Heart Sounds & Murmurs Guide by Dr. Vitrag Shah

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Heart Sounds & Murmurs

Dr.Vitrag Shah
First year resident,MD Medicine
April-2012
GMC,Surat

Dr.Vitrag Shah - www.medicalgeek.com

Different areas for auscultation of heart


I. Auscultatory Valve Area

 1. MV: apex, fifth left intercostal
space, medial to the
midclavicular line
 2. PV: second left intercostal space
 3. AV: second right intercostal space
 4. AV2: left third intercostal
space(Neoaortic/Erb’s area)
 5. TV: lower part of left sternal border
 6. Other part


Auscultatory order
 ApexPV AV AV2 TV
Or
 ApexTV AV2PV AV

Content of auscultation
1. Heart rate
2. Heart rhythm
3. Heart sound
4. Heart murmurs


Function of the valves
 Valves prevent the back flow of blood.

 The papillary muscles will not close the
valves,they will maintain the closure of the
valves.

 The importance of chordea tendinei attached
to the papillary muscles is because during
ventricular contraction the ventricle size
decreases and the papillary muscle must
contract to shorten the chordea tendinei to
prevent the leakage of valves

Heart sounds
 The bell and diaphragm of the stethoscope accentuate sounds of
different pitches. The bell emphasizes low-pitched sounds such
as normal heart sounds and the diastolic murmur of mitral
stenosis. The diaphragm filters these sounds and helps to
identify high-pitched sounds such as the early diastolic murmur
of aortic regurgitation or a pericardial friction rub.

 Normal heart valves make a sound when they close but not when
they open. The classic 'lub-dub' sounds are caused by closure of
the atrioventricular (mitral and tricuspid) valves followed by the
outlet (aortic and pulmonary) valves.

 the first and second heart sounds
 extra heart sounds (third and fourth, heard in diastole)
 additional sounds, e.g. clicks and snaps
 pericardial rubs
 murmurs in systole and/or diastole.


Cause of the heart sounds
 Slapping of the valves leaflets is not enough to
generate a heart sound.

The causes of the 1st heart sound:
 During systole the AV valves are closed &
blood tries to flow back to the atrium back
bulging the AV valves. But the taut chordae
tendinae stop the back bulging and causes the
blood to flow forward.
 This will cause vibration of the valves, blood &
the walls of the ventricles which is presented
as the 1st heart sound.


The causes of the 2nd heart
sound:
 During diastole, blood in the blood vessels
tries to flow back to the ventricles cause the
semilunar valves to bulge. But the elastic
recoil of the arteries cause the blood to
bounce forward which will vibrate the blood
the valves and the ventricle walls.
 This is presented as the 2nd heart sound.


Difference between the 1st and
2nd heart sounds
 The 1st sound lasts longer because the AV
valves are less taut than the semilunar valves
which will enable them to vibrate for longer
time.

The 2nd heart sound had higher frequency due to

 The semilunar valves are more taut
 The great elastic coefficient of the taut arteries
which provides the principle vibrations of the
2nd heart sound

First heart sound
 The first heart sound (S1), 'lub', is caused by
closure of the mitral and tricuspid valves at
onset of ventricular systole and is best heard
at the apex.

 Components of S1

 Mitral Valve Closure
 Best Heard: Apex

 Tricuspid Valve Closure
 Best heard: Lower Left Sternal Boarder


Abnormalities of intensity of the
first heart sound
Quiet
 Low cardiac output
 Poor left ventricular function
 Long P-R interval (first-degree heart block)
 Rheumatic mitral regurgitation , Calcified MS

Loud
 Increased cardiac output
 Large stroke volume
 Mitral stenosis
 Short P-R interval
 Atrial myxoma (rare)

Variable
 Atrial fibrillation
 Extrasystoles
 Complete heart blockDr.Vitrag Shah - www.medicalgeek.com

S1

 Wide Splitting
 RBBB
 PVC from Left Ventricle
 Single Sound
 Normal
 LBBB
 PVC from Right Ventricle
 Paced Beats


Second Heart Sound
 The second heart sound (S2), 'dub', is caused by closure of
the pulmonary and aortic valves at the end of ventricular
systole and is best heard at the left sternal edge.
 It is louder and higher-pitched than the first sound, and
the aortic component is normally louder than the pulmonary
one.
 Physiological splitting of the second heart sound occurs
because left ventricular contraction slightly precedes that of
the right ventricle so that the aortic valve closes before the
pulmonary valve.
 This splitting increases at end-inspiration because the
increased venous filling of the right ventricle further delays
pulmonary valve closure.
 This separation disappears on expiration.Splitting of the
second sound is best heard at the left sternal edge.
 On auscultation, you hear 'lub d/dub' (inspiration) 'lub-dub'
(expiration).


Abnormalities of the second heart sound
Quiet
 Low cardiac output
 Calcific aortic stenosis
 Aortic regurgitation
Loud
 Systemic hypertension (aortic component)
 Pulmonary hypertension (pulmonary component)
Split Widens in inspiration (enhanced physiological splitting):
 Right bundle branch block
 Pulmonary stenosis
 Pulmonary hypertension
 Ventricular septal defect
Fixed splitting (unaffected by respiration):
 Atrial septal defect
Widens in expiration (reversed splitting):
 Aortic stenosis
 Hypertrophic cardiomyopathy
 Left bundle branch block
 Ventricular pacing


Physiological splitting of S2


Fixed splitting of S2


Reversed splitting of S2


Third heart sound
 A third heart sound (S3) is a low-pitched early
diastolic sound best heard with the bell at the apex. It
coincides with rapid ventricular filling immediately
after opening of the atrioventricular valves and is
therefore heard after the second as 'lub-dub-dum'.
 0.12~0.18'' after S2, frequency  intensity.
 A third heart sound is a normal finding in children, in
young adults and during pregnancy.
 A third heart sound is usually pathological after the
age of 40 years.
 The most common causes are left ventricular failure,
when it is an early sign, and mitral regurgitation. In
heart failure S3 occurs with a tachycardia and S1 and
S2 are quiet (lub-da-dub).

Causes of a third heart sound
Physiological
 Healthy young adults
 Athletes
 Pregnancy
 Fever
Pathological
 Large, poorly contracting left ventricle
 Mitral regurgitation


Fourth heart sound
 A fourth heart sound (S4) is less common. It is
soft and low-pitched, best heard with the bell of
the stethoscope at the apex. It occurs just before
the first sound (da-lub-dub). 0.11'' prior to S1
 It is always pathological and is caused by
forceful atrial contraction against a non-
compliant or stiff ventricle.
 A fourth heart sound is most often heard with left
ventricular hypertrophy (due to hypertension,
aortic stenosis or hypertrophic obstructive
cardiomyopathy). It cannot occur when there is
atrial fibrillation.
 Both a third and a fourth heart sound cause a
'triple' or 'gallop' rhythm.

Added Sounds


Pericardial Friction Rub
 Three Phases
○ Mid Systolic, Mid Diastolic, Pre Systolic
 Scratchy, Leathery
 Best Heard
○ With Diaphragm of Stethoscope
○ Left Sternal Boarder Leaning over at End Expiration
 Apposition of Abnormal Visceral and Parietal Pericardium
 Confused with Hamman’s Sign in Post Open Heart Surgery
(Crunch Sound from Mediastinal Air)
 It may be audible over any part of the precordium but is often
localized. It is most often heard in acute viral pericarditis and
sometimes 24-72 hours after myocardial infarction. Pericardial rubs
vary in intensity over time, and with the position of the patient.
 A pleuro-pericardial rub is a similar sound that occurs in time with the
cardiac cycle but is also influenced by respiration and is pleural in
origin. Occasionally a 'crunching' noise can be heard caused by air in
the pericardium (pneumopericardium).

Early Systolic Sounds
 Ejection Sound- Usually High Frequency
 Aortic Valve- Aortic Stenosis, Bicuspid Aortic
Valve
 Pulmonary Valve-Pulmonic Stenosis Vary with
Respirations
 Prosthetic Valves- Mechanical, Not
Bioprosthetic


Mid-Late Systolic Sounds

 Click
 High Frequency Sound Found in Mitral Valve
Prolapse
 Occurs Earlier with Valsalva Maneuver or
Squatting to Standing


Early Diastolic Sounds
 Opening Snap of Mitral Stenosis (MS)
○ High pitched-Left Lateral Decubitus Position, Apex.
0.04-0.12 sec after A2 (S3 occurs 0.12 sec after A2)
○ Occurs after S2, before S3
○ MS More Severe with Short A2-OS Interval & softer
OS or absent OS
 Paricardial Knock
○ Chronic Constrictive Pericarditis
○ Mitral Regurgitation
○ Atrial Myxoma
○ Older Model Prosthetic Mitral Valve


Mechanism of OS
 Stenotic anterior mitral valve leaflet
suddently bulging download into the left
ventricular cavity like a dome, with a
snapping sound when the mitral valve is
rapidly opened during diastole. So OS is
heard only if AML of mitral valve is
mobile.
 OS occurs when movement of AMV
suddenly stops, at point when LVP drops
below that of LAP.


