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

Gan Chee Wei
041303031
Group B2

Cardiac Cycle

• systolic pressure refers to the peak pressure reached during systole.
• diastolic pressure refedrs to the lowest pressure during diastole.

Mechanical events of the cardiac cycle:
A)Events in late Diastole

• mitral & tricuspid valves are open
• aortic & pulmonary valves are closed
• blood filling of the atria & ventricles
• the rate of filling declines as the ventricles become distended
• cusps of the atrioventricular(AV) drift to closed position

B)Atrial Systole

• contraction of the atria propels some additional blood into ventricles
• 70% of the ventricular filling occurs passively during diastole

C)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)

D)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.

CHUA LAUSANNE
041303019

Cardiac cycle

Phase 1 – Atrial contraction

· As the atria contract, the pressure within the atrial chambers increases
· more blood flow across the open atrioventricular (AV) valves, leading to a rapid flow of blood into the ventricles
· However, atrial contraction does produce a small increase in venous pressure that can be noted as the "a-wave" of the left atrial pressure (LAP).
· A heart sound is sometimes noted during atrial contraction (fourth heart sound, S4). This sound is caused by vibration of the ventricular wall during atrial contraction.
· it is noted when the ventricle compliance is reduced ("stiff" ventricle) as occurs in ventricular hypertrophy and in many older individuals.
· Represents p wave in the ECG, which represents electrical depolarization of the atria.

Phase 2 – Isovolumeric contraction

· The AV valves close as intraventricular pressure exceeds atrial pressure.
· Closure of the AV valves results in the first heart sound (S1).
· Ventricular volume does not change because all valves are closed during this phase. Contraction, therefore, is said to be "isovolumic" or "isovolumetric."
· The "c-wave" noted in the LAP may be due to bulging of mitral valve leaflets back into left atrium.
· Represent by QRS complex in ECG, which represents ventricular depolarization.

Phase 3 – Rapid filling

· initial and rapid ejection of blood into the aorta and pulmonary arteries from the left and right ventricles
· Ejection begins when the intraventricular pressures exceed the pressures within the aorta and pulmonary artery, which causes the aortic and pulmonic valves to open.
· No heart sounds are ordinarily noted during ejection because the opening of healthy valves is silent.
· The presence of sounds during ejection (i.e., ejection murmurs) indicate valve disease or intracardiac shunts.

Phase 4 – Reduced filling

· Left atrial and right atrial pressures gradually rise
· due to continued venous return from the lungs and from the systemic circulation
· ventricular repolarization occurs as shown by the T-wave of the ECG

Phase 5 – Isovolumeric relaxation

· When the intraventricular pressures fall sufficiently at the end of phase 4, the aortic and pulmonic valves abruptly close
· It cause the second heart sound (S2) and the beginning of isovolumetric relaxation.
· Valve closure is associated with a small backflow of blood into the ventricles and a characteristic notch (dicrotic notch) in the aortic and pulmonary artery pressure tracings.
· Although ventricular pressures decrease during this phase, volumes remain constant because all valves are closed.
· The volume of blood that remains in a ventricle is called the end-systolic volume and is ~50 ml in the left ventricle.
· The difference between the end-diastolic volume and the end-systolic volume is ~70 ml and represents the stroke volume.

Phase 6 – Rapid filling

· When intraventricular pressures fall below atrial pressures. the AV valves rapidly open and ventricular filling begins.
· The opening of the mitral valve causes a rapid fall in LAP. The peak of the LAP just before the valve opens is the "v-wave."
· Ventricular filling is normally silent.
· When a third heart sound (S3) is audible, it may represent tensing of chordae tendineae and AV ring during ventricular relaxation and filling.
· This heart sound is normal in children; but is often pathological in adults and caused by ventricular dilation.

Phase 7 – Reduced filling

· As ventricles continue to fill with blood and expand, they become less compliant and the intraventricular pressures rise.
· Aortic pressure and pulmonary arterial pressures continue to fall during this period.

