CARDIAC CYCLE

DR RAKESH JAIN
SR Cardiology
Govt. Medical College, Calicut.

Cardiac Cycle

Def: The cardiac events that occur from

beginning of one heart beat to the beginning
of the next.
first assembled by Lewis in 1920 but first
conceived by Wiggers in 1915

Atria act as PRIMER PUMPS for

ventricles & ventricles provide major
source of power for moving the blood
through the vascular system.
Initiated by spontaneous generation of
AP in SA node (located in the superior lateral wall of
the right atrium near the opening of the superior vena cava)

Electrical System: Brief

Action potentials originating
in the sinus node travel to
AV node (1m/s) in 0.03 sec.

1. AV nodal delay of 0.09 sec before the impulse

enters the penetrating portion of the A-V bundle
2. A final delay of another 0.04 sec occurs mainly in
this penetrating A-V bundle

total delay in the A-V nodal and A-V bundle

system is about 0.13 sec
A total delay of 0.16 sec occurs before the excitatory
signal finally reaches the contracting muscle of the
ventricles from its origin in sinus node.

Delay in AV node (0.13sec)

Why delay?
Diminished numbers of gap junctions Between
successive cells in the conducting pathways.

Significance?
Delay allows time for the atria to empty their blood
into the
ventricles before ventricular contraction
begins

Rapid Transmission in the Purkinje

System (1.5 to 4.0 m/sec)
i.e.

About 6x that in ventricular muscle

About 150x that in A-V nodal fibers

allowing almost instantaneous

transmission of the cardiac impulse
throughout the ventricular muscle

(B/c of very high level of permeability of the gap

junctions)

Summary of Cardiac Impulse

Transmission

Mechanical Phase

Cardiac cycle basically

describes
1.
2.
3.

Pressure
Volume, and
Flow phenomenon
in ventricles as a function of time

Basics

1 Beat = 0.8 sec (800 msec)

Systole = 0.3 sec
Diastole = 0.5 sec
In tachycardia, Diastolic phase decreases
more than systolic phase

Phases of cardiac cycle

LV Contraction
Isovolumic contraction (b)
Maximal ejection (c)
LV Relaxation
Start of relaxation and reduced ejection (d)
Isovolumic relaxation (e)
LV Filling
Rapid phase (f)
Slow filling (diastasis) (g)
Atrial systole or booster (a)

Time Intervals
Total ventricular systole
0.3 sec
Isovolumic contraction (b)
0.05 sec
RV)

(0.015sec for

Maximal ejection (c)

0.1 sec
Reduced ejection (d)
0.15 sec
Total ventricular diastole
0.5 sec
Isovolumic relaxation (e)
0.1 sec
Rapid filling phase (f)
0.1 sec
Slow filling (diastasis) (g)
0.2 sec
Atrial systole or booster (a) 0.1 sec
GRAND TOTAL (Syst+Diast) = 0.8 sec

Physiologic Versus Cardiologic

Systole and Diastole
PHYSIOLOGIC
SYSTOLE
Isovolumic
contraction
Maximal
ejection
PHYSIOLOGIC
DIASTOLE
Reduced
ejection
Isovolumic
relaxation
Filling phases

CARDIOLOGIC
SYSTOLE
From M1 to A2,
including:
Major part of
isovolumic contraction
Maximal ejection
Reduced ejection
CARDIOLOGIC
DIASTOLE

20msec

A2-M1 interval
(filling phases included)
Physiological systole

cardiologic systole, demarcated by

heart sounds rather than by physiologic
events, starts fractionally later than
physiologic systole and ends significantly
later.
Cardiologic systole> physiologic systole

Description of Cardiac cycle

phases
1.
2.
3.
4.

Pressure & Volume events

ECG correlation
Heart sounds
Clinical significance

Atrial Systole
A-V Valves Open; Semilunar Valves Closed

Blood normally flows

continually from
great veins into atria
80% flows directly
thr atria into
ventricle before the
atria contracts.
20% of filling of
ventricles atrial
contraction
Atrial contraction is
completed before
the ventricle begins
to contract.