OS S2 S3
Area Just inside 2nd & 3rd left ICS Only Apex
apex/entire
chest wall
Relation to A2-OS interval A2-P2 interval Disappear of
posture wides on narrows on sitting
standing standing
Intensity on Remain Decreases -
standing same/intensified
Relation to A2-OS interval Split increase None
respiration constant on respiration
throught
respiration
Intensity on Same - RVS3 Load
respiration during
inspiration
A2-OS/A2- - A2-P2 interval A2-S3 interval is
P2/A2-S3 shorter than A2- longer than A2-
interval OS interval OS interval
Pitch High(Best heard High Low (With Bell)
with diaphtagm)

Auscultation-
Timing of A2 to OS Interval
Say Timing Severity Other
seconds of MS HS’s
Prrr  0.06 Severe
Pada .07-.08 Mod-
severe
Pata .08-.09 Mod
Papa  0.10 Mild PK
0.1-0.110
Tu-  .12 A2-S3
huh 0.12-0.18

Gallop:
1)Three or four sounds are spaced to
audibly resemble the center of a horse,
the extra sounds occurs after S2.


• Protodiastolic gallop rhythm
• S3 gallop, ventricular gallop
rhythm.
• S1 + S2 + pathologic S3


 In early diastole, the blood through
into ventricle from atrium in failing
myocardium, the ventricular wall
tension is poor, produce vibration.
Reflex that the ventricular function
 Auscultation character of S3 gallop:
 lower in pitch
 After S2
 Best hear at apex
 Loudest at the end of expiration.


 S3 gallop: differ from normal S3
 Occur in severe organic heart disease
 HR>100 bpm
 The interval time between S1 and S2
are almost equal, mimicking quality,
normal S3 is nearer from S2
 Normal S3 will disappear in standing
or sitting position


 Late diastolic gallop
 S4 gallop, atrium gallop
○ At late diastole, related to atrial contraction.
In LVEDP  compliance Artial
contraction
occur precede S1, far from S2
low-pitch; best heard at apex
○ Tensity: end of expiration(from LA)
end of inspiration (from RA)


• Occur in pressure overload,LVH, in
myocardial damaged , LV compliance
, such as BP, IHSS, CHD.


 Summation gallop
 Overlapping of S3G and S4G while HR


Mid Diastolic Sounds
 S3
 Occurs During Rapid Filling of Left
Ventricle (LV) related to LV Volume
 Low Frequency Best Heard
○ At the Apex w/Bell
○ Pt in Left Lateral Decubitus Position
 Can Be Normal to Age 40???
 Can be Pathognomonic for Congestive Heart
Failure


Late Diastolic Sounds
 S4
 During Atrial Phase of LV Filling
○ Consequence of Ventricular Stiffness
 Absent in Atrial Fibrillation or Ventricular
Pacing
 Low Frequency Sound Best Heart
○ At the Apex
○ Pt in Left Lateral Decubitus Position
 HTN, Aortic Stenosis, Ischemic Heart Disease


Diastolic Sounds
 Right Sided S3, S4
 Left Lower Sternal Boarder
 Intensity Varies with Respiration due to Right
Heart Filling (Carvallo’s Sign)
 Summation Gallop
 Occurrence of an Over Lapping S3 and S4 due
to Tachycardia


Murmurs (Latin word)
 Sudden deceleration of blood produces
heart sounds while Heart murmurs are
produced by turbulent flow (Raynold’s
number >2000) across an abnormal valve,
septal defect or outflow obstruction, or by
increased volume or velocity of flow
through a normal valve.
 Murmurs may occur in a healthy heart.
These 'innocent' murmurs occur when
stroke volume is increased, e.g. during
pregnancy, and in athletes with resting
bradycardia or children with fever.

