Lecture 41
Functi
on
of
Heart
as a
Pump
Dr. Khaled Ibrahim
By the end of this session, the student should be able to:
1) Illustrate and discuss the action potential of contractile cardiac
fibers.
2) Describe the excitability changes during cardiac action potential.
3) Describe excitation-contraction coupling of the cardiac muscle.
4) Describe the intrinsic regulation of the cardiac pumping.
5) Describe the effect of various extrinsic factors on cardiac
pumping (nervous, physical and chemical).
Guyton & Hall Textbook of Physiology - 12th ed. P.
103-104 & 110-112.

CONTRACTILITY
Definition:
 It is the ability of the cardiac muscle to convert the stored
chemical energy of fuel (ATP) into mechanical energy or work.
 In case of cardiac muscle, contractility is manifested by:
pumping & circulation of blood (cardiac contraction gives the
blood its velocity).
Ionic basis of action potential of cardiac muscle (contractile muscle fibers):
Q? Why does the action potential of cardiac muscle have a plateau, while that of
skeletal muscle does not?
1- A moderate quantity of Ca2+ diffuses to the inside of cardiac
muscle fiber during the action potential and for a prolonged time.
The plateau occurs during this prolonged influx of Ca2+. But very
little amount of Ca2+ diffuses in skeletal muscle
2- Immediately after the onset of action potential, the permeability
of cardiac muscle for K+ decreases 5 folds. It is believed that this is
due to excess Ca2+ influx. The  permeability to K+ ----->  K+ efflux
which prevents rapid repolarization -----> plateau. This effect that
does not occur in skeletal muscle
Relation between the mechanical response (contraction) and
Electrical response (action potential)
Contraction (systole) starts just after depolarization and reaches
its maximum by the end of the plateau.
Relaxation (diastole) starts with the rapid phase of repolarization.
Repolarization is complete by the end of the first half of diastole
Excitability changes during the action potential
Following the application of a threshold stimulus, excitability passes by the
following phases
1- Absolute refractory period (ARP)
 During this period, the excitability of the cardiac muscle is completely
lost.
 No other stimulus, whatever its strength can excite the cardiac muscle.
 It coincides (corresponds) with: the phase of rapid depolarization and
the repolarization till the end of plateau (= during systole of cardiac
muscle).
 Significance: Due to this long ARP, tetanus cannot be produced in
cardiac muscle. Tetanization of cardiac muscle is fatal because the heart as
a pump must contract and relax to fill with blood.
N.B.: ARP in skeletal muscle is
very short and equals only the
latent period, so tetanus can
occur to increase the tension
of the muscle to move or carry
objects
2- Relative refractory period (RRP)
 During this period, the excitability gradually recovers until it
reaches the normal value.
 A stronger stimulus applied during the RRP would produce a
weaker systole.
 This period coincides with the rapid repolarization (= the first half
of diastole).
 Significance: This is the phase where extrasystole occurs
3- Supernormal phase (SNP)
 During this phase, the excitability rises above the normal.
 A weaker stimulus is needed to excite the cardiac muscle, and a
stronger contraction is produced.
 It coincides with the second half of diastole. (= after the end of
action potential).
 Significance:
Physiologically: Stimuli adjusted to occur during the SNP of the
preceding cycles, would produce systoles of increasing strength.
This
is
called
phenomenon”.
the
“staircase
phenomenon”
or
“treppe
 Excitation-contraction coupling in the myocardial muscle fibers:
 It is the mechanism by which the action potential causes the
myofibrils of the muscle to contract.
Mechanism:
 Rules controlling contractility :
= intrinsic regulation of the cardiac pumping
1-All or non rule:
* When a cardiac muscle unit is stimulated by an adequate stimulus
(minimal or threshold), it responds maximally giving maximal
contraction But when it is stimulated by an inadequate stimulus, it
does not respond at all.
* This is due to its syncytial nature. The two atria form a syncytium
while the two ventricles form another syncytium. Impulses travel from
the atrial to the ventricular syncytium only through the AV bundle.
2- Staircase phenomenon or Treppe phenomenon:
* If the cardiac muscle is stimulated by successive maximal stimuli, the 1st
few contractions show gradual  in magnitude which is represented
graphically as a staircase. After that, the strength of contraction becomes
stable at its normal level.
* Mechanism:
1) The first stimulus produces thermal (warming of the muscle),
chemical ( activity of the muscle enzymes) & ionic changes ( Ca2+
inside the muscle) which improve the physiological state of the
cardiac muscle (i.e., better physiological conditions).
2) The second stimulus fall in the supernormal phase of excitability.
Question:
Does the staircase phenomenon contradicts the All or
none rule?
No. Because For the all or none rule to be applied, all
physiological conditions should remain constant.
3- Starling's low of the heart:
 It was studied by Starling in the isolated denervated heart.
 It states that: WITHIN CERTAIN LIMIT, THE GREATER THE INITIAL
LENGTH OF THE CARDIAC MUSCLE FIBER, THE GREATER THE FORCE OF
MYOCARDIAL CONTRACTION.
 The initial length of cardiac muscle fiber is determined by the degree of
diastolic filling i.e. End Diastolic Volume (EDV) (It is the volume of the
blood in the ventricles at the end of diastole).
 According to starling's law: excess venous return (amount of blood
returning to the atria from the peripheral veins) e.g. during muscular
exercise --->  the initial length of muscle fibers (EDV) ---->  the force of
ventricular contraction.
 Significance: This prevents stagnation of blood in venous side.
WHILE, Overstretching of the muscle fibers, e.g., heart failure causes
marked  contractility.
 Normally, the pericardium allows optimal increase in diastolic volume
and prevents overstretching.
 Mechanism of Starling's law: It is myogenic in nature through  the
overlappement between thin & thick filaments.
Inotropism
Definition:
an effect on myocardial contractility.
A +ve Inotropic effect is that which  myocardial contractility.
A -ve Inotropic effect is that which  myocardial contracility.
I- Nervous
+ ve Inotropic factor
- ve Inotropic factor
Sympathetic Stimulation
Parasympathetic (vagal) Stimulation
It  the contractilty of atrial but not
factors
the ventricular muscle, as the vagus
does not supply the ventricles.
Mechanism:
Norepinephrine
Mechanism:
binds
to
β1- Acetylcholine
binds
to
M2
adrenergic receptors ---->  the (muscarinic) receptors ----->  the
permeability of the sarcolemma permeability of the sarcolemma
to Ca2+.
to Ca2+ ions.
+ ve Inotropic factor
- ve Inotropic factor
II. Physical
Mild warming
Mechanism:
factors
1) Accelerate the metabolic By an opposite mechanism.
reactions
Mild cooling
Mechanism:
needed
to Sever warming (denaturation of
produce the ATP.
muscle
proteins)
&
sever
2)  the viscosity of the cooling (stoppage of chemical
sarcoplasm ----> facilitating reactions) ---->  myocardial
the sliding of thin over thick contractility.
filaments.
3)  the kinetic energy of ions
---->  Ca2+ influx into the
myocardial fibers.
+ ve Inotropic factor
- ve Inotropic factor
III. Chemical
factors
1. Hormones
Catecholamines:
e.g. adrenaline & noradrenaline.
Glucagon
Thyroxine
2- pH
Alkalosis
Acidosis
favoring systole. This is due to favoring diastole. this is due to
increasing the affinity of troponin C depression
to Ca.
of
the
affinity
of
troponin C to Ca.
Severe alkalosis  the force of Severe acidosis stops the heart in
myocardial contractility and may diastole.
stop the heart in systole.
3- Inorganic
ions
+ ve Inotropic factor
- ve Inotropic factor
Excess Ca2+
Excess K+ (in ECF)
it produces stronger systoles Favor diastole, So, marked 
and
shorter
incomplete in K concentration may stop
diastoles) favoring systole.
Marked increase of Ca2+ may
stop the heart in systole, a
condition called calcium rigor
(irreversible contraction).
Accordingly , I.V. injection of
Ca2+ should be administered
very slowly.
the heart in diastole.
+ ve Inotropic factor
4- Drugs: a- Digitalis:
Mechanism: It inhibits the Na+K+ pump at the myocardial
sarcolemma ----> cytosolic Na+ ----> activation of the Na+-Ca2+
exchanger to transport Na+ out,
and Ca++ into the cell -----> 
cytosolic Ca2+ -----> stronger
myocardial contraction.
b- Xanthines i.e. caffeine and
theophylline:
Mechanism: They stimulate
myocardial contractility by
inhibiting the breakdown of
cyclic AMP and increasing its
intracellular concentration.
- ve Inotropic factor
Quinidine, procainamide and
barbiturates:
They decrease myocardial
contractility by decreasing
the influx of depolarizing Ca2+
into the myocardial cell.
Toxins:
Bacterial toxins as diphtheria
or typhoid toxins weaken the
myocardial contractility by
direct action on the
contractile mechanism.