Transcript MURMURS AND DYNAMIC AUSCULTATION By Dr Ankur

MURMUR AND
Dynamic Auscultation
OF Cardiovascular System
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.
2.
3.
4.
5.
6.
Respiration
Postural Change
Valsalva maneuver
Exercise
Change in Cardiac Cycle length
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 respiration
3. 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.
STANDING
Auscultation 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
standing
All 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 POSITION
PASSIVE 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 Position
Causes 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 MANEUVER
Forced 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
pressure
 Reflex 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
toincrease 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 EXERCISE
Use 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 pressure
Heart rate
Cardiac output
LV filling pressure
LV 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 reduced
5. 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 )
AS
PS
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 Inhalation
Inhalation of Amyl Nitrate
Crush ampoule in towel
take 3-4 deep breaths over 10 – 15 secs
Changes 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 COSM 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
Diminishes
Aortic stenosis
Mitral regurgitation
Pulmonary stenosis
TOF
Tricuspid regurgitation Mitral regurgitation
Mitral stenosis
Austin Flint
Pulmonary regurgitation Aortic Regurgitation
Phenylephrine
↑ BP & SVR ↓ CO & HR – last for 35mts
Reduces intensity of S1, A2-OS may widen
Augments the murmurs of VSD, PDA, MR, AR,
TOF, Systemic AVF
Diminishes AS, MS & functional murmurs
ESM of HOCM diminishes
Click & murmur of MVP get delayed
Methoxamine & Phenylephrine
Opposite effect of Amyl Nitrate
Phenylephrine - due to short duration of action
Systolic pressure elevated by 30 mm Hg
for 3 to 5 mts
EFFECT
1. Increases systemic arterial pressure
2. Reflex Bradycardia , decrease CO, decrease
Contractility
Caution : Not to be used in patients with CHF or
Systemic hypertension.
Methoxamine & Phenylephrine
AR , MR , VSD , TOF – Louder
SM OF AS, PS and DM of PR and TS show no changes
LV size increases HOCM – Softer
Click 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 S 2 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 S 1
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, MR,AR
musical
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 ishemia
ii. Infective endocarditis -destruction of leaflet tissue, chordal
rupture, or both
iii. R u p t u r e o f t h e c h o r d a e t e n d i n e a e i n m y x o m a t o u s
mitral valve disease
i v. B l u n t c h e s t w a l l t r a u m a - p a p i l l a r y m u s c l e
contusion and rupture, chordal detachment, or
leaflet avulsion.
2.Congenital, small ventricular septal defect ventricular size decrease and septum thickness
increases which seals off defect
3 . V S D w i t h h i g h PA p r e s s u r e high pulmonary resistance will decrease the late
shunting
4 . T r i c u s p i d r e g u r g i t a t i o n w i t h n o r m a l PA p r e s s u r e s The murmur is soft (grade 1 or 2), best heard at
t h e l o w e r l e f t s t e r n a l b o r d e r, a n d m a y i n c r e a s e i n
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 tract
2. Functional: dilation of aortic root, pulmonary trunk increase flow into aorta and
pulmoary artery
3. 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.
2.
3.
4.
Aortic sclerosis
Bicuspid aortic valve
Dilated aorta
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 A2
Slow rising and delayed
pulse
Ejection click
S4
Narrow pulse pressure
Decreased S1
Laterally displaced diffuse
PMI
S3
POST PVC
INCRESES
NO CHANGE
Isometric 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 p2
Delayed in onset
Usu extends throughout diastole
Short duration
Features of PAH present
Usually absent
Mid Diastolic Murmur
RV
LV
- TS
- MS
- TR
- Austin Flint murmur
- ASD
- Carey-Comb's
- VSD
- PDA
- MR
OTHERS
-Atrial Myxoma
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 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,
Diastolic Pr., Flow rate and gradient across valve]
– LLSB
RV
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]
• CauseIncreased 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 elicited
Concentrate on the first few cycles after
maneuvres
Realize that each maneuvre induces more
than one alterations in hemodynamics
Systolic murmur
Diastolic murmur
early systolic
mid systolic
late systolic
pan/holo systolic
early diastolic
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.
SHAPE
crescendo, 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.