‫سورة البقرة آية ‪32‬‬

LECTURE OBJECTIVES
•BYTHE END OF THIS LECTURE YOU
SHOULD BE ABLE TO:-
1.PROPERTIES OF CARDIAC MUSCLE.
• EXCITABILITY.
• AUTORRHYTHMICITY.
• CONDUCTIVITY.
• CONTRACTILITY.
 Properties of cardiac muscle:

• EXCITABILITY: ABILITY TO
RESPOND TO ADEQUATE
STIMULATION.
• AUTORRHYTHMICITY: ABILITY TO
GENERATE A REGULAR RHYTHM.
• CONDUCTIVITY: ABILITY TO
CONDUCT CARDIAC IMPULSE.
• CONTRACTILITY: ABILITY TO
CONTRACT.
 PROPERTIES OF
CARDIAC MUSCLE
1-CONTRACTILITY

THIS IS THE ABILITY OF CARDIAC

MUSCLE TO CONTRACT (ISOTONIC OR
ISOMETRIC).
THE FACTORS THAT AFFECT
CONTRACTILITY (+ OR -) = INOTROPIC
FACTORS
FACTORS AFFECTING CARDIAC CONTRACTILITY
A-MECHANICAL FACTORS

1-Preload:
It is the load that determines the initial
length of the resting ms before contraction.
In heart= EDV or EDP.
EDV   tension & velocity of shortening
 stronger contraction.
Maximal contractility occurs at sarcomere
length 2.2  (L-max) [ no. of cross bridges
&  sensitivity of contractile proteins to bind
to Ca++].
The length-tension relationship is the basis
of Starling Law.
 Frank Starling Law

Within limits, the force of

myocardial contraction is
directly proportional to the
initial length of the cardiac ms
fibers (preload or EDV).
SIGNIFICANCE:
IT IS AN INTRINSIC MECHANISM THAT ALLOWS HETEROMETRIC (CHANGE
IN LENGTH) AUTOREGULATION OF MYOCARDIAL CONTRACTILITY, IN:
1-NORMAL HEART: MATCH THE VENTRICULAR OUTPUT TO CHANGES IN
THE VR .
2-INCREASE AORTIC PRESSURE:   SV OF LV   EDV OF NEXT BEAT 
FORCEFUL CONTRACTION.
3-IN DENERVATED HEARTS (TRANSPLANTED HEARTS): MAIN
MECHANISM THAT ADJUSTS THE PUMPING CAPACITY OF THE HEART.
4-FAILING HEART: WEAK VENTRICULAR CONTRACTION   EDV  
MYOCARDIAL CONTRACTILITY.
EDV= 130 ml (volume of blood in
ventricle at end of diastole.
ESV = 55 ml (volume of blood in
ventricle at end of systole).
SV= 75 ml = EDV – next ESV
DFV= 75 ml = EDV – preceding
ESV
 2-AFTERLOAD
It is the load that the muscle fibers
faces when it begins to contract.
Afterload= aortic pressure, arterial
wall rigidity, blood viscosity.
Change in the afterload  affects
mainly the velocity of shortening of
cardiac
FORCE VELOCITY RELATIONSHIP:
1-EFFECT OF AFTERLOAD:
A-INITIAL VELOCITY  1
MAGNITUDE OF AFTERLOAD
B- 0 AFTERLOAD  MAXIMAL VELOCITY (V MAX).
C-AT CRITICAL AFTERLOAD (L0)  0 VELOCITY  ISOMETRIC
CONTRACTION.
2-EFFECT OF PRELOAD:
 VR   PRELOAD   INITIAL VELOCITY OF SHORTENING AT ANY
GIVEN AFTERLOAD, BUT NOT VMAX (MIDDLE CURVE).
3-EFFECT OF MYOCARDIAL CONTRACTILITY STATE:
+VE INOTROPIC DRUGS (EPINEPHRINE)   INITIAL & MAXIMUM
VELOCITY OF SHORTENING (UPPER CURVE= UP & TO RIGHT).
B-CARDIAC (INTRINSIC) FACTORS
1-MYOCARDIAL MASS:
LOSS (ISCHEMIA)   FORCE OF MYOCARDIAL
CONTRACTILITY
2-HEART RATE:
FORCE FREQUENCY RELATIONSHIP:
FREQUENCY (TACHYCARDIA)   FORCE OF
MYOCARDIAL CONTRACTILITY (+VE INOTROPIC) DUE TO 
INTRACELLULAR CA++ CONTENT, AND VICE VERSA.
3-THE CARDIAC INOTROPIC STATE:
IT IS DETERMINED BY QUANTITY OF CA++ DELIVERED TO
CONTRACTILE PROTEINS.
 2-Automaticity & Rhythmicity

•AUTOMATICITY: PROPERTY OF SELF EXCITATION

(SPONTANEOUS GENERATION OF AP).
RHYTHMICITY: REGULAR GENERATION OF THESE AP.
HOWEVER, ALL PARTS OF THE CONDUCTING SYSTEM OF THE
HEART ARE CAPABLE OF AUTORRHYTHMICITY, BUT THE NORMAL
1RY PACEMAKER IS SAN (SINUS RHYTHM = 100-110/MIN), THE 2RY
IS AVN (=NODAL RHYTHM = 45-60/MIN) (ACTS WHEN SAN IS
BLOCKED), 3RD IS PURKINJE SYSTEM (= IDIOVENTRICULAR
RHYTHM = 25-40/MIN) (ACTS WHEN AVN IS BLOCKED).
THE FACTORS THAT AFFECT AUTORHYTHMICITY (+ OR -) =
CHRONOTROPIC FACTORS.
THE PACEMAKER AP = SLOW RESPONSE•
1-RMP = -55 TO -60 MV, UNSTABLE = PREPOTENTIAL DUE TO  K+
EFFLUX, ITS LATE PART DUE TO  CA++ INFLUX (T-TYPE).
2-DEPOLARIZATION IS SLOW UP TO + 10 MV (SMALL AMPLITUDE)
DUE TO CA++ INFLUX (L- CHANNELS)
3-NO PLATEAU, AP= 200-250 MSEC.
4-REPOLARIZATION IS GRADUAL DUE TO K+ EFFLUX.
EFFECT OF PARASYMPATHETIC  -VE CHRONOTROPIC, ACH ACTS
ON M2 MUSCARINIC RECEPTORS   K+ EFFLUX 
HYPERPOLARIZATION .
EFFECT OF SYMPATHETIC  +VE CHRONOTROPIC, NE ACTS ON 2
ADRENERGIC RECEPTORS   K+ EFFLUX  DEPOLARIZATION &
ACTIVATES L TYPE CA++ CHANNELS   SLOPE OF
PREPOTENTIALS .
Slow Response (SAN & AVN):
 3-Excitability
•Excitability: this is the ability to response
to stimulation.
•2 types:
1-Slow response (SAN, AVN).
2-Fast response (atria, ventricle, purkinje
system).
•The fast response (300-400 msec):
1-Phase 0 = upstroke, rapid depolarization,
overshoots to + 20 mv (rapid Na+ influx=
voltage gated, fast).
2-Phase 1= partial repolarization (inactivation
of Na+ channels, Cl-influx, K+ efflux).
3-Phase 2= plateau, prolonged repolarization
(Ca++ influx, L type, balances K+ efflux).
4-Phase 3 = rapid repolarization ( K+ efflux &
closure of Ca++ channels).
5-Phase 4 = complete repolarization &
restoration of RMP ( K+ efflux & Na+K+ pump
that restores the normal ionic distribution).
 Excitability Characteristics
in fast and slow responses:
ARP RRP
Excitability = 0 Stimuli > threshold 
Strong stimulus = local propagated AP (slow
response (effective RP rising & low
=ERP). amplitude).
Fast: phase 0 to 1/2 of Fast: The remain of
phase 3. phase 3.
Slow: phase 0 to late Slow: phase 4 =
of phase 3. postrepolarization
refractoriness.
A 3rd phase of excitability occurs only in fast
response = supernormal phase (=phase 4), weak
stimulus  propagated AP (low amplitude=
because although the Na channels able to produce a
propagated response, remain partially inactivated),
is called vulnerable period, dangerous, since
stimulation at this time  ventricular fibrillation.
Supernormality is apparent in His-Purkinje cells,
absent in AV, atria & ventricles. So, it is simply
lowered threshold.
Summary of types of action potentials
in different regions of heart:

