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

MECHANISMS-DIFFERENT HEART SOUNDS AND MURMURS.

First Heart Sound
-'Lub' sound--due to closure of atrio-ventricular (A-V) valves at the beginning of systole.

Second Heart Sound
-'Dub' sound--due to closure of semilunar valves (aortic and pulmonary) at the end of systole.
-marks beginning of diastole.

The normal pumping heart of the heart is considered to start when the A-V valves close at the onset of ventricular systole.

Third Heart Sound
-occasionally a weak,rumbling third heart sound is heard at the beginning of the middle-third of diastole.
-logical but unproved explanation--it is the sound of blood back and forth between the walls of the ventricles initiated by inrushing blood from the atria.
-the frequency of this sound is usually so low that the ear cannt hear it, yet it can be often be recorded in the phonocardiogram.

Fourth Heart Sound
-aka atrial heart sound.
-can sometimes be recorded in the phonocardiogram, can almost never be heard with a stethoscope beacuse of its weakness and very low frequency--usually 20cycles/sec or less.
-occurs when the atria contracts--presumably caused by the inrush of blood into the ventricles which initiates vibration.

Mitral Stenosis
-diastolic murmur
-blood passes with difficulty through the stenosed mitral valve from the left atrium (LA) to the left ventricle (LV)
-also bcos the presure in the LA seldom rises above 30mmHg, thus a large pressure differential forcing blood from LA to LV does not develop.

Mitral Regurgitation
-systolic murmur.
-blood flows backward through the mitral valve into the LA during systole.
-causes a high frequency blowing, swishing sound (similar to aortic regurgitation but occurs in systole rather than diastole)
-sound transmitted most strongly in LA, but LA is deep within chest--difficult to hear over the atrium-- sound transmitted to chest wall mainly thru LV to the apex of the heart.
-Principal cause : Rheumatic disease

Mitral Valve Prolapse (MVP)
-When the mitral valve does not open and close properly, the flaps may 'billow' backward slightly into the upper chamber during the heart's contraction.
-Sometimes small amounts of blood may leak backward into the upper chamber of the heart because the valve does not close normally.
-common causes of mild mitral regurgitation.
-caused by congenital anomalies or degenerative myxomatous changes and is sometimes a feature of Ct disorders (Marfan's Synd)
-progressive elongation of chordae tendinae--increasing mitral regurgitation.
Chordal rupture--sudden, severe regurgitation.
-can predispose to infective endocarditis.
-MVP also assoc with typically benign arrythmias, atypical chest pain and very small risk of embolic stroke or TIA.
-overall long term prognosis is good.

Aortic Stenosis
-systolic murmur
-blood is ejected from LVthrough only a small fibrous opening of the aortic valve.
-Resistance to ejection--high pressure of blood in LV (300 mmHg), but pressure in aorta is still normal.
Thus a 'nozzle' effect is craeted during systole,with blood jetting at tremendous velocity thru the small opening of the valve ---> severe turbulence of blood at the root of aorta.
-a loud murmur is transmitted throughout the superior thoracic aorta and even the large arteries of the neck.
-may produce sound vibrations--thrill.

Aortic Regurgitation
-diastolic murmur
-no abnormal sound heard on systole, but on diatole, blood flows backward from the high pressere aorta into the LV.
-the murmur results from turbulence of blood jetting backward.

Tricuspid Regurgitation
-structural incompetence of the valve.
-the incompetent nature of the valve can result from primary structural abnormalities of the leaflets and chordae or from secondary myocardial dysfunction and dilatation.
-causes blood to leak back through the tricuspid valve from the right ventricle into the right atrium of the heart. In a healthy heart, no blood is allowed back through a valve once it has passed through. Leaking decreases the heart's efficiency and often leads to heart failure.
-Common cause : Rheumatic disease.



