Automaticity phase 4 diastolic depolarisation

Pacemaker fibres in the SA node and latent (also subsidiary or secondary) pacemakers spontaneously depolarise during phase 4 towards threshold for regenerative excitation -termed "automaticity".

Sinus node automaticity

The SA nodal action potential with underlying currents is shown in Fig 3.7.20 From a maximum diastolic potential of - 50 to - 60 mV, the cell undergoes slow diastolic (phase 4) depolarisation. This phase merges smoothly with the AP upstroke (phase 0), and there is no distinct AP overshoot, phase 1, or phase 2 (Fig 3.7).

SA node automaticity must be the result of a net gain in intracellular positive charges during diastole.1 2 Contributing to this change is a voltage dependent channel activated at membrane potentials negative to -50 to -60 mV, with a reversal potential of around -20 mV.This pacemaker current (If) is carried mostly by monovalent cations (Na+, K+). Hyperpolarisation increases the If rate of activation, so that it carries only about 20% of phase 4 depolarising current in SA nodal cells. Therefore, automaticity is primarily dependent on Ik, Ica l, Ica T, and an unidentified background current (Ib). Repolarisation results in the closure or deactivation of the K+ channels (Ik) opened during the preceding

AP. This causes K+

Pacemaker Current

Fig 3.7 Membrane currents underlying SA node automaticity and the modulation of automaticity. Inward currents (black) include the pacemaker current (If), background current (Ib), transient Ca2+ current (ICa T), and long lasting Ca2+ current (ICa L). Outward currents include two inward rectifying K+ currents - the delayed rectifier (IK) and a hyperpolarising K+ current that is activated by vagal stimulation (IACh). (1) The rate of SA node discharge can be increased by increasing the slope of phase 4 depolarisation. (2) The rate can be slowed by reducing the slope of phase 4 depolarisation, (3) reducing threshold potential (TP), or (4) by increasing maximum diastolic potential (MDP).

Fig 3.7 Membrane currents underlying SA node automaticity and the modulation of automaticity. Inward currents (black) include the pacemaker current (If), background current (Ib), transient Ca2+ current (ICa T), and long lasting Ca2+ current (ICa L). Outward currents include two inward rectifying K+ currents - the delayed rectifier (IK) and a hyperpolarising K+ current that is activated by vagal stimulation (IACh). (1) The rate of SA node discharge can be increased by increasing the slope of phase 4 depolarisation. (2) The rate can be slowed by reducing the slope of phase 4 depolarisation, (3) reducing threshold potential (TP), or (4) by increasing maximum diastolic potential (MDP).

conductance to decline during phase 4, contributing to net depolarising current. The proposed Na+ background current (Ib) is carried by a voltage independent channel in SA nodal cells - one that is different from the one responsible for I^. Finally, 7Ca L and 7Ca t contribute to the SA node AP upstroke.

Purkinje fibre automaticity

The MDP of automatic Purkinje fibres is hyperpolarised ( - 70 to - 90 mV) compared with that of SA nodal cells.1 2 Consequently, If is the major pacemaker current in automatic

Purkinje fibres, and 7^ is also the primary carrier for the AP upstroke.

Modulation of automaticity

The intrinsic rate of SA nodal pacemaker discharge is determined by: (1) maximum diastolic potential (MDP); (2) threshold potential (TP); and (3) the slope of phase 4 depolarisation (Fig 3.7). Vagal stimulation slows SA node automaticity by: (1) activation of inward rectifying, hyperpolarising K+ current (I^ACh), (2) reduction of I^l, and (3)

reduction of If.28 iKACh hyperpolarises MDP and shortens AP duration. This, together with the reduction in If, slows the rate of phase 4 depolarisation, causing it to take longer to reach TP for a regenerative AP (Fig 3.7). Reduced IcaL slows the rate of phase 0

depolarisation. Catecholamines accelerate automaticity by moving the potential for If activation to a more positive value, and by increasing IK and ICa - both increase the slope of phase 4 depolarisation.

Subsidiary (latent) pacemakers

In addition to Purkinje fibres, cells in certain portions of the atria (sulcus terminalis, Bachman's bundