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Cardiac action potential
By: Hina Shaikh
May 8th 2009
Introduction
• Action potential
• Cardiac muscle action potential
• Clinical correlations
Introduction
• Action potential can be defined as the rapid
changes in the membrane potential.
• These changes occur due to the change in
membrane permeability to ions.
• There is a reversal of membrane charge that
moves down the axon causing an electrical
impulse to be transmitted.
Introduction
• In the extracellular fluid we see
a high concentration of sodium
ions with a low concentration
of potassium ions.
• Intracellularly there is high
concentration of potassium
ions and a low concentration of
sodium ions.
• The sodium-potassium pump
present on the membrane,
regulates the respective
concentration of these ions.
• As we know from before
this pump uses ATP to
extrude 3 Na+ ions out of
the cell and 2 K+ into the
cell thus creating an
environment in which
intracellularly the cell is
negatively charged and
extracellularly it is
positively charged.
Phases
• There are 5 phases, numbered
(0-4)
• Phase 4: Is the resting
membrane potential.
• Phase 0: is immediate/rapid
depolarization
• Results from a Na+ ion influx
into the cell by the fast channels
opening.
• The fast Na+ channels opening
is depending on the membrane
potential at the time of excitation.
Action potential generated by
the ventricular cardiomyocyte
• - If the membrane potential is at
its baseline (about -85 mV), all the
fast Na+ channels are closed, and
excitation causes them to open.
This allows a greater influx of Na+
• If, however, the membrane
potential is less negative, some of
the fast Na+ channels will be
opened earlier, causing a lesser
response to excitation.
• Phase 1: slight repolarization, is
due to closure of the fast Na+
channels, causing an end to
depolarization.
• Phase 2: plateau of action
potential
• Phase 3: The potassium channels
are open which cause potassium
ions to go into the extracellular
compartment. The is net loss of
positive charge causes the cell to
repolarize.
• Phase 4: back to resting
membrane potential will remain in
this state unitl anoter action
potential is generated.
Differences
• 1) Longer action potential
• 2) Plateau
Comparison
• In skeletal muscle the opening
of “fast sodium channels”
causes generation of action
potential.
• These channels are termed
“fast” as they open for
thousandths of a second and
immediately close.
• After closure, repolarization
occurs.
• In cardiac muscle there are
fast sodium channels as well as
slow calcium channels which
open slowly.
• These channels are open for
tenths of a second. In this time
period calcium and sodium
ions enter into the cell
elongating the depolarization
period thus causing the
appearance of a plateau.
• In additon, after the action
potential is generated, the
permeability of potassium ions
to the membrane decreases.
• This is not seen in skeletal
muscle.
• Decreased permeability of
potassium ions and the
discontinued entering of
sodium and calcium ions into
the cell restores the resting
membrane potential.
Fast and Slow response
1) Fast Response:
Also known as nonpacemaker action potentials
Rapid depolarization
Found throughout the heart
except for the pacemaker
cells.
Happens in Phase 0, the fast
sodium channels open causing
rapid depolarization to occur.
Fast sodium currents cause
depolarization.
In this same instance
potassium channels are
closed.
2) Slow Response:
- Are known to be the pacemaker
cells of the heart
- i.e. SA node and AV node
- Slower depolarization.
- Slow calcium currents cause
depolarization.
- Initailly open at Phase 4, which
initiates depolarization, giving
rise to Phase 0 where there is
depolarization.
- The rate of movement of these
ions are slow, thus a slower rate
of depolarization.
Clinical aspect
• There are certain cells of the
heart that can undergo
spontaneous depolarization,
in which an action potential is
generated without any
influence from nearby cells.
This is also known as
automaticity.
• Automaticity is due to the
spontaneous electrical activity
of the SA node. Electrical
impulses generated from the
SA node spread through the
heart via a nodal tissue.
• The normal activity of the
pacemaker cells of the heart is
to spontaneously depolarize at
a regular rhythm, generating
the normal heart rate.
• Abnormal automaticity
involves the abnormal
spontaneous depolarization of
cells of the heart.
Clinical aspect cont..
• Disorder of irregular or
abnormal heart rhythms are
called Arrhythmia.
• Normally the SA node sends
the electrical signal
throughout the heart where it
goes to the AV node AV
bundle Purkinjie fibres.
• However, if this pathway is
disrupted, it can result in
abnormal heart rhythms.
• It can be in the form of:
• 1) Tachycardia: more than
100 beats/min
• 2)Bradycardia: less than 60
beats/min
Symptoms:
i) Bradycardia:
• Fatigue
• dizziness
• light headedness
• fainting or near-fainting spells
ii) Tachycardia:
• Palpitations
• Rapid heart action
• chest pain
• dizziness
• Light headedness
• fainting or near fainting
Causes and Factors:
Causes:
- Normal pathway disrupted
- Another part of the heart acts
as the pacemaker
- Development of abnormal
heart rate
Factors:
• Coronary artery disease
• High blood pressure
• Diabetes
• Smoking
• Excess alcohol or caffeine
• drug abuse and
• stress.
Fibrillation
• Arhythmias can develop into a more severe
state, known as fibrillation.
• There are two types of fibrillation:
1) Atrial Fibrillation
2) Ventricular Fibrillation
1) Atrial Fibrillation:
- Atria quiver
- Fail to push out enough blood
into ventricles
- The remaining blood in the
atria forms a clot
- A fragment of this clot can
travel and obstruct an artery
causing stroke.
Treatment:
- Anticoagulant
- Electric shock to revert heart
rhythms back to normal
- Antiarrhythmic agents
2) Ventricular Fibrillation:
- ventricles quiver
- unable to pump enough blood
to vital organs (i.e. brain)
- Leaving untreated can lead to
death
• Treatment:
- Defribillator: applies electric
shock that reverts it to the
normal heart beat
- Antiarrhythmic agents:
supress fast heart rhythms
References
• http://outreach.mcb.harvard.edu/animations/actionpotential.swf
• http://www.chemistrydaily.com/chemistry/Cardiac_action_potential
• http://www.phschool.com/science/biology_place/biocoach/cardio1/electri
cal.html
• http://www.americanheart.org/presenter.jhtml?identifier=4469
• http://www.chemistrydaily.com/chemistry/Cardiac_arrhythmia
• http://library.thinkquest.org/C003758/Function/The%20Cardiac%20Acti
on%20Potential.htm
• http://www.nlm.nih.gov/MEDLINEPLUS/ency/imagepages/1056.htm
• http://www.nlm.nih.gov/MEDLINEPLUS/ency/article/001101.htm
• http://www.medicinenet.com/atrial_fibrillation/page4.htm#tocm
• http://www.cvphysiology.com/Arrhythmias/A010.htm
• http://www.doctorslounge.com/cardiology/drugs/antiarrhythmic/
• Guyton