CARDIAC CYCLE
-is the cardiac events tht occur from the beginning of one heartbeat to the beginning of the next.
-each cycle is initiated by spontaneous generation of an action potential in the sinus node.
-consists of a period of relaxation-diastole (during which the heart fills with blood) and a period of contraction-systole.
-de-oxygenated blood from the SVC(superior vena cava) and IVC(inferior vena cava) flows into the right atrium. The open atrioventricular (AV) valves allow blood to pass through to the ventricles. The SA node contracts triggering the atria to contract. The right atrium empties its contents into the right ventricle. The tricuspid valve prevents the blood from flowing back into the right atrium.
-AV valves close and the semilunar open. The de-oxygenated blood is pumped into the pulmonary artery.
-pulmonary artery carries the blood to the lungs. There the blood picks up oxygen and is returned to the left atrium of the heart by the pulmonary veins.
-diastole period-the semilunar valves close and the AV valves open. Blood from the pulmonary veins fills the left atrium. (Blood from the vena cava is also filling the right atrium.) The SA node contracts again triggering the atria to contract. The left atrium empties its contents into the left ventricle. The mitral valve prevents the oxygenated blood from flowing back into the left atrium.
-During systole, the AV valves close and the semilunar valves open. The left ventricle receives impulses from the Purkinje fibers and contracts. Oxygenated blood is pumped into the aorta. The aortic valve prevents the oxygenated blood from flowing back into the left ventricle.
-The aorta branches out to provide oxygenated blood to all parts of the body. The oxygen depleted blood is returned to the heart via the vena cava.

The cardiac cycle has four phases

I Ventricular filling
II Isometric contraction
III Ejection
IV Isovolumetric relaxation

• Ventricular filling

Ventricular diastole lasts for nearly two thirds of the cycle at rest. There is an initial phase of rapid filling lasting aprrox. 0.15 sec. As ventricular volume increase with blood the ventricular pressure is actually decreasing due to the elastic recoil of the heart. As the ventricle reaches its natural volume the rate of filling decreases and further filling requires further distension of the ventricles. In the final third of the filling phase, the atria contract and force some blood into the ventricles. The volume of blood in the ventricles at the end of diastole is the approx. 120 ml and is called end diastolic pressure.

• Isovolumetric Contracture

Ventricular systole lasts 0.35s and is divided into a brief isovolumetric phase and a longer ejection phase. As soon as the ventricular pressure rises above the atrial pressure, the atrioventricular valves are forced shut. The ventricle is now a closed chamber.

• Ejection

When ventricular pressure rises above that of the arterial circulation the outflow valves are opened and ejection begins. Three quarters of the stroke volume is ejected in the first half of the ejection phase. As systole weakens and the rate of ejection slows down, the rate at which blood flows away through the arterial system begins to exceed the ejection rate, so pressure begins to fall. Valve closure creates a brief pressure rise in arterial pressure trace called the dicrotic wave. The ventricles do not empty completely but only about by two thirds.

• Isovolumetric relaxation

With closure of the aortic and pulmonary valves, each ventricle once again becomes a closed chamber. Ventricular pressure falls very rapidly owing to the mechanical recoil of collagen fibres within the myocardium. When ventricular pressure has fallen just below atrial pressure, the atrioventricular valves open and blood flows in from the atria, which have been refilling during ventricular systole.



THIRD HEART SOUND

Common in young people and is caused by the rush of blood into the relaxing ventricles during early diastole.


FOURTH HEART SOUND

Occurs just before the first and is caused by atrial systole



MURMURS

There are two fundamental classes of valvular abnormality, incompetence and stenos is. Incompetence is failure of the valves to close tightly, thus allowing a regurgitation of blood. Stenosis is the narrowing of the valve. A high pressure gradient is required to force blood through a stenosed valve. In aortic stenosis ventricular systole pressure is raised, increasing the work of the ventricle, while at the same time aortic pressure is reduced.
With either abnormality, blood passes through the valve in a turbulent jet, setting a high frequency vibration which is heard as a murmur. There are eight basic murmurs of valvular origin. For example, in mitral valve incompetence there is regurgitation into the left atrium, producing a murmur throughout systole(pansystolic) that sounds the loudest over the mitral auscultation area. The heart sound may then be represented as ‘lu-shshshsh-tupp’.

