In Greek, systole means contraction and diastole means to send apart. The start of systole can be regarded as (1) the beginning of isovolumic contraction when LV pressure exceeds the atrial pressure or (2) mitral valve closure (M1). These correspond reasonably well because mitral valve closure actually occurs only about 20 milliseconds after the crossover point of the pressures. Thus, in practice, the term isovolumic contraction often also includes this brief period of early systolic contraction even before the mitral valve shuts, when the heart volume does not change substantially. Physiologic systole lasts from the start of isovolumic contraction (where LV pressure crosses over atrial pressure, Fig. 24-18) to the peak of the ejection phase, so that physiologic diastole commences as the LV pressure starts to fall (Table 24-4). This concept fits well with the standard pressure-volume curve. Physiologic diastole commences as calcium ions are taken up into the SR, so that myocyte relaxation dominates over contraction, and the LV pressure starts to fall as shown on the pressure-volume curve. In contrast, cardiologic systole is demarcated by the interval between the first and second heart sounds, lasting from the first heart sound (M1) to the closure of the aortic valve (A2). The remainder of the cardiac cycle automatically becomes cardiologic diastole. Thus, For the cardiologist, protodiastole is the early phase of rapid filling, the time when the third heart sound (S3) can be heard. This sound probably reflects ventricular wall vibrations during rapid filling and becomes audible with an increase in LV diastolic pressure, wall stiffness, or rate of filling.
Clinical improvement leads to splitting of A2&P2 in 1st box
first and second heart sounds
PG IN GENERAL MEDICINE
• The cardiac events that occur from beginning
of one heart beat to the beginning of the next
are called the cardiac cycle.
• the temporal sequence of events in the
• The three basic events are LV contraction, LV
relaxation, and LV filling…
• Duration 0.1 sec
• During ventricular relaxation
blood flows from atria to
• When both atria contracts almost
simultaneously and pumps
remaining 25% of blood flows in
respective ventricles .
• Contraction of atria increases
pressure inside atria to 4-6 mmHg
in right atrium and abt
7-8mmHg in left atrium.
LEFT VENTRICULAR CONTRACTION.
• LV pressure starts to build up when the arrival of
calcium ions at the contractile proteins starts to
trigger actin-myosin interaction.
• Soon after, LV pressure in the early contraction
phase builds up and exceeds that in the left atrium
(normally 10 to 15 mm Hg), followed about 20
milliseconds later by M1.
• The exact relation of M1 to mitral valve closure is
open to dispute.
• Although mitral valve closure is often
thought to coincide with the crossover point
at which the LV pressure starts to exceed the
left atrial pressure, in reality mitral valve
closure is delayed because the valve is kept
open by the inertia of the blood flow.
• Duration 0.05 sec
• At beginning of this phase AV valve
are closed but semilunar valves are
not yet opened.
• Volume of blood inside both
ventricles remains the same hence
this phase is called as isovolumic
phase of contraction.
• When pressure in left ventricle is
slightly above 80 mmHg and right
ventricular pressure slightly above 8
mmHg then the ventricular
pressures push the semilunar valves
Rapid ejection phase
• The duration of this phase is
abt 0.11 sec.
• Abt.2/3rd of stroke volume is
ejected in this rapid ejection
• The pressure inside the left
ventricle rises to 120mmHg
during this phase.
• The end of rapid ejection
phase occurs at abt the peak
of ventricular pressure
• The right ventricle ejection
begins before that of left and
continues even after the left
ventricular ejection is
Reduced ejection phase
• Duration 0.14 sec.
• Rest one third stroke volume is ejected.
• As the cytosolic ca2+ ion concentration
starts to decline because of uptake of
calcium into the SR more and more
myofibers enter the state of relaxation,
and the rate of ejection of blood from
the left ventricle into the aorta falls.
• During this phase, blood flow from the
left ventricle to the aorta rapidly
diminishes but is maintained by aortic
recoil, the Windkessel effect. The
pressure in the aorta exceeds the falling
pressure in the left ventricle.
• At the end of ventricular systole ventricles start
relaxing allowing rapid fall in the intraventricular
• This is the period of protodiastole which lasts for
• At the end of this phase elevated pressure in
distended arteries (Aorta and Pulmonart artery)
immediately pushes the blood back toward the
ventricles which snaps the aortic and pulmonary
semilunar valves .
