Cardiac cycle - concept, origin of heart sounds, murmurs and other sounds

From ; Cham Chun Yoong (041303012) semester6 /batch 15 /group B1


The Cardiac Cycle
The cardiac cycle is divided into four separate periods, two of the periods occurring during the relaxation phase (Diastole) of the cardiac muscle, and two periods occurring during the contraction phase (Systole) of the cardiac muscle. The first phase of the cardiac cycle is the Ventricular Filling Period (VFP) duringdiastole. At the start of VFP, the heart is in a polarized state and blood is moving through the atria past the heart valves and into the ventricles. As an electrical stimulus occurs from the S-A node, the myocardial cells of the atria depolarize which causes the atria to contract. This atrial contraction forces additional blood past the tricuspid and bicuspid valves, filling the ventricles. This atrial contraction is recorded on the ECG as the p wave. The second phase of the cardiac cycle is the isovolumetric Contraction Period (ICP) which begins systole for the cardiac cycle. The ICP is the beginning of ventricular contraction. Blood is not being ejected from the ventricles during ICP, but pressure is building in the ventricles in order to force the semilunar valves of the Aorta and pulmonary artery open. The pressure in the ventricle must exceed the pressure in the Aorta for blood to be ejected from the heart. The third period of the cardiac cycle is the Ventricular Ejection Period(VEP) which is a continuation of the systolicphase of the cardiac cycle. During VEP, pressure within the ventricles has increased well above the pressure in the Aorta and pulmonary vein. The pressure differential forces the semilunar valves open and blood is ejected from the ventricles into the arteries. Blood will be flow past the semilunar valves until the pressure gradient in the arteries exceeds the pressure of the contracting ventricles. Upon equillibrium of the pressures between the ventricles and arteries, the semilunar valves will shut, and blood flow from the ventricles will cease. The electrical recording for both ICP and VEP are illustrated on the ECG as the QRS complex The final period of the cardiac cycle is the Isovolumetric Relaxation Period (IRP) and occurs during diastole. The ICP is characterized as the resting phase of the cardiac cycle when the ventricles are repolarizing and all valves (bicuspid, tricuspid, and semilunar) are closed. The electrical recording for IRP is illustrated on the ECG as the t wave .

Heart sound



First heart sound, or S1, "lub"

The first heart tone, or S1, is caused by the closure of the atrioventricular valves, mitral and tricuspid, at the beginning of ventricular contraction, or systole. When the pressure in the ventricles rises above the pressure in the atria, these valves close to prevent regurgitation of blood from the ventricles into the atria.

Second heart sound, or S2 (A2 and P2), "dub"

The second heart tone, or S2, is caused by the closure of the aortic valve and pulmonic valve at the end of ventricular systole. As the left ventricle empties, its pressure falls below the pressure in the aorta, and the aortic valve closes. Similarly, as the pressure in the right ventricle falls below the pressure in the pulmonary artery, the pulmonic valve closes.

Third Heart Sound S3

Description:
Low frequency sound in early diastole, 120 to 180 ms after S2

Clinical Significance:
Results from increased atrial pressure leading to increased flow rates, as seen in congestive heart failure, which is the most common cause of a S3. Associated dilated cardiomyopathy with dilated ventricles also contribute to the sound.
Less commonly, valvular regurgitation and left to right shunts may also result in a S3 due to increased flow.
May be normal physiological finding in patients less than age 40.


Fourth Heart Sound S4

Description:
Low frequency sound in presystolic portion of diastole,

Clinical significance:
Seen in patients with stiffened left ventricles, resulting from conditions such as hypertension, aortic stenosis, ischemic or hypertrophic cardiomyopathy.
In patient with mitral regurgitation, suggestive of acute onset of regurgitation due to the rupture of the chorda tendinae that anchor the Valvular leaflets.


Heart murmurs


Definition :An unusual heart sound which may be innocent or reflect disease.

Systolic Murmurs


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

Aortic stenosis


Loudest in aortic area; radiates along the carotid arteries
Intensity varies directly with Cardiac output
A2 decreases as the stenosis worsens
Other conditions which may mimic the murmur of aortic stenosis without obstructing flow:
1. Aortic sclerosis
2. Bicuspid aortic valve
3. Dilated aorta
4. Increased flow across the valve during systole

Mitral regurgitation (MR), also known as mitral insufficiency, is the abnormal leaking of blood through the mitral valve, from the left ventricle into the left atrium of the heart.