 Mechanism
 Blood velocity
 Blood vascosity
 Valve: narrowed or incompetent;
organic or relative
 Abnormal connection
 Vibration of loose structure
 Diameter of vessel or 


Points to be examined in murmur
 Timing
 Shape
 Intensity
 Duration
 Location of maximum intensity
 Character
 Pitch
 Radiation
 Variation with respiration
 Variation with position
 Variation with other maneuvers
 Best heard with bell or diaphram

Common Murmurs and
Timing

Systolic Murmurs
 Aortic stenosis
 Mitral insufficiency
 Mitral valve prolapse
 Tricuspid insufficiency
Diastolic Murmurs
 Aortic insufficiency
 Mitral stenosis

S1 S2 S1

Describing a heart murmur
1. Timing
 murmurs are longer than heart sounds
 HS can distinguished by simultaneous palpation of the
carotid arterial pulse
 systolic, diastolic, continuous
2. Shape
 crescendo (grows louder), decrescendo, crescendo-
decrescendo, plateau
3. Location of maximum intensity
 is determined by the site where the murmur originates
 e.g. A, P, T, M listening areas


Describing a heart murmur con’t:
4. Radiation
 reflects the intensity of the murmur and the direction
of blood flow
5. Intensity
 graded on a 6 point scale
○ Grade 1 = very faint
○ Grade 2 = quiet but heard immediately
○ Grade 3 = moderately loud
○ Grade 4 = loud
○ Grade 5 = heard with stethoscope partly off the chest
○ Grade 6 = no stethoscope needed
*Note: Thrills are assoc. with murmurs of grades 4 - 6


Describing a heart murmur con’t:
6. Pitch
 high, medium, low depending upto high/medium/low
velosity jet
7. Quality
 blowing, harsh, rumbling, and musical
8. Others:
i. Variation with respiration
○ Right sided murmurs change more than left sided
ii. Variation with position of the patient
iii. Variation with special maneuvers
○ Valsalva/Standing => Murmurs decrease in length and intensity
EXCEPT: Hypertrophic cardiomyopathy and Mitral valve prolapse


Levine & Freeman’s Grading

Grades of intensity of murmur
 Grade 1 Heard by an expert in optimum
conditions
 Grade 2 Heard by a non-expert in optimum
conditions
 Grade 3 Easily heard; no thrill
 Grade 4 A loud murmur, with a thrill
 Grade 5 Very loud, often heard over wide
area, with thrill
 Grade 6 Extremely loud, heard without
stethoscope


 Physiological maneuver
1) Change the body position
- Left recumbent: MS
- Sitting, leaning forward: AI
- Squatting from standing, supine position,
raising two legs may increase venous
return, SV CO
- Murmur of MI, AI
- Murmur of IHSS


2) Respiration
- Deep inspiration: thorax pressure
venous return, pulmonary circulation
clockwise rotation of heart make
murmur
of TI, TS ,PI
- Expiration:
- Valsalva maneuver: thorax pressure
venous return M of IHSS


3) Exercise:
- HR
- Blood volume
- Blood velocity
make the murmur of MS

Left sided murmurs increases on expiration
while right sided murmur increased on
Inspiration.

Basal (Aortic & Pulmonary) murmurs increases
on sitting and leaning forward while apical (Mitral &
Tricuspid) murmurs increases on left lateral position.


Systolic Murmurs
Derived from increased turbulence associated
with:
1. Increased flow across normal SL valve or into a
dilated great vessel
2. Flow across an abnormal SL valve or narrowed
ventricular outflow tract - e.g. aortic stenosis
3. Flow across an incompetent AV valve - e.g. mitral
regurg.
4. Flow across the interventricular septum


Holosystolic vs Pansystolic
murmur
 A holosystolic murmur is one which lasts
from the end of S1 to the beginning of S2.
 A pansystolic murmur is one which lasts
from the beginning S1 to the end of S2,
and therefore obscures these heart
sounds.
 The difference between them is academic
in terms of the diagnosis. Pansystolic
murmurs are often louder and more
significant.


