1. CARDIAC ACTION POTENTIALS

2.  The function of the heart is to pump blood through the circulation.
 To serve as a pump, the ventricles must be electrically activated and
then contract.
 In cardiac muscle, electrical activation is the cardiac AP, which normally
originates in the sinoatrial (SA) node.
 AP initiated in the SA node are conducted to the entire myocardium in a
specific, timed sequence.
 “Sequence” is especially critical because the atria must be activated and
contract before the ventricles, and the ventricles must contract from
apex to base for efficient ejection of blood.

3. PHYSIOLOGY OF CARDIAC MUSCLE

4. PHYSIOLOGY OF CARDIAC MUSCLE
The atrial and ventricular
types of muscle contract in
much the same way as
skeletal muscle, except
that the duration of
contraction is much longer.
cardiac muscle fibers
arranged in a latticework

5. PHYSIOLOGY OF CARDIAC MUSCLE
The specialized
excitatory and
conductive fibers
contract slowly
because they contain
few contractile fibrils;
they cause automatic
rhythmical electrical
discharge in the form
of action potentials

6. PHYSIOLOGIC ANATOMY OF CARDIAC MUSCLE
 cardiac muscle is
striated as in skeletal
muscle.
 cardiac muscle has
typical myofibrils that
contain actin and
myosin filaments
almost identical to
those found in skeletal
muscle;

7. CARDIAC MUSCLE AS A SYNCYTIUM
 intercalated discs are cell
membranes that separate
individual cardiac muscle cells
from one another.
 At each intercalated disc the
cell membranes add with one
another in way that they form
permeable junctions (gap
junctions) that allow rapid
diffusion of ions.
 ions move with ease in the
intracellular fluid so that action
potentials travel easily from one
cardiac muscle cell to the next.

9. The atria are
separated from the
ventricles by fibrous
tissue that surrounds
the atrioventricular (A-
V) valvular openings
between the atria and
ventricles.

10. Normally, potentials are
not conducted from the
atrial syncytium into the
ventricular syncytium
directly through this
fibrous tissue.
they are conducted only
by way of a specialized
conductive system
called A-V bundle

11. This division of the muscle of
the heart into 2 functional
syncytiums allows the atria to
contract a short time ahead of
ventricular contraction, which is
important for effectiveness of
heart pumping.

12. heart
Contractile cells
• atria and ventriculum
• the working cells of the
heart.
• AP lead to contraction .
Conducting cells
• SA node, the atrial internodal tracts, the AV node, the bundle of His, and the
Purkinje system.
• specialized muscle cells - they function to rapidly spread AP over the entire
myocardium.
• Another feature of the specialized conducting tissues is their capacity to
generate action potentials spontaneously.

13. CARDIAC ACTION POTENTIALS

14. SINUS NODE, OR SINO-ATRIAL NODE, SA NODE
 AP of the heart is initiated in the
SA node, which serves as the
pacemaker.
 After the AP potential is initiated
in the SA node, there is a very
specific sequence and timing for
the conduction of AP to the rest
of the heart.
 The sinus node is located in the
superior wall of the right atrium
immediately below to the
opening of the superior vena
cava.
 The fibers of this node have
almost no contractile muscle

15. ATRIAL INTERNODAL TRACTS AND ATRIA
 AP potential spreads
from the SA node to the
right and left atria via
the atrial internodal
tracts.
 Simultaneously, AP is
conducted to the AV
node.

16. AV NODE
 Conduction velocity through the
AV node is slower than in the
other cardiac tissues.
 Slow conduction through the AV
node ensures that the ventricles
have sufficient time to fill with
blood before they are activated
and contract.
 Increases in conduction velocity
of the AV node can lead to
decreased ventricular filling and
decreased stroke volume and
cardiac output.

17. BYNDLE OF HIS, PURKINJE SUSTEM, VENTRICLES
 From the AV node, AP enters the
specialized conducting system of the
ventricles.
 AP is first conducted to the bundle of His
through the common bundle.
 It divides in the left and right bundle
branches and then the
smaller bundles of the Purkinje system.
 Conduction through the His-Purkinje
system is extremely fast,
and it rapidly distributes AP to the
ventricles.
 AP also spreads from one ventricular
muscle cell to the next, via lowresistance
pathways between the cells.
 Rapid conduction of AP throughout the
ventricles is essential and allows for
efficient contraction and ejection of

18. The term normal sinus rhythm
means that the pattern and
timing of the electrical
activation of the heart are
normal. To qualify as normal sinus
rhythm, the following three
criteria must be :
(1) The action potential must
originate in the SA node.
(2) The SA nodal impulses must
occur regularly at a rate of 60 to
100 impulses per minute.
(3) The activation of the
myocardium must occur in the
correct sequence and with the
correct timing and delays

19. AP OF VENTRICLES, ATRIA, PURKINJE SYSTEM
 The ionic basis for the action potentials in the
ventricles, atria, and Purkinje system is
identical.