Heart sounds

First heart sound, S1
· Produced by the closure of AV valves simultaneously
· Indicates the onset of ventricular systole
· Loudest at apex
· Immediately precedes / coincides with the apex

Second heart sound, S2

· Produced by closure of aortic and pulmonary valves
· Physiological splitting
§ During inspiration(-ve intrathoracic pressure), there is increase venous return which delays the right heart emptying
§ Causing pulmonary valve closes later than aortic valve
§ As a result S2 is heart as 2 component , A2 and P2
§ Common in children and young adults

Third heart sound, S3

· Produced by rapid filling of the ventricle during early diastole, leading to sudden limitation of the expansion of ventricle causing vibration
· Heard immediately after S2 , with bell of stethoscope
· Can be physiological in- healthy young adults, athletes, pregnancy

Fourth heart sound, S4

· Occurs during the atrial contraction phase
· Caused by surge of the ventricular filling that accompanies atrial systole
· Heard immediately before S1
· Pathological in young adults- increased ventricular stiffness associates with HTN, AS and acute MI

Murmurs

· Due to vibrations produced by the turbulent flow at –
§ The region of the valve
§ Near the valve
§ Abnormal communication within the heart
· Mechanism of production:
§ Increase flow through a normal valve
§ Normal or decreased flow through abnormal valve
§ Regurgitation of blood through a leaking valve
· 3 classification:
§ Systolic
§ Diastolic
§ Continuos

Systolic murmurs:

·Ejection systolic murmur
§ Heard separately from the S1 and S2
§ Crescendo-decresendo
§ Eg: AS and PS (due to obstruction to the ventricular outfow cause by stenotic valve)
· Pansystolic murmur
§ Extend from the S1 to S2
§ Constant intensity throughout the whole systole
§ Generated whenever pressure difference btw the 2 chambers is high throughout the systole and blood flow becomes turbulent
§ Eg: MR, TR and VSD
· Late-systolic murmur
§ Separated from the S1 but extend up to S2
§ Eg: mitral valve prolapsed, papillary muscle dysfunction

Diastolic murmurs:

· Early diastolic murmur
§ Starts after S2 and gradually decreases in intensity
§ due to flow of blood back into left ventricle may partially obstruct mitral valv
§ Eg: PR and AR
· Mid-diastolic murmur
§ Begins well after S2 and persist to the next heart sound
§ Eg : MS, TS

Continuous murmur

· Begins in after S1 and continues without interruption through S2
· Due to blood flow without interruption from a vascular bed of higher resistance into vascular bed of lower resistance without interruption btw systole and diastole
· Eg : AV fistula, PDA

2 important components of cardiac cycle :
i)diastole
ii)systole

• Diastole of cardiac cycle

-The cardiac cycle begins with a period of rapid ventricular filling.
-The right atrium fills with deoxygenated blood from the superior vena cava, the inferior vena cava, and the coronary venous return (e.g., the coronary sinus and smaller coronary veins).
-At the same time, the pulmonary veins return oxygenated blood from the lungs to the left atrium.
-During the early diastolic phase of the cardiac cycle, both ventricles relax and fill from their respective atrial sources.
-The atrio-ventricular valves (the tricuspid valve is located between the right atrium and right ventricle; the mitral valve is between the left atrium and left ventricle) open and allow blood to flow from the atria into the ventricles.
-The flow of blood through the atrio-ventricular valves is unidirectional and as volume related pressure increases within the ventricles, the atrioventricular valves close to prevent backflow from the ventricles into the atria.

