Last edited: 3/14/2022

HEART SOUNDS
Heart Sounds Medical Editors: Aldrich, Camille, Ilia & May

OUTLINE
I) HEART VALVES: AUSCULTATION LOCATIONS III) S2 HEART SOUND SPLITTING
II) S1 AND S2 HEART SOUNDS IV) EXTRA HEART SOUNDS (S3 + S4)
S1 + S2 HEART SOUNDS OVERVIEW V) ADDITIONAL HEART SOUNDS
S1 HEART SOUND
S2 SOUND

I) HEART VALVES: AUSCULTATION LOCATIONS

(A) OBJECTIVE

[Link]

Know the location of auscultation [Link]

o Where should we listen for heart sound
Correlate the location with the particular valves
(B) AUSCULTATION LOCATIONS
Mnemonic
o All Physicians Earn Too Much
(1) Aortic valve (4) Tricuspid valve
Location: Right 2nd intercostal space (ICS) parasternal Location: Left 4th intercostal space parasternal border
border (PSB) o Go down one more spot from Erb’s point
o Between the 2nd and 3rd rib
(5) Mitral valve
(2) Pulmonic valve
Location: Left 5th intercostal space midclavicular line
Location: Left 2nd intercostal space parasternal border
o Other side of the aortic valve auscultation location Table 1. Auscultation locations
Auscultation Location

Location: Left 3 intercostal space parasternal border

rd Aortic valve Right 2nd ICS PSB
o Go down one more spot from pulmonic valve Pulmonic valve Left 2nd ICS PSB
auscultation location
Erb’s point Left 3rd ICS PSB
Good overview of all heart sounds and murmurs
o Especially aortic regurgitation murmur Tricuspid valve Left 4th ICS PSB
Left 5th ICS midclavicular
Mitral valve
line

Heart Sounds CARDIOVASCULAR PATHOLOGY: Note #21. 1 of 13

 II) S1 AND S2 HEART SOUNDS

S1 + S2 HEART SOUNDS OVERVIEW

[Link]

(A) S1 HEART SOUND → VENTRICULAR SYSTOLE (B) S2 HEART SOUND → VENTRICULAR DIASTOLE
When the ventricles are contracting Ventricles are done with systolic time period → they’re
Ventricles in their contractile stage, they’re depolarized going to start relaxing (diastole)
o They’re electrically stimulated → ready to rock and o We want blood to actually go into the ventricles from
roll and start blasting blood out of the ventricles the atria
When this happens  We want them to fill with blood so that they can
o Think about the particular valves that are going to be push blood out
closing → atrioventricular valves We need tricuspid valve and mitral valve to open for
 Tricuspid valves blood to come down into the ventricles from the atria
 Mitral valves The valves that we don’t want to open are aortic valve
[Link]
We only want blood to only go from the ventricles to their and pulmonic valve
respective arteries o So that blood doesn’t flow backward into the
o Pulmonary artery ventricles
o Aortic artery o Remember the purpose of valves → provide one-way
flow prevent backflow
Tricuspid valve and mitral valve should close →
indication of S1 heart sound What happens is
o When the ventricles relax
S1 indicates the closure of atrioventricular valves → Blood will actually come backward
o Tricuspid valve and mitral valve → And then snap the aortic valve and pulmonic
o When the valves close, it should give a nice little
valve
“click sound” or “lub” type of sound
o That’s when we get S2 heart sound
Once S1 starts from the point of S1 until the second heart
(C) QUICK RECAP
sound
o Indicative of ventricular systole (1) S1 → onset of ventricular systole
Auscultation + carotid artery palpation Closure of mitral valve and tricuspid valve
o In this situation, mitral valve should close first
Sometimes it’s difficult when we’re listening to the heart
because it’s a high-pressure system
sound
o The patient’s heart are going really fast, difficult to From that point until we get into the next heart sound →
discern which one is it ventricular systole
Sometimes what we can do is palpate their carotids (2) S2 → Represent closure of the aortic and pulmonic
when we’re listening to their heart valve
When we palpate and feel the upstroke of the carotid
Aortic valve is under higher pressure → should also
o Beat that’s pulsating on our actual fingertip
close first
Carotid upstroke is kind of telling us that we’re in the o We refer this as “dub” type of sound
period of ventricular systole
This should correlate with the carotid downstroke
Anatomy-wise explanation o Because blood should be trying to recoil back to the
heart
When the ventricles contract → they push blood into the
o We don’t want it to go back into the heart → so aortic
aorta → carotid artery
valve closes and so does the pulmonic valve
So, we’re going to feel that rapid upstroke with the S1
o It will happen just right after the S1 Refer to minute 11:56 of the lecture to listen for the
normal heart sound
If we feel it during the next part (downstroke) → S2

