MURMUR AND Dynamic Auscultation OF Cardiovascular System ANKUR KAMRA.
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Transcript of MURMUR AND Dynamic Auscultation OF Cardiovascular System ANKUR KAMRA.
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.