• Systole

-At the onset of the systolic phase, specialized cardiac muscle fibers within the sino-atrial node (S-A node) contract and send an electrical signal propagated throughout the heart.
-In a sweeping fashion, the right atrium contracts and forces the final volume of blood into the right ventricle.
-The left atrium contracts and contributes the final 20% of volume to the left ventricle.
-The SA node signal is delayed by AV node to allow full contraction of atria that allow ventricle to reach their maximum volumes.
-A sweeping right to left wave of ventricular contraction then pumps blood into the pulmonary and systemic circulatory systems.
-The semilunar valves that separate the right ventricle from the pulmonary artery and the left ventricle from the aorta open shortly after the ventricles begin to contract.
-The opening of the semilunar valves ends a brief period of isometric (constant volume) ventricular contraction and initiates a period of rapid ventricular ejection.
-After emptying, both ventricles collapse to undergo a period of repolarization and refilling.
-At the outset, ventricular pressures remain greater than atrial pressures and the atrioventricular valves remain closed.
-The cardiac cycle is complete with the onset of another period of rapid ventricular filling that takes place when atrial pressures exceed ventricular pressures and the atrio-ventricular valves open to allow rapid filling.

Dinesh Ranaweera 041303025

s3 ( third heart sound)

This is a low pitched sound,produced in the ventricle about 0.14-0.16 seconds after A2, at the termination of rapid filling,,
It is normal in children and in people with high cardiac output.
In people more than 40 years of age, it indicates impairment of ventricular function,AV valve regurgitation,conditions which increases rate/volume of ventricular filling.

Physiological S3-

Occurs in early ventricular diastole.
Due to vibration of ventricular walls as blood rushes in.

Pathological S3-
Possibly due to thud of blood hitting non compliant ventricular walls at the start of ventricular filling.Such as when there is myocardial damage.

S4 ( fourth heart sound)

This is also a low pitched sound,it is a presystolic sound produced in the ventricle during ventricular filling.It is associated with inaffective atrial contraction.This sound is best heard with the bell piece of the stethascope.
It is absent in atrial fibrillation.
Occurs due to diminished ventricular compliance increases the resistence to ventricular filling.
This type of heart sound is present in persons with systemic hypertension,Aortic stenosis,hypertrophic cardiomyopathy,Ischeamic heart disease and acute mitral regurgitation.
It is also accompanied by visible and palpable presystolic distension of the left ventricle.
Loudest at the apex and in left lateral position.
It is also accentuated by mild isotonic or isometric exercise in supine position.


Heart Murmurs

Heart murmurs are found where there is turbulent flow, and their radiation follows the direction of blood flow.Murmurs maybe palpable and produce precordial thrills.

Causes of murmurs-
Generated by a high velocity jet of blood,Eg stenotic or regurgitant jet,passing from a high pressure to a low pressure chamber or vessel.
May occur with increased flow velocity in a normal vessel or with flow into a dilated or distorted vessel.
Murmurs does not always indicate valve pathology.
It may indicate high flow.as in pregnancy.

Description of murmurs-
Murmurs are described in terms of
a)Timing with cardiac cycle-systolic/diastolic.
b)Influence of respirarion
c)Low pitched/high pitched
d)Character-soft blowing,rumbling
e)Presence of thrill
f)Point of maximum intensity and direction of selective propagation
g)Any specific manoeeuvres/body positions which make the murmur more prominent.

Systolic Murmurs

Ejection murmurs-
Has characteristics of crescendo(getting gradually louder) and decresendo(gettin gradually softer)
Flows across a stenotic aortic/pulmonary valve or flow into a dilated aorta or pulmonary artery.
Also occurs with increased flow across pulmonary/aortic valves.
Commences after 1st heart sound.
Peaks in mid systolic
Stops at second heart sound.There is also a definite gap in between mumur and S1 and S2.

Pan systolic murmurs-
Generated by jets passing from a high pressure to a low pressure chamber throughout systole.
Begins with S1 and ends with S2.
Intensity of murmur is uniform throughout the systole...Eg mitral regurgitation,tricuspid regurgitation,ventricular septal defect.

Late systolic Murmurs-
Begins well after S1 and continues up to S2,it is also often preceded by a midsystolic click.
Eg mitral valve prolapse,papillary muscle dysfunction.

Diastolic Murmurs-

Mitral and Tricuspid mid diastolic Murmurs
This is a low pitched murmur.which is best heard with the bell of the stethscope.
It is w well localized murmur,which is accentuated by the patient being in the left lateral position.
If short it can be confused with S3.
It begins well after S2 and may persist upto the next S1.
Eg-Mitral stenosis,Tricuspid stenosis

Early diastolic murmur
Starts just after S2 and gradually decreases with intensity.It is a high piched kind of murmur,which can be short or persist throughout diastole.
Eg-Aortic regurgitation.