Diastolic Murmurs
 Almost always indicate heart disease

 Two basic types:
 The term early diastolic murmur is misleading because the murmur usually
lasts throughout diastole, but it is loudest in early diastole.
1. Early decrescendo diastolic murmurs
 signify regurgitant flow through an imcompetent semilunar valve
○ e.g. aortic regurgitation

2. Rumbling diastolic murmurs in mid- or late diastole
 suggest stenosis of an AV valve
○ e.g. mitral stenosis


Classification and causes of diastolic murmur


Continuous Murmurs
 Begin in systole, peak near s2, and continue into all or
part of diastole.
1. Cervical venous hum
 Audible in kids; can be abolished by compression over the IJV
2. Mammary souffle
 Represents augmented arterial flow through engorged breasts
 Becomes audible during late 3rd trimester and lactation
3. Patent Ductus Arteriosus
 Has a harsh, machinery-like quality
4. Pericardial friction rub
 Has scratchy, scraping quality


Non-Audible murmurs at apex
and pulmonary area


Functional Murmur:
 short and soft SEM
 Normal S1 and S2
 Normal cardiac impulse
 No evidence for hemodynamic
abnormality


Innocent or Normal Murmurs-
Systolic
 Vibratory Systolic Murmur (Still’s Murmur)
 Pulmonic Systolic Murmur (Pulmonary Trunk)*
 Mammary Soufflé*
 Peripheral Pulmonic Systolic Murmur (Pulmonary
Branches)
 Supraclavicular or Brachiocephalic Systolic
Murmur
 Aortic Systolic Murmur
*common in pregnancy

 Still’s Murmur
○ Medium Frequency, Vibratory, Originating from
Leaflets of Pulmonic Valve

Innocent or Normal Murmurs-
Continuous
 Venous Hum
 Continuous Mammary Soufflé


Changing murmurs
 Murmurs which change in character or
intensity from moment to moment.
 Carey-coombs’ murmur
 Infective endocarditis
 Atrial Thrombus
 Atrial Myxomas


The Carey Coombs murmur or
Coombs murmur
 A clinical sign which occurs in patients with
mitral valvulitis due to acute rheumatic fever.
 It is described as a short, mid-diastolic rumble
best heard at the apex, which disappears as
the valvulitis improves.
 It is often associated with an S3 gallop rhythm,
and can be distinguished from the diastolic
murmur of mitral stenosis by the absence of
an opening snap before the murmur.
 The murmur is caused by increased blood flow
across a thickened mitral valve.


Named murmurs
 Carey Coombs murmur- Mid diastolic murmur, in
rheumatic fever
 Austin Flint murmur- mid- late diastolic murmur,in
Aortic Regurgitation.
 Graham- Steel murmur- high pitched, diastolic,
inpulmonary regurgitation.
 Rytands murmur - mid diastolic atypical murmur, in
Complete heart block.
 Docks murmur-diastolic murmur, Left Anterior
Descending(LAD) artery stenosis.
 Mill wheel murmur- due to air in RV cavity following
cardiac catheterization.
 Stills murmur- inferior aspect of lower left sternal
border, systolic ejection sound,vibratory/musical
quality,in subaortic stenosis, small VSD
 Gibson’s murmur: continous machinary murmur of PDA


Gallaverdin Phenomenon:
 The Gallavardin phenomenon is a clinical sign found in
patients with aortic stenosis. It is described as the dissociation
between the noisy and musical components of the systolic
murmur heard in aortic stenosis.
 The harsh noisy component is best heard at the upper right
sternal border radiating to the neck due to the high velocity jet
in the ascending aorta. The musical high frequency
component is best heard at the cardiac apex.
 The presence of a murmur at the apex can be misinterpreted
as mitral regurgitation. It is presumably due to high frequency
vibrations traveling to the apex from the calcific aortic valve.
 However, the apical murmur of the Gallavardin phenomenon
does not radiate to the left axilla and is accentuated by a
slowing of the heart rate (such as a compensatory pause after
a premature beat) whereas the mitral regurgitation murmur
does not change.
 The sign is named after Louis Gallavardin, having been
described by Gallavardin and Ravault in 1925.


Dynamic Auscultation
All patients with a new murmur should
undergo dynamic auscultation:
 Respiration:
 right sided murmurs are louder during
inspiration, expiration has the opposite effect
 Valsalva manoeuvre:
 Postural Changes
 Isometric exercise
 Squatting:
 Vasoactive agents – Amyl Nitrite


Respiration
 Expiration :A2,P2 of second Heart sound separated
<30ms ;single sound
 Inspiration: Splitting interval widens ;A2,P2 heard as 2
distinct sounds
DIASTOLIC & EJECTION SOUNDS:
 S3 & S4 from Rt ventricle;augment in inspiration ;diminish
during exhalation.
 Opening Snap of MV- soft in inspiration;loud in exhalation
 Inspiration decreases intensity of ejection sounds in PS ,
No effect on aortic ejection sounds.
MURMURS
 Inspiration: Diastolic murmur of TS,Pulmonary
regurgitation murmur,systolic murmur of TR,pre-systolic
murmur of Ebstein anomaly are accentuated
 Mid-systolic click, systolic murmur of MVP accentuated.