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S1 HEART SOUND

Sometimes S1 may sound a little bit louder, but sometimes S1 sound can be softer
o They can test this on exam
And we should be able to recognize if it’s actually louder or softer
o Know the differentials for having loud and soft S1
Remember more significant component of S1 is mitral valve
o Tricuspid valve to a smaller degree
o But mitral valve shuts really hard
 It’s going to produce large vibrations → cause S1 heart sound to be heard

(A) LOUD S1
Causes
Hyperdynamic states
Shortening of the PR interval
Mild/moderate mitral stenosis
(1) Hyperdynamic state

During hyperdynamic state Hyperdynamic states can be found in patients with

o Imagine left ventricle is smashing blood, trying to
push them out of the aorta Fevers
[Link]
o When it does that, it smashes the valves really hard Septic
 Valve shuts and produces the vibration → cause o Sometimes our body’s sympathetic nervous system is
the loud S1 on overdrive
o Causing the heart to pump harder to generate and
push and meet all the demands of the body
High T3 + T4
o Condition whenever T3 + T4 levels are so high that it’s
causing toxic effects in the body → thyrotoxicosis
Exercising
Severe anemia
Pregnancy
o They have higher volume → heart has to pump really
hard

Heart Sounds CARDIOVASCULAR PATHOLOGY: Note #21. 3 of 13

(2) PR interval is really short
Lower likelihood but definitely want to think about it

Refer to minute 16:15-16:51 of the lecture for better

visualization for the valve leaflet momentum explanation

Valve leaflet momentum

Normally when blood is in the ventricles
o What it will do is blood will try to push the leaflets
together to one another
Imagine the distance of the leaflet are quite closer or
farther away from one another
o Which one will produce the louder sound?
Remember we have SA node → AV node → bundle  It’d be the one that farther away from one another
branch system → Purkinje There’s not a lot of blood that’s filling up to push them
AV node receives electrical activity and says [Link]
closer to one another
o “Let me hold onto this electrical activity for just a o So if they’re farther distance from one another, when
second” the ventricles contract
o The whole purpose of it is to giving the ventricles
The leaflets are going to slam shut harder because
enough time to relax
they have generated momentum
When the PR interval is short o Due to the farther distance of mitral valve leaflets
o AV node is like “Oh, hot potato” and throws the
Short PR interval can be seen in patient with Wolff
electrical activity down into the ventricles to
Parkinson’s White (WPW) syndrome
depolarize
o Ventricles don’t have time to relax
 Decrease diastolic filling time
→ Less left ventricular in diastolic volume
• Less volume in the heart when it relax
(3) Mild/moderate mitral stenosis

[Link]

Remember mitral stenosis is where the mitral valves kind of really fibrotic and calcified → less pliable

In this case, we want to classify this mitral stenosis to mild or moderate category
o Meaning that they still have a little bit of pliability and movement
o If the leaflets are not moving, they’re not going to give you loud S1
 They’ll actually cause soft or absent of S1
Normal condition
Valve super stenotic → difficult to be able to push
blood through Let’s say left arial pressure is 10mmHg
The pressure inside atria increases o The left ventricular pressure has to be greater than
o Because it has to accommodate for all of the 10mm to close the mitral valve
volume that’s sitting inside of it
Patient with mitral stenosis
o Also because it has to push blood down
The atria then become bulk up Because of the stenosis, their left atrial pressure is way
o Become hypertrophic and generate high higher than normal
pressures and push blood down o Let’s say left atrial pressure is 30mmHg
Now the left ventricular pressure has to be greater
o Remember from cardiac cycle video than 30mmHg
 How do we actually close the mitral valve? o For it to overcome the left atrial pressure to push the
• The left ventricular pressure has to be greater mitral valve close
than left atrial pressure The mitral valve is going to get hit with 30mmHg of
pressure
o When they get hit with high pressure
 It’s going to snap those valves closed hard if
they have some pliability → produce loud S1
sound
o Imagine getting hit with a rock vs getting hit with a
pebble

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(B) SOFT S1

Relatively easy because we’ve already covered all the ones for the
loudest one
o Guess what? Flip it!

