Cardiac Action Potential

Explain the ionic basis of spontaneous electrical activity of cardiac muscle cells

Describe the normal and abnormal processes of cardiac excitation and electrical activity

An action potential is a propagating change in the membrane potential of an excitable cell, used in cellular communication and to initiate intracellular processes. It is caused by altering the permeability of a membrane to different ions.

Pacemaker Potential

This pattern of electrical activity is seen in the SA and AV nodes. It has no resting state, and is continually depolarising.

Phases of the Pacemaker Potential

  • Phase 0
    At the threshold potential of -40mV, voltage-gated L-type (long-lasting) Ca2+ channels open, causing an inward movement of ions. The membrane potential peaks at 20mV.
  • Phase 3
    Ca2+ channels close and K+ channels open, leading to repolarisation. The nadir is called the maximum diastolic potential and is -65mV.
  • Phase 4
    Phase 4 consists of:
    • The funny current
      A steady influx of Na+/K+ which gradually depolarises the cell.
      • Sympathetic stimulation increases the funny current, increasing the rate of depolarisation.
      • Parasympathetic stimulation increases K+ permeability, hyperpolarising the cell and flattens the gradient of phase 4.
    • Calcium current
      In phase 4, this is the transient calcium current, driven by T-type calcium channels. They open when the membrane potential reaches ~-50mV, also causing depolarisation.

Ventricular Action Potential

To prevent tetanic contraction (which would be bad) ventricular muscle has a long plateau prior to repolarisation, which lengthens the absolute refractory period to 250ms. The relative refractory period is 50ms.

Phases of the Ventricular Action Potential

  • Phase 0: Depolarisation
    At the threshold potential, voltage-gated fast-Na+ channels open briefly, causing depolarisation. The membrane potential peaks at 30mV.
  • Phase 1: Partial Repolarisation
    The closure of Na+ channels results in K+ fleeing the cell down its electrochemical gradient, causing a slight drop in voltage called partial repolarisation.
  • Phase 2: Plateau
    L-type Ca2+ channels open, causing a slow inward Ca2+ current which maintains depolarisation and facilitates muscle contraction.
  • Phase 3: Repolarisation
    Membrane permeability normalises, and outward potassium current returns the membrane potential to normal.
  • Phase 4: Resting Potential
    Membrane potential returns to its resting -85mV.

Propagation of the Cardiac Action Potential

Pacemaker cells:

  • Are responsible for automaticity and rhythmicity of the heart
  • The fastest pacemaker is the focus for myocardial conduction
    This is typically the SA node.
    • Should the SA node fail, the next fastest pacemaker will take over
    • This provides an element of redundancy

Conduction pathway:

  • Atrial Conduction
    From the SA node, the impulse travels at ~1m.s-1, depolarising the atria.
    • Current travels down Bachmann's Bundle, which connects the right atrium to the left atrium
  • AV node
    The AV node is the only (normal) site of connection between the atria and ventricles. AV nodal cells:
    • Transmits with a delay of 0.1s
      This allows time for atrial contraction to finish before ventricular contraction begins.
    • Have a prolonged refractory period and cannot conduct more than 220 impulses per minute
      • This period is prolonged by vagal stimulation, which increases potassium permeability and hyperpolarises the cell
      • Conversely, sympathetic stimulation increases calcium permeability and allows more rapid transmission
    • Conducts via three pathways:
      • Bachmann Pathway
        Also conducts to the LA.
      • Wenckebach pathway
      • Thorel pathway
  • Ventricular Conduction
    From the AV node, the signal propagates:
    • Initially via the Bundle of His to the right and left bundles
    • Secondly via the Purkinje fibres which conduct at 1-4m.s-1
      Purkinje fibres have a long refractory period, and spontaneously depolarise with an intrinsic rate of 30-40 bpm.
    • Lastly, ventricular muscle is depolarised
      Endocardium, papillary muscle and septum contract first, followed by apex, followed by the chambers.

Autonomic Control

  • Parasympathetic Innervation
    • SA node by the right vagus
      There is continual PNS input ("Vagal tone") via inhibitory ACh GPCR, reducing the SA node from its intrinsic rate of 90-120bpm to a more sedate 60-100bpm.
    • AV node by the left vagus
    • The atria are innervated by parasympathetic neurons, whilst the ventricles are only minimally innervated
      PNS stimulation therefore has little effect on inotropy, but does affect chronotropy.
      • PNS stimulation may have no direct effect on inotropy, instead acting indirectly via changes in chronotropy
  • Sympathetic Innervation
    • SNS activity causes release of noradrenaline (at post-ganglionic synapse) and adrenaline from adrenal medulla which stimulate cardiac β1 receptors causing:
      • Positive chronotropy at the SA node
      • Positive inotropy at ventricular muscle
      • Positive luisotropy
      • Shorter action potential duration (due to opening of rectifying K+ channels
      • Increased AV conduction

Cardiac Transplant

The transplanted heart has no vagal/parasympathetic innervation but still expresses β1 receptors, so it:

  • Defaults to a resting heart rate of ~100bpm
  • Becomes highly preload dependent as it cannot respond quickly to changes in SVR
  • Not responsive to parasympatholytics (atropine, glycopyrrolate) or ephedrine (as this is indirectly-acting) to increase chronotropy - isoprenaline may be used
  • Gradual response to demands in exercise (lacks local SNS innervation, but will still respond to circulating catecholamines)
  • Increased sensitivity to catecholamines due to increased expression of β1 receptors


  1. Kam P, Power I. Principles of Physiology for the Anaesthetist. 3rd Ed. Hodder Education. 2012.
  2. Chambers D, Huang C, Matthews G. Basic Physiology for Anaesthetists. Cambridge University Press. 2015.
  3. Matsuura W, Sugimachi M, Kawada T, Sato T, Shishido T, Miyano H, Nakahara T, Ikeda Y, Alexander J Jr, Sunagawa K. Vagal stimulation decreases left ventricular contractility mainly through negative chronotropic effect. Am J Physiol. 1997 Aug;273.
Last updated 2017-10-05

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