LEC(4)

ELECTRICAL EXCITABILITY AND ACTION POTENTIAL

Dr. Radwa Abdel-Rhman Abdulla
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Types of Cardiac Muscles.

Action potential phases

in cardiac muscles

AGENDA

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 ❑ Atrial muscle - Ventricular muscle:

The Atrial and ventricular types of muscle contract in much the same
way as skeletal muscle - duration of contraction is much longer.
❑ Excitatory and conductive muscle:

The specialized excitatory and conductive fibers contract only weakly

-TYPES OF CARDIAC because they contain few contractile fibrils.
MUSCLES:

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 Autorhythmic cells

• Autorhythmic cells (1%)

• do not contract
• generate and conduct action potentials
CARDIAC • Generate action potentials that drive contractile cells.
• Do not have a resting potential, instead, they slowly
MUSCLE CELLS depolarize, hence ‘pacemaker cells.

Contractile cells

•99% of cardiac muscle cells

•do mechanical work of pumping
•have a different looking action potential from other nerve
cells due to calcium channels

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CARDIAC MUSCLE CELLS:

-Heart has pacemaker cells [Sino-Atrial (SA) node] which

generate action potentials spontaneously; this sets the
rhythmic heart rate.

-The signal for the cardiac muscle fibers (cardiac

myocytes) to contract comes not directly from the nervous
system , but from pacemaker cells of SA node.

-Cells of the SA node depolarize the atrial myocytes.

-Cardiac myocytes which generate force are connected to
each other by gap junctions, so depolarization of one cell
quickly spreads to the neighboring cells, action potentials
are generated by membranes of atrial myocytes

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 ‫نظام التوصيل الكهربائي للقلب‬
INTRINSIC CONDUCTION
SYSTEM
Autorhythmic cells:
1-Initiate action potentials
2-Have “drifting” resting potentials
called pacemaker potentials
3-membrane slowly depolarizes “drifts” to
threshold, initiates action potential, membrane
repolarizes to -60 mV.
4-Use calcium influx (rather than sodium) for
rising phase of the action potential

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Cardiac conduction system:

❑ Sinoatrial (SA) node normally generates the action potential,

i.e., the electrical impulse that initiates contraction.
❑ The SA node excites the right atrium (RA), travels
through Bachmann’s bundle to excite left atrium (LA).
❑ The impulse travels through internodal pathways in RA to
the atrioventricular (AV) node.
❑ From the AV node, the impulse then travels through the bundle
of His and down the bundle branches, fibers specialized
for rapid transmission of electrical impulses, on either side of
the interventricular septum.
• Right bundle branch (RBB) depolarizes the right ventricle
(RV).
• Left bundle branch (LBB) depolarizes the left ventricle
(LV) and interventricular septum.

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 ❑ Both bundle branches terminate
in Purkinje fibers, millions of small
fibers projecting throughout the
myocardium.
 Specialized cardiac fibers called Purkinje
fibers carry an electrical stimulation or
impulse that enables the heart to contract
in unison.
 An organized rhythmic contraction of the
heart requires adequate propagation of
electrical impulses along the conduction
pathway.

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  ACTION POTENTIAL PHASES IN CARDIAC MUSCLES.

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ACTION POTENTIAL PHASES :

 Phase 4: The resting phase

• The resting potential in a cardiomyocyte is −90 mV
due to a constant outward leak of K+ through inward
rectifier channels.
• Na+ and Ca2+ channels are closed at resting TMP.

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 Phase 0: Depolarization
• An action potential triggered in a neighboring
cardiomyocyte or pacemaker cell causes the TMP to
rise above −90 mV.
• Fast Na+ channels start to open one by one and
Na+ leaks into the cell, further raising the TMP.
• TMP approaches −70mV, the threshold potential in
cardiomyocytes, i.e. the point at which enough fast
Na+ channels have opened to generate a self-
sustaining inward Na+ current.
• The large Na+ current rapidly depolarizes the TMP to
0 mV and slightly above 0 mV for a transient period
of time called the overshoot; fast Na+ channels close
(recall that fast Na+ channels are time-dependent).
• L-type (“long-opening”) Ca2+ channels open when
the TMP is greater than −40 mV and cause a small
but steady influx of Ca2+ down its concentration
gradient.
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 Phase 1: Early repolarization

• TMP is now slightly positive.

• Some K+ channels open briefly and an outward
flow of K+ returns the TMP to approximately 0
mV.

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 Phase 2: The plateau phase

• L-type Ca2+ channels are still open and there is a

small, constant inward current of Ca2+. This
becomes significant in the excitation-contraction
coupling process described below.
• K+ leaks out down its concentration gradient
through delayed rectifier K+ channels.
• These two countercurrents are electrically
balanced, and the TMP is maintained at
a plateau just below 0 mV throughout phase 2.

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 Phase 3: Repolarization

• Ca2+ channels are gradually inactivated.

• Persistent outflow of K+, now exceeding
Ca2+ inflow, brings TMP back towards resting
potential of −90 mV to prepare the cell for a new
cycle of depolarization.
• Normal transmembrane ionic concentration
gradients are restored by returning Na+ and
Ca2+ ions to the extracellular environment, and
K+ ions to the cell interior. The pumps involved
include the sarcolemmal Na+-
Ca2+ exchanger, Ca2+-ATPase and Na+-K+-
ATPase

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 PACEMAKER CELLS:
 Pacemaker cells are cells that generate electrical impulses (action potential) by
themselves.
 The impulses are generated with a certain rhythm, creating the heart pulse.
 Thus, in contrast to neurons and other muscle cells, the pacemaker cells need no
external stimuli to depolarize..
 The nervous system regulates the heart’s rhythm and contractility.

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  1-Automaticity: unlike other cardiomyocytes, pacemaker
cells do not require external stimulation to initiate their action
potential; they are capable of self-initiated depolarization .
 This property is known as Automaticity, whereby the cells
undergo spontaneous depolarization, and an action potential
**PROPERTIES OF
is triggered when threshold voltage is reached.
CARDIAC
 2-Unstable membrane potential: Pacemaker cells have an
PACEMAKER CELLS:
unstable membrane potential, and their action potential is not
usually divided into defined phases.
 3-No rapid depolarization phase: Pacemaker cells have
fewer inward rectifier K+ channels than do other
cardiomyocytes, so their TMP is never lower than −60 mV.

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 ACTION POTENTIALS OF PACEMAKER CELLS IN THE HEART.

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 https://derangedphysiology.com/main/cicm-primary-exam/required-reading/cellular-
physiology/Chapter%20118/mechanisms-responsible-cell-resting-membrane-potential
 https://app.pulsenotes.com/medicine/cardiology/notes/electrophysiology

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 Dr. Radwa Abdel Rhman .
Lecturer -Medical Equipment Department
Faculty of Applied Health Sciences Technology

Room-G.224

Sunday(2.30 pm-4.30) - Wednesday(1.30pm-2.30pm)

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