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7/30/2019 15 Electrical Activity-Cardiac Action Potential 2012-1
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CARDIAC ACTION POTENTIAL
Howard Mass, Ph.D.
2012
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The SA node originates an actionpotential that subsequently spreads
through the cardiac chambers. Thenumbers on the heart illustrate inmilliseconds the elapsed timeinterval between the origin of thedepolarization at the SA node andthe appearance of thedepolarization in the differentregions of the heart. The tracing onthe right shows the temporalrelationship between themyocardial action potentials and theECG. The P wave represents atrialmuscle depolarization, the QRScomplex represents ventricularmuscle depolarization, and the Twave represents ventricular musclerepolarization.
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Membrane Channels
Ungated Potassium
Voltage-Gated Sodium
Voltage-Gated Calcium
Voltage-Gated Potassium
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Voltage-Gated Potassium (cont.)
Inward rectifying
Delayed Rectifying
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-80 mV
+60 mV
Phase 0(upstroke)
Phase 2 (plateau)
Phase 1(early repolarization)
Phase 4 (diastole)
Phase 4 (diastole)
Phase 3 (repolarization)
Phases of the Cardiac Action Potential
(AP)
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10/2010
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Nodal Action Potential
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Phase 4
Phase 0
Phase 3
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What ions/currents are responsible for the nodal action potential?
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Autonomic Control of Cardiac Function and
the Cardiac Action Potential
Effects of Autonomic NS control:
Chronotropic
Dromotropic
Inotropic
Lusitropic
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Chronotropy
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Dromotropy
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Inotropy
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Channel Gatingmechanism
Functional role
K+
channel (inward rectifier)
Voltage
Maintains high K+
permeability during phase 4
Its decay contributes to diastolic depolarization
Its suppression during phases 0 to 2 contributes to plateau
Na+
channel (fast)
Voltage
Accounts for phase 0 of action potential
Inactivation may contribute to phase 1 of action potential
K+
channel (transient outward)Voltage
Contributes to phase 1 of action potential
Ca2+ channel (slow inward, L channels) BothContributes to phase 2 of action potential
Inactivation may contribute to phase 3 of action potential
Is enhanced by sympathetic stimulation and
-adrenergic agents
K+ channel (delayed rectifier) VoltageCauses phase 3 of action potential
Is enhanced by increased intracellular Ca2+
K+
channel (ATP-sensitive)Increases K
+permeability when [ATP] is low
K+ channel (acetylcholine-activated) Ligand
Responsible for effects of vagal stimulation
Decreases diastolic depolarization (and the heart rate)
Hyperpolarizes resting membrane potential
Shortens phase 2 of the action potential
Na+ (pacemaker current) Both
Is activated by hyperpolarization and contributes to the
diastolic depolarization
Is enhanced by sympathetic stimulation and
beta-adrenergic agentsIs suppressed by vagal stimulation
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Effect of Ion Disturbances on the
Action Potential:
Hyperkalemia
Hypercalcemia
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