Atrial contraction normally accounts for

about 10%-15% of LV filling at rest,
however, At higher heart rates, atrial
contraction may account for up to 40%
of LV filling referred to as the "atrial
kick
The atrial contribution to ventricular
filling varies inversely with duration of
ventricular diastole and directly with
atrial contractility

Atrial Systole
Pressures & Volumes

a wave atrial
contraction, when atrial
pressure rises.
Atrial pressure drops
when the atria stop
contracting.

After atrial contraction is complete

LVEDV typically about 120 ml
(preload)
End-diastolic pressures of
LV = 8-12 mmHg and
RV = 3-6 mmHg

AV valves floats upward (preposition)

Abnormalities of a wave

Elevated a wave
Tricuspid stenosis
Decreased ventricular compliance (ventricular failure,
pulmonic valve
stenosis, or pulmonary hypertension)

Cannon a wave
Atrial-ventricular asynchrony
valve)

(atria contract against a closed tricuspid

complete heart block, following premature ventricular

contraction, during ventricular tachycardia, with ventricular
pacemaker

Absent a wave
Atrial fibrillation or atrial standstill
Atrial flutter

Why blood does not flow back in to

SVC/PV while atria contracting, even
though no valve
in between?

Wave of contraction through the atria

moves toward the AV valve thereby
having a "milking effect."
Inertial effects of the venous return.

Atrial Systole
ECG

p wave atrial depolarization

impulse from SA node results in
depolarization & contraction of atria ( Rt
before Lt )
PR segment isoelectric line as
depolarization proceeds to AV node.
This brief pause before contraction allows
the ventricles to fill completely with blood.

Atrial Systole
Heart Sounds

S4 (atrial or presystolic gallop) - atrial emptying after

forcible atrial contraction.
appears at 0.04 s after the P wave (late diastolic)
lasts 0.04-0.10 s
Caused by vibration of ventricular wall during
rapid atrium emptying into non compliant
ventricle

Causes of S4

Physiological;
>60yrs (Recordable, not audible)

Pathological;

All causes of concentric LV/RV hypertrophy

Coronary artery disease
Acute regurgitant lesions
An easily audible S4 at any age is generally
abnormal.

Clinical Facts about S4

In contrast to S3, which may mean ventricular

failure, the presence of S4 does not indicates
heart failure. It only signify hardworking
ventricle.
The presence of S4 correlate with a gradient of
at least 50mmHg across LVOT in suspected
LVOT obstruction.
(This correlation is not applicable in HCM)

In setting of MI, an audible S4 indicates that at

least 10% of myocardium is at jeopardy.
In presence of Shock, S4 indicates that
hypovolemia is unlikely as PCWP will be
>18mmHg.
S4 can be heard when RVEDP >12mmHg on Rt
or LVEDP > 15mmHg on Lt side. If EDP is very
high i.e. >25 mmHg, S4 may be absent b/c of
insufficient atrial functions.

JVP: x descent

Prominent x descent
1 Cardiac tamponade
2 Constrictive pericarditis
3 Right ventricular ischemia with preservation of
atrial
contractility

Blunted x descent
1 Atrial fibrillation
2 Right atrial ischemia

Beginning of Ven.Systole
Isovolumetric Contraction
All Valves Closed

Isovolumetric Contraction
Pressure & Volume Changes

The AV valves close when

the pressure in the
ventricles (red) exceeds the
pressure in the atria
(yellow).
As the ventricles contract
isovolumetrically -- their
volume does not change
(white) -- the pressure
inside increases,
approaching the pressure in
the aorta and pulmonary
arteries (green).
JVP: c wave- d/t Right
ventricular contraction
pushes the tricuspid valve
into the atrium and
increases atrial pressure,
creating a small wave into
the jugular vein. It is
normally simultaneous with

Ventricular chamber geometry changes considerably as

the heart becomes more spheroid in shape;
circumference increases and atrial base-to-apex length
decreases.
Early in this phase, the rate of pressure development
becomes maximal.This is referred to as maximal
dP/dt.
Ventricular pressure increases rapidly
LV ~10mmHg to ~ 80mmHg (~Aortic pressure)
RV ~4 mmHg to ~15mmHg (~Pulmonary A pressure)
At this point, semilunar (aortic and pulmonary) valves open
against the pressures in the aorta and pulmonary artery

LV Torsion

eft-handed helix in subepicardium

right-handed helix in subendocardium

Figure: Schematic Drawing of LV Torsion

The image on the left shows the myofiber directions. Solid lines epicardial region;
dashed lines endocardial region. The image on the right shows untwisting.
ED end-diastole; ES end-systole; LV left ventricle.

