Influence of Membrane Resting Potential on Action Potential Properties

on 7.7.05 with 0 comments



  • The extent and synchrony of sodium channel activation is dependent on the resting membrane potential.

    • Inactivation gates of sodium channels close in the membrane potential range of -75 to -55 mV (less channels available for sodium ion inward current)

    • For example: less intense sodium current if the resting potential is - 60 mV compared to -80 mV

    • Consequences of reduced sodium activation due to reduced membrane potential (less negative)

      • reduced of velocity upstroke (Vmax) [phase 0] (maximum rate of membrane potential change)

      • reduced excitability

      • reduced conduction velocity-- a significant cause of arrhythmias

      • prolongation of recovery:-- an increase in effective refractory period

  • Plateau Phase:

    • Plateau phase -- Na channels mostly inactivated

    • Repolarization (h gates reopen)

    • "Refractory period": time between phase 0 and phase 3 -- during this time the stimulus does not result in a propagated response

    • Altered refractoriness may cause or suppress arrhythmias

  • Factors that reduce the membrane resting potential & reduce conduction velocity

    • Hyperkalemia

    • Sodium pump block

    • Ischemic cell damage

  • Conduction in severely depolarized cells

    • With decreased membrane potentials (e.g., -55 mV), sodium channels are inactivated

    • Under some circumstances, increased calcium permeability or decreased potassium permeability allow for slowly conducted action potentials with slow upstroke velocity

    • Ca2+-inward current-mediated action potentials are normal for the specialized conducting SA nodal and AV nodal tissues, which have resting membrane potentials in the -50 to-70 mV range.

Factors that may precipitate or exacerbate arrhythmias
  • Ischemia

  • Hypoxia

  • Acidosis

  • Alkalosis

  • Abnormal electrolytes

  • Excessive catecholamine levels

  • Autonomic nervous system effects (e.g., excess vagal tone)

  • Excessive catecholamine levels

  • Autonomic nervous system effects (e.g., excess vagal tone)

  • Drug effects: e.g., antiarrhythmic drugs may cause arrhythmias)

  • Cardiac fiber stretching (as may occur with ventricular dilatation in congestive heart failure)

  • Presence of scarred/diseased tissue which have altered electrical conduction properties

Category: Physiology Notes

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