SA node Slow response

Atrium Fast response
AV node Slow response
Bundle of His Fast response
Purkinje fiber Fast response
Ventricle Fast response
Relation Between the mechanical response and
AP in fast response fibers:
•The mechanical response starts just after the
depolarization phase (phase 0) of AP, it
continues for relatively longer period.
•The systole reaches maximum at the end of
plateau (phase 2).
•The 1st half of diastole coincides with phase 3.
•The 2nd half of diastole coincides with phase 4.
Importance of long ARP in cardiac muscle:
•The ARP in cardiac muscle > ARP in
skeletal muscle.
•It occupies whole systole + early part of
diastole.
•Its importance:
The heart during systole cannot be
stimulated, so cardiac tetanization would
not occur.
It provides rest periods for cardiac ms,
so the hear t can continue contracting
without fatigue
 4-Conductivity
Conductivity: this is the ability of cardiac ms
to transmit AP from 1 fiber to adjacent
fibers.
The last parts to be activated are the
posterobasal portion of LV and the
pulmonary conus of right ventricle.
The average speed of conduction:
1-SAN, AVN (fibers are small & poor gap J)
0.05 m/sec.
2-Atrial pathway, ventricular ms, bundle of
His  1 m/sec.
3-Bundle branches & purkinje network
(fibers are large & rich gap J)  4 m/sec.
The AV nodal delay:
1-The AN (=atrionodal) region : between
atrium and upper part of node.
2-The N (=nodal) region: mid portion of node.
3-The NH (=nodal His) region: when the
nodal fibers merge with bundle of His.

Characters of AV nodal delay:

1 way conduction: From AV node  bundle of
His (prevents re-entry).
AV nodal delay: 0.1 sec, mainly in AN region
(allows atria to contract and empty their
contents of blood into the ventricle before the
latter depolarize and contract.
 LECTURE OBJECTIVES
•BYTHE END OF THIS LECTURE YOU
SHOULD BE ABLE TO:-

2. ECG
• ECG LEADS.
• CONNECTION & CALIBRATION.
• SPREAD OF CARDIAC EXCITATION.
• NORMAL ECG.
 Recording of the ECG (ECG leads):
ECG is the recording of the electric
currents generated by the cardiac
muscle, by electrodes placed on skin
surface.

The apparatus is called

electrocardiograph.

A standard ECG consists of 12 different

leads, that record the same electric
cardiac events (but from different views).
 3 types of leads
1-Bipolar limb leads (standard limb leads
of Einthoven):
Measure the difference in potential
between 2 limbs.
Lead I: left arm – Right arm (LA- RA or
VL - VR), v= voltage.

Lead II: Left leg- Right arm (LL- RA, or

VF- VR), f= foot.

Lead III: Left leg- left arm (LL- LA, VF-

VL).
 Einthoven's triangle
It is an equilateral triangle, the sides of
which represent the 3 bipolar limb
leads, and heart lies at its centre.
Einthoven's law

voltage in lead II=

voltage in lead I + voltage in lead III.
2)Unipolar leads:
These measure the absolute (actual)
potential at a certain point.
These are 2 types:
a-Unipolar limb leads:
VR (reflect the electrical
activities of cavities).
VL (reflect the electrical activities
of the left side of the heart).
VF (reflect the electrical activities
of inferior surface of heart).
b-Unipolar chest leads:
V1: at right margin of sternum in
4thright intercostal space.
V2: at left margin of sternum in 4th
left intercostal space.
V3: midway between V2 and V4.
V4: Left mid-clavicular line in 5th
intercostal space.
V5: left anterior axillary line in 5th
intercostal space.
V6: left midaxillay line in 5th
intercostal space.
3)Augmented unipolar limb leads
(Goldberg's leads):

These are unipolar limb leads that

have magnified amplitude by about
50% without any change in their
configuration (aVR, aVL, aVF).
 Connections and Calibration

It is arranged so that an upward

deflection (+ve) is produced when
a depolarization wave is moving
toward the exploring electrode or
a repolarization wave is moving
away.
 Spread of cardiac excitation
Depolarization initiated at SA node
spreads through the atria from the right to
the left, then in the interventricular septum
(mid-part) from left to right.

In the ventricular wall, it spreads from

the endocardial to the epicardial surface.

Last parts to be depolarized (posterobasal

portion of the left ventricle, pulmonary
conus, upper most part of the
interventricular septum.
CONDUCTING SYSTEM OF HEART
 Normal ECG
It consists of 5 main waves : P, Q, R,
S, T, sometimes there is U wave.
These waves are separated by
segments, and each starts and ends at
the isoelectric line.
 P wave
Caused by atrial depolarization.
Amplitude 0.1- 0.25 mv, duration 0.08-
0.11 sec.
+ve in leads facing left ventricle.
The 1st part is due to right atrial
activation, while the terminal part is due to
left atrial activation.
Abnormalities: left atrial hypertrophy P
mitrale, in M.S.
Right atrial hypertrophy P pulmonale, A-V
nodal rhythm inverted, Atrial fibrillation
disappear.
 Normally, there is no wave for
depolarization of SA node since its
excitation does not generate
electrical activity to reach the body
surface.