Diastolic Murmurs


Almost always indicate heart disease
Two basic types:
1. Early decrescendo diastolic murmurs
•signify regurgitant flow through an incompetent semilunar valve
e.g. aortic regurgitation
2. Rumbling diastolic murmurs in mid- or late diastole
•suggest stenosis of an atriventricular valve
e.g. mitral stenosis

Aortic Regurgitation


Best heard in the 2nd intercostal space at the left sternal edge
High pitched, decrescendo
Radiation:
i. Left sternal border = associated with primary valvular pathology;
ii. Right sternal edge = associated with primary aortic root pathology
Other associated murmurs:
i. Midsystolic murmur
ii. Austin Flint murmur





Mitral Stenosis


Two components:
1. Middiastolic - during rapid ventricular filling
2. Presystolic - during atrial contraction; therefore, it disappears if atrial fibrillation develops.
Is low-pitched and best heard over the apex (with the bell)
Little or no radiation
Murmur begins after an Opening Snap; S1 is accentuated


Summary

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

CARDIAC CYCLE


LATE DIASTOLE

- AV valves are open (aortic and pulmonary valves are closed)
- rate of ventricular filling is decreasing due to the distended ventricles
-AV valve cusps drift to closed position


ATRIAL SYSTOLE

-atrium contracts
-to propel additional blood into the ventricles


VENTRICULAR SYSTOLE

-AV valves close

-intraventricular pressure increases (due to contraction of myocardium)
[ISOVOLUMETRIC VENTRICULAR CONTRACTION- 0.05s]

-pressure in ventricles exceed pressure in aorta (80mmHg)
and pulmonary artery (10mmHg)

-aortic and pulmonary valves open

-ventricular ejection of blood into aorta and pulmonary artery

-intraventricular pressure rises to maximum (right ventricle-25mmHg,
left ventricle-120mmHg)

-intraventricular pressure starts declining

-in late systole, aortic pressure is more than the left ventricle, but blood \
still flows from the ventricle into the aorta due to momentum



EARLY DIASTOLE


-ventricles are fully contracted

-therefore, intraventricular pressure drops more rapidly
[PROTODIASTOLE-0.04s]

-momentum of ejected blood is overcome

-aortic and pulmonary valves close

-intraventricular pressure drops further
[ISOVOLUMETRIC VENTRICULAR RELAXATION]

-intraventricular pressure less than atrial pressure

-AV valves open

-blood flows from the atrium into the ventricles




HEART SOUNDS

S1

-corresponds to the closure of AV valves at the onset of systole
-accentuated in mitral stenosis


S2

-corresponds to the closure of aortic and pulmonary valve after
ventricular ejection
-physiological splitting of S2 is seen because increased venous return to
the right side of the heart during inspiration causes delay in closure of
pulmonary valve (inspiration causes decreased intrathoracic pressure,
therefore increasing venous return)
-S2 split into A2 and P2
-S2 split dissappears during expiration
-fixed splitting of S2 seen in ASD


S3

-due to rapid filling of ventricles during diastole
-physiological in young children and adults under 40years
-can also occur in high output states like anemia, pregnancy
and thyrotoxicosis
-pathological after 40years-indicate left ventricular failure


S4

-caused by atrial contraction in late diastole
-seen in hypertrophic cardiomyopathy, hypertension, aortic stenosis




HEART MURMURS

MID-SYSTOLIC (EJECTION) MURMUR

-due to turbulence in the left or right ventricular outflow tracts
during ejection
-starts following opening of aortic or pulmonary valves
-reaches crescendo in mid-systole
-disappears before 2nd heart sound

-eg : 1. aortic stenosis
-heard loudest in aortic area
-radiation to the carotids

2. pulmonary stenosis
-heard in pulmonary area

3. "Innocent murmurs"
-unrelated to any heart disease
-always mid-systolic
-may be due to hyperkinetic conditions like anaemia,
pregnancy or thyrotoxicosis


PANSYSTOLIC MURMURS

-due to regurgitation of blood through incompetent AV valves
-audible through out systole from 1st to 2nd heart sound

-eg : 1. mitral regurgitation
-heard loudest at cardiac apex
-radiates to the axilla
-best heard with diaphragm of the stethoscope,
with patient lying in left lateral position

2. tricuspid regurgitation
-loudest at lower left sternal edge
-louder during inspiration due to increased venous return to
the right side of the heart during inspiration



LATE SYSTOLIC MURMUR

-seen in mitral valve prolapse
-mid-systolic click, followed by late systolic murmur



EARLY DIASTOLIC MURMUR

-due to regurgitation of blood through incompetent aortic and
pulmonary valves during diastole
-high pitched
-start immediately after 2nd heart sound
-fading away in mid-diastole
-heard using diaphragm of stethescope
-with patient leaning forward

-eg : 1. aortic regurgitation
-better heard in Erb's area ( left 3rd intercostal space)

2. pulmonary regurgitation
-heard in pulmonary area



MID-DIASTOLIC MURMUR

-due to turbulent flow through AV valves
-start relatively late after 2nd heart sound

