Cardiac Action Potentials

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0 2 3 4 Slow Response 0 100 200 300 0 100 200 300 Diastolic Depolarization Threshold CA PERMIABILITY K PERMIABILITY 0mv -60mv -40mv 1 2 3 4 PLATEAU K PERMIABILITY CA PERMIABILITY PLATEAU -90mv 0mv Fast Sodium Channels Responsible for Depolarization IK1 Inward Rectifying Potassium channel -High resting K+ Permeability -Responsible for -90mv resting potential Threshold Diastolic Depolarization (DD) Decrease in K+ efflux through Ikr + Iks channels -in Slow Response Fibers these progressivly close during DD Increase permeability to Sodium Sodium enters through If channels that open at -60mv Increase permeability to calcium L-type begin to open as membrane approaches threshold Sodium Channel Blocker Slows rate of depolarization Slows conduction Velocity Treats V-tach + A-fib Potassium Channel Blocker Acts on IKr + IKs Prolong the duration of AP Treats: V-tach + A-Fib Calcium Channel Blocker Suppresses activity of SA + AV node (Depolarization caused by calcium channels) -Slows rate of diastolic depolarization = slower HR Treats: Arrhythmias due to early and late afterpolarizaitons Also Decreases cardiac contractility + SVR so used to treat Angina + Hypertension Activation Gate Inactivation Gate Inactivation Gate Activation Gate Na Activation Gate Inactivation Gate Less than 1ms Later Inactivation Gate Closes Activation Gate Inactivation Gate Fast sodium channels open and cause Phase 0: Depolarization Fast Sodium Channels Reset to “resting” configuration as membrane potential goes from -50 -> -90mv CC: pathological conditions exist membrane potentia does not repolarize enough and inactivation gate does not reset, fiber assumes Slow Response characteristics Inward rectifying Potassium Channel Closes during Deplarization Ik1 reopens at -40mv and contributes to last phase of repolarization K Outward Transient Rectifying Channel Ito1 Depolarization breifly opens these channel They contribute to partial repolarization (phase1) K K Outward Delayed Rectifying Channels IKr + Iks: Closed by depolarization They determine the Beginning of Repolarization Outward Delayed Rectifying Channels IKr + IKs Closed by depolarization Ca Ca L-Type Calcium Channel Voltage Gated, Opens at threshold Open for a L-ong time Responsible for plateau Closes during repolarization L-Type still open L-Type Closes during Repolarization K K Activation Gate Inactivation Gate K Effective Refractory period last between Depolarization a half way through Repolarization It is caused by the INACTIVATION GATES of Fast Sodium Channels IK1 Inward Rectifying Potassium channel are expressed at a much lower level in slow fibers Explains -60mv resting potential DO NOT OPEN IN SLOW FIBERS Outward Delayed Rectifying Channels IKr + IKs Contribute to DD in Slow Fibers by progressivle clossing K K Na Ca If: Funny sodium Channels Open when membrane reaches Maximum Negative potential (-60mv) and close approaching Threshold Funny Sodium Channels Close at threshold Fast Sodium Channels Non functional bc Inactivation Gate wont reset <--(Permanent Conformation) Activation Gate Inactivation Gate X X Ca L-type Calcium Contribute to the End of DD Begin to open near threshold Ca L-Type Closes during Repolarization K K IKR IKS Outward delayed rectifying potassium channels repsonsible for repolarization Outward Delayed Rectifying IKr + IKs channels close at threshold Ca X X

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Transcript of Cardiac Action Potentials

  • 02

    3

    4

    Slow Response

    0 100 200 300

    0 100 200 300

    Diasto

    lic Depo

    larizat

    ion

    Threshold

    CA PERMIABILITYK PERMIABILITY0mv

    -60mv

    -40mv

    1 2

    3

    4

    PLATEAU

    K PERMIABILITY CA PERMIABILITY

    PLATEAU

    -90mv

    0mv

    Fast Sodium ChannelsResponsible for Depolarization

    IK1 Inward Rectifying Potassium channel-High resting K+ Permeability

    -Responsible for -90mv resting potential

    ThresholdDiastolic Depolarization (DD) Decrease in K+ eux through Ikr + Iks channels -in Slow Response Fibers these progressivly close during DD Increase permeability to Sodium Sodium enters through If channels that open at -60mv Increase permeability to calcium L-type begin to open as membrane approaches threshold

    Sodium Channel BlockerSlows rate of depolarizationSlows conduction VelocityTreats V-tach + A-b

    Potassium Channel BlockerActs on IKr + IKsProlong the duration of APTreats: V-tach + A-Fib

    Calcium Channel BlockerSuppresses activity of SA + AV node (Depolarization caused by calcium channels)-Slows rate of diastolic depolarization = slower HRTreats: Arrhythmias due to early and late afterpolarizaitonsAlsoDecreases cardiac contractility + SVR so used to treat Angina + Hypertension

    Activation Gate

    Inactivation GateInactivation

    Gate

    Activation

    Gate

    Na

    Activation Gate

    Inactivation Gate

    Less than 1msLater Inactivation

    Gate Closes

    Activation Gate

    Inactivation Gate

    Fast sodium channelsopen and cause

    Phase 0: Depolarization

    Fast Sodium ChannelsReset to resting congurationas membrane potentialgoes from -50 -> -90mv

    CC: pathological conditions existmembrane potentia does not repolarizeenough and inactivation gate does not reset, ber assumes SlowResponse characteristics

    Inward rectifying Potassium ChannelCloses during Deplarization

    Ik1 reopens at -40mvand contributes to lastphase of repolarization

    K

    Outward TransientRectifying Channel Ito1

    Depolarization breiy opens these channel

    They contribute to partialrepolarization (phase1)

    K K

    Outward Delayed Rectifying ChannelsIKr + Iks: Closed by depolarization

    They determine the Beginning of Repolarization

    Outward Delayed Rectifying Channels IKr + IKsClosed by depolarization

    Ca

    Ca

    L-Type Calcium ChannelVoltage Gated, Opens at threshold

    Open for a L-ong timeResponsible for plateau

    Closes during repolarization

    L-Type still open

    L-Type Closes during Repolarization

    K

    K

    Activation Gate

    Inactivation Gate

    K

    Eective Refractory period last between Depolarization a half way through RepolarizationIt is caused by the INACTIVATION GATES of Fast Sodium Channels

    IK1 Inward Rectifying Potassium channelare expressed at a much lower level in slow bersExplains -60mv resting potentialDO NOT OPEN IN SLOW FIBERS

    Outward Delayed Rectifying Channels IKr + IKsContribute to DD in Slow Fibersby progressivle clossing

    K KNa

    Ca

    If: Funny sodium ChannelsOpen when membrane reachesMaximum Negative potential(-60mv) and close approachingThreshold

    Funny Sodium ChannelsClose at threshold

    Fast Sodium ChannelsNon functional bc InactivationGate wont reset


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