AMY SUZANA AHMAD SAUFI SASIDHARAN
041303006

-CARDIAC CYCLE-


MECHANICAL EVENTS

Late diastole
-mitral and tricuspid valves are open
-aortic and pulmonary valves are closed
-blood flows into heart throughout diastole filling atria and ventricles
-ventricles become distended
-pressure in ventricles remains low
-70% of ventricular filling occurs passively


Atrial systole
-contraction of atria propels additional blood to the ventricles
-contraction of atrial muscle that surrounds the orifices of the superior & inferior vena cava and pulmonary veins narrows their orifices
-inertia of blood moving towards heart tends to keep blood in it

Ventricular systole
-at beginning, mitral and tricuspid (AV) valves close
-intraventricular pressure rises sharply as myocardium presses on the blood in ventricle
-this period of isovolumetric (isovolumic, isometric) ventricular contraction lasts for 0.05s until pressures in left & right ventricles exceed pressures in aorta and pulmonary artery
-aortic and pulmonary valves open--- AV valves bulge into atria causing small rise in atrial pressure
-phase of ventricular ejection begins
-ejection rapid at first, intraventricular pressure rises to a maximum and declines before ventricular systole ends
-AV valves pulled down by contraction of ventricular muscle—atrial pressure drops
-amount of blood ejected by each ventricle per stroke at rest = 70-90mL
-EDV = 130mL
-EF = 50mL

Early diastole
-once ventricular muscle fully contracted, ventricular pressure drops rapidly
-period of protodiastole, lasts about 0.04s
-ends when momentum of ejected blood is overcomed and aortic and pulmonary valve close
-isovolumetric ventricular relaxation
-AV valves open permitting the ventricles to fill
-atrial pressure continues to rise

-HEART SOUNDS-

1st heart sound (S1)
-represents closure of mitral (M1) and tricuspid (T1) valves
-splitting in inspiration may be heard and its normal
Loud S1
-In mitral stenosis, because the narrowed valve orifice limits ventricular filling, there is no gradual decrease in flow towards the end of diastole
-the valves are therefore at their maximum excursion at the end of diastole and so shut rapidly leading to a loud S1 (the ‘tapping’ apex)
-S1 is also loud if diastolic filling time is shortened Eg: if the PR interval is short, and in tachycardia
Soft S1
-S1 is soft if the diastolic filling time is prolonged Eg: if the PR interval is prolonged or if the mitral valve leaflets fail to close properly (ie mitral incompetence)

2nd heart sound (S1)
-represents aortic (A2) and pulmonary valve (P2) closure
-A2 is said to be loud in tachycardia, hypertension, transposition
-P2 is loud in pulmonary hypertension and soft in pulmonary stenosis
-splitting in inspiration is normal and mainly due to the variation with respiration of right heart venous return, causing the pulmonary component to move
-a single S2 occurs in Fallots tetralogy, severe aortic or pulmonary stenosis, pulmonary atresia

3rd heart sound (S3)
-may occur just after the S2
-low pitched and best heard with the bell of stethoscope
-pathological after the age of 30yrs
-loud S3 occurs in dilated left ventricle with rapid ventricular filling Eg: mitral regurgitation, VSD or poor LV function
-in constrictive pericarditis or restricitive cardiomyopathy it occurs early and more high-pitched (pericardial knock)

4th heart sound (S4)
-occurs just before S1
-always abnormal �* it represents atrial contraction against a ventricle made stiff by any cause Eg: aortic stenosis, hypertensive heart disease