(J Am Coll Cardiol Img 2009;2:648

Isovolumetric Contraction
ECG

The QRS complex is due to ventricular

depolarization, and it marks the
beginning of ventricular systole.

Isovolumetric Contraction
Heart Sounds

S1 is d/t closure and after

vibrations of AV Valves. (M1
occurs with a definite albeit
20 msec delay after the LVLA pressure crossover.)
S1 is normally split (~0.04
sec) because mitral valve
closure precedes tricuspid
closure.
(Heard in only 40% of normal
individuals)

S1 heart sound

low pitch and relatively longlasting

lasts ~ 0.12-0.15 sec
frequency ~ 30-100 Hz
appears 0.02 0.04 sec after the
beginning of the QRS complex

Some Clinical facts about S1

S1 is a relatively prolonged, low

frequency sound, best heard at apex.
Normally split of S1 (~40%)is heard only
at tricuspid area.(As tricuspid
component is heard only here.)
If S1 is equal to or higher in intensity
than S2 at base, S1 is considered
accentuated.

Variable intensity of S1 and jugular venous

pulse are highly specific and sensitive in the
diagnosis of ventriculoatrial dissociation during
VT, and is helpful in distinguishing it from
supraventricular tachycardia with aberration.
Value of physical signs in the diagnosis of ventricular tachycardia. C J
Garratt, M J Griffith, G Young, N Curzen, S Brecker, A F Rickards and A J Camm,
Circulation. 1994;90:3103-3107

Causes of
Loud S1
1.
2.
3.
4.
5.
6.
7.

Exercise
Emotinal excitibility
Mitral stenosis
Hyperkinetic circulation
Atrial septal defect
Sinus tachycardia
Short P-R interval

Soft S1
1.
2.
3.
4.
5.
6.
7.
8.
9.

Sinus tachycardia
Mitral regurgitation
Severe AR
Ventricular aneurysm
Acute MI
Myocarditis
Cardiomyopathy
Prolonged P-R interval
Calcific MS

Ejection
Aortic and Pulmonic Valves Open; AV Valves Remain
Closed

The Semilunar valves ( aortic ,

pulmonary ) open at the
beginning of this phase.

Two Phases

Rapid ejection - 70% of the blood

ejected during the first 1/3 of
ejection
Slow ejection - remaining 30% of
the blood emptying occurs during
the latter 2/3 of ejection

Rapid Ejection
Pressure & Volume Changes

When ventricles
continue to contract ,
pressure in ventricles
exceed that of in aorta
& pul arteries & then
semilunar valves
open, blood is pumped
out of ventricles &
Ventricular vol
decreases rapidly.

Ventricular contraction: RV v/s LV

Rapid Ejection

ECG & Heart Sounds

In rapid ejection part of

the ejection phase there
no specific ECG
changes / heart sounds
heard.

Slow Ejection
Aortic and Pulmonic Valves Open; AV Valves
Remain Closed

Blood flow from the

left ventricle to the
aorta rapidly
diminishes but is
maintained by aortic
recoil, the
Windkessel effect
At the end of
ejection, the
semilunar valves
close. This marks
the end of
ventricular systole
mechanically.

Slow Ejection

ECG & Heart Sounds

T wave slightly
before the end of
ventricular
contraction
it is d/t ventricular
repolarization
heart sounds :
none

Beginning of Diastole
Isovolumetric relaxation
All Valves Closed

At the end of systole, ventricular

relaxation begins, allowing intraventricular
pressures to decrease rapidly (LV from
100mmHg to 20mmHg & RV from
15mmHg to 0mmHg), aortic and pulmonic
valves abruptly close (aortic precedes
pulmonic) causing the second heart
sound (S2)
Valve closure is associated with a small
backflow of blood into the ventricles and a
characteristic notch (incisura or dicrotic
notch) in the aortic and pulmonary artery
pressure tracings
After valve closure, the aortic and
pulmonary artery pressures rise slightly
(dicrotic wave) following by a slow
decline in pressure

Isovolumetric
relaxation

Volumes remain constant because all

valves are closed
volume of blood that remains in a
ventricle is called the end-systolic
volume (LV ~50ml).
pressure & volume of ventricle are low
in this phase .