- eg : 1. mitral stenosis
-best heard in cardiac apex
-using bell of stethoscope
-with patient in left lateral position

2. tricuspid stenosis
- heard in lower left sternal edge
-accentuated by inspiration


***in both these conditions, atrial systole produces a presystolic
murmur immediately before S1 (perceived as an accentuation
of the mid-diastolic murmur)



CONTINUOUS MURMURS

-heard during systole and diastole

- eg : 1. patent ductus arteriosus
-flow from the high pressure aorta to the low pressure
pulmonary artey continues through out cardiac cycle
-producing a murmur over the base of the heart
-continuouly audible, but loudest at end of systole and
diminishes during diastole

Gan Chee Wei
041303031
group B2

Heart Sounds
A) first heart sound

• produced by the closure of mitral & tricuspid valve simultaneously
• indicate the onset of ventricular systole
• heard as a LUB while auscultating
• immediately precedes with carotid pulse
• heard loudest at the apex

B)Second heart sound

• produced by the closure of aortic valve(A2) & pulmonary (P2) valves
• pulmonary valve closes later & aortic valve closes earlier due to early raise of left ventricular pressure and early activation of the LV
• heard as 2 components A2,P2
• heard as DUB
• follows the carotid pilse
• better heard at pulmonary & aortic areas

C)third heart sound

• low-pitched
• produced in ventricle after A2,at the termination of rapid filling
• best heard with bell piece of stethscope at left ventricular apex during expiration & in left lateral position
• physiological S3:-occur in early ventricular diastole

-due to vibration of ventricular walss as blood rushes in

• pathological S3:-due to the "thud" of blood hitting noncompliant ventricular walls at the start of diastole

-Eg: myocardial damage

• normal in children & persons with high cardiac output

D)Fourth heart sound

• low-pitched
• presystolic sound produced in the ventricle during diastole
• associated with an effective atrial contraction
• best heard with bell piece
• absent in atrial fibrillation
• occurs when diminished ventricular compliance increase the resistance to ventricular filling
• presents in systemic hypertension, aortic regurgitation,hypertrophic cardiomyopathy,ischaemic heart diseases
• accompanied by visible & palpable presystolic distensionof left ventricle
• loudest at left ventricular apex& in left lateral position
• is accentuated by mild isotonic or isometric exercise in supine position

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What is Cardiac cycle?- The cardiac events that occur from the beggining of one heart beat to the beggining of the next heart beat.

properties of Cardiac muscle-
myocardial fibers hav a resting membrane potencial of -90mv.Individual fibers are seperated by a membrane, but depolarization spreads radially through them as if they were a syncytium because of the presence of gap junctions.
The transmembrane action potencial of a single cardiacmuscle cell is characterized by rapid depolarization, a plateau and then slow repolarization.
Initail depolarization is due to Na ion influx, because of rapidly opening Na ion channels.
The Ca ion influx, By slowly opening Ca ionchannels.
Repolarization by the net efflux of pottasium through multiple ion channels.
mechanical events of cardiac cycle.
Events of Late diastole

In late diastole, mitral and tricuspid valves are open and the aortic and pulmonary valvesare closed.
Blood flowsinto the heart filling the atria and the ventricles.Rate of filling declines as the ventricles become distended , especially when the heart rate becomes low.

Atrial systole
Contraction of the atria propels additional blood into the ventricles but about 70% ventricular filling occurs passively during diastole.
Contration of the atria,decreases the size of the orrifices,of the superior venacava,inferior venacava, and ther pulmonary veins and thus decreases the regurgitation.

Ventricular systole

At the start of ventricular systole the AV valves close.Intraventricular pressure rises,myocardium presses on the blood in the ventricles. This period is called ISOVOLUMETRIC VENTRICULAR CONTRATION PHASE, and lasts about 0.05 secs. Pressure in the left and right ventricle exceeds the pressure in the aorta 80mmhg and pulmonaryartery 10mmhg...When this happens the aortic and the pulmonary valves open.
When the aortic and pulmonary valves open the ventricular ejectioin begins.Ejection is rapid initially then slows down.Ventricular pressure rises to a maximum before ventricular systole ends.Peak left ventricular pressure is about 120 mmhg, and peak right ventricular pressure is about 25mmhg.

Early diastole
Ventricular muscle fully contracted...when this happens the ventricular pressure drops rapidly.this is called the preiodof protodiastole.Lasts for about 0.04 secs.Aortic and pulmonary valves close.Pressure continues to drop rapidly during the period of ISOVOLUMETRIC VENTRICULAR RELAXATION.This period of relaxation ends when the ventricular pressure falls below the atrial pressure.Then the AV valves open and the ventricles fill up.