CARDIAC MURMURS

-CHARACTER & TIMING
Ejection-systolic murmur
-usually originates from the outflow tract and waxes & wanes with the intraventricular pressure
-may be innocent
-common in children and high output states Eg: tachycardia, pregnancy
-organic causes: --aortic stenosis and sclerosis, pulmonary stenosis


Pansystolic murmur
-is of uniform intensity and merges with S2
-usually organic and occurs in mitral or tricuspid regurgitation or VSD
-mitral valve prolapse may produce a late systolic murmur ± midsystolic click


Early diastolic murmur
-high pitched, easily missed
-occurs in aortic and pulmonary regurgitation
-if pulmonary regurgitation is secondary to pulmonary hypertension (which is itself due to mitral stenosis) then its called Graham Steell murmur


Mid-diastolic murmur
-low pitched and rumbling
-occur in mitral stenosis, rheumatic fever (Carey Coombs murmur), aortic regurgitation (Austin Flint murmur)

-GRADES
1/6: very soft, only heard after listening for a while
2/6: soft, but detectable immediately
3/6: clearly audible, but no thrill palpable
4/6: clearly audible, palpable thrill
5/6: audible with sthethoscope only partially touching chest
6/6: can be heard without placing sthetoscope on chest

-AREA LOUDEST
-mitral murmurs tend to be loudest over the apex, in contrast to the area of greatest intensity from the lesions of the aortic (right 2nd intercostals space), pulmonary (left 2nd intercostals space) and tricuspid (left sternal edges) valves

-RADIATION
-ESM of aortic stenosis classically radiates to the carotids
-PSM of mitral regurgitation radiates to axilla