Murmur
Def:blowing,whooshing or rasping sounds produced by turbulent flow through the heart valves or near the heart.

-murmur can occur when heart valves not closed tightly
eg:mitral valves regurgitation
tricuspid regurgitation
aortic regurgitation
pulmonary regurgitation

-murmur can occur when blood flow thru a narrow opening or stiff valves
eg:mitral stenosis
tricuspid stenosis
aortic stenosis
pulmonary stenosis


classification of murmur into : systolic
diastolic
continuos

• Systolic murmur is due to

1. increased flow thru a normal valve
2.normal or decreased flow thru a stenosed valve
3.systolic leak from high to low pressure

Different type - ejection systolic
Late systolic
Pansystolic or Hollow systolic
Ejection murmur
*commences after 1st heart sound
*peak in midsystolic
*stop before 2nd heart sound
*definite gap betw. the murmur and the 1st n 2nd heart sound
*phonocardiogram : diamond shape
eg : aortic stenosis and pulm.stenosis

Late systolic
*murmur begins well after first heart sound and continues up to 2nd heart sound
eg: mitral valve prolapse
papillary muscle dysfunction

Pansystolic murmur
*murmurs begin with the 1st heart sound and end with 2nd heart sound
eg:Mitral regurgitation , Tricuspid regurgitation,VS

• Diastolic murmurs

- heard after 2nd heart sound and before the subsequent 1st heart sound

Types : Early diastolic
Mid diastolic

Early diastolic murmur
*murmur start just after the 2nd heart sound and gradually decreases in intensity - persists up to opening of mitral and tricuspid valve
eg:aortic regurgitation
Pulmonary regurgitation

Mid diastolic murmur
*murmurs begin well after 2nd heart sound and may persist up to the next 1st heart sound
eg:mitral stenosis
tricuspid stenosis
Austin-Flint murmur

• Continuous murmur

*murmur begins in the systole and continues w/o interruption thru the 2nd heart sound into all part of diastole
eg:Patent ductus arteriosus
AV fistula

CARDIAC CYCLE :
- the activity of heart follows a cyclical pattern.

- the atria contracts first, followed by the ventricle after some delay.

- one contraction (systole) and one relaxation (diastole) together forms a cardiac cycle.

- each cycle repeats itself about 70 times a minute.

- duration of cardiac cycle : 0.8sec
* ventricular systole (aka systole) : 0.3sec
* ventricular diastole (aka diastole) : 0.5sec

- when heart rate increases, duration of cardiac cycle decreases (with more reduction in duration of diastole than that of systole).

- events in a cardiac cycle :
* in late diastole, mitral and tricuspid valves between atria and ventricles are open and the aortic and pulmonary valves are closed. Blood flows into the heart throughout diastole, filling the atria and ventricles. The rate of fillling declines as ventricles become distended, and the cusps of atrioventricular (AV) valves drift toward the closed position. Pressure in ventricles remain low.
* in atrial systole, contraction of atria propels some additional blood into ventricles (but most of ventricular filling occurs passively during diastole). Contraction of atrial muscle that surrounds the orifices of SVC, IVC and pulmonary veins narrows their orifices, and the inertia of blood moving towards the heart tends to keep blood in it. However, there is some regurgitation of blood into the veins during atrial systole.
* at the start of ventricular systole, the mitral and tricuspid valves close. Ventricular muscles shorten relatively little initially, but intraventricular pressure rises sharply as the myocardium presses on the blood in the ventricle. The pressure in left and right ventricles exceeds the pressures in the aorta (80mmHg) and pulmonary artery (10mmHg) and the aortic and pulmonary valves open. During the contraction, the AV valves bulge into atria and causes a small but sharp rise in atrial pressure. When the aortic and pulmonary valves open, ventricular ejection begins with ejection being rapid initially and slowing down as systole progresses. Late in systole, the aortic pressure actually exceeds the ventricular, but for a short period momentum keeps the blood moving forward. The AV valves are pulled down by contractions of ventricular muscle, and atrial pressure drops.
* early diastole : once the ventricular muscle is fully contracted, the already falling ventricular pressures drop more rapidly. It ends when momentum of the ejected blood is overcome and the aortic and pulmonary valves close, setting up transient vibrations in the blood and blood vessel walls. After the valves are closed, pressure continues to drop rapidly. This ends when ventricular pressure falls below atrial pressure and the AV valves open, permitting the ventricles to fill. Filling is rapid at first, then slows as the next cardiac contraction approaches. Atrial pressure continues to rise after the end of ventricular systole until the AV valves open, then drops and slowly rises again until the next atrial systole.


