return to pre valsalva a transient overshoot of systemic arterial

pressureReflex bradycardia

PHASE BP HR

1 INCREASE DECREASE

2 DECREASE INCRESAE

3 DECREASE INCREASE

4 INCREASE DECREASE

EFFECTS ON MURMUR

• PHASE1 –as stroke volume fall there is decrease in –

systolic murmur of AS, PS, MR, TR diastolic murmur of AR PR MS TS PHASE2- reduction in LV volume and size leads

to- increase in systolic murmur of HOCM increase in degree of MVP prolapse

• PHASE 3- sudden increase in SVR leads to increase in right side murmurs

• PHASE 4-left side murmur comes to control levels and may transiently increase.

• ASD, MS and CHF – Phase 1 and 3 are normal but there is absence of decrease in arterial pressure tracing during phase 2 and overshoot of BP does not occur in phase 4 that leads to SQUARE WAVE RESPONSE ie. Instead of four phases there is only two phase.

The Muller Maneuver

Converse of Valsalva Maneuver

Less frequently employed

Forcibly inspires while the nose is held closed and mouth is firmly sealed for about 10 sec.

Augments murmur and filling sound originating in right side of the heart.

ISOMETRIC EXERCISEUse calibrated handgrip device

or tennis ball or rolled up BP cuff.

Measure the maximum effort.Patient exerts 70 – 100% of this

maximum for about 30 seconds

Simultaneous handgrip using both hands

Valsalva maneuver during handgrip should be avoided

ISOMETRIC EXERCISE

Hemodynamic changes:Significant increase in

Arterial pressureHeart rateCardiac outputLV filling pressureLV size

Isometric Exercise

1. Systolic Murmur of AS reduced due to reduced gradient across aortic valve

2. AR , MR , VSD – increased due to increase systemic vascular resistance

3. MDM of MS – increased due to Increased CO

4. Syst Murmur of HOCM reduced5. MVP murmur + click delayed

ISOMETRIC EXERCISE

• Avoid in those with ventricular arrhythmias and myocardial ischemia

• Contraindicated in recent myocardial infarction, uncontrolled hypertension, cerebrovascular disease, suspected aortic dissection

Cardiac cycle length changes post PVC and AF

• ↑ preload will increases ventricular filling and size

• Also in addition there is secondry increase in ventricular contractibilty of new beat and transient increase in arterial pressure.

Cardiac cycle length changes

Increased ( L or R vent ejection murmurs )ASPS

HOCM(there is inc in SM but also decrese volume of pulse known as BROCKENBROUGH PHENOMENA)

No change for MR , TR DM of AR increases due to transient rise in

arterial pressure

Amylnitrite InhalationInhalation of Amyl Nitrate

Crush ampoule in toweltake 3-4 deep breaths over 10 – 15 secsChanges observed- < 30 secs : Systemic vasodilatation 30 – 60 secs : increase HR & CO However majority of auscultaory changes are

observed in first 30 sec

• Due to increse in CO- SM of AS and PS SM of TR All functional SM DM of MS and TS DM of PR

• Due to decrease in SVR following murmur are decreased-

SM of MR DM and austin flint murmur of AR SM of TOF Due to decrease LV volume and size – SM of HCM increases early appearance of MVP click and murmur but

softening of murmur occur due to decrease resistance to LV resistance

Amyl Nitrite Inhalation

Augments DiminishesAortic stenosis Mitral regurgitationPulmonary stenosis TOFTricuspid regurgitation Mitral regurgitationMitral stenosis Austin FlintPulmonary regurgitation Aortic Regurgitation

Phenylephrine↑ BP & SVR ↓ CO & HR – last for 3-

5mtsReduces intensity of S1, A2-OS may widenAugments the murmurs of VSD, PDA, MR, AR,

TOF, Systemic AVFDiminishes AS, MS & functional murmursESM of HOCM diminishesClick & murmur of MVP get delayed

Methoxamine & Phenylephrine

Opposite effect of Amyl NitratePhenylephrine - due to short duration of actionSystolic pressure elevated by 30 mm Hg for 3 to 5 mts

EFFECT

1. Increases systemic arterial pressure2.Reflex Bradycardia , decrease CO, decrease

Contractility Caution : Not to be used in patients with CHF or

Systemic hypertension.