1st heart sound

Low, slightly prolonged "lub" caused by the closure of the AV valves during systole,

2nd Heart sound

Shorter,high pitched "dup" caused by the closure of Aortic and Pulmonary valves,just after the end of the ventricular systole.

CARDIAC CYCLE
Cardiac cycle is the sequence of changes in the pressure and flow in the heart chambers and blood vessels in between 2 subsequent cardiac contractions.

Normal duration: 0.8 sec at heart rate of 75/min

Atrial systole: 0.3 sec
Atrial diastole:0.7 sec
Ventricular systole: 0.3 sec
Ventricular diastole: 0.5 sec

ATRIAL DIASTOLE
atrial muscles relax and atrial pressure increases due to continuous venous return.

ATRIAL SYSTOLE (ATRIAL CONTRACTION)
Following the impulse generation from SAN (sino-atrial node),atrial muscle contracts and atrial pressure increases;ie left atrial pressure rises 4-6mmHg whereas left atrial pressure rises 7-8mmHg.
it propels 30% addittional blood into ventricles.

VENTRICULAR SYSTOLE
Ventricular contraction begins and ventricular pressure exceeds atrial pressure very rapidly causing closure of AV valves with production of first heart sound.(S1)

When the pressure in LV exceeds the pressure in the aorta,and the pressure in the RV exceeds the pressure in the pulmonary artery,opening of semilunar valves occur.

70-80ml of blood is ejected out by each ventricle at rest.this is called the stroke volume.

VENTRICULAR DIASTOLE
Due to atrial systole,blood fills the ventricle.The ventricle relaxes. the semilunar valves close and and produce the second heart sound(S2)

S1
The first heart sound is produced due to closure of the AV valves and markes the onset of ventricular systole.
Low pitch, producing loud sound.It sounds like the syllable L-U-B-B.
It can be heard all over the chest but best heard over mitral and tricuspid areas.

S2
The second heart sound is due to closure of semilunar valves and markes the onset of ventricular diastole. It is high -pitched,producing sharp sound. It sounds like the syllable D-U-B.
It can be heard all over the chest but best heard over the pulmonary and aortic areas.

S3
The third heart sound is due to vibrations of the cardiac walls produced by the rapid filling phase of the ventricles during ventricular diastole proper.
Not usually heard in normal people.
It is low pitced, has low intensity and of 0.1 sec duration

S4
The fourth heart sound is due to atrial systole,characterized by low frequency and low amplitude.
Normally inaudible.

MITRAL STENOSIS

• Nearly always due to rheumatic heart disease, but rarely maybe congenital.
• the blood being filled into the left ventricle through the narrowed mitral valve produce the murmur.

Auscultation: ABNORMAL SOUNDS
loud S1, opening snap, apical early diastolic rumbling murmur, which fades in mid-diastole and often with presystolic accentuation. It should be noted that the murmur is variable in severe stenosis; when the valve is mobile and not calcified the murmur persists throughout diastole and S1 and the opening snap remain loud; when the valve is heavily calcified, the murmur is often difficult to hear and S1 and the opening snap become soft and may be absent
Well localised to apex.

MITRAL REGURGITATION

• due to patency of the mitral valve,the blood that was fileed into the left ventricle regurge back into the left atrium, producing the murmur.
• Incomplete systolic closure of the mitral orifice resulting in backflow of blood from the left ventricle to the left atrium
• Caused by an abnormality of the mitral apparatus, which includes the valve leaflets, annulus, chordae tendineae, papillary muscles, and wall of the left ventricle

MURMUR
High-pitched ,blowing, pansystolic murmur best heard at the apex.
commonly radiates to axilla and back.
increases during expiration, sustained hand grip and transient exercise. the murmur is unchanged or decreases during inspiration.

MITRAL VALVE PROLAPSE
More common in females.
redundant mitral leaflet tissue and chordae tendinae.
Myxomatous degenaration of mitral valve, predominantly affecting the posterior mitral leaflet (PML)

MURMUR
Mid or late systolic clicks occur >0.14seconds after S1
mid-systolic or late systolic apical murmur (rarely whooping and honking)
the systloic murmur of mitral valve prolapse increases during standing and valsalva menouvre, but decreases during squatting and isometric exercise.

AORTIC STENOSIS
The normal aortic valve area averages 2.5cm2 and there should normally be no gradient.
a valve area of less than 0.8cm2 or a gradient of more than 50mmHg represents critical stenosis.

MURMUR
Loud harsh ejection systolic murmur best heard at the second left intercostal space(pulmonary area) radiating towards the left shoulder.
the murmur increases with inspiration and decreases with expiration.

