Heart murmurs & Dynamic Auscultation

Heart murmurs & Dynamic Auscultation

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?

[Re >4000 turbulent flow] L = linear dimension (internal diameter In pipes) Q = V1*A1= V2*A2 V = mean fluid velocity Q = P/R Q = volumetric flow rate A = pipe cross-sectional area Re => Turbulence m = dynamic viscosity of => murmur the fluid

n = kinematic viscosity [m/ r] r = density of the fluid 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 4 RICS

th 4th L cos. cart. in L St. border 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

Systolic murmur Diastolic murmur Continuous murmur early systolic mid systolic late systolic pan/holo systolic early diastolic mid diastolic pre systolic Site of murmur Systolic

Diastolic Apex MR MS, Flow mur. LLSB TR, VSD TS, Flow mur.


URSB AS Others Continuous Intensity- Grading FREEMAN & LEVINE GRADING GRADE 1- faintest murmur which can be heard only with special effort. GRADE 2- soft but readily audible GRADE 3- loud without thrill GRADE 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 factors 1. Pressure difference or gradient- Gr pitch 2. Amount of Flow- Flow pitch PITCH Hz

LOW Flo w Pr Gr QUALIT Y E.g.: 25125

rumblin g MDMMS MEDIU M 125300 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 Systolic murmur

Diastolic murmur Continuous murmur early systolic mid systolic late systolic pan/holo systolic early diastolic mid diastolic pre systolic Systolic Murmurs Midsystolic murmur

Most common murmur heard in everyday practice. Starts at an interval after S1 and ends before S2. It could be 5 settings

PATHOLOGICAL INNOCENT/PHYSIOLOGICAL 1. Ventricular outflow obstruction 2. Dilation of aorta and pulmonary trunk 3. Accelerated systolic flow into aorta or pulmonary trunk 4. Innocent midsystolic murmur( including those due to morphological changes of valve with no obstruction) 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 S4

Reverse splitting S2 Harsh, crescendodecrescendo 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 AS Gallaverdin phenomenon/ hourglass phenomenon Lower n (aortic) vs. Higher n (mitral) periodic vibrations of stiffened non calcific aortic valve MR AS MR Differentiating from

[ 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 BP difference Thrill Ejection sound

Murmur Maximum Assoc AR Supra valvular Sub valvular nil RUL > LUL Nil

Max 2 RICS; Supra sternal & carotids Max Right carotid Mid LSB Present Absent Absent 2 RICS

1 RICS Mid LSB +/- 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 marfans 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 Stills murmur Pulmonary mid systolic murmur Peripheral pulmonary systolic murmur Supraclavicular or brachiocephalic systolic murmur Aortic sclerosis Systolic mammary souffl

Physiological murmurs Stills 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 Souffl 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 Holosystolic Early systolic

Late systolic Sometimes 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 Carvallos sign- Increased VR, increased RV volume Increased SV velocity of regurgitant flow Sometimes TR heard only during inspiration Carvallos 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 TR Tall 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 LSM MVP Barlows syndrome refers to the spectrum of symptoms caused by MVP [click or murmur alone to palpitations,

chest pain, or syncope] 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 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 Short mur. early

equalization of diastolic pressures C/C AR Long mur. Medium n High n velocity less rapid and pressure gradient lower 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 obstruction Abnormal 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 Murmur OTHERS RV LV - TS - TR

-Atrial Myxoma - MS - Austin Flint murmur - Carey-Comb's - 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 AFsevere 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., across valve]

LLSB Flow rate and gradient 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 2 & 3 LICS maximum intensity. 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 Coombs 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 CabotLocke 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. Docks 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 KeyHodgkin 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. Rytands 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 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 arteries 3. Disturbances in flow patterns in veins Connection b/w high pressure

chamber/vessel & low pressure chamber/ vessel 1. From the aorta a. Persistent ductus arteriosus b. Aorto-pulmonary window c. RSOV 2. From the coronary artery: 1. Coronary arteriovenous fistulae draining into RA, RV, PA 2. ALCAPA 3. Other arteriovenous communications 1. Broncho-pulmonary collaterals 2. Chest wall arteriespulmonary vessels 3. Peripheral A-V Fistula

4. Others 1. Lutembacher syndrome with restricted ASD PDA Gibsons murmur At 1 or 2 LICS NR- high frequency soft murmur peaks around S2 Mod R- loud coarse machinery murmur with eddy sounds S E

V E R I T Y 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 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 - LA- ULSB rad to Lt ant RA- RLSB or RUSB ax line CS- back b/w spine & Lt scapula - Lt SVC- upper to mid RV inflow- LLSB LSB 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. Do not peak at S2 Usu LUSB or RUSB I/C flow] Disturbance in flow patterns in arteries AV Fistula Murmur heard in the venous side

Due to rapid blood flow- cervical venous hum, mammary souffl, hyperthyroidism, hemangioma, hyperemia of neoplasm (HCC, RCC, Pagets 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 Decubitus LV 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 expiration AR & PR EDM

C. Sitting with legs dangling Further reduces venous return If S2 fails to fuse on sitting D. Elbow Knee Position Pericardial 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 Neck Venous hum H. Passive elevation of both legs Transiently increases venous return, increase S3 Physical Maneuvers Inspiration

Expiration Left Rightsided sidedevents eventsbecome becomemore moreprominent prominent Diff S2 split AR & appreciable PR Pericardial RVs3 RVs4 prominent friction rub [exhalation & supine]

Tricuspid Innocent pulm sys &mid dia sys Murmurmur increased becomes more prominent becos of reduced AP diameter Pulm ejection sound reduced Valsalva Maneuver 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 initial pulm VR = SV I/T Pr directly transmitted to aorta. I/T Pr = BP Sudden BP

VR = sympathetic tone HR sudden return of peripherally pooled blood to the vasoconstricted arterial system (20 to the increased sympathetic tone) I/T Pr = Valsalva Maneuver 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 IVincreased Right murmurs Valsalva Maneuver PHASE I/T Pr = VR = II BP sympathetic tone HR MAXIMAL SYMPATHETIC

ACTIVATION FLAT PART OF STARLINGS CURVE PHASE sudden return IV of peripherally pooled blood to the vasoconstricted arterial system (20 to the increased sympathetic tone) HEART FAILURE ASD MS

Isometric Exercise Calibrated Handgrip device or a handball. Better to carryout bilaterally, sustained for 20-30 secs Not to be done in arrhythmia / Ischemia Transient but significant increase in SVR, BP, HR , CO , LV filling pressure , Heart size 1. LVS3 & LVS4 increases 2. Systolic Murmur of AS reduced reduced gradient across aortic valve 3. AR , MR , VSD increased 4. MDM of MS increased 5. Syst Murmur of HOCM reduced 6. MVP murmur + click delayed Isotonic Exercise 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 Pharmacological Maneuvers Inhalation of Amyl Nitrate [Crush ampoule in towel, 3-4 deep breaths over 1015 s] First 30 secs 30 to 60 secs > 60 secs

Decreased Sys Art Pressure Reflex Tachycardia Increased CO, HR Lasts 2 minutes No reduction in stroke volume as seen in NTG 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 Anatomy The 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 1015 s]

First 30 secs 30 to 60 secs > 60 secs Decreased Sys Art Pressure Reflex Tachycardia Increased CO, HR S1 Augmented A2 Diminished

OS Becomes louder A2-OS interval shortens S3- Either ventricles augmented AS , PS , HOCM , TR , Functional murmurs All augmented

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