CARDIAC CYCLE

•Cardiac cycle means 1 complete heart beat.

•Each heart beat consist of 1 systole or contraction &
• 1 diastole or relaxation .
•Duration of cardiac cycle is 0.8 seconds.
 EVENTS IN CARDIAC CYCLE
•A) PHASES OR EVENTS IN SYSTOLE
•1) isovolumetric contraction of the ventricles (0.03 sec)
•2) rapid ventricular ejection (0.08 sec)
•3) slow ventricular ejection (0.16 sec)

•B) PHASES OR EVENTS IN DIASTOLE

•1) Isovolumetric relaxation (0.05 sec)
•2) rapid ventricular filling (0.16 sec)
•3) slow ventricular filling (diastasis) (0.18 sec)
•4) atrial systole. (0.14 sec)
1) ISOVOLUMETRIC CONTRACTION OF THE
VENTRICLES (0.03 sec)
• Ventricles start contracting
• Intraventricular pressure rises
• This causes the closure of AV valves , results in Ist heart
sound.
• The pressure in ventricles rises further but less than that of
aorta therefore the semilunar valves remains clised
• Thus no blood enters or leave the ventricle therefore no
change in volume occurs.
• There is RS wave on ECG
2) rapid ventricular ejection (0.08 sec)
• In this phase contraction of the ventricles continues
• This results in greater pressure in ventricles than that of
great arteries.
• This causes opening of semilunar valves, blood leaves the
ventricles with great force entering the aorta & pulmonary
arteries
• The intraventricular pressure reaches its peak.
• About 70% of the ventricular emptying will take place
during this phase
3) slow ventricular ejection (0.16 sec)
•After attaining maximum ejection , further contraction slows
down & weaker than that of during rapid ejection phase.
•The blood is continually pumped into the large arteries till the
final systole comes to an end.
•This phase is responsible for 30% of ventricular ejection.
•
•1) Isovolumetric relaxation (0.05 sec)
•In this phase ventricles start relaxing
•Intraventricular pressure falls steeply
•The pressure in the ventricle falls to a level lower than in aorta
& pulmonary artery
•Ejection of blood in these arteries has resulted in their
distension & now the distended vessel undergo elastic recoil.
•In large arteries blood flow may reverse momentarily , but
semilunar valve becomes closed due to high pressure in large
arteries as compared to intraventricular pressures.
• this closure of semilunar valves results in 2nd heart sound &
the back flow of blood is prevented.
•In spite of ventricular relaxation the intraventricular pressure
remains high as compared to atria , thus the AV valve remains
closed during this phase.
•Due to this the ventricle will remain a close cavity with no
blood entering or leaving them.
•Because of this there is no change in volume during this phase.
•2) rapid ventricular filling (0.16 sec)
•Ventricle diastole continues resulting in enlargement of the
ventricular cavities.
•This causes the pressure within the ventricle to fall further i.e. a
level lower than in atria.
•Thus due to high pressure in atria as compared to ventricles,
results in opening of AV valves
•The blood that has earlier accumulated in atria due to closure
of AV valves now rushes into the ventricles.

•3) slow ventricular filling (diastasis) (0.18 sec)

•As most of the blood has already entered , the ventricular
filling decreases.
•At this time atria & ventricle act as a chamber , i.e. any blood
reaching the atria immediately enters the ventricles.
•Thus atria acting as a conduit or pipes .
•This stage is also called diastasis.
•4) atrial systole. (0.14 sec)
•In this phase while the ventricles are in the fina stage of the
diastole , atrial muscle fibres contract & push blood into the
ventricles
•Atral systole results 4th heart sound
•Atrial systole provides 25% of the ventricular filling.
•This phase is followed by the beginning of the new cardiac
cycle which is marked by the beginning of the isovolumetric
contraction causing the closure of AV valves.
PRESSURE CHANGES IN LEFT VENTRICE DURING CARDIAC
CYCLE
•1) isovolumetric contraction of the ventricles (0.03 sec)
•At its start pressure in the ventricle is about 0-10 mmhg
•As the ventricle start contracting intraventricular start rising &
may reach to 80 mmhg. At the end of this phase.
•2) rapid ventricular ejection:
•At this stage pressure rises further & exceed that in aorta thus
causes opening of the aortic valve.
•During this phase the pressure rises at its peak & reaches to 120
mmhg.
•3) slow ventricular ejection.
•Ventricular emptying continues but but lower than that of
previous phase
•And the pressure in ventricle is equal or slightly less than that
of aorta , but the inertia of the blood keeps the blood flowing
from ventricles into the aorta.
•4) isovolumetric relaxation
•Ventricles undergo relaxation
•Size of the cavity increases
•Ventricle is now a close cavity with no blood entering or leaving
the lung.
•By the end of this phase the pressure in the ventricle is about
few mmhg or above 0
•5) rapid ventricular filling:
•The pressure in the ventricle falls further due to increase in size
of the ventricle.
•6) slow ventricular filling
•Pressure falls urther.
7) Atrial systole:
•Due to atrial systole there is slight rise in pressure.