TRICUSPID REGURGITATION
MURMUR
Blowing pansystolic murmur best heard at the lower left sternal border (tricuspid area), radiating to lower left right sternal border or pulmonary area. It may be heard up to the apex, but never beyond it.
the murmur is intensified during inspiration and decreases during expiration
(De Carvallo's Sign)

Cardiac Cycle
sequence of changes in the pressure and flow in the heart chambers and blood vessels in between two subsequent cardiac contractions.
normal duartion-0.8s at heart rate of 75/min
vent. systole-0.3s
vent.diastole-0.5s
atrial systole - 0.1s
atrial diastole - 0.7s

EVENTS IN THE CARDIAC CYCLE
at the beginning of cardiac cycle , characteristics feats during diastole are:-

a.Atrial Systole(atrial contraction phase)
atrial muscles contract
duration 0.1s
propels approx 30%of blood
narrows orifice of IVC ,SVC and pulmonary , which causes decresed venous return to the heart

b.Ventricular systole
duration 0.3s
two major phases:-
1.Isovolumetric(isometric)Ventricular Contraction
-duration 0.05s
-ventricles contract and pressure in the ventricles exceed the atrium , causding the A-V valve to closed , causing the first heart sound
2.Ventricular systole proper
duration 0.25s
blood is ejected out from the ventricles
with the opening of the semilunar valves there follows the ejection phase-during this phase , arterial and ventricular pressures follow each other closely.this phase is divided in 3 divisions:-
1.Rapid ejection phase , duration 0.1s
2.Summit
3.Slow ejection phase , duration 0.15s

the amount of blood by each ventricle per stroke at rest is 70-80ml and this is called Stroke Volume.
this is approx 65%of End diastolic ventricular blood volume(EDV) (normal - 120-140 ml) and leaves approx 50ml in each ventricle at the endof systole.this is called end systolic blood volume

c.Ventricular diastole
duration 0.5s
4 major phases:-
1.protodiastole-0.04s
2.Isometric ventricular relaxation phase-0.08s
3.ventricular diastole proper-0.28s
4.last rapid filling phase due to atrial systole-0.1s

d.Atrial Diastole
duration-0.7s
during this phase , atrial muscles relax and atrial pressure gradually increases due to continous venous drop to almost 0mmhg with the opening of the A-V valve


Heart sounds
-first heart sound
*at the beginning of ventricular systole
*due to closure of the A-V Valve
*"Lubb"
-second heart sound
*at the end of ventricular diastole
*due to closure of aortic and pulmonary valves
*"Dub"
-third heart sound
*due to vibrations of the cardiac walls produced by rapid filling phase of the ventricles during ventricular diastole proper.
-fourth heart sound
*due to atrial systole



Murmurs
produced due to vibrations produced by turbulent flow at:-

*region of the valve
*near the valve
*abnormal communication within the heart

Systolic murmurs
mechanism:-
1.increased flow thru normal valve e.g. flow murmurs
2.normal or decresed flow thru stenotic valve e.g. aortic/pulmonary stenosis
3.systolic leak from high to low pressure chambers

early systolic - acute MR , acute TR , small VSD , VSD with severe pulmonary hypertension
mid systolic(ejection) - aortic stenosis , pulmonary stenosis , AR , PR , systemic and pulmonary hypertension.
late sysytolic- mitral valve prolapse , papillary muscle dysfunction]
pan(holosystolic) - MR , TR , VSD

Diastolic murmurs
heard after 2nd heart sound and before subsequent first heart sound.

early diastolic - AR , PR(Graham Steell's murmur of pulm hypertension)
mid diastolic - MS , TS , Austin Flint murmur , Carey-Coomb's murmur


Continuous Murmurs
*Patent ductus arteriosus-Gibson's murmur
*Arterio-venous fistula
*Coronary AV fistula

CARDIAC CYCLE :
- the events of the cardiac cycle can be divided into events occuring during : late diastole , atrial systole , ventricular systole and early diastole .

1)Events in late diastole : -the mitral and tricuspid valves open and the
aortic and pulmonary valves are closed .
-blood flows into the atria and ventricls
througout diastole.
-the rate of filling declines as the ventricles
become distended.
-the pressure in the ventricles remain low.

2)Events in atrial systole : -contraction of the atria propels some
additional blood into the ventricles
( but about 70% of ventricular filling
occurs passively during diastole ) .
-there is some regurgitation of blood
into the veins during atrial systole .