-ACCENTUATING MANOUVRES
-movements that bring that relevant part of the heart closer to the sthethoscope
accentuate murmurs Eg: leaning forward for aortic regurgitation, left lateral position for mitral stenosis
-Expiration increases blood flow to the left side of the heart therefore accentuates left sided murmurs (inspiration has opposite effect)
-Valsalva manouvre (forced expiration against a closed glottis) decreases systemic venous return, accentuation mitral valve prolapse but softening mitral regurgitation and aortic stenosis (squatting has exactly the opposite effects)
-Exercise accentuates mitral stenosis



~~~~~~~~~~~~~~~goodnite~~~~~~~~~~~~~~~~~~~~~~~~~

Name: Semantha Chia Peck Sin
Roll No.: 041303015
Batch 15 (Group B2)

Heart Sounds
First Heart Sound (S1)
ØProduced by the closure of mitral and tricuspid valve simultaneously, so heard as a single sound.
ØIndicates the onset of ventricular systole.

Second Heart Sound (S2)
vProduced by the closure of aortic valve and pulmonary valves.
vPulmonary valve closes later and the aortic valve closes earlier due to early rise of Left ventricular pressure and early activation of the left ventricle.
vAs a result, S2 is heard as 2 components, aortic and pulmonary components.

Third Heart Sound (S3)
·Produced due to the rapid filling of the ventricle during early diastole leading to sudden limitation of expansion of the ventricle causing vibrations.
·Characteristics: Low frequency sound, heard better with the bell of the stethoscope.
·Rarely, there may be a third heart sound S3.
·Also called as “Protodiastolic sound” . It is not of valvular origin, as it occurs at the beginning of diastole just after S2.
·This sound occurs when the left ventricle is not very compliant, and at the beginning of diastole the rush of blood into the left ventricle causes vibration of the valve leaflets and the chordae tendinae.
·The third heart sound is normal in children and young adults, but disappears before middle age. Abnormal reemergence of this sound late in life indicates a pathological state, often a sign of a failing left ventricle as in dilated congestive heart failure (CHF). This sound is called a “Protodiastolic Gallop”, a type of gallop rhythm.

Fourth Heart Sound (S4)
§Characteristics: Low frequeny sound, heard in the later part of diastole in patients with sinus rhythm. Better felt than auscultated. Disappears in patients with atrial fibrillation.
§The rare fourth heart sound (S4) is sometimes audible in healthy children, but when audible in an adult is called a “Presystolic Gallop”.
§This gallop is a sign of a pathologic state, usually a failing left ventricle.
§This sound occurs just after atrial contraction ("atrial kick") and is the sound of blood being forced into a stiff or hypertrophic left ventricle.
§The combined presence of S3 and S4 is a quadruple gallop. At rapid heart rates, S3 and S4 may merge to produce a summation gallop.

Murmurs
Genesis of Murmurs
vMurmurs are due to the vibrations produced by the turbulent flow at:-
1)The region of the valve
2)Near the valve
3)Abnormal communication within the heart.
vMurmurs which are produced on the right side of the heart are more prominent on inspiration.

Grades of Murmurs

Grade

Description

1

Very faint, heard only after listener has "tuned in"; may not be heard in all positions

2

Quiet, but heard immediately after placing the stethoscope on the chest.

3

Moderately loud.

4

Loud, with palpable thrill.

5

Very loud, with thrill. May be heard when stethoscope is partly off the chest.

6

Very loud, with thrill. May be heard with stethoscope entirely off the chest.

Types of Murmurs
Systolic Murmurs
§Early Systolic Murmur
§Begins with S1 and diminishes in intensity and stops well before S2.
§Eg: Acute mitral regurgitation, acute tricuspid regurgitation, ventricular septal defect.

Ejection (Mid-Systolic) Murmur
ØCharacteristics:-
oCommences after S1, peaks in mid-systole.
oStops before S2.
oThere will be a definite gap in between the murmur and S1 and S2.
ØPhonocardiogram records the murmur as diamond-shaped.

Late Systolic Murmur
üBegins well after S1 and continues up to S2.
üEg: Mitral valve prolapsed, papillary muscle dysfunction.

Pan (Holosystolic Murmurs)
·Murmur begins with S1 ends with S2 or its components.
·S1 is usually muffled, intensity of murmur is uniform thoughout the sytole.
·Eg: Mitral or tricuspid regurgitation and ventricular septal defect.

Diastolic Murmurs
Early Diastolic Murmur
vStarts just after S2 and gradually decreases in intensity.
vEg: Aortic Regurgitation, pulmonary regurgitation.

Mid-Diastolic Murmur
oBegins well after S2 and may persist up to the next S1.
oEg: Mitral stenosis, tricuspid stenosis, Austin Flint murmur, Carey-Coombs’ murmur.

