7. electrical activity of the heart

8/3/2019 7. Electrical Activity of the Heart

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Cardiac Action Potentials


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The Cardiac Action Potential Types

Are Either Fast Or Slow Response

Fast-response action potentials

Atrial myocardial fibers

Ventricular myocardial fibers

Purkinje fibers

Slow-response action potentials

Sinoatrial node

Atrioventricular node


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Differences between fast andslow cardiac action potentials:

RMP Slow > Fast

Slope of upstroke Fast > Slow

Amplitude of action potential Fast > Slow

Overshoot of action potential Fast > Slow


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Fast Response Action

Potential


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Phases of theFast Response Action Potential

Phase 0 = Depolarization

Phase 1 = PartialRepolarization

Phase 2 = Plateau

Phase 3 = Repolarization

Phase 4 = RestingMembrane Potential


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Phase 0

The characteristics ofthe upstroke of theaction potential

depend almostentirely on inwardmovement of Na+


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Fast Na+

Current

Phase 0


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Phase 1

Inactivation of Na+channels ends

Transient outward K+current


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Na+

Current

Na+ current ends

Outward K+current


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Phase 2 (Plateau)

What produces theplateau?

Slow inward Ca++

currents (L-typecalcium channels)

Counterbalanced by: Outward K+ currents


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Action potential and ionic fluxes


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Phase 2 (Plateau)

Ventricular contraction persists throughoutthe action potential, so the long plateauproduces a long action potential to ensure

forceful contraction of substantial duration


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Calcium-Induced CalciumRelease

When the myocyte is depolarized calciumenters the cell via L-type calciumchannels. The amount of calcium that

enters the cell is small, but this triggers therelease of a large amount of calcium intothe cytosol from the sarcoplasmic

reticulum which results in binding ofmyosin to actin and contraction of themyocyte.


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Phase 3

Outward K+ current is mainly responsiblefor repolarization

Na+ channel recovery begins duringRelative Refractory Period


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= Outward K+ Current

Na+ ChannelRecovery

Na+ ChannelConfiguration

Change


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Phase 4

Restoration of ionicconcentrations

Na+,K+-ATPase

Na+-Ca++ Exchanger ATP-driven Ca++

Pump


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Restoration of Ionic Gradients


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Ca++ Out

Na+ In

Cell

ECFExcess Ca++ions from CICR

Excess Ca++ ions from actin-myosin dissociation

Na/Ca Exchanger


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Resting Membrane Potential inCardiac Cells

Depends mainly on the conductance of K+

Determined mainly by the ratio of intracellular

to extracellular concentration of K+

Measured value is slightly less negative thanpredicted because of small but finite

conductance of Na+ Na+,K+-ATPase


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Slow Response Action

Potentials


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Slow Response Action Potential

Phase 0

Phase 2

Very brief

Phase 3 Not separated clearly

from phase 2

Phase 4

Note: Phase 1 isabsent

4

0

3


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Slow Response Action Potential:Phase 0

Depolarization ismainly by Ca++ influx


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Cations froman adjacentdepolarizing

cell ordiastolic

depolarization

Ca++ channelsactivated

K+ effluxcauses

repolarization

Ca++ channelrecovery

RelativeRefractory

Period


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Refractory Periods:Effective (ERP) and Relative (RRP)


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Automaticity(Pacemaker Cells)

DiastolicDepolarization

Inward Na+ (not viatypical Na+ channels)

Ca++ influx

K+ efflux (opposeseffects of other ions)


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Autonomic neurotransmitters


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Autonomic neurotransmitters


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Conduction System


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Sinus Rhythm

The SA (Sinus) Node is the heartsdominant pacemaker.

The ability of a focal area of the heart togenerate pacemaking stimuli is known asAutomaticity.

The depolarization wave flows from the SANode in all directions.


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Overdrive Suppression


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SA Node

Atrial Foci (60-80 bpm)

Junctional Foci (40-60 bpm)

Ventricular Foci (20-40 bpm)



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Automaticity of pacemaker cells becomesdepressed after a period of excitation at a highfrequency

Due to activity of Na+, K+-ATPase.

At higher heart rates more Na+ is extruded than K+enters the cell > tends to hyperpolarize the cells

Slow diastolic depolarization requires more time toreach threshold


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THE END

7. electrical activity of the heart

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