There is no wave of atrial

repolarization because it is masked
by QRS at same time (more potent).
 QRS complex

Caused by ventricular depolarization,

duration 0.06- 0.1 sec.

Q wave= depolarization of
interventricular septum, R= 10 mm,
1 mv due to depolarization of apex,
S= due to depolarization of
posterobasal part of left ventricle.
 T wave
Due to ventricular repolarization.
Amplitude = 0.2- 0.4 mv, duration
0.2- 0.25 sec.
It is normally +ve in leads facing the
left ventricle, last part to depolarize, is
the first part to repolarize (from the
epicardium to the endocardium).
Abnormality: inverted in myocardial
ischemia, increased activity in
sympathetic overactivity, muscular
exercise.
 P-R interval
From the start of P to the start of
R= 0.12- 0.21 second.
It involves conduction of cardiac
impulse through the AV node.
Prolonged in : 1st degree heart
block, increase vagal tone.
Shortened in: AV nodal rhythm,
sympathetic activity, Wolff-Parkinson
White Syndrome.
 Q-T interval
From the onset of Q to the end of T wave=
0.36- 0.42 sec.
QT  1/ HR.
Called electrical systole.
T-Q interval
From the end of T to the onset of Q = 0.4
sec.
Called electrical diastole.
It is shortened before atrial and ventricular
extrasystoles, but it is prolonged after
ventricular extrasystoles due to conpensatory
pause.
 ST segment
From the end of S to start of T =
0.12 sec.