3)Events in ventricular
systole : -mitral and tricuspid valves (AV valves) close .
-isovolumetric ventricular contraction occurs
for about 0.05s.
-then , pressures in the left and right
ventricles exceed the pressures in the aorta
(80mmHg) and the pulmonary artery
(10mmHg) .
-aortic and pulmonary valves open .
-ventricular ejection begins.Peak left
ventricular pressure is about 120mmHg and
peak right ventricular pressure is 25 mmHg .
-towards the end of systole , the aortic
pressure exceeds the ventricular , but for a
short period , momentum keeps the blood
flowing forward .
-*amount of blood ejected by each ventricle
per stroke at rest : 70-90 ml
*and diastolic ventricular volume : 130ml
*end systolic ventricular volume :50ml
*ejection fraction :65%

4)Events in early diastole : -ventricular pressure drops even more rapidly
once the ventricle is fully contracted
(protodiastole-lasts for 0.04s) .
-this ends when the momentum of ejected
blood is overcome and the aortic and
pulmonary valves close .
-pressure continues to drop rapidly
(isovolumetric ventricular relaxation) .This
ends when ventricular pressure falls below the
atrial pressure .
-AV valves open and ventricles fill up .



HEART SOUNDS AND MURMURS

1st heart sound : -occurs due to sudden closure of mitral and tricuspid
valves .
-it is a low pitched and slightly prolonged sound .

2nd heart sound : -occurs due to closure of aortic and pulmonary valves .
-it is a high pitched but shorter sound .
-physiological splitting may occur during the 2nd heart
sound due to an interval between aortic and pulmonary
valve closure during inspiration .

3rd heart sound : -occurs due to inrush of blood during rapid ventricular
filling .
-this sound occurs in many normal young individuals at
1/3 of the way through diastole .
-it is a soft and low pitched sound .

4th heart sound : -occurs due to ventricular filling when the atrial
pressure is high or the ventricle is stiff as in ventricular
hypertrophy .

Abnormal sound in mitral stenosis : -mid diastolic murmur.
-occurs due to turbulent flow through
the AV valves .
-it starts following valve opening and ,
relatively late after the 2nd heart
sound and continues for a variable
period during mid diastole .
-it is best heard in the apex ,using the
bell of the stethoscope .

Abnormal sound in mitral regurgitation : -pansystolic murmur
-occurs due to regurgitation of
blood through incompetent AV
valves .
-heard best at the apex with the
diaphraghm of the stethoscope
and the patient lying on his left .

Mitral valve prolapse : -pansystolic murmur dur to regurgitation of blood
through incompetent AV valves .
-systolic click - occurs due to pliant valve cusps .

Aortic stenosis : -mid systolic murmur due to turbulence ini the right and
left ventricular outflow tracts during ejection .
-best heard in the aortic and pulmonary areas .

Aortic regurgitation : -mid systolic murmur due to increased stroke volume
and velocity of ejection .
-early diastolic murmur due to regurgitation of blood
through incompetent aortic valves .

Tricuspid regurgitation : -pansystolic murmur due to regurgitation of blood
through incompetent tricuspid valves .

Choo Wei Chong
Source: William F. Ganong (Review of Medical Physiology)
The Cardiac Cycle

1) Late diastole, the mitral and tricuspid valves are open and the aortic
and pulmonary valves are closed. Blood flows thoroughout diastole, filling the atria and ventricles.
The filling declines as ventricles become distended and the AV valves drift toward closed position, note the pressure in ventricles remains low. In this stage, 70% of ventricular filling occur, passively.

2) Atrial systole, atria contraction propels additional 30% of blood into the ventricles.
Atrial contraction narrows the IVC and SVC orifices, and the inertia of blood towards heart - keep blood in it. But, in the pulmonary veins, some regurgitation of blood occurs.

3) Ventricular systole, in this stage, the AV valves close. And the ventricular muscle shortens relatively little, but intraventricular pressure rises sharply (isovolumic ventricular contraction) until the pressure excees that of aortic(80mmHg) and pulmonary(10mmHg) pressure and their corresponding valves opens.
During the isovolumic ventricular contraction stage, AV valves bulge into atria cause small rise in pressure.
Upon opening of the aortic and pulmonary valves, the phase of ventricular ejection begins. Initial ejection is rapid, slowing down as systole progresses. (Peak LV pressure: 120mmHg ; RV pressure 25mmHg)
In late ventricular systole, pressure in aorta exceeds that of left ventricle but the momentum of blood keeps the flow momentarily.
Ejection fraction = 65% (70-90mL) of end-diastolic ventricular volume(130mL)
Thus, about 50mL of blood remains at the end of systole (end-systolic ventricular volume)

4) Early diastole, once the ventricular muscle is fully contracted, the already falling vent. pressur drop more rapidly(protodiastole). This end when the momentum of the ejected blood is overcome and the aortic and pulmonary valves close.
After the valves are closed, pressure continues to drop rapidly (isovolumic ventricular relaxation). This phase end when the ventricular pressure falls below the atrial pressure and the AV valves opens; and ventricular filling begins rapidly.
Atrial pressure continue to rise after end of ventricular systole until AV valves open, then drop and slowly rises again until the next atrial systole.