Causes
Hypodynamic states
Prolonged PR interval
Very severe mitral stenosis
Mitral regurgitation

(1) Hypodynamic states (3) Very severe mitral stenosis

Condition where the heart is not really pumping very Remember the mitral valve in very severe mitral
much → not having high stroke volume stenosis is not pliable
Can be found in patient with heart failure o They’re really fibrotic so they don’t move very much
o Not going to be pushing on mitral valve with as much during systole and diastole
force There’s very short distance between the leaflets →
→ Not going to close them shut as hard means very soft S1 sound
→ Produce soft S1
(4) Mitral regurgitation
(2) Prolonged PR interval
When we’re pumping blood
Remember AV node receives the extra electrical activity, o We’re supposed to pumping it out into the aorta
it says
o “I’m gonna let them wait” Sometimes, the mitral valve leaflets don’t really close
o “All right, here you go ventricles” together
o The ventricles have a lot of time to fill o One of the valve leaflets aren’t coming close together
→ Not sealing together
Prolonged PR interval increases diastolic filling  Causes blood to backflow into left atrium
o If they fill longer → increase left ventricular end o No good seal between the leaflets
diastolic volume (LVEDV) → Doesn’t slap together
o If we increase their LVEDV, we’re going to have → Doesn’t produce very much sound
more blood in the ventricles
In mitral regurgitation, the blood gets pushed into the left
Imagine the blood’s seeping around the valves → it’s atrium and then go back to the left ventricle
going to kind of lift the valve leaflets o Now the left ventricle is going to get volume
o Now the valve leaflets are in closer distance to one overloaded
another compared to normal condition
Now imagine the leaflets that are sitting on the blood
If that’s the case column
o When the ventricle has to squeeze and push blood o Remember the blood is bringing the leaflets
out, it has to push the small distance closer together
o Close distance of mitral valve leaflets → soft S1
sound High left ventricular diastolic volume → cause small
distance between the leaflets
Prolonged PRi can be found in patient with heart Problematic issue because the blood is accumulating
blocks (AV blocks)
[Link] o Because every time the left ventricle is supposed to
o Commonly in 1st degree and 2nd degree heart block pump blood into the aorta
→ It pumps up into left ventricle
→ Then back down to left ventricle
o Left ventricle keeps getting more volume
 Bring the leaflets closer to one another
 Short distance → we don’t get a lot of momentum
→ produce soft S1 sound

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S2 SOUND

Remember S2 is telling us about ventricular diastole We only want the blood come from atria
o A period of when the ventricle is relaxing o We don’t want the blood come from the arteries that
 The ventricle is being filled with blood just pushed the blood into
So, the valves that they push the blood into should
actually shut
o Shut off aortic valve and pulmonic valve → S2
sound
(C) LOUD S2

High pressure within the respective artery

(1) High pulmonary artery pressure (2) High pressure within the aorta
When we push blood from the right ventricle into the Due to systemic hypertension
pulmonary circuit o May also be due to coarctation of aorta
o When the artery receives the blood, it is kind of elastic When we push blood from the left ventricle into the aorta
→ Accommodates and recoil, push the blood out into o The aorta is going to expand, accommodate that
the respective circulation volume
o But some of it should come back down → the  And then recoil and push it down into the
good ol’ valve snap shut to prevent backflow descending aorta, branches of the aortic arch
Imagine having a high pressure system which is pushing o Also push some of the blood back down
down → It’s going to really slam that aortic semilunar
o The blood coming back down pushes with a lot of valve close very hard → very loud S2
force → snaps the pulmonic valve very hard
Can be seen in patient with pulmonary hypertension