All ventricular fibers are

depolarized, so it is normally
isoelectric and its upward or
downward deviation indicates
myocardial damage.
 LECTURE OBJECTIVES
• BY THE END OF THIS LECTURE YOU
SHOULD BE ABLE TO:-
3. CARDIAC CYCLE
• ATRIAL SYSTOLE.
• ISOVOLUMETRIC CONTRACTION.
• RAPID EJECTION.
• REDUCED EJECTION.
• EARLY VENTRICULAR DIASTOLE.
• ISOVOLUMETRIC RELAXATION.
• RAPID VENTRICULAR FILLING
• REDUCED VENTRICULAR FILLING.
 The cardiac events that occur
from the beginning of one heart
beat to the beginning of the next
are called the cardiac cycle. Each
cycle is initiated by spontaneous
generation of an action potential
in the sinus node.
The cardiac cycle consists of one systole-
diastole (i.e. contraction-relaxation) sequence
of the heart, and it lasts about 0.8 second
(when the heart rate is 75/ minute). It
starts by atrial systole followed by
ventricular systole then by diastole of the
whole heart, passing in the following phases:
1)Atrial systole (0.1 second) [coincident
with late ventricular diastole].
2)Ventricular systole (0.3 second), this
includes 3 phases:
a-Isometric contraction phase (0.05 second).
b-Maximum ejection phase (0.15 second).
c-Reduced ejection phase (0.1 second).
3) Early ventricular diastole (0.2
second), this includes 3 phases:
a- Protodiastolic phase (0.04 second).
b-Isometric relaxation phase (0.06
second).
c- Rapid filling phase (0.1 second).
4) Mid-ventricular diastole (= slow
filling phase) (0.2 second).
5) Late ventricular diastole (coincident
with atrial systole).
ATRIAL SYSTOLE - HEART
 ATRIAL SYSTOLE
PRESSURES & VOLUMES
 1-Atrial systole
In this phase, both atria contract leading to blood
evacuation into the ventricles. Its events include
a-Atrial pressure: This initially increases (a. contraction)
it decreases again (passage of blood to v)
b-Ventricular pressure: This initially increases slightly
then it decreases again (late v. diastole)
c-Ventricular volume: This increases slightly .
d-Valves: The A-V valves are open while the semilunar
valves are closed.
e-Aortic pressure: This decreases gradually.
f-Sounds: 4th heart sounds.
g-ECG: P wave starts 0.02 second before this phase,
while the main part of P and PR segment and Q wave
occur .
ISOVOLUMETRIC CONTRACTION
HEART
ISOVOLUMETRIC CONTRACTION
PRESSURES & VOLUMES
 2-Ventricular systole
Isometric (isovolumetric) contraction phase: 0.05 sec
a-Atrial pressure: a slight increase (bulge of cusps).
b-Ventricular pressure: the ventricular pressure rises
sharply (to 80 mmHg in left ventricle, and 10
mmHg in right ventricle).
c-Ventricular volume: unchanged.
d-Valves: The A-V valves and the semilunar valves are
closed.
e-Aortic pressure: This decreases to a minimum (80
mmHg) at the end of this phase.
f-Sounds: The early component of the first heart
sound is heard due to closure of the AV valves
g-ECG: Q wave starts 0.02 second before this phase,
while the R and S waves occur during it.
RAPID EJECTION
HEART
 RAPID EJECTION
PRESSURES & VOLUMES
Maximum (rapid) ejection phase: 0.15 sec
a-Atrial pressure: This is initially decreased (descent
cusps), then it gradually increases (VR).
b-Ventricular pressure: the ventricular pressure rises
to maximum (to 120 mmHg in left ventricle, and
25 mmHg in right ventricle).
c-Ventricular volume: This rapidly decrease.
d-Valves: The A-V valves remain closed, while the
semilunar valves open.
e-Aortic pressure: This markedly increases to a
maximum (120 mmHg= systolic blood pressure).
f-Sounds: The second component of the first heart
sound.
g-ECG: The S-T segment is present in this phase,
while the T wave starts in the late phase.
RAPID EJECTION
ECG
REDUCED EJECTION
HEART
 REDUCED EJECTION
PRESSURES & VOLUMES
Reduced (slow) ejection phase: 0.1 sec:
a-Atrial pressure: This is still increasing
(VR).
b-Ventricular pressure: This slightly
decreased.
c-Ventricular volume: This further decreased.
d-Valves: The A-V valves remain closed,
while the semilunar valves are still open.
e-Aortic pressure: This slightly decreases.
f-Sounds: There are no sounds in this phase.
g-ECG: Most of the ascending limb and the
top of the T wave occur during it.
 3- Early ventricular diastole = 0.2 sec
Protodiastolic phase: 0.04 sec
a-Atrial pressure: This is still increasing.
b-Ventricular pressure: This decreases at more rapid
rate (V pr  aortic pr, but blood continues to reach
the aorta by momentum, when the momentum is
overcomed, blood in aorta flow back to close the
valve).
c-Ventricular volume: This remains almost constant.
d-Valves: The A-V valves remain closed, while the
semilunar valves are still open, but they are closed
at the end of this phase.
e-Aortic pressure: This decreases rapidly.
f-Sounds: The 2nd heart sound, is heard at the end
of this phase.
g-ECG: Most of the descending limb of the T wave
occur during it.
ISOVOLUMETRIC RELAXATION
HEART
Isometric (isovolumetric) relaxation phase:
0.06 sec
a-Atrial pressure: This is still increasing.
b-Ventricular pressure: the ventricular
pressure falls sharply (to 0-5 mmHg).
c-Ventricular volume: unchanged.
d-Valves: The A-V valves and the semilunar
valves are closed.
e-Aortic pressure: This initially increases
producing the dicrotic wave. Then gradually
decreases
f-Sounds: The 2nd heart sound.
g-ECG: The T wave ends in this phase.
ISOVOLUMETRIC RELAXATION
PRESSURES & VOLUMES
RAPID VENTRICULAR FILLING
HEART
RAPID VENTRICULAR FILLING
PRESSURES & VOLUMES
Rapid (maximal) filling phase: 0.1sec
a-Atrial pressure: This initially decreases slightly
(blood passes to v), then it increases gradually
(VR).
b-Ventricular pressure: This initially decreases (v.
relaxation), then it increases gradually (filling ~
0 mmHg because of synchronous relaxation of
v).
c-Ventricular volume: This increases markedly .
d-Valves: The A-V valves open, while the
semilunar valves remain closed.
e-Aortic pressure: This decreases gradually.
f-Sounds: The 3rd heart sound.
g-ECG: The early part of T-P segment is present
in this phase.
REDUCED VENTRICULAR FILLING
HEART
REDUCED VENTRICULAR FILLING
PRESSURES & VOLUMES
 4-Slow (reduced) filling phase= 0.2 sec
Mid ventricular diastole
a-Atrial pressure: This increases gradually.
b-Ventricular pressure: This increases
gradually.
c-Ventricular volume: This increases
gradually.
d-Valves: The A-V valves open, while the
semilunar valves remain closed.
e-Aortic pressure: This still decreasing.
f-Sounds: There are no sounds at this phase.
g-ECG: The late part of T-P segment, and
the start of the P wave are present in this
phase.