• It also causes dicrotic notch in the down slope
of aortic pressure called Incisura.
• Incisura indicates end of systole and the onset
Isovolumetric relaxation phase
• The ventricles continue to relax
as closed chambers as semilunar
valves are closed and AV valves
are not yet open.
• This causes rapid fall of pressure
inside ventricles (from 80mmHg
to abt 2 to 3 mmHg in left
• This phase lasts for 0.06 sec.
• Because the ventricular volume
remains constant this phase is
called isovolumic relaxation
Rapid filling phase
• As LV pressure drops below that in the
left atrium, just after mitral valve
opening, the phase of rapid or early
filling occurs to account for most of
• Active diastolic relaxation of the
ventricle may also contribute to early
• Such rapid filling may cause the
physiologic third heart sound (S3),
particularly when there is a hyperkinetic
Reduced filling phase
• After the rapid filling
ventricles rises slowly,
• As pressures in the atrium
and ventricle equalize, LV
filling virtually stops
2nd RAPID FILLING PHASE
• Renewed filling requires that the
pressure gradient from the
atrium to the ventricle increase.
This is achieved by atrial systole
(or the left atrial booster),
• which is especially important
when a high cardiac output is
required, as during exercise, or
when the left ventricle fails to
relax normally, as in LV
PHYSIOLOGIC SYSTOLE CARDIOLOGIC SYSTOLE
Isovolumic contraction From M1 to A2, including:
Maximal ejection Major part of isovolumic
PHYSIOLOGIC DIASTOLE CARDIOLOGIC DIASTOLE
Reduced ejection A2-M1 interval (filling
demarcated by heart
sounds rather than
• starts fractionally
later than physiologic
systole and ends
Cause of S1 --theories
• 2 THEORIES
• LUISADA et.al
• Onset of isovolumetric contraction results in
prominent tensing of LV walls,septum,mitral
valve apparatus which produces transient
• 2nd audible component due to ejection
component coincident with opening of aortic
• CRAIGE,LEATHAM et.al
• First component reflects sudden tensing of
closed mitral leaflets ,which sets the
surrounding cardiac structures and blood into
• Second component produced due to tricuspid
HOW TO LISTEN TO S1
• Just precedes carotid upstroke
• S1 will appear to initiate the outward LV thrust of
• Medium to high frequency but lower pitch than S2
• Q-M1 60ms
• Q-T1 90ms
• M1-T1 30ms
• Splitt s1 can be appreciated in tricuspid area
• Loud M1 at apex may mask T1
• Tricuspid area
• Low frequency
• Not palpable
• Best during inspiration
DD of split S1
S4 Vs Split S1
• Low pitched generally,with bell,localised
• Often palpable
• LV S4 is audible at apex in left lateral
position,on expiration,isometric hand grip
• RV S4 audible at tricuspid area,during
inspiration,straight leg raising
When apparent splitting of S1 heard at
base we should suspect presence of an
ejection sound or early midsysolic
click.• Aortic click
• Discrete, snappy
• Occur later S1
• BEST at aortic area
• Heard all over chest
• LVH features
• Systolic thrill at aortic
• Pulmonary click
• Better heard in
• Localised to pul area
• Systolic thrill at
• Best at apex
• Widely audible
• High frequency
• Not palpable
• Loud and earlier on standing
FIRST HEART SOUND
Intensity determined by
• Structural integrity of mitral valve
• Postion of AV valves at time of ventricular
• Integrity of isovolumetric systole
• Heart rate
• P-R interval
• Myocardial contractility
The mitral annulus
• The mitral annulus is a fibrous ring that connects
with the leaflets.
• appears to be more D-shaped, rather than
circular as prosthetic valves
• The annulus functions as a sphincter that
contracts and reduces the surface area of the
valve during systole to ensure complete closure
of the leaflets. Thus, annular dilatation of the
mitral valve causes poor leaflet apposition, which
results in mitral regurgitation.
• the mitral valve as a continuous veil inserted
around the circumference of the mitral orifice.
• The free edges of the leaflets have several
• Two of these indentations, the anterolateral
and posteromedial commissures, divide the
leaflets into anterior and posterior.