1st heart sound (0.15sec)
- low, slightly prolonged "lub"
- caused by vibrations set up b sudden closure of mitral and tricuspid valves at the start of ventricular systole


2nd heart sound(0.12sec)
- shorter, high-pitched "dup"
- caused by vibrations associated with closure of the aortic and pulmonary valves just after the end of ventricular systole


3rd heart sound (0.1sec)
- soft, low-pitched
- heard about 1/3rd of the way through diastole
- coincides with rapid ventricular filling and is probably due to vibrations set up by the inrush of blood


4th heart sound
- sometimes (but rarely) heard immediately before 1st sound when atrial pressure is high or the ventricle is stiff in conditions such as ventricular hypertrophy
- is due to ventricular filling


Murmurs(or bruits)
- are abnormal sounds heard in various parts of vascular system, with the term "murmur" being more commonly used to denote noise heard over the heart than over the blood vessels

- major causes of cardiac murmurs are diseases of the heart valves :
* when the orifice of a valve is narrowed (stenosis), blood flow through it in the normal direction is accelerated and turbulent
* when a valve is incompetent, blood flows backward through it (regurgitation or insufficiency), again through a narrow orifice that accelerates flow.

- timing of the murmur (either systolic or diastolic) can be predicted from cardiac cycle :
* aortic or pulmonary stenosis - systolic
* aortic or pulmonary insufficiency - diastolic
* mitral or tricuspid stenosis - diastolic
* mitral or tricuspid insufficiency - systolic
* congenital interventricular / interatrial septal defect - systolic


MITRAL & TRICUSPID STENOSIS
- produces a mid-diastolic murmur : murmur begins well after 2nd heart sound and may persist upto the next 1st heart sound (during passive ventricular filling)


MITRAL & TRICUSPID REGURGITATION
- in acute MR and TR, there will be an early systolic murmur : murmur begins with 1st heart sound and diminishes in intensity and stops well before 2nd heart sound (mid-diastole)
- in MR and TR as such, there will be a pansystolic (holosystolic) murmur : murmur begins with 1st heart sound and ends with 2nd heart sound or its component. 1st heart sound is usually muffled ; intensity of murmur is uniform throughout the systole.


MITRAL VALVE PROLAPSE
- produces a late systolic murmur : murmur begins well after 1st heart sound (clear gap between the murmur and 1st heart sound) and continues upto 2nd heart sound.


AORTIC & PULMONARY STENOSIS
- produces an ejection systolic (mid-systolic) murmur : murmur commences after 1st heart sound, peaks in mid-systole and stops before 2nd heart sound. There is a definite gap in between the murmur and the 1st and 2nd heart sound.


AORTIC & PULMONARY REGURGITATION
- produces an early diastolic murmur : murmur starts just after 2nd heart sound and gradually decreases in intensity (persists upto opening of mitral and tricuspid valves)
- may also produce an ejection systolic murmur in cases where there is ejection of blood into dilated aorta or pulmonary arteries.

Cardiac cycle..

Sequence of events that occur when the heart beats. Each cycle lasts for approximately 0.8s.