(D) SOFT S2

We have small little space → try to push through it and

the valve barely opens
o Whenever we want to close → the leaflets are
actually close to one another → soft S2

Less pliable valve

o Less pliable valve is not opening well and closing
well
o Giving the soft S2 heart sound
 May see this in aortic stenosis and pulmonic
Aortic valve is the most common type of valvular stenosis (less common)
disease  Differentiate these with different maneuvers or
Imagine somebody has aortic stenosis location
Super calcified, fibrotic, sclerotic → super immobile • Aortic → right upper sternal border
o Doesn’t want to allow blood to be able to go through • Pulmonic → left upper sternal border
 It’s ability to close is not good

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 III) S2 HEART SOUND SPLITTING
When you listen to a normal heart, you hear “lub” and “dub” in succession, which corresponds to:
o S1 and S2
o Ventricular Systole and Ventricular Diastole
Recall: S2 corresponds to the closure of the pulmonic and aortic valves
In certain pathologies, S2 can be split, wherein you can hear the pulmonic and aortic components separately

(A) PHYSIOLOGICAL SPLIT S2 (B) WIDE SPLIT S2

(1) Mechanism during Expiration (1) Mechanism
During expiration, there is more blood flow to the During expiration, S2 splitting is noticeable
pulmonary circulation and left side of the heart o A2 and P2 are heard separately
o Left atrium  left ventricle  aorta During inspiration, intrathoracic pressure decreases,
o Recall: The left ventricle has a stronger contractile directing blood to the right side of the heart
force than the right ventricle o Due to the increased blood volume, right ventricular
The aorta fills with blood, expands, and recoils contraction and pulmonic valve closure [Link]
delayed
o Blood is pushed to the systemic circulation; or o This causes a more exaggerated S2 splitting
o Blood is pushed back towards the left ventricle,
(2) Causes
snapping the aortic valve shut
During expiration, there is less blood flow to the right side High Preload in the Right Ventricle
of the heart o Increased blood volume delays ventricular contraction
o Right atrium  right ventricle  pulmonary aorta and pulmonic valve closure
o Recall: The right ventricle has a weaker contractile High Afterload in the Right Ventricle
force than the left ventricle o Right ventricular contraction encounters resistance
The pulmonary artery fills with blood, expands, and due to:
recoils  Increased pressure in the pulmonary artery
o Blood is pushed to the pulmonary circulation; or (pulmonary hypertension, pulmonary embolism)
o Blood is pushed back towards the right ventricle,  Defective valve impairs blood flow, increasing right
snapping the pulmonic valve shut ventricular pressure (pulmonary valve stenosis)
 Since there is less blood volume, the pulmonic o RV contraction and pulmonic valve closure are
valve does not shut as quickly delayed, resulting in S2 splitting

During expiration, the aortic valve sound (A2) comes Right Bundle Branch Block
before the pulmonic valve sound (P2), but the delay is o Recall: Right bundle branch supplies electrical activity
almost negligible
[Link] to the right ventricle, allowing it to depolarize and
o A2 is more intense and louder than P2 subsequently contract
o The splitting of S2 is not as noticeable o Damage to the right bundle branch will prolong RV
depolarization and contraction
(2) Mechanism during Inspiration  RV contracts later, causing delayed closure of the
During inspiration, intrathoracic pressure decreases, pulmonic valve
directing blood to the right side of the heart  Results in S2 splitting
o Due to the increased blood volume, right ventricular Wolf-Parkinson-White (WPW) Syndrome (Type A)
contraction and pulmonic valve closure are delayed o An accessory pathway runs into the left ventricle via
o This causes the P2 sound to come after A2 the bundle of Kent
During inspiration, there is less blood flow to the left side  The bundle of Kent runs between the left atrium
of the heart and left ventricle
During inspiration, there is physiologic splitting of S2, o This causes quicker depolarization of the left ventricle
with A2 coming before P2  LV contracts earlier, causing earlier closure of the
o The splitting of S2 is more noticeable aortic valve
 Results in S2 splitting