Other Murmurs
Innocent Murmurs
§Systolic murmur.
§Present in persons with normal CVS and normal carotid, brachial and femoral arteries.
§Eg: Young children (3-8 years old) – Still’s murmur, adult (more than 50 years old) – Ejection systolic murmur.

Continuous Murmurs
üDiastolic murmur.
üMurmur begins in the systole and continues without interruption through S2 into all or part of the diastole.
üEg: Patent ductus arteriosus – Gibson’s murmur, arterivenous fistula, Coronary AV fistula.

Name: Semantha Chia Peck Sin
Roll No.: 041303015
Batch 15 (Group B2)

The Cardiac Cycle
Definition: The cyclical events that take place in the heart during each heart beat.
nConsists of precisely timed rhythmic electrical and mechanical events that propel blood into the systemic and pulmonary circulations.

Events:-
[IMG]file:///C:/DOCUME%7E1/YULITA%7E1/LOCALS%7E1/Temp/msohtmlclip1/01/clip_image002.gif[/IMG]

Phases of Cardiac Cycle
Phase 1:-
üAtrial systole (0.1 second)
üAtria contract (systole), ventricles are relaxed (diastole).
üThe atrioventricular (AV) valves are open; the semilunar valves are closed.
üBlood enters to the ventricles through the AV valves.
Phase 2:-
üAtria relax (diastole), ventricles contract (systole).
üThe AV valves close (“Lubb-Dubb”); the semilunar valves open.
üBlood moves from the right ventricle to the pulmonary trunk through the pulmonary semilunar valve.
üBlood moves from the left ventricle to the aorta through the airtic semilunar valve.

Phase 3:-
üAtrial and ventricular diastole (0.4 second).
üThe AV opens, the semilunar valves closed.
üBlood enters the right atrium through the vena cavae, and the left atrium through the pulmonary veins.

Cardiac Cycle

Definition
The cyclical events that take place in the heart during each heart beat.
Heart rate = Cycle operation = 75 beats/min

Duration
75 beats in 60sec, 1 beat = 60/75 = 0.8sec/cycle
Out of 0.8sec, 0.3sec is the duration for systole while 0.5sec is for diastole
If heart rate increases, cardiac cycle duration decreases (Diastole duration reduces more than systole)

Ventricular Systole
i. Isovolumetric Contraction Phase
Duration – 0.05sec
Aortic & pulmonary valves are closed previously
AV (Atrio-ventricular) valves close, producing 1st heart sound
Left ventricular pressure increases till it exceeds aortic pressure (80mmHg), then aortic valve opens
Right ventricular pressure increases till it exceeds pulmonary pressure (10mmHg), then pulmonary valve opens
Tricuspid valve bulge into atria, producing c wave in Jugular Vein

• Rapid Ejection Phase

Duration – 0.10sec
Initial blood flow from Left ventricular to aorta is rapid

• Slow Ejection Phase

Duration – 0.15sec
Ejection of blood from Left Ventricle to aorta slows down
Left ventricular pressure increases till 120mmHg before it decreases
Right ventricular pressure increases till 25mmHg before it decreases
Momentum keeps blood flowing
AV valves are pulled down by ventricular muscle contraction
Blood ejected per stroke at rest is 70–90mL
End-diastolic ventricular volume = 130mL
End-systolic ventricular volume = 50mL
Ejection fraction = 65% (Index of ventricular function)

Ventricular Diastole
iv. Proto Diastole
Duration – 0.04sec
Once ventricular muscle is fully contracted, IVP (intra-ventricular pressure) decreases further
When aortic pressure exceeds that of IVP, semilunar valves close

• Isovolumetric Relaxation Phase

Duration – 0.10sec
All valves are closed, IVP continue to decrease

• Rapid Filling Phase

Duration – 0.10sec
70% of ventricular filling occurs in this phase

• Slow Filling Phase

Also known as ‘Diastasis’
Duration – 0.20sec
IVP decreases further

viii. Filling due to atrial systole
Duration – 0.10sec

Heart Sounds

3rd Heart Sound
- low pitched sound, heard best with bell of stethoscope
- may be normal in younger people, but almost always pathologic if it occurs in people older than 40.
- S3 occurs in early diastole, about 0.12-0.20sec after S2
- S3 is sometimes referred to as a protodiastolic gallop
- When originating from LV, S3 is best heard at the apex
- Turning the patient into the left lateral position may augment S3 detection
- When originating from RV, S3 is heard at the 4th left intercostals space adjacent to the sternum
- S3 occurs at the end of early ventricular fillinf when the ventricle reaches its elasctic limit
- S3 occurs when the ventricle reaches its elastic limit during early diastolic filling. S3 may be produced when normal or subnormal amounts of flow enter an already over-filled ventricle (congestive heart failure), or when very rapid filling occurs in a more normal ventricle (valvular regurgitation & high output states)