• These commissures can be accurately
identified by the insertions of the commissural
chordae tendineae into the leaflets
• The anterior leaflet is located posterior to the aortic root
• large and semicircular in shape.
• free edge with few or no indentations.
• The 2 zones on the anterior leaflet are referred to as rough and clear
zones, according to the chordae tendineae insertion.
• 2 zones are separated by a prominent ridge on the atrial surface of
the leaflet, which is the line of the leaflet closure.
• The prominent ridge is located approximately 1 cm from the free
edge of the anterior leaflet.
• Distal to the ridge is a rough zone that has a crescentic shape.
• During systole or mitral valve closure, the rough zone of the anterior
leaflet will appose to the rough zone of the posterior leaflet.
• The rough zone is thick and has chordae tendineae insertions on the
• The posterior leaflet is the section of the mitral valve that is
located posterior to the 2 commissural areas
• It has a wider attachment to the annulus than the anterior
• It is divided into 3 scallops by 2 indentations or clefts.
• The middle scallop is larger than the other two.
• The 3 zones on the posterior leaflets are referred to as rough,
clear, and basal zones, according to the chordae tendineae
• The rough zone is distal to the ridge of the line of the leaflet
• Like that of the anterior leaflet, the clear zone has no chordae
tendineae insertion. It is located in the middle part of the
posterior leaflet, between the rough zone and the basal zone.
• The basal zone is located between the clear zone and the
mitral valve annulus.
• Small fibrous strings that originate either from
the apical portion of the papillary muscles or
directly from the ventricular wall and insert into
the valve leaflets or the muscle.
• 2 types
• Commisural chordae
• Leaflet chordae
• Commissural chordae
• Commissural chordae are the chordae that
insert into the commissures
• Two types of commissural chordae exist.
Posteromedial commissural chordae insert into
the posteromedial commissural area;
anterolateral commissural chordae insert into
the anterolateral commissural area.
• the chordae that insert into the anterior or
• Two types of chordae tendineae are connected
to the anterior leaflet.
• The first is rough zone chordae, which insert into
the distal portion of the anterior leaflet known as
the rough zone.
• The second is strut chordae, which are the
chordae that branch before inserting into the
• The posterior leaflet has 3 types of chordae
• The first is rough zone chordae, which are the
same as that of the anterior leaflet.
• The second is basal chordae, insert into the
basal zone of the posterior leaflet.
• The third type of chordae is cleft chordae,
these insert into the clefts or indentations of
the posterior leaflet, which divide the
posterior leaflet into 3 scallops
• Unlike the anterior leaflet, the posterior
leaflet does not have strut chordae.
• arise from the apex and middle third of the left ventricular
• The anterolateral papillary muscle is normally larger than
the posteromedial papillary muscle and is supplied by the
left anterior descending artery or the left circumflex artery.
• The posteromedial papillary muscle is supplied by the right
• Extreme fusion of papillary muscle can result into mitral
• rupture of a papillary muscle, usually the complication of
acute myocardial infarction, will result in acute mitral
• Chronically, rheumatic fever leads to
commissural fusion, valve thickening, and
calcification. The appearance of the mitral
valve with shortened, fused chordae and
scarred commissures has been likened to the
mouth of a catfish (fish-mouth deformity).
S1 in mitral stenosis
• Loud snapping s1 is one of the hallmark of MS
• Loud s1 is due to
• LA,LV pressure cross over occurs after LV pressure has begun to rise.
• Rapidly increasing LV pressure in early systole contribute to loud s1
• Persistent LA,LV gradient in late diastole keeps the leaflets wide open.
• Increased distance the cusps must travel during their closing motion
contributes to loud s1
• Thickened leaflets and chordae may resonate
with high amplitude than normal valve.
MS with soft s1
• Extensive mitral valve calcification
• Congestive heart failure
• Large right ventricle,
• Severe pulmonary hypertension
• Very mild mitral stenosis
• MS plus MR with dominant MR
• MS with AR
Rate of rise of LV
pressure falls steeply
resulting in decreased
velocity of closure of
Loud S1 in MR
• Associated MS
• MR of MVP
• Rheumatic MR with well preserved AML
• Severe TR for MS mistaken as MR
• Loud ejection click of AS
Produced by –
• Sudden deceralation of retrograde flow of blood
column in aorta and pulmonary artery when the
elastic limits of tensed leaflets are met –create
vibration in cardiohemic system.
