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Understanding Cardiac Action Potential

The cardiac action potential follows a repeating cycle in cardiac myocytes. It begins with phase 4, the resting state of the cell. Phase 0 is the upstroke of rapid depolarization as sodium channels open. Phase 1 is early repolarization by potassium channels. Phase 2 is the plateau phase maintained by calcium influx. Phase 3 is final rapid repolarization as calcium channels close and potassium channels remain open. The cell then returns to phase 4 to prepare for the next action potential firing and contraction of the heart muscle. The movement of ions across the cell membrane underlies the changes in electrical potential recorded as an electrocardiogram.

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0% found this document useful (0 votes)
126 views17 pages

Understanding Cardiac Action Potential

The cardiac action potential follows a repeating cycle in cardiac myocytes. It begins with phase 4, the resting state of the cell. Phase 0 is the upstroke of rapid depolarization as sodium channels open. Phase 1 is early repolarization by potassium channels. Phase 2 is the plateau phase maintained by calcium influx. Phase 3 is final rapid repolarization as calcium channels close and potassium channels remain open. The cell then returns to phase 4 to prepare for the next action potential firing and contraction of the heart muscle. The movement of ions across the cell membrane underlies the changes in electrical potential recorded as an electrocardiogram.

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Jiehah Rudy
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CARDIAC ACTION POTENTIAL

HAMDAN IBRAHIM
 The heart has Cardiac Myocytes (muscle cells). The contraction of

these cells is initiated by electrical impulses known as “Action

Potential”

 Impulses start from small group of myocytes called Pacemaker cells

and responsibility for initiating & conduction action potential

 Various states of membrane action potential and recording of

depolarization and repolarization as waveform.


The movement of ions across the myocardium cell can be

described using two terms :

Depolarization – myocardial contraction

Repolarization – myocardial relaxation

RE polarization = RE laxation
Electrical activity occurs in the body as the result of movement of
positive and negative ions cell
The hearts conduction system produces systolic contraction and
diastolic relaxation of myocardium.
The electrical activity of the heart can be graphically on an
ELECTROCARDIOGRAM (ECG).
4 steps of cardiac conduction
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Step 1 : Pacemaker Impulse Generation
SA Node contracts, generating nerve impulses travel to the heart cause both
atria contract.
Step 2 : AV node Impulse Conduction
Impulse reach AV Node, delayed for about 0.10 sec to allows atria to
contract and empty blood into the ventricle.
Step 3 : AV Bundle Impulse Conduction
Impulses are carried down the center of the heart to left & right ventricle
Step 4 : Purkinje fibers Impulse Conduction
Impulses reach these fibers & trigger the muscle fibers in the ventricle to
contract
Anatomy of the Action Potential in the heart
 Mechanical events of the heart triggered by changes in the
electrical of the cardiac cells.
 Under normal circumstances, electric impulse generated
spontaneously via conduction system of the heart
 Surface of ECG can be simply described as P,QRS and T waves
and its summation action potential event.
 Cells are stimulated by the impulses and electric potential of cell
membrane drastically changed
 This change in the membrane potential is termed “action
potential”
EXCITATION-CONTRACTION COUPLING
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 Process by which an electrical action potential leads to


contraction of cardiac muscle cells
 Converting a chemical signal into mechanical energy via
the action of “contractile proteins”
 Calcium is the mediator couples electrical excitation to
physical contraction by cycling in and out myocytes
cytosol.
10 CONTRACTILE PROTEINS
Main contractile elements:-
a)Myosin – thick filaments contains myosin ATPase
b)Actin –thin filaments
Regulatory elements
a)Tropomyosin – prevents contraction resting state
b)Troponin – have 3 subunits
- troponin T TnT (ties troponin to actin)
- troponin I TnI (inhibits activity ATPase)
- troponin C TnC (binds calcium ions)
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CALCIUM-INDUCED CALCIUM RELEASE (CICR)

Initial influx of Ca+ into myocytes during phase 2 is

insufficient to trigger contraction

This signal amplified by the CICR mechanism which

triggers much greater.


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CONTRACTILE CYCLE
Ca+ binds to Tnc – TnI is inhibit – conformational change
tropomyosin

MYOCYTE RELAXATION
Ca+ channels inactivate end of phase 2
Ca+ ions dissociate from TnC
 Action potential follows a fixed time and voltage
 Changes in cardiac action potential may induce cardiac
arrhythmias

Ion channel Syndrome Arrythmias


Natrium N+ Brugada VF
Natrium N+ Long QT 3 Torsades de Pointes
Kalium K+ Short QT syndrome Atrial arrhythmias
Long QT 1 Torsades de Pointes
Long QT 2
Calcium C+ Cathecolaminergic Bidirectional VT
Ventricular Tachycardia
The action potential in typical cardiomyocytes composed of 5 phases (0-4) , beginning and ending with phase 4

PHASE 0 – Upstroke of rapid depolarization

Voltage gated Na+ channels open reponse to depolarization

Positive feedback mechanism cause fast and step depolarization

Very rapid and it lasts for about 2m/sec (0.002 sec)

PHASE 1 – Early repolarization

Immediately after depolarization

The end of rapid repolarization represented “notch”

K+ ion channel open rapidly repolarize the cell


PHASE 2 – Plateau

C+ ion channel open and excitation contraction coupling process is balance

Correlated with S-T segment on ECG

PHASE 3 – Final rapid repolarization

C+ ion channel close but K+ ion channel remain open

Correlated with T wave on ECG

Prepare cell for new cycle of depolarization

PHASE 4 – Resting membrane

N+ and C+ ions channel are closed

K+ ions channel keeps membrane positive outside and negative charge

inside the cell


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