The Heart Sounds

First sound ('lub') is caused by the vibrations set up by the sudden closure of AV valves at the beginning of ventricular systole. Duration- 0.15s, frequency- 25-45Hz.
Second sound ('dub') caused by vibrations accociated with closure of aortic and pulmonary valves just after the end of ventricular systole. Duration 0.12s, frequency 50Hz. It is loud and sharp when the diastolic pressure in the aorta/pulmonary artery is elevated, causing a brisk shut at the end of systole.
Third sound is heard about one-third of the way through diastole in many young individuals. This coincides with the period of rapid ventricular filling and is probably due to vibrations set up by the inrush of blood. Duration 0.1s
Fourth sound can sometimes be heard before the first sound when atrial pressure is high or ventricle is still in conditions such as ventricular hypertrophy-due to ventricular filling.


Murmurs & Bruits

Normally, the blood flow is laminar and nonturbulent up to a critical velocity; above this velocity, blood flow becomes turbulent and creates sounds. Blood flow speeds up when an artery or a heart valve is narrowed.
Bruits are vascular sounds heard due to turbulent flow. Some causes include atherosclerosis, aneurysm, AV fistula, patent ductus arteriosus.
The major but certainly not the only cause of cardiac murmurs is valvular heart disease.

Valve Abnormality Timing of murmur
Aortic or pulmonary stenosis systolic
regurgitation diastolic
Mitral or tricuspid stenosis diastolic
regurgitation systolic

Murmur due to aortic or pulmonary valves disease are heard best at the base of heart. And murmurs due to mitral disease are heard best at the apex.
Interventricular septal defect causes systolic murmur when blood frow from left to right.
Soft murmur may or may not be heard in interatrial septal defect. Soft innocent murmurs are common is children who have no cardiac disease.
In anemic patients, systolic murmurs are common.

Choo Wei Chong
Source: William F. Ganong (Review of Medical Physiology)
The Cardiac Cycle

1) Late diastole, the mitral and tricuspid valves are open and the aortic
and pulmonary valves are closed. Blood flows thoroughout diastole, filling the atria and ventricles.
The filling declines as ventricles become distended and the AV valves drift toward closed position, note the pressure in ventricles remains low. In this stage, 70% of ventricular filling occur, passively.

2) Atrial systole, atria contraction propels additional 30% of blood into the ventricles.
Atrial contraction narrows the IVC and SVC orifices, and the inertia of blood towards heart - keep blood in it. But, in the pulmonary veins, some regurgitation of blood occurs.

3) Ventricular systole, in this stage, the AV valves close. And the ventricular muscle shortens relatively little, but intraventricular pressure rises sharply (isovolumic ventricular contraction) until the pressure excees that of aortic(80mmHg) and pulmonary(10mmHg) pressure and their corresponding valves opens.
During the isovolumic ventricular contraction stage, AV valves bulge into atria cause small rise in pressure.
Upon opening of the aortic and pulmonary valves, the phase of ventricular ejection begins. Initial ejection is rapid, slowing down as systole progresses. (Peak LV pressure: 120mmHg ; RV pressure 25mmHg)
In late ventricular systole, pressure in aorta exceeds that of left ventricle but the momentum of blood keeps the flow momentarily.
Ejection fraction = 65% (70-90mL) of end-diastolic ventricular volume(130mL)
Thus, about 50mL of blood remains at the end of systole (end-systolic ventricular volume)

4) Early diastole, once the ventricular muscle is fully contracted, the already falling vent. pressur drop more rapidly(protodiastole). This end when the momentum of the ejected blood is overcome and the aortic and pulmonary valves close.
After the valves are closed, pressure continues to drop rapidly (isovolumic ventricular relaxation). This phase end when the ventricular pressure falls below the atrial pressure and the AV valves opens; and ventricular filling begins rapidly.
Atrial pressure continue to rise after end of ventricular systole until AV valves open, then drop and slowly rises again until the next atrial systole.


The Heart Sounds

First sound ('lub') is caused by the vibrations set up by the sudden closure of AV valves at the beginning of ventricular systole. Duration- 0.15s, frequency- 25-45Hz.
Second sound ('dub') caused by vibrations accociated with closure of aortic and pulmonary valves just after the end of ventricular systole. Duration 0.12s, frequency 50Hz. It is loud and sharp when the diastolic pressure in the aorta/pulmonary artery is elevated, causing a brisk shut at the end of systole.
Third sound is heard about one-third of the way through diastole in many young individuals. This coincides with the period of rapid ventricular filling and is probably due to vibrations set up by the inrush of blood. Duration 0.1s
Fourth sound can sometimes be heard before the first sound when atrial pressure is high or ventricle is still in conditions such as ventricular hypertrophy-due to ventricular filling.