• MEDIUM TO HIGH PITCHED
• 2 components aortic and pulmonary
• A2 P2 Each coincide with incisura of great arterial pressures i.e
peak deacceleration of blood mass followed by rebound
• The time interval from crossover of pressures
to actual occurrence of sounds is called
hang out interval.
• As aorta has high resistance and low
complaince , recoil from ejected blood is early
so less hangout period.
• PA hangout period is 2-5 times more than that
• PA- 80ms, A-30ms
• This difference produces normal split of S2.
• Normal S2 split in inspiration and single sound
• Split heard in 2-3 left ICS
• Frequency both components same
• Amplitude A2 > P2
• P2 only heard at II left ICS
• A2 is heard at Rt II nd ICS,Lt parasternal
Splitting during inspiration
• Decrease in intrathoracic pressure,incresed blood flow to
RV,increased RV ejection time
• Decreased pulmonary venous return , decreased Q-A2 interval
• Decreased pulmonary vascular resistance
,increased hangout period ,increased Q-P2 interval
• Internal to apex
• Widely audible
• High pitched
• Not palpable
• No variation with
• LVS3 or RVS3
• Low pitch
Wide & fixed splitting
• Acute and
• Sev. PAH
• RBBB with
increase in RV
& LV filling
• Marked increase in pulmonary capacitance
prolongs hang out interval to its limit
• RV stroke volume is not influenced by
• Phasic changes in systemic venous return
during respiration is associated with reciprocal
changes in L -> R shunt
REVERSED OR PARADOXICAL SPLIT
• Maximum split in expiration that narrows or
disappears on inspiration.
• From base to apex there will be softening of p2
• Valsalva maneuver
CAUSES OF REVERSED SPLITT
• Left bundle branch
• Right ventricular
• PVCs of right
• WPW syndrome
• Severe AS
• Severe systemic hypertension
• Acute MI
• During episode of angina
• Severe AR
• large PDA
• Aneurysm of ascending aorta
• Post stenotic dilatation in AS
Pseudo paradoxical split
• Actually s2 split in expiration and inspiration.
• But during inspiration COPD patient lung will
• So that single S2 will be heard in inspiration
• Artifactual muffling of P2
• Severe PAH - Hang out interval is encroached
by loss of pulmonary capacitance
• Murmur obscuration
• Pulmonary atresia
• Severe TOF
• Tricuspid atresia
• Eisenmenger VSD
with single ventricle
• severe calcified AS
• Severe pulmonary
• Truncus arteriosus
Intensity is influenced by
1. Pressure beyond the valve
2. Flow across the valve
3. Size of vessel beyond the valve
4. Stenosis of the valve
5. Regurgitation of the valve
• In AR due to aortic root disease ( syphilis,
ankylosing spondylitis )A2 is accentuated.
• In AR due to aortic valve disease ( rheumatic) A2
is diminished or absent
Causes of loud P2
• Normal in infants & children
• Adults with chest deformity or thin chests
• Pulmonary arterial hypertension
• Left to right shunts
• Hyperkinetic circulatory states
Causes of diminished & absent P2
• Normal in elderly
• Thick chested adults
• Pulmonary stenosis
• Dysplastic valve
• Tetrology of fallot
• Transposition of great
• Truncus arteriosus
• Pulmonary atresia
• Absent pulmonary valve
• The pulmonic sound is considered accentuated if
it is equal to aortic sound in the pulmonary area
• The pulmonic sound is localised to the pulmonary
area and the aortic component is widely audible
• Even in the pulmonary area A2 is louder than P2.
• Accentuation of pulmonic sound is graded as
mild(+), moderate(++) , severe(+++)
Grading of pulmonic sound intensity
Grading of pulmonic
basis Correlation to PA
normal Pulmonic sound less
normal PA pressure
Systolic < 30
Mild or + Pulmonic sound
equal to A2
Systolic 30 – 35
Moderate or ++ Louder than A2 Moderate PAH
Systolic 40 – 75
Severe or +++ Very loud / banging Severe PAH
Systolic > 75