- Maneuvers that increase venous return (leg elevation) tend to increase the intensity of S3 & move it closer to S2, while things that decrease cardiac filling cause the S3 to decrease in intensity & move farther away from S2

4th Heart Sound
- low pitched sound, heard best with the bell of stethoscope
- S4 occurs in late diastole approximately 0.04-0.12sec prior to S1.
- Hence, S4 is sometimes referred to as a presystolic gallop
- When originating from left heart, S4 is best heard at apex
- Turning the patient to left lateral position may augment detection of a left sided S4
- When originating from the right heart, S4 is best heard at the 4th left intercostal space adjacent to the sternum, or at the xiphoid
- Apparently normal men over age 50 may have audible s4 gallops
- An S4, when pathologic, is produced by atrial contraction against a stiff, non-compliant ventricle. Stiff ventricles are characteristic of ventricular hypertrophy, & as such are commonly seen in pulmonary or systemic hypertension. Pulmonic or aortic stenosis, & scarring secondary yo previous myocardial infarction
- S4 increases in intensity & moves farther away from S1 with maneuvers that increase venous return or with increased sympathetic stimulation
- S4 often decreases to the point of inaudibility with standing
- S4 is dependent on atrialcontraction & is always absent in patient with atrial fibrillation
- A left sided S4 can be distinguished from a split S1 by location (S1 is loudest at the LSB, while S4 is loudest at the apex) & the fact that the S4 should disappear with firm pressure on the diaphragm

Cardiac cycle is the term referring to all or any of the events related to the flow of blood that occur from the beginning of one heartbeat to the beginning of the next.Every single 'beat' of the heart involves three major stages: atrial systole, ventricular systole and complete cardiac diastole.
Atrial systole is the contraction of the heart muscle (myocardia) of the left and right atria. Normally, both atria contract at the same time. As the atria contract, the blood pressure in each atrium increases, forcing additional blood into the ventricles. The additional flow of blood is called atrial kick. Atrial kick is absent if there is loss of normal electrical conduction in the heart, such as during atrial fibrillation, atrial flutter, and complete heart block.
Ventricular systole is the contraction of the muscles (myocardia) of the left and right ventricles.The closing of the mitral and tricuspid valves (known together as the atrioventricular valves) at the beginning of ventricular systole cause the first part of the "lub-dub" sound made by the heart as it beats. The second part of the "lub-dub" (the Second Heart Tone, or S2), is caused by the closure of the aortic and pulmonic valves 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.
Cardiac Diastole is the period of time when the heart relaxes after contraction in preparation for refilling with circulating blood. Ventricular diastole is when the ventricles are relaxing, while atrial diastole is when the atria are relaxing. During ventricular diastole, the pressure in the (left and right) ventricles drops from the peak that it reaches in systole. When the pressure in the left ventricle drops to below the pressure in the left atrium, the mitral valve opens, and the left ventricle fills with blood that was accumulating in the left atrium.
Pathogenesis of 3rd heart sound
Sound is produced due to rapid filling of ventricle during early diastole leading to sudden limitation of expansion ventricle causing vibration.
· Causes
A.Physiology
1.healthy young adult
2.athleta
3.pregnancy
4.fever
B.Pathology
1.cardiac failure
2.mital regurgitation
3.dilated cardiomyopathy
Pathophysiology 4th heard sound
In condition wih decreased ventricular compliance,there will b increased atrial contraction producing ventricular distension causing sound during presystolic phase
Causes: condition ass wf LVH n RVH

myocardial fibers hav resting membrane fibers and potencial 90mv.Individual separate membrane, but depolarization spreads radially through them as if they were syncytium because the presence of the difference between the interfaces. transmembrane cell cardiacmuscle potencial single action is characterized by a rapid depolarization, a plateau and then a slow repolarization. Initail depolarization is due to Na ions flowing just the opening of ion channels, Na. flow of Ca, Ca ionchannels slowly opening. Repolarization who left without pottasium through a series of ion channels.

This is really very important to know more about this. The position of the valves when the ventricles contract can have a big effect on the first heart sound. If the valves are wide open when the ventricule contracts, a loud S1 is heard. This can occur with anemia, fever or hyperthyroid.


casino spel