Valsalva Maneuver
 Deep inspiration followed by forced exhalation
against a closed glottis for 10-20 secs.
 Phase 1:transient rise in systemic arterial
pressure.
 Phase 2:decrease in systemic venous
return,systolic pressure & pulse pressure;
reflex tachycardia.
 Phase 3:abrupt transient decrease in arterial
pressure.
 Phase 4: overshoot of systemic arterial
pressure & reflex bradycardia.

Phase 2:
 S3 & S4 attenuated.
 A2-P2 interval narrows
 Systolic murmurs of AS & PS;MR,TR diminish.
 Diastolic murmurs of AR &PR;TS,MS-soften.
 Lt ventricular volume decreases;systolic murmur of
HOCM amplifies ;click,late systolic murmur of MVP
begins earlier.
Phase 3:
 Sudden increase in systemic venous return;wide split
of S2;augmentation of murmurs & filling sounds Rt
side heart.
Phase 4:
Murmurs & filling sounds Lt side return to control &
transiently increase.

Postural changes & Exercise:
 Lying from standing/passive elevation of
both legs :
 Widening of S2 split
 Augmentation of Rt S3 & S4; Lt S3,S4
 Systolic murmurs of PS,AS,MR,TR& VSD
augmented
 Lt ventricular EDV increased;systolic
murmur of HOCM diminished & mid-systolic
click,late systolic murmur of MVP are
delayed /attenuated.


Squatting
 Increase in venous return & systemic resistance
simultaneously;Stroke volume and arterial pressure
rise-transient reflex bradycardia.
 Augmentation of S3 & S4 (both ventricles)
 Systolic murmurs of PS & AS ;diastolic murmurs of
TS & MS become louder.(Rt sided preceding Lt)
 Elevated arterial pressure;increases blood flow
through Rt ventricular outflow tract in TOF
 Systolic murmur of VSD increases.
 The combtn of increase in arterial pressure and
increase in venous return increases Lt ventricular
size which decreases obstruction to outflow;intensity
of HOCM murmur ;mid-systolic click,late systolic
murmur of MVP delayed.


Left Lateral recumbent position

 Accentuates S1,S3,S4 from Lt side of the heart.
 OS,murmurs of MS,MR;Mid-systolic click and late systolic
murmur of MVP.

Isometric Exercise

 Increase in systemic vascular resistance,arterial
pressure,HR,CO,Lt ventricular filling pressure and heart
size.
 S3 & S4 on Lt side is accentuated.
 Systolic murmur of AS decreases.(reduced pr gradient
across aortic valve.)
 Diastolic murmur of AR,systolic murmur of MR ,VSD
increase in intensity.
 Diastolic murmur of MS –louder.
 Systolic murmur of HOCM decreases & systolic click, late
systolic murmur of MVP is delayed.(increase in LV volume)


Amyl Nitrite
 Marked vasodilatation;redtn in systemic arterial
pressure;reflex tachycardia;increase in CO and
HR
 S1 augmented;A2 diminished
 OS of mitral and tricuspid valve become louder
 A2/OS interval shortens
 S3 augmented
 Systolic murmurs of AS,PS,HOCM,TR and
functional systolic murmurs are accentuated.


Murmur Analysis with Dynamic Auscultation


Back to the Basics
1. When does it occur - systole or diastole
2. Where is it loudest - A, P, T, M
I. Systolic Murmurs:
1. Aortic stenosis - ejection type
2. Mitral regurgitation - holosystolic
3. Mitral valve prolapse - late systole

II. Diastolic Murmurs:
1. Aortic regurgitation - early diastole
2. Mitral stenosis - mid to late diastole


Summary
A. Presystolic murmur
 Mitral/Tricuspid stenosis
B. Mitral/Tricuspid regurg.
C. Aortic ejection murmur
D. Pulmonic stenosis (spilling
through S20
E. Aortic/Pulm. diastolic
murmur
F. Mitral stenosis w/ Opening
snap
G. Mid-diastolic inflow murmur
H. Continuous murmur of PDA

THANK YOU


Heart Sounds & Murmurs Guide by Dr. Vitrag Shah

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