Electrical conduction of the cardiovascular system

Physiology : cardiovascular 

 Electrical conduction:

SA node (pacemaker) creates an action potential → signal spreads across atria and causes their contraction 

 → signal reaches AV node and is slowed down → AV node conducts the signal to bundle of His down the interventricular septum to Purkinje fibers in myocardium → they carry the signal across the ventricles → the ventricles contract (electromechanical coupling)

—The electrical activity of the heart can be recorded through electrocardiography. See ECG for an overview of ECGs and their interpretation.


Heart excitation:


  1. Pacemaker cells (e.g., sinus node) of the conduction system of the heart autonomously and spontaneously generate an action potential (AP).
  2. The conduction system transmits the AP throughout the myocardium.
  3. The electrical excitation of the myocardium results in its contraction (see electromechanical coupling and filament sliding theory in muscle tissue).
  4. The phase of relaxation prevents immediate re-excitation (refractory period).

Cardiac calcium channels and calcium pumps :

1.  Calcium channels :    2 types :

a. L-type voltage-gated calcium channel :

  • Long-acting, high-voltage channels that are responsible for electromechanical coupling
  • Activation via depolarization (– 40 mV) triggers Ca2+ influx into the cells, which in turn stimulates the release of Ca2+ from the sarcoplasmic reticulum .

    b.  T-type voltage-gated calcium channel :

     voltage-gated calcium channel that is opened by low-voltage depolarization potentials

    c. Ryanodine receptor : 

    ca2+ channel that opens after binding of Ca2+ .

    d . SERCA (sarcoplasmic Ca2+-ATPase):
    Ca2+ pumps and exchangers that are responsible for terminating a contraction.

    c. Na+/Ca2+ exchanger.

    e. Funny channels : 
    Nonselective cation channels (e.g., for Na+, K+) in pacemaker cells that open as the membrane potential becomes more negative (hyperpolarized).



    Fast sodium channels  :
    Na+ channels that rapidly open and close following depolarization.

    Action potential of the heart :

    1. phase 0 : 
    a- myocardial action potential :

    • Upstroke: An action potential from a pacemaker cell or adjacent cardiomyocyte causes the transmembrane potential (TMP) to rise above −90 mV.
    • Depolarization: Fast voltage-gated Na+ channels open at -65 mV → rapid Na+ influx into the cell → TMP rises further until slightly above 0 mV.

    b- pacemaker action potential : 
    Upstroke: At TMP -40 mV (threshold potential of pacemaker cells), L-type Ca2+ channels open → TMP increases to +40 mV
    • No rapid depolarization phase because fast voltage-gated Na+ channels are inactivated in pacemaker cells 

       → results in slower conduction velocity between atria and ventricles

    2. phase 1 :
    a- myocardial action potential :
    • Inactivation of voltage-gated Na+ channels.
    • Transient Kchannels start to open (outward flow of K+ returns TMP to 0 mV).

    b- pace maker action potential :
    absent  .

    3. phase 2 : 
    a- myocardial action potential:
    • K+ efflux through delayed rectifier K+ channels and Ca2+ influx through voltage-gated L-type Ca2+ channels, which triggers Ca2+ release from the sarcoplasmic reticulum (i.e., Ca2+-induced Ca2+ release) 

       → contraction of the myocyte

    • TMP is maintained at a plateau just below 0 mV.

    b- pace maker action potential :

    4. phase 3 :
    a- myocardial action potential :
    • Inactivation of voltage-gated Ca2+ channels
    • K+ efflux through delayed rectifier K+ channels continues: Persistent outflow of K+ exceeds Ca2+ inflow and brings TMP back to -90 mV.
    • The sarcolemmal Na+-Ca2+ exchangerCa2+-ATPase, and Na+-K+-ATPase restore normal transmembrane ionic concentration gradients (Na+ and Ca2+ ions return to extracellular space, K+ to intracellular space

    b- pacemaker action potential :
    • Closure of voltage-gated Ca2+ channels and
    • Opening of delayed rectifier K+ channels → Kefflux (TMP returns to -60 mV)

    5. phase 4 :
    a- myocardial action potential :
    • Resting membrane potential stable at -90 mV due to a constant outward flow of K+ through inward rectifier channels
    • Na+ and Ca2+ channels closed

    b- pacemaker action potential :
    No resting phase (unstable membrane potential)

    • Gradual Na+/K+ entry via funny channels If (funny current or pacemaker current) → slow spontaneous depolarization (TMP raises above -60 mV); no external action potential needed (automaticity of SA and AV nodes)
      • At TMP -50 mV: T-type Ca2+ channels open.

    important points :

    Pacemaker cells have no stable resting membrane potential. Their special hyperpolarization-activated cation channels (funny channels) ensure a spontaneous new depolarization at the end of each repolarization and are responsible for the automaticity of the heart conduction system! In sympathetic stimulation, more If channels open, increasing the heart rate.

    Upstroke and depolarization of a pacemaker cell are caused by the opening of voltage-activated L-type calcium channels. In other muscle cells and neurons, upstroke and depolarization are caused by fast sodium channels!

    The duration of action potentials differs in the various structures of the conduction system and increases from the sinus node to the Purkinje fibers.


    Refractory period

    • Effective refractory period (ERP): a recovery period immediately after stimulation, during which a second stimulus cannot generate a new AP in a depolarized cardiomyocyte. The Na+ channels are in an inactivated state until the cell fully repolarizes (phases 1–3).
      • See ‘Refractory period’ in resting potential and action potential for details.
    • Phases (determined based on the number of sodium channels ready to be reactivated)
      • Absolute refractory period: time interval in which no new AP can be generated because fast Na+ channels are deactivated (plateau phase)
      • Relative refractory period: time interval in which some Na+ channels can be reactivated but have a higher threshold potential; only a strong impulse can trigger a new, low amplitude AP
    • Effect
      • Ensures sufficient time for chamber emptying (during systole) and refilling (during diastole) before the next contraction
      • Prevents re-excitation of cardiomyocytes during this period to avoid circulatory excitation, which would lead to arrhythmia and tetany of cardiac muscle



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