Murmurs & Bruits

Normally, the blood flow is laminar and nonturbulent up to a critical velocity; above this velocity, blood flow becomes turbulent and creates sounds. Blood flow speeds up when an artery or a heart valve is narrowed.
Bruits are vascular sounds heard due to turbulent flow. Some causes include atherosclerosis, aneurysm, AV fistula, patent ductus arteriosus.
The major but certainly not the only cause of cardiac murmurs is valvular heart disease.

Valve Abnormality Timing of murmur
Aortic or pulmonary stenosis systolic
regurgitation diastolic
Mitral or tricuspid stenosis diastolic
regurgitation systolic

Murmur due to aortic or pulmonary valves disease are heard best at the base of heart. And murmurs due to mitral disease are heard best at the apex.
Interventricular septal defect causes systolic murmur when blood frow from left to right.
Soft murmur may or may not be heard in interatrial septal defect. Soft innocent murmurs are common is children who have no cardiac disease.
In anemic patients, systolic murmurs are common.

Gan Chee Wei
041303031
group B2

Heart Sounds
A) first heart sound

• produced by the closure of mitral & tricuspid valve simultaneously
• indicate the onset of ventricular systole
• heard as a LUB while auscultating
• immediately precedes with carotid pulse
• heard loudest at the apex

B)Second heart sound

• produced by the closure of aortic valve(A2) & pulmonary (P2) valves
• pulmonary valve closes later & aortic valve closes earlier due to early raise of left ventricular pressure and early activation of the LV
• heard as 2 components A2,P2
• heard as DUB
• follows the carotid pilse
• better heard at pulmonary & aortic areas

C)third heart sound

• low-pitched
• produced in ventricle after A2,at the termination of rapid filling
• best heard with bell piece of stethscope at left ventricular apex during expiration & in left lateral position
• physiological S3:-occur in early ventricular diastole

-due to vibration of ventricular walss as blood rushes in

• pathological S3:-due to the "thud" of blood hitting noncompliant ventricular walls at the start of diastole

-Eg: myocardial damage

• normal in children & persons with high cardiac output

D)Fourth heart sound

• low-pitched
• presystolic sound produced in the ventricle during diastole
• associated with an effective atrial contraction
• best heard with bell piece
• absent in atrial fibrillation
• occurs when diminished ventricular compliance increase the resistance to ventricular filling
• presents in systemic hypertension, aortic regurgitation,hypertrophic cardiomyopathy,ischaemic heart diseases
• accompanied by visible & palpable presystolic distensionof left ventricle
• loudest at left ventricular apex& in left lateral position
• is accentuated by mild isotonic or isometric exercise in supine position

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Heart murmurs

• found where there is turbulent flow, &their radiation follows the direction of blood flow
• murmurs may be palpable & produce precordial thrills

Causes of murmurs:

• a high -velocity jet,eg: a stenotic or regurgitant jet,passing from a high -pressure to a lower pressure chamber or vessels
• may occur with increased flow velocity in a normal vessel or with flow into a dilated or distorted vessel
• do not always indicate valve pathology
• may indicate a high flow eg : pregnancy

Description of murmurs:
murmurs are described in term of :

• timing with cardiac cycle-systolic/distolic
• relation with respiration
• low pitched/high pitched
• character:soft,blowing,rumbling
• presence of thrill
• point of maximum intensity & direction of selective propagation
• any specific manoeuvres/body position which make the murmur more prominent
• grade

Grade of murmur:

• I :heard with great difficulty under ideal condition
• II : easily heard
• III :loud without thrill
• IV :with thrill
• V :very loud
• VI : extremely loud

Systolic murmurs:
A)Ejection murmurs

• crescendo-decrescendo
• flow across a stenotic aortic/pulmonary valve or flow into a dilated aorta or pulmonary artery
• also happens with increased flow across pulmonary/aortic valves
• commences after S1
• peaks in mid-systole
• stops before S2
• a definite gap in between murmur & S1,S2

B)Pansystolic murmurs

• generated by jets passing from a high pressure to a low pressure chamber throughout systole
• begins with S1 & ands with S2
• eg:Mitral regurgitation,tricuspid regurgitation,ventricular septal defect

C)Late systolic murmur

• begins well after S1 & continues up to S2
• preceded by a midsystolic click
• eg:MVP,papillary muscle dysfunction

Diastolic murmurs
A)mitral & tricuspid mid-diastolic murmur

• low-pitched
• rumbling murmurs starting after the opening snap
• best heard with bell
• are localised
• accentuated by left lateral position
• can be confused with S3
• start well after S2 & may persist up to next S1
• Eg:Mitral stenosis,tricuspid stenosis,Austin Flint murmur

B)Early diastolic murmurs

• begins just after S2 & gradually decrease intensity
• high pitched
• can be short or persist throughout diastole
• Eg:aortic regurgitation,pulmonary regurgitation