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(C) FIXED SPLIT S2 (D) PARADOXICALLY SPLIT S2

Splitting of S2 is the same distance during both inspiration P2 sound comes before A2
and expiration Left ventricular contraction is prolonged/delayed, causing
There is an abnormal communication within the heart that A2 to come after P2
is equalizing the pressure within the heart
(1) Causes
(1) Atrial Septal Defect
High afterload in the Left Ventricle
Recall: In normal patients, left atrial pressure (LAP) is o Left ventricular contraction encounters resistance due
higher than right atrial pressure (RAP) to:
o This allows more blood to flow from the left atrium to  Increased pressure in the aorta (hypertension)
the left ventricle during expiration  Defective valve impairs blood flow, increasing left
The presence of an atrial septal defect will change the ventricular pressure (aortic valve stenosis)
normal pressures within the heart  Narrowing of the blood vessels impedes blood
Recall: During expiration, blood flow is increased in the flow and increases LV pressure (coarctation of
left side and decreased in the right side. the aorta)
o With the ASD, the relatively higher LAP will push o Consequently, A2 is delayed and comes after P2
blood into the right atrium Left Bundle Branch Block
o There is increased blood volume in the right ventricle, o Recall: Left bundle branch supplies electrical activity
causing delayed P2 to the left ventricle, allowing it to depolarize and
Recall: During inspiration, blood flow is decreased in the subsequently contract
left side and increased in the right side. o Damage to the left bundle branch will prolong LV
o There is less volume of blood in the LAP, so less depolarization and contraction
blood is pushed into the right atrium via the ASD  LV contracts later, causing delayed closure of the
o However, there is still more volume of blood aortic valve
(increased venous return) in the right side, which will  Results in A2 coming after P2
still result in delayed P2 Wolf-Parkinson-White (WPW) Syndrome (Type B)
Thus, during both expiration and inspiration, there is still a o An accessory pathway runs into the right ventricle via
fixed distance between A2 and P2 the bundle of Kent
 For this rarer type, the bundle of Kent runs
between the right atrium and right ventricle
o This causes quicker depolarization of the right
ventricle
 RV contracts earlier, causing earlier closure of the
pulmonic valve
 Results in P2 coming before A2
(2) Expiration vs Inspiration
During expiration, the distance between P2 and A2 is
wider
o Recall: There is increased blood flow to the left side,
further prolonging A2
During inspiration, the distance between P2 and A2 is
relatively less wide, compared to during expiration
o Recall: There is decreased blood flow to the left side;
however, increased pressure/decreased
depolarization still delays A2

[Link]

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(E) ABSENT SPLIT S2 (F) TEST YOUR KNOWLEDGE

Also called “single S2” Identify the types of S2 splitting below, based on the
Only the P2 sound is audible temporal distribution of S2 components during inspiration
Severe Aortic Stenosis and expiration
o The aortic valve needs to close to produce the A2
sound Table 2. Test Your Knowledge
o In severe aortic stenosis, the valve is very stiff and Graph Description
immobile due to fibrosis or calcification
o As a result, the aortic valve cannot close, and the
A2 sound is absent
P2 comes before A2
The distance between
the two S2 components
is wider during
expiration

Answer: Paradoxical
Splitting of S2

A2 comes before P2
The distance between
the two S2 components
are the same during
expiration and
inspiration

Answer: Fixed Split S2

A2 comes before P2
No true splitting during
expiration
Splitting during
inspiration only

Answer: Physiologic
Splitting S2

A2 comes before P2
There is splitting during
both expiration and
inspiration
More exaggerated split
during inspiration

Answer: Wide Split S2

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IV) EXTRA HEART SOUNDS (S3 + S4)

