Heart murmurs & Dynamic Auscultation Dr Nithin P G.
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Transcript of Heart murmurs & Dynamic Auscultation Dr Nithin P G.
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Heart murmurs & Dynamic Auscultation
Dr Nithin P G
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Outlay of Seminar
• Definition
• What to look for/ how to describe a murmur
• Classification of murmurs
• Types of murmurs
• Dynamic Auscultation
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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.
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How is a murmur produced and heard?
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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
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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
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Auscultation of murmur
Other factors affecting auscultation of murmur
• Distance from chest wall, position of patient
• Underlying soft tissue, lung, fluid
• Quality of apparatus
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Auscultation of murmur
Upper 3rd L St-C Jn
4th L cos. cart. in L St. border4th RICS
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How to describe a murmur?
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Description of a Murmur
• Position in the cardiac cycle
• Site of murmur [max. intensity]
• Intensity
• Quality & Pitch
• Conduction
• Dynamic changes
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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
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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
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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.
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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
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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
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Classification & types of murmurs
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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
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Systolic Murmurs
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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
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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)
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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
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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
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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 =
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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.
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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 +/-
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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
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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
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PS
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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
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Other causes of MSM
OS-ASD• Rapid flow across pulmonary valve to
dilated pulmonary trunk
Pure AR• Due to Accelerated LV ejection
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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
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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
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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
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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
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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
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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
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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
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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
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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
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Other PSM
• Aorto Pulmonary Window with PAH– Otherwise continuous murmur– Diastolic component reduced with increasing PAH
• PDA with PAH– Similar mechanism
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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
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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
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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]
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Diastolic Murmurs
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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
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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
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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
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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
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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
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Mid Diastolic MurmurRV- TS
LV- MS- Austin Flint murmur
- Carey-Comb's
OTHERS-Atrial Myxoma
- TR
- ASD
- VSD- PDA- MR
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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]
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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
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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
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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
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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
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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
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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]
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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
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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.
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Continuous murmur
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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
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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
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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
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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]
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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
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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
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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
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Dynamic Auscultation
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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 .
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Intervention
• Position
• Physical maneuvers
• Pharmacological
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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
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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
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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
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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
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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)
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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
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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
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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
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• 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
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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
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Amyl Nitrate inhalation
• AS vs. MR
• TR vs. MR
• PS vs. TOF
• MS vs. Austin F
• PR vs. AR
• HOCM vs. MVP [n/c]
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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
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Thank you
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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
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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
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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