cardiac_cycle_from first week to delivery.ppt

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. Pressure
2. Volume, and
3. 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 (0.015sec for RV)
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
CARDIOLOGIC
SYSTOLE
Isovolumic
contraction
Maximal
ejection
From M
1
to A
2
,
including:
Major part of
isovolumic contraction
Maximal ejection
Reduced ejection
PHYSIOLOGIC
DIASTOLE
CARDIOLOGIC
DIASTOLE
Reduced
ejection
Isovolumic
relaxation
Filling phases
A
2
-M
1
interval
(filling phases included)
20msec
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.Pressure & Volume events
2.ECG correlation
3.Heart sounds
4.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 (pre-position)

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 (atria contract against a closed tricuspid valve)
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 the
carotid pulse.


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
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;2:648–55)
left-handed helix in subepicardiumright-handed helix in subendocardium

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 LV-LA
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 long-lasting

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 Soft S1
1.Exercise
2.Emotinal excitibility
3.Mitral stenosis
4.Hyperkinetic circulation
5.Atrial septal defect
6.Sinus tachycardia
7.Short P-R interval
1.Sinus tachycardia
2.Mitral regurgitation
3.Severe AR
4.Ventricular aneurysm
5.Acute MI
6.Myocarditis
7.Cardiomyopathy
8.Prolonged P-R interval
9.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 are closed .

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 120-160
msec.

Correlates of S3
Anatomical Dilated ventricle
Functional Systolic dysfunction
(EF<40%)
Hemodynamics
LVEDP
Cardiac index
Symptoms
Doppler flow across AV
valve
>25 mmHg
<2 L/min/m
2
Dyspnea, PND, Orthopnea
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, 11
th
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 1/5
th

of LV because pressures
are so much lower on right

RV v/s LV
Rt Ventricular
•Pressure wave 1/5
th

•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 1/5
th
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.Guyton and Hall Textbook of Medical Physiology, 11th Ed. Arthur C.
Guyton, John E. Hall.
2.Cardiovascular Physiology Concepts Second Edition, Lippincott Williams
& Wilkins, 2011
3.Clinical Methods in Cardiology By Soma Raju, Second Edition, orient
longman
4.Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, ninth
edition
5.Harrison's Principles of Internal Medicine, 19
th
edition, McGraw-Hill Book Co
6.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 the isovolumic contraction of the
left ventricle in the heart?
A. F
B. B
C. H
D. D
2.

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

6. 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