OVERVIEW

(1) Cardiac cycle

The S1 sound represents the closure of During ventricular diastole there are three phases
o The mitral valve 1) Early diastolic filling
o The tricuspid valve Characterized by rapid entry of blood into the ventricles
The S2 sound represents the closure of o This blood is located in the atria at the beginning of
o The aortic semilunar valve diastole
 A2 component 2) Middle diastolic filling
o The pulmonic semilunar valve
 P2 component Characterized by slower entry of blood into the
ventricles
From S1 to S2 is the period of ventricular systole o This blood is located in the channels outside the atria
o Contraction  Superior vena cava
From S2 to S1 is the period of ventricular diastole  Inferior vena cava
o Relaxation  Pulmonary veins
o S3 and S4 can be heard only during ventricular 3) Atrial kick (late diastolic filling)
diastole
 Considered to be diastolic extra heart sounds Characterized by atrial contraction that pushes out the
[Link] blood remaining in the atria at the end of ventricular
diastole (10-20%)

S3 SOUND
 Systolic heart failure
(2) Only occurs in the early (rapid) phase
(6) Examination
of diastolic filling
The S3 sound is a very low pitch
(3) Mechanism
o Better heard with the bell of the stethoscope
The S3 sound is caused by More common on the left side of the heart
o Increased venous return o Can be heard at the left lower sternal border
o High compliance of the ventricles  Around the fifth left intercostal space
 More particularly in the left ventricle
Best position for the patient is left lateral decubitus
The moving blood becomes turbulent due to position (on their left side)
o Increased amount of blood entering o This way the mitral valve is brought closer to the
o Large, more compliant ventricles chest wall and it is easier to hear the S3 sound
This gives off the S3 heart sound
(4) Physiological causes
Pregnancy
o Larger volume of blood
 Enough for both the mother and the fetus
Young athletic individuals
o Good venous return
o The heart is naturally compliant
 Due to the very good contractility
(5) Pathological causes
Excessive left ventricular dilation
o This can be seen in
 Aortic regurgitation
 Mitral regurgitation
 Dilated cardiomyopathy

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S4 SOUND

(1) Only occurs in the atrial kick (late) phase (4) Examination
of diastolic filling The S4 sound is a very low pitch
o Better heard with the bell of the stethoscope
(2) Mechanism
More common on the left side of the heart
The S4 is caused by o Can be heard at the left lower sternal border
o Increased atrial kick which is caused by  Around the fifth left intercostal space
 Left atrial hypertrophy
Best position for the patient is left lateral decubitus
Hypertrophic left atrium contracts harder and generates position (on their left side)
more force o This way the mitral valve is brought closer to the
chest wall and it is easier to hear the S4 sound

(3) Pathological causes

The S4 sound is always pathological
Atrial hypertrophy
o Due to mitral stenosis
 It restricts the blood flow from the LA into the LV
[Link]

Increased left ventricular end diastolic pressure (LVEDP)

o Requires the left atrium to generate higher pressure
 Blood flows from areas with high pressure to areas
with low pressure

o Causes of increased LVEDP

 Hypertension
 Aortic stenosis
 Hypertrophic obstructive cardiomyopathy
• The septum is hypertrophic and causes
difficulties with pushing blood out the heart
 Ischemic cardiomyopathy
• After multiple myocardial infarcts the damaged
myocardial tissue is replaced with fibrous tissue

TEST YOUR KNOWLEDGE

You examine a patient You examine another patient
o Laying in a left lateral decubitus position You examine a patient
On the left lower sternal border o Laying in a left lateral decubitus position
o Around the fifth intercostal space On the left lower sternal border
 With the bell of the stethoscope o Around the fifth intercostal space
• You hear a low pitch extra sound  With the bell of the stethoscope
o In the early phase of diastole • You hear a low pitch extra sound
When you hear this, you know that the patient is o In the late phase of diastole
o Pregnant or o Right before the onset of the S1 sound
o A young athlete or When you hear this, you know that this is
o Has a condition that causes left ventricular o Due to left atrial hypertrophy
dilation  Caused by increased left atrial pressure
You say this sound is S3, caused by You say this sound is S4, caused by
o Rapid ventricular filling o High left ventricular end diastolic pressure (LVEDP) or
 Due to a very compliant left ventricle or dilated  Mitral stenosis
left ventricle o Thick and tough ventricular walls with decreased
compliance
 Hypertension
 Aortic stenosis
 Hypertrophic obstructive cardiomyopathy
 Ischemic cardiomyopathy

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V) ADDITIONAL HEART SOUNDS

There are extra types of sounds that can be present in systole, diastole, or both.