20. AP OF VENTRICLES, ATRIA, PURKINJE SYSTEM
 Long duration of AP. AP
duration varies from 150 msec in
atria, to 250 msec in ventricles, to
300 msec in Purkinje fibers.
 AP in nerve and skeletal muscle
(1 to 2 msec).
 Duration of the AP also
determines the duration of the
refractory periods: The longer AP,
the longer refractory period.
 Thus, atrial, ventricular, and
Purkinje cells have long
refractory periods compared
with other excitable tissues

21. STABLE RESTING MP.
The cells of the atria,
ventricles, and Purkinje system
exhibit a stable, or constant,
resting membrane potential.
AV nodal and Purkinje fibers
can develop unstable resting
membrane potentials, and
under special conditions, they
can become the heart’s
pacemaker.

22. PLATEAU.
 AP of the atria, ventricles, and Purkinje
system is characterized by a plateau.
 The plateau is a sustained period of
depolarization, which accounts for the long
duration of AP and, consequently, the long
refractory periods

23.  There are AP in a ventricular muscle fiber and an atrial
muscle fiber.
 AP in a Purkinje fiber would look similar to that in the
ventricular fiber, but its duration would be slightly longer.

24. ACTION POTENTIALS IN CARDIAC MUSCLE
Phase 0, upstroke.
 In ventricular, atrial, and Purkinje fibers,
AP begins with a phase of rapid
depolarization, or the upstroke.
 Upstroke is caused by a increase in Na+
conductance, produced by depolarization-
induced opening of activation gates on the
Na+ channels.
 as in nerve, the inactivation gates on the
Na+ channels close in response to
depolarization.
 the Na+ channels open briefly and then
close.
 At the peak of the upstroke, the membrane
potential is depolarized to a value of about
 +20 mV

25. PHASE 1, INITIAL REPOLARIZATION.
 Phase 1 in ventricular, atrial, and Purkinje fibers is a brief period of
repolarization, which follows the upstroke.
 for repolarization to occur, there must be a net outward current.
 There are 2 explanations for the occurrence of the net outward current.
 First, the inactivation gates on the Na+ channels close in response to
depolarization. When these gates close, gNa decreases, and the inward
Na+ current ceases.
 Second, there is an outward K+ current: At the peak of the upstroke, both
the chemical and the electrical driving forces
favor K+ movement out of the cell .
 Because the K+ conductance (gK) is high,
K+flows out of the cell, down this
electrochemical gradient

26. PHASE 2, PLATEAU.
 During the plateau, there is a
long period (150 to 200 msec)
of relatively stable,
depolarized MP, particularly in
ventricular and Purkinje fibers.
(In atrial fibers, the plateau is
shorter than in ventricular
fibers.)
 For the membrane potential to
be stable, inward and outward
currents must be equal such
that there is no net current
flow across the membrane.

27. PHASE 2, PLATEAU.
 There is an increase in Ca2+ conductance (gCa) during plateau, which
results in an inward Ca2+ current.
 Inward Ca2+ current is also called slow inward current, because of the
slow Ca2+(compared with the fast Na+ channels).
 The Ca2+ channels are L-type channels (“L,” for long-lasting) and are
inhibited by the Ca2+channel blockers nifedipine, diltiazem, and
verapamil.

28. PHASE 2, PLATEAU.
 To balance the inward Ca2+ current, there is an outward K+ current.
 During the plateau, the inward Ca2+ current is balanced by the outward
K+ current, the net current is O, and the membrane potential remains at a
stable depolarized value.
 The significance of the inward Ca2+ current extends beyond its effect on
membrane potential.
 This Ca2+ entry during the plateau of the action potential initiates the
release of more Ca2+ from sarcoplasmic reticulum for excitation-
contraction coupling.
 This process of so-called Ca2+-induced Ca2+ release.

29. PHASE 3, REPOLARISATION
 Repolarization begins gradually at the end of
phase 2, and then there is rapid repolarization
to the resting MP membrane potential.
 Repolarization occurs when outward currents
are greater than inward currents.
 During phase 3, repolarization results from a
combination of a decrease in gCa and an
increase in gK (to even higher levels than at
rest).
 The reduction in gCa results in a decrease in
the inward Ca2+ current, and the increase in
gK results in an increase in the outward K+
current.
 At the end of phase 3, the outward K+ current is
reduced because repolarization brings the
membrane potential closer to the K+
equilibrium potential, thus decreasing the
driving force on K+.

30. PHASE 4, RESTING MP, ELECTRICAL DIASTOLE
 The membrane potential returns to the resting
level of - 85 mV after repolarisation.
 During phase 4, the membrane potential is
stable again, and inward and outward currents
are equal.
 The resting MP potential approaches, but does
not fully reach, the
K+ equilibrium potential, that means the high
resting conductance to K+.
 The K+ channels, and the resulting K+ current,
responsible for phase 4 are different from those
responsible for repolarization in phase 3.
 In phase 4, the K+ conductance is called gK1.
 The high conductance to K+ produces an
outward K+ current.
 The inward current that balances this outward
current is carried by Na+ and Ca2+, even
though the conductances to Na+ and Ca2+ are

31. ACTION POTENTIALS IN THE SA NODE
 The configuration and ionic basis for SA action potential differ from AP in
atrial, ventricular, and Purkinje fibers.
 1) The SA node exhibits automaticity; that is, it can spontaneously
generate AP without neural input.
 2) It has an unstable resting MP, in contrast to cells in atrial, ventricular,
and Purkinje fibers.
 3) It has no sustained plateau.

32. AUTOMATIC ELECTRICAL RHYTHMICITY OF THE
SINUS FIBERS
cardiac fibers have the
ability of self-excitation, a
process that cause
automatic rhythmical
discharge and
contraction.
This is true of the fibers of
the heart's specialized
conducting system,
including the fibers of the
sinus node.
the sinus node ordinarily
controls the rate of beat of
the entire heart.

33. PHASE 0, UPSTROKE
 Phase 0 is the upstroke of the action potential.
 The upstroke is not quite as rapid or as sharp as in the other types of
cardiac tissues.
 The ionic mechanism for the upstroke in the SA node is different.
 In the SA nodal cells, the upstroke is the result of an increase in gCa and
an inward Ca2+ current.
 This inward Ca2+ current is carried
Predominantly in T-type Ca2+ channels
(“T,” for transient, in contrast to the L-type
channels responsible for the plateau in
ventricular cells). The T-type channels are
not inhibited by L-type Ca2þ channel blockers
Such as verapamil.
Phases 1 and 2 are absent.

34. MECHANISM OF SINUS NODAL RHYTHMICITY
the "resting membrane
potential" of the sinus
node is about -55 to -60
millivolts,
in comparison with -85
to -90 millivolts for the
ventricular muscle fiber.

35. MECHANISM OF SINUS NODAL RHYTHMICITY
The reason of
this lesser
negativity is that
the membranes
of the sinus
fibers are leaky
to Na+ and
Ca2+ ions,
and positive
charges of the
entering Na+
and Ca2+
neutralize some
of the
intracellular
negativity.

36.  At the level of -55 millivolts, the fast
Na+ channels have already become
"inactivated," - they have become
blocked.
 Therefore, only the slow Na-Ca
channels can open (i.e., can
become "activated") and cause the
action potential.
 As a result, the atrial nodal action
potential is slower to develop than
the action potential of the ventricular
muscle.
 return of the potential to its negative
state occurs slowly rather than that
occurs for the ventricular fiber.

37. SELF-EXCITATION OF SINUS NODAL FIBERS
 Because of the high Na+
concentration in the
extracellular fluid outside
the nodal fiber, Na+ from
outside the fibers tend to
leak to the inside.
 between heartbeats, influx
of Na+ causes a slow rise
in the resting membrane
potential in the positive
direction.
 the "resting" potential
gradually rises and
becomes less negative
between each 2
heartbeats.

38. SELF-EXCITATION OF SINUS NODAL FIBERS
 When the potential reaches a threshold
voltage of about -40 millivolts,
 the Na-Ca channels become "activated," thus
causing the action potential.
 the inherent leakiness of the sinus nodal
fibers to Na+ and Ca2+ ions causes their
self-excitation.

39. WHY DOES THIS LEAKINESS TO NA+ AND CA2+ IONS NOT CAUSE
THE SINUS NODAL FIBERS TO REMAIN DEPOLARIZED ALL THE
TIME?
two events occur during
the the action potential
to prevent this.
the Na-Ca channels
become inactivated (i.e.,
they close) within about
100 to 150 milliseconds
after opening,
at about the same time,
greatly increased
numbers of K+ channels
open.

40.  Therefore, influx of positive Ca2+ and Na+ ions
through Na-Ca channels ceases,
 at the same time large quantities of positive K+
diffuse out of the fiber.
 Both of these effects reduce the intracellular
potential back to its negative resting level and
therefore terminate the action potential.

41.  K+ channels remain open for another few
tenths of a second, temporarily continuing
movement of positive charges out of the cell,
with resultant excess negativity inside the fiber;
 this is called hyperpolarization.
 The hyperpolarization state initially carries the
"resting" membrane potential down to about -55
to -60 millivolts at the termination of the action
potential.