Methoxamine & Phenylephrine

AR , MR , VSD , TOF – LouderSM OF AS, PS and DM of PR and

TS -show no changes LV size increases HOCM – SofterClick and Murmur of MVP -

Delayed

Some general points about murmur before discussing individual murmurs

Timing

– Sometime it is difficult to identify the timing of murmur

– Murmur can be timed by simultaneous palpation of the carotid arterial pulse or by identifying S2S2 at base

– Inching technique of Harvey and Levine

– In tachycardia carotid sinus massage can slow down heart rate

– In case of extra systole indentify the beat that follows pause and then first sound after pause will be S1

LENGTH

• It generally reflect the pressure difference b/w two sites and this is true for all stenotic lesions like MS, AS, PS or TS

• In regurgitant lesion length has no correlation with severity.

• In AR length of murmur correlates better then MR but still not as reliable as stenotic lesions

CHARACTER • High frequency murmur occur when pressure

difference b/w two chambers are high and low pressure difference has low frequency and pitch.

• As a general rule regurgitant lesions are high frequency and stenotic are rough or low frequency. Murmur of AV stenosis are of low frequency while semilunar are of mixed frequency

• High frequency or soft component of murmur is more widely audible this is reason why AS soft component is audible at apex and mistaken for MR

• While low frequency or rough component is audible at site of best audibility of murmur.

PITCH Hz Pr Gr QUALITY E.g.:

LOW 25-125 Less Rumbling,rough

MDM-MS

MEDIUM 125-300

mix Harsh, rough

AS

HIGH >300 high Blowing, soft, musical

MR,AR

Systolic Murmurs

Early Systolic murmurs

Early systolic murmurs begin with S1 and extend for a variable period of time, ending well before S2

1. Acute severe mitral regurgitation◦ Regurgitation occurs into a normal-sized, relatively noncompliant

left atrium and as LV-LA pressure gradient is abolished during late systole, termination of retrograde flow occurs well before S2.

◦ best heard at apical impulse ◦ Caused by:

i. Papillary muscle rupture due to ishemiaii. Infective endocarditis -destruction of leaflet tissue, chordal rupture, or both

iii. Rupture of the chordae tendineae in myxomatous mitral valve diseaseiv. Blunt chest wall trauma-papillary muscle contusion and rupture,

chordal detachment, or leaflet avulsion.

2.Congenital, small ventricular septal defect- ventricular size decrease and septum thickness increases which seals

off defect3. VSD with high PA pressure- high pulmonary resistance will decrease the late shunting4. Tricuspid regurgitation with normal PA pressures- The murmur is soft (grade 1 or 2), best heard at the lower left

sternal border, and may increase in intensity with inspiration (Carvallo's sign). Regurgitant "c-v" waves may be visible in the jugular venous pulse.

Midsystolic (ejection) murmurs

Mid-systolic murmurs begin at a short interval following S1, end before S2

Murmur is due to flow across LV or RV outflow tract when flow proceeds , murmur increase in in crescendo and when it decrease murmur decrease in decrescendo.

Intensity of murmur depend on cardic output. So when flow and cardic output changes like in various maneuver murmur changes.

Causes are:1. Innocent: due to flow across normal ventricular outflow tract2. Functional: dilation of aortic root, pulmonary trunk increase flow into aorta and

pulmoary artery3. Pathologic

are secondary to structural CV abnormalities e.g. Aortic stenosis, Hypertrophic cardiomyopathy, Pulmonic stenosis

Aortic stenosis

• Harsh, medium pitch, loudest in aortic area; radiates along the carotid arteries and apex.

• Intensity varies directly with CO

• Severity varies with murmur may have an early peaking and short duration or late peaking and prolonged duration.