(A) ADDITIONAL SYSTOLIC HEART SOUNDS

(1) Ejection Clicks
Involves two vessels:
o Pulmonary trunk
o Aorta Mitral Valve Prolapse
Occurs during early to midpoint of ventricular AKA Barlow Syndrome, Floppy Valve Syndrome
systole (S1 to S2) May be associated with:
o Marfan syndrome
o Ehlers-Danlos syndrome
Weakening of the chordae tendineae due to connective
tissue defects
o Chordae tendineae helps anchor down the leaflets
o Myxomatous degeneration of the mitral valve leaflets
Normal: mitral valve is supposed to close during
ventricular systole
[Link] Mid-systolic click
In MVP, the valve bows upward into the left atrium during
ventricular systole
Bowing of mitral valve produces a clicking sound during
the middle to late systolic phase
Ventricles are contracting Holosystolic murmurs
o Due to mitral regurgitation
o Since the bowed leaflet doesn’t click with the other
Right ventricle pumps blood up into the pulmonary trunk
valve leaflet, blood can easily regurgitate back into
o In Pulmonary Stenosis
the left atrium  causes an associated murmur
 Patient has a stenotic pulmonic valve
o May have a little crescendo
• Valves are fibrotic; sometimes calcified
o Usually heard in late systole
• Difficult for valves to open and difficult for it to o Sound intensity can be changed with maneuvers
allow blood to flow o Will be discussed during the Heart Murmur lecture
o Bowing
 When blood is pushed inside, the valves bow
 Bowing creates a clicking sound
Left ventricle pumps blood up into the aorta
o Aortic Stenosis
o Same concept as pulmonary stenosis
o Bowing

Precipitates the occurrence of a crescendo de

crescendo type of murmur
Due to blood trying to flow through the bowed valve Prosthetic Valves
o A lot of blood flows through the valve at first, causing
the crescendo Systolic clicks are normally (and should be) heard in
o The amount of blood flowing through the valve patients with prosthetic valves
lessens, causing the de crescendo o Absence of click indicates a potential prosthetic valve
malfunction

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(B) ADDITIONAL DIASTOLIC HEART SOUNDS

(1) Opening Snaps (2) Pericardial Knock
o Heard primarily in patients with:
 Mitral Stenosis Heard in constrictive pericarditis
 Tricuspid Stenosis Excessive fibrosis of the pericardial cavity
o Ventricles only get blood flow during early diastole
Normal physiology:
The rigid pericardium blocks the ventricles from relaxing
o During ventricular diastole (S2 to S1), blood flows from
o This causes a sudden cessation of blood flow, which
the atria into the ventricles
produces the pericardial knock
 Ventricles are in a relaxation state: opening up
and allowing blood to fill them No associated murmur
Difficult to differentiate with an s3 heart sound
Opening snaps are due to two situations: o Pericardial knock has a slightly higher pitch than S3
o Mitral Stenosis  Hence, may not be heard using the bell of a
 Fibrotic and calcified valves stethoscope
 Blood is supposed to move through the valves and
into the ventricles
 The high pressure generated to open the valves
causes the valves to quickly open, producing the
sound of an opening snap
 When blood is pushed from the atria into the
[Link]
ventricles

Happens at the beginning of diastole

Associated with decrescendo murmur
o “Diastolic rumble”
o Right after the valve opens, there’s a high amount of
blood flowing through it, which eventually decreases
o This is what differentiates the opening snap from S3
and S4

(C) ADDITIONAL CONTINUOUS HEART SOUNDS

Pericardial Friction Rub
o Heard in patients with pericarditis
 Inflammation of visceral and/or parietal pericardium
 When the ventricles go through the cycles of contracting and relaxing, the visceral and parietal pericardium rub against
each other
o Triphasic heart sound: Can be heard during:
 Atrial systole
 Ventricular systole
 Ventricular diastole
Continuous heart sound: happens all throughout ventricular systole (S1 to S2) and ventricular diastole (S2 to S1)
A scratching type of sound

Heart Sounds CARDIOVASCULAR PATHOLOGY: Note #21. 13 of 13