•VOLUMES IN THE VENTRICLE

•1) end-diastolic volume: (110-120ml)
•It is the filling of the ventricle during diastole
•2) stroke volume: (70 ml)
•It is the ejected bood during systole
•3) end- systolic volume: (40-50 ml)
•It is remaining blood at the end of the systole
•4) ejection fraction: (60%)
•The fraction of end-diastolic volume that is ejected is called the
E.F.
Pressure changes in the atria (the a, c & v waves)
1) A wave:
• It is due to atrial contraction
• Right atrial pressure is 4-6 mmhg
• Left atrial pressure is 7-8 mmhg
2) C wave :
• It occurs when the begin to contract
• Occurs due to bulging of AV valves into the atria
3) V wave:
• Occurs towards the end of ventricular contraction.
• Occurs due to slow flow of blood into the atria from the
veins while the AV valves are closed.
 GRAPHICAL ANALYSIS OF
VENTRICULAR PIMPING
• 2 important pressures
• Systolic pressure &
• Diastolic pressures
• ALSO KNOWN AS VOLUME- PRESSURE CURVES.
• DIASTOLIC PRESSURE CURVE:
• Measure the maximum filling (volume) of ventricle or END-
DIASTOLIC PRESSURE
• SYSTOLIC PRESSURE CURVE:
• Shows relationship between ventricular contraction & filling.
 Phase I:
• Period of filling
Phase II:
• Period of iso-volumic contraction

Phase III:
• Period of ejection

Phase IV
• Period of isovolumic relaxation
PRE-LOAD: (Pressure during filling of the ventricle)
•It is considered to be the end-diastolic pressure when the
ventricles has become filled & it is the degree of tension in the
muscles when they begin to contract.
•AFTER-LOAD.(arterial pressure against which muscle
contracts)
•It is the pressure in the arteries that arises from the ventricle or
it is the resistance in the circulation & It is the load against
which ventricular muscle exerts its contractile force.
 REGULATION OF CARDIAC PUMPING
•At rest heart pumps 4-6 liters of blood
•During exercise , it pumping is increased to 7-8 times.
•This pumping is resulted by:
•1) intrinsic regulation of heart pumping
•2) control of heart rate by ANS.

•1) intrinsic regulation of heart pumping (Frank- Starling

mechanism)
•Cardiac pumping depends upon the rate of blood flow from
veins into the heart i.e Venous return for e.g venous return that
occurs in case of exercise will cause increase in cardiac out put.
•This intrinsic ability of the heart to adapt to increasing volume
of inflowing blood is called the Frank starling mechanism of
the heart.
•This mechanism states that under normal physiological limits
heart pumps all the that comes in it by means of veins i.e. the
greater the filling or stretching of the heart the greater or more
is the contraction.
CONTROL OF HEART BY A.N.S.
•EFFECT OF SYMPTHETIC NERVOUS SYSTEM
•It increases the heart rate & force of contraction
•Strong sympathetic stimulation can increase the heart rate
from 72 beats/min to 180 to 200 beats’min

•EFFECT OF PARASYMPTHERTIC STIMULATION

•It decreases the heart rate & force of contraction.
 EFFECT OF IONS ON HEART FUNCTION
•EFFECT OF K ION
•Excess K ion in the ECF causes to heart to dilate & flaccid &
HR is also decreased.
•It also blocks the conduction from atria into the ventricle
through AV node.
•This is due to the fact that inc. K ion decreases the RMP in the
cardiac muscle fiber . This decreases the intensity of action
potential that makes the heart progressively weaker.

•EFFECT OF CALCIUM IONS

•Increase in Ca ion in the ECF cause the heart to go in spastic
contraction
•Deficiency of Ca ion causes flaccidity similar to that of inc. Ca
ions
EFFECT OF TEMPERATURE
•Increase in temperature as in case of fever increases the heart
rate
•Whereas hypothermia has the opposite effect.
CONDUCTING SYSTEM OF HEART
•S.A. node is responsible for generating the electrical impulses
that brings about the mechanical activity i.e. contraction of the
heart.
•It is called the PACE MAKER of the heart.
•It is small flattened ellipsoid non-contrctile, specialized
cardiac muscle about 3 mm wide, 15 mm long & 1 mm thick
located on superio-lateral wall of the right atrium just beneath
the opening of superior vana cava.
•It has the property of self excitation a process that cause
automatic rhythmical discharge & contraction.
•The action potential in heart muscle is also called cardiac
impulse & like action potential in nerve fibers it travels from :
•S.A. node it spreads to both atria and than reaches another
specialized structure called A.V. node.
•The A.V. node lies on the lower part of the inter-atrial septum
on the right side near the coronary sinus
•The impulse from SA node reach the AV node through anterior,
posterior & middle internodal pathway.
•The impulse from SA node reach at AV node in 0.03 secs.
•after reaching here there is a delay of 0.09 seconds.
•The cause of slow conduction in AV node & AV bundle is its
small size and few gap junctions between the cells which causes
resistance to conduction of ions. From cell to cell.
•From AV node the impulse goes to AV bundle
•The impulse reach here in 0.04 secs (therfore total duration is
0.16 secs.)
•From AV bundle it travels to right & left bundle branch of
pirkinjee fibers that innervate the ventricular muscles.
 S.A. NODE

INTER NODAL PATHWAY

A.V. NODE (0.03+ delay of 0.09 secs)

A.V. BUNDLE (0.04 total delay is 0.16 sec)

RT. & LT. BUNDLE BRANCHES OF

PIRKINJEE FIBERS
 Action potential in S.A. node
•R.M.P. is -55 to – 60 mv.
•Depolarization is due to calcium & sodium leaky channels
•Repolarization of due to K leaky channels.
•Apart from SA node other parts of the conductive system that
exhibits rhythmic self excitation are A.V. nodes & pirkinjee
system(40-60 times/min) .
•In normal conditions SA node controls the heart rhythmicity in
contrast to AV node & pirkinjee system because the discharge
rate of SA node is more (70-80) as compared AV node or
Pirkinjee system
•But in abnormal conditions when the there is a block in
conduction of impulse from SA to AV node then the AV node
starts generating nerve impulses (ectopic pace maker)
•Effects of sympathetic & Para Sympathetic nervous asystem
•Parasympathetic nervous system decreases the excitation of SA
node by causes hyperpolarization
•Sympathetic nervous system Sa nodal discharge & in turn heart
rate by causing increase permeability of Ca & Na at SA node