Two phases:

a)Diastole (relaxation phase)

b) Systole (contraction phase)

Diastole:
Both atrium and ventricles are relaxed.. Atrio-ventricular valve (AV) is open. De-oxygenated blood from superior vena cava (svc) & Inferior vena cave (IVC) flows into right atrium. Since the AV valve is open, the blood will then flow into right ventricle. The pressure in right ventricle increases and this will shut the AV valve.
SA node generated an impulse and this results in contraction on right atrium (Atrial systole) and additional blood will be pushed into right ventricle thru AV valve. The high pressure in right ventricle and low pressure in right atrium makes sure that no blood flows back into right atrium.

Systole:

Now, both AV valves and Semilunar valves are closed. Heart is a closed chamber now. Right ventricle receives impulses form purkinje fibers and contracts. Since all exits are closed, the pressure in right ventricle rises above the pressure in pulmonary artery (10mmHg) and semilunar valve opens.
Blood the flows into pulmonary artery and this results in fall of right ventricular pressure below pulmonary artery pressure and hence semilunar valve will close.
This blood will be carried to lungs for oxygenation and the oxyegnated blood is carried back to left atrium via pulmonary veins.


Diastole:
In the next diastole, the semilunar valves close and the atrioventricular valves open. This allows blood to flow into left atrium from pulmonary veins. At the same time blood from IVC and SVC is filling right atrium.
SA node releaese an impulse again triggering the atria to contract.
Left atrium empties its contents into the left ventricle and pressure in left ventricle rises above pressure in left atrium hence closing the mitral valve.

Systole:

Now mitral valve is closed and so is semilunar valve (aortic valve). Heart is again a closed chamber and ventricles are contracting. Since the blood has no where to flow, this rises the pressure in left ventricle above that in aorta... Once the pressure exceeds 80mmHg, semilunar valve opens and blood flows into aorta and is carried to whole body.

This cycle repeats itself for about 70-90 times per minute.



Pathophysiology of 3rd and 4th heart sound:

3rd heart sound:

Due to increased atrial pressure leading to increased flow rates.
Commonly seen in congestive cardiac failure.



4th heart sound:

Due to blood being forced into a hypertrophic left ventricle.

• S3 (Third heart sound)

*produced due to rapid filling of the ventricle during early diastole leading to sudden limitation of the ventricle causing vibrations.
*heard over apex ,while patient is in suspine or left lateral position
*Characteristic : early diastolic low frequency extra heart sound
heard with bell of stethescope
increase with inspiration , leg elevation and with
increase venous return
Physiological : healthy young adults
Athlete
Pregnancy
Fever

Pathological : after 40yrs
cardiac failure
mitral regurgitation
dilated cardiomyopathy

• S4 (fourth heart sound)

*due to decreased ventricular compliance there will be increased atrial contraction producing ventricular distension causing the sound during the presystolic phase
*occur during atrial filling phase of the ventricular diastole
Characteristic :
-Low pitch extra heart sound at late diastole or early systole.
-Increases with forced inspiration, exercise, elevation of legs, and with increased venous return.
-better felt than auscultated
-disappears in patients with atrial fibrillation
-better heard at apex

Causes : left ventricular hypertrophy
right ventricular hypertrophy

CARDIAC CYCLE

Mechanical events occuring in the cardiac cycle :

Late diastole
- mitral and tricuspid valves are open
- aortic and pulmonary valves are closed
- blood fills the atria and ventricles
- as the ventricles distend, the cusps of the atrioventricular valve move
to closed position
- end-diastolic volume = 130 ml

Atrial systole
- contraction of the atria pushes more blood into the ventricles (30%)
- contraction of the atrial muscles surrounding the orifice of the superior
and inferior vena cava prevents regurgitation

Ventricular systole
- mitral and tricuspid valves close = FIRST HEART SOUND
- ISOVOLUMETRIC CONTRACTION : The ventricles contract against a
fixed volume as the aortic and pulmonary valves are closed. The intra-
ventricular pressure continues to rise until it finally exceeds that of the
aorta and pulmonary artery, causing the aortic and pulmonary valves to
open. Initially, the atrioventricular valves bulges into the atria.
- VENTRICULAR EJECTION : Blood is forced into the aorta and pulmonary
artery. As the intraventricular pressure rises, the atrioventricular valves
get pulled into the ventricles.
- Amount of blood ejected : 70-90 ml
- End-systolic volume = 50 ml