• A/W parvus et tardus

• Other conditions which may mimic the murmur of aortic stenosis w/o obstructing flow:1. Aortic sclerosis

2. Bicuspid aortic valve

3. Dilated aorta

4. Increased flow across the valve during systole

Hypertrophic cardiomyopathy

Loudest b/t left sternal edge and apex; Grade 2-3/6 Does NOT radiate into neck; carotid upstrokes are brisk and

may be bifid The murmur will classically increase in intensity with

maneuvers that result in increasing degrees of outflow tract obstruction, such as a reduction in preload or afterload (Valsalva, standing, vasodilators) or to an augmentation of contractility (inotropic stimulation). Maneuvers that increase preload (squatting, passive leg raising, volume administration) or afterload (squatting, vasopressors) or that reduce contractility (-adrenoreceptor blockers) decrease the intensity of the murmur

MANEUVERS FIXED LVOT DYNAMIC LVOT

RESPIRATION NO CHANGE MAY INC WITH EXPIRATION

STANDING DECREASES INCREASES

SQUATTING INCREASES DECREASES

VALSALVA DECREASES INCREASES

BROCKENBROUGH NORMAL POSTIVE

AS MR

Location Aortic area Apex

Radiation Neck Axilla

Shape Diamond Holosystolic

Pitch Medium High

Associated signs Decreased A2Slow rising and delayed pulseEjection clickS4Narrow pulse pressure

Decreased S1Laterally displaced diffuse PMIS3

POST PVC INCRESES NO CHANGEIsometric Exercise DECREASES INCREASES

Amyl Nitrate INCREASES DECREASES

MVP HCM

CLICK PRESENT ABSENT

POST ECTOPIC BEAT DO NOT CHANGES DECREASES

AMYL NITRATE BI PHASIC INCREASES

Pansystolic (Holosystolic) Murmurs• Are pathologic• Murmur begins immediately with S1 and continues up to S2• 1. Mitral valve regurgitation

– Loudest at the left ventricular apex– Radiation reflects the direction of the regurgitant jet– i. To the base of the heart = anterosuperior jet (flail

posterior leaflet)– ii. To the axilla and back = posterior jet (flail anterior

leaflet– Also usually associated with a systolic thrill, a soft S3, and a

short diastolic rumbling (best heard in left lateral decubitus• 2. Tricuspid valve regurgitation• 3. Ventricular septal defect

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

-Austin Flint murmur

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 p2Delayed in onset

Usu extends throughout diastole Short duration

Features of PAH present Usually absent

Mid Diastolic MurmurRV- TS

LV- MS

- Austin Flint murmur

- Carey-Comb's

OTHERS-Atrial Myxoma

- TR

- ASD

- VSD- PDA- MR

MS

• Low pitch 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

Austin Flint Murmur• Severe AR regurgitant jet directed toward

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

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

• To differentiate from MS– No OS– Amyl nitrate inhalation

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

Valsalva Maneuver

DYNAMIC AUSCULTATION

Proper assessment requires• Good stethoscope• Quiet room• Cooperative patient• Bare chest• Intact autonomic function and normovolemia• Knowledge about the maneuver and the

changes expected

THE CAVEATS ARE………Avoid dynamic auscultation in sick patients When postures are changed, transition

should be abrupt Continuous auscultation is required, when

maneuvres are being elicitedConcentrate on the first few cycles after

maneuvresRealize that each maneuvre induces more

than one alterations in hemodynamics

early systolic mid systolicSystolic murmur late systolic pan/holo systolic early diastolicDiastolic murmur mid diastolic pre systolic

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 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

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.

SHAPEcrescendo, decrescendo, crescendo-decrescendo, plateau

1.The crescendo (grows louder) Configuration of the murmur of chronic AS can be understood in terms of the progressive increase

in the systolic pressure gradient between the left ventricle and aorta.

2. Decrescendo Configuration(decreasing) of the murmur of chronic AR can be understood in terms of the progressive decline

in the diastolic pressure gradient between the aorta and the left ventricle.

3.The crescendo-decrescendo(increasing-decreasing or diamond shape) configuration of the murmur of AS reflects the changes in the systolic pressure gradient between the left ventricle and the

aorta as ejection occurs, 4.The plateau(even or unchanged) configuration of the murmur of

chronic rheumatic MR is consistent with the large and nearly constant pressure difference between the left ventricle and the left

atrium.