Isovolumetric relaxation

Throughout this and the

previous two phases,
the atrium in diastole
has been filling with
blood on top of the
closed AV valve,
causing atrial pressure
to rise gradually
JVP - "v" wave occurs
toward end of
ventricular contraction
results from slow flow of
blood into atria from
veins while AV valves

Isovolumetric relaxation
ECG & Heart Sounds

ECG : no
deflections
Heart Sounds : S2
is heard when the
semilunar vlaves
close.
A2 is heard prior
to P2 as Aortic
valve closes prior
to pulmonary
valve.

Why A2 occurs prior to P2 ?

Hangout interval is longer for

pulmonary side (~80msec),compared to
aortic side (~30msec).
Hangout interval is the time interval from
crossover of pressures (ventricle with their
respective vessel) to the actual occurrence of
sound.

Due to lower pressure and higher

distensibility, pulmonary artery having
longer hangout interval causing delayed
PV closure and P2.

S2 heart sound

Appears in the terminal period of

the T wave
lasts 0.08 0.12s

Some clinical facts about S2

Normal split: Two components heard during

inspiration and is single sound during
expiration.
(A2-P2 ~20- 50 msec in inspiration)

Clinically split is defined as wide, if it is heard

well in standing position, in expiration (normally
not heard as the split is 15 msec, which can not be
heard by human ears)

Single S2: absence of audible split in either

phase of respiration.

Fixed split: two components fails to

move with respiration.
Reverse split: Inaudible split during
inspiration and audible split during
expiration. (recognized by wider split in expiration)

Common causes of wide split S2

RBBB
Sev PAH
ASD
Idiopathic dilatation of pul artery
Sev right heart failure
Moderate to severe PS
Severe MR
Normal variant

Common causes of wide fixed split

S2

ASD
All causes of wide split with
associated severe right ventricular
failure.

Common causes of single S2

Truncus arteriosus
Pulmonary atresia
Aortic atresia
TGA
AS, PS
Single loud P2 in extreme PAH

Causes of reverse split S2

LBBB
RV pacing
RV ectopy
Severe AS
Acute MI
WPW type B
Severe TR
Aneurysm of ascending aorta
Severe systemic hypertension

JVP: V wave

Elevated v wave
1 Tricuspid regurgitation
2 Right ventricular heart failure
3 Reduced atrial compliance (restrictive myopathy)

a wave equal to v wave

1 Tamponade
2 Constrictive pericardial disease
3 Hypervolemia

Rapid Inflow ( Rapid Ven. Filling)

A-V Valves Open

Once AV valves are open

the blood that has
accumulated in atria
flows into the ventricle.

Rapid Inflow

Volume changes

Despite the inflow of blood

from the atria,
intraventricular pressure
continues to briefly fall
because the ventricles are
still undergoing relaxation
JVP: Seen as y-descent.

Rapid Inflow ( Rapid Ven. Filling)

ECG & Heart Sounds

ECG : no deflections
Heart sounds : S3 is heard,
lasts 0.02-0.04 sec
(represent tensing of chordae
tendineae and AV ring during
ventricular relaxation and filling)

Whatever the mechanism,

a sudden inherent
limitation in the long axis
filling movement of the LV
is consistently observed.

Clinical facts about S3

In presence of HF, S3 correlates well

with ventricular end diastolic pressure
and is usually >25mmHg on left side.
Right sided S3 correlate well with rapid
y descend in neck veins.
Normal A2-S3 interval is between 120160 msec.

Correlates of S3
Anatomical

Dilated ventricle

Functional

Systolic dysfunction
(EF<40%)

Hemodynamics
>25 mmHg
LVEDP
<2 L/min/m2
Cardiac index
Symptoms
Doppler flow across AV Dyspnea, PND, Orthopnea
valve
Tall E wave compare to A wave

Gallop rhythm
A gallop rhythm is a grouping of three heart sounds
that together sound like hoofs of a galloping horse.

Protodiastolic gallop or ventricular gallop or S3 gallop

addition of an S3 to the physiological S1 and S2
creates a three-sound sequence, S1-S2-S3.
Presystolic gallop rhythm or atrial gallop
addition of an S4 to the physiological S1 and S2
creates a three-sound sequence, S4-S1-S2.
(during tachycardia S4-S1 can fuse, producing a summation
gallop )

Causes of S3

Physiological: Childrens & young adults <40 yrs

(nearly 25%)
(Not heard in normal infants & adult >40
yrs.)

Pathological:
Ventricular failure
Hyperkinetic state (anemia, thyrotoxicosis, beri-beri)
MR, TR
AR, PR
Systemic AV fistula

JVP: y descent

Prominent y descent
1 Constrictive pericarditis
2 Restrictive myopathies
3 Tricuspid regurgitation

Blunted y descent
1 Tamponade
2 Right ventricular ischemia
3 Tricuspid stenosis

Diastasis
A-V Valves Open

remaining blood
which has
accumulated in
atria slowly flows
into the ventricle.

Diastasis
Volume changes

Ventricular volume
increases more slowly
now. The ventricles
continue to fill with blood
until they are nearly full.

Diastasis

ECG & Heart Sounds

ECG : no deflections
Heart Sounds : none

The Lewis or wiggers cycle, Guyton & Hall. Textbook of Medical Physiology, 11th
Edition

Volumes

End diastolic vol

: During diastole, filling

of ventricle increases vol of each

ventricle to
~ 110 -120 ml

Stroke Vol : amount of blood pumped

out of ventricle during systole. ~ 70 ml

End systolic vol : the remaining amount

of blood in ventricle after the systole.

~40 -50 ml

Pressure-Volume Loop

Pressure-volume loop of RV
is same as that of LV,
however the area is only
1/5th
of LV because pressures
are so much lower on right

RV v/s LV
Rt

Ventricular
Pressure wave 1/5th
dp/dt is less
Isovolumic
contraction &
relaxation phases are
short.

Timing of Cardiac EVENTS

1. RA start contracting before
LA
2. LV start contracting before
RV
3. TV open before MV,
so RV filling start before
LV.
4. RV peak pressure 1/5th of
LV.
5. RV outflow velocity smooth
rise & fall, while Lt side
initial
peak followed by quick
fall.

The First cardiac catheterization

Cardiac catheterization was first attempted by Dr
Werner Forssmann in 1929, at the age of 25 yrs only,
when he was a resident in a hospital at Eberswalde, near
Berlin. He was his own subject. A fellow resident who
agreed to pass the catheter, got scared and abandoned
the effort by the time the catheter reached the axilla.
Forssmann completed the task himself with radiographer
holding the mirror infront of screen. Forssmann catheterize his
heart safely nine times till he had no more peripheral veins
left to try. But this was not enough to convince the medical
world about the safety of the procedure. After being
banished from academics, frustrated Forssmann settled for
medical practice in a small town.
It was extensive studies with catheterization by Dr
Andre Cournand & Dr Dickinson Richard Jr. and eventually the
novel prize for physiology & medicine was awarded jointly to
Forssmann, Cournand & Richard in 1956.
The history of cardiac catheterization illustrates
what reckless idealism of youth can achieve and the long time
(here 27 yrs) might take the world to realize the value of even
something of great significance.

References
1.
2.
3.
4.
5.
6.

Guyton and Hall Textbook of Medical Physiology, 11th

Ed. Arthur C. Guyton, John E. Hall.
Cardiovascular Physiology Concepts Second Edition,
Lippincott Williams & Wilkins, 2011
Clinical Methods in Cardiology By Soma Raju, Second
Edition, orient longman
Braunwald's Heart Disease: A Textbook of
Cardiovascular Medicine, ninth edition
Harrison's Principles of Internal Medicine, 19th edition,
McGraw-Hill Book Co

Understanding Medical Physiology: A Textbook for

Medical Students: By R.L. Bijlani, M.D., RL Bijlani MD
SM DSc (Hon Causa) FAMS, S. Manjunatha,4 th edition

7.

Medical Physiology E-Book:By Walter F. Boron, Emile

L.Boulpaep, Second Edition
8.
Value of physical signs in the diagnosis of ventricular
tachycardia. C J Garratt, M J Griffith, G Young, N
Curzen, S Brecker, A F Rickards and A J Camm,
Circulation. 1994;90:3103-3107
9.
Color Atlas of Physiology. Stefan Silbernagel,
Agamemnon Despopoulos. 6th Edition.
10. Jacc: cardiovascular imaging, Vol.2 No. 5, 2009. May
2009: 648-55.

QUIZ
1.

Which letter indicates the point in

the cardiac cycle that the mitral
valve opens?
A. A
B. B
C. C
D. D

2. In a normal cardiac cycle , true is

A. RA ejection precedes LA ejection
B. RV contraction starts before LV contraction
C. LV ejection starts before RV ejection
D. Pulmonary valve closes before aortic valve

3. Which letter in the image represents

2.
the isovolumic
contraction of the left
ventricle in the heart?
A. F
B. B
C. H
D. D

4. Which of the following pairs is INCORRECT?

A. P wave: atrial depolarization
B. QRS complex: ventricular depolarization
C. T wave: ventricular repolarization
D. QT interval: Measure of duration of atrial
action
potential

5. Isovolumic contraction phase correspond to

A. AV opening to AV Closure
B. MV closure to MV opening
C. MV closure to AV opening
D. AV opening to MV opening

Left ventricular end-diastolic volume is:

A. 30-50 mls
B. 50-70 mls
C. 70-120 mls
D. 120-150 mls

7. Prominent y descent in JVP seen in all except

A. Constrictive pericarditis
B. Restrictive cardiomyopathies
C. Tricuspid regurgitation
D. Cardiac temponade

8. All are true about S3 except

A. Right sided S3 correlate well with rapid y descend
in neck veins.
B. S3 normally heard in normal infants
C. S3 usually indicates systolic dysfunction
D. S3 correlates well with ventricular end diastolic
pressure usually >25mmHg on left side

9. Cardiac apex is palpable during which phase

of cardiac cycle
A. Isovolumic contraction phase
B. Isovolumic relaxation phase
C. Rapid ejection phase
D. Atrial systole phase

10. Sensitive & specific sign of ventricularterial

dissociation in VT are
A. Variable intensity of S1
B. Variable jugular venous pulse
C. Both A & B
D. None of the above

Answers
1.

Which letter indicates the point in

the cardiac cycle that the mitral
valve opens?
A. A
B. B
C. C
D. D

2. In a normal cardiac cycle , true is

A. RA ejection precedes LA ejection
B. RV contraction starts before LV contraction
C. LV ejection starts before RV ejection
D. Pulmonary valve closes before aortic valve

3. Which letter in the image represents

2.
the isovolumic
contraction of the left
ventricle in the heart?
A. F
B. B
C. H
D. D

4. Which of the following pairs is INCORRECT?

A. P wave: atrial depolarization
B. QRS complex: ventricular depolarization
C. T wave: ventricular repolarization
D. QT interval: Measure of duration of atrial
action
potential

5. Isovolumic contraction phase correspond to

A. AV opening to AV Closure
B. MV closure to MV opening
C. MV closure to AV opening
D. AV opening to MV opening

Left ventricular end-diastolic volume is:

A. 30-50 mls
B. 50-70 mls
C. 70-120 mls
D. 120-150 mls

7. Prominent y descent in JVP seen in all except

A. Constrictive pericarditis
B. Restrictive cardiomyopathies
C. Tricuspid regurgitation
D. Cardiac temponade

8. All are true about S3 except

A. Right sided S3 correlate well with rapid y descend
in neck veins.
B. S3 normally heard in normal infants
C. S3 usually indicates systolic dysfunction
D. S3 correlates well with ventricular end diastolic
pressure usually >25mmHg on left side

9. Cardiac apex is palpable during which phase

of cardiac cycle
A. Isovolumic contraction phase
B. Isovolumic relaxation phase
C. Rapid ejection phase
D. Atrial systole phase

10. Sensitive & specific sign of ventricularterial

dissociation in VT are
A. Variable intensity of S1
B. Variable jugular venous pulse
C. Both A & B
D. None of the above

THANK YOU