Early diastole
- PROTODIASTOLE : Once the ventricles have fully contracted, the
already falling intra-ventricular pressure falls even more rapidly. Once
the momentum of ejected blood has been overcome, the aortic and
pulmonary valves close = SECOND HEART SOUND.
- ISOVOLUMETRIC RELAXATION : the intra-ventricular pressure
continues to drop. THis phase ends when the intraventricular pressure
drops to below the atrial pressure causing the atrioventricular valves to
open.
- PASSIVE VENTRICULAR FILLING

DURATION OF EVENTS :
Systole - 0.27 sec
DIastole - 0.53 sec
Total cycle - 0.80 sec


ORIGIN OF HEART SOUNDS
1st heart sound - vibrations set up by the sudden closure of the mitral
and tricuspid valves at the start of ventricular systole.
- low pitched, prolonged sound

2nd heart sound - vibrations associated with the closure of the aortic
and pulmonary valves just after the end of ventricular
systole
- high pitched, shorter sound

3rd heart sound - vibrations set up by the inrush of blood during rapid
ventricular filling
- soft, low pitched sound

4th heart sound - ventricular filling when the ventricular wall is stiff and
cannot expand, or when atrial pressure is high
- seen in ventricular hypertrophy


MURMURS
Mitral Stenosis
Clinical findings : tapping apical impulse, diastolic thrill at apex, loud S1,
mid -diastolic murmur, opening snap.

Mid-diastolic murmur is caused by turbulent flow through the stenotic atrioventricular valve. It is best heard with the bell of the stethoscope with patient in left lateral position.


Mitral regurgitation
Clinical findings : high volume pulse, hyperdynamic apical impulse, systolic thrill at the apex, soft S1, pan-systolic murmur.

Pan-systolic murmur is caused by regurgitation throught the incompetant atrioventricular valve. It is loudest at the apex and radiates to the left axilla.

Mid-diastolic murmur may also be heard due to increased flow across the non-stenotic mitral valve.


Aortic Stenosis
CLinical findings: low volume pulse, heaving apical impulse, systolic thrill, ejection click, ejection systolic murmur

Ejection systolic murmur is caused by turbulence in the ventricular outflow during ejection. It is best heard with the diaphragm with the patient sitting forward. Sometimes, it is heard at the apex with a different quality : Gallaverdin phonomenon.


Aortic regurgitation
Clinical findings : hyperdynamic / heaving apex, diastolic thrill in aortic area, loud S2, early diastolic murmur, austin-flint murmur, ejection systolic murmur.

Early diastolic murmur is caused by regurgitation through the incompetant aortic valve. Best heard using the diaphragm with the patient sitting forward. Radiates to the left sternal edge.

Austin-Flint murmur is a soft mid-diastolic murmur. The preclosure of the anterior leaflet of the mitral valve by the regurgitant jet produces mitral turbulence.

Ejection systolic murmur is caused by increased stroke volume and velocity of ejection. This is due to the increased amount of blood in the ventricles caused by the regurgitant blood from aorta in addition to the normal volume that entered from the atria.


Mitral Valve Prolapse
Clinical findings : Mid-systolic click, late-systolic murmur.

Mid-systolic click occurs due the prolapse of the mitral valve in mid-systole.

Late-systolic murmur occurs due to the regurgitant jet flowing across the prolapsed mitral valve.


Tricuspid Regurgitation
Clinical Findings : Pansystolic murmur , right-sided S3, prominent JVP, pulsatile liver

Pansystolic murmur is caused by the regurgitant flow of blood across the incompetant tricuspid valve. The murmur is accentuated during inspiration as the increase in venous return to the right side of the heart increases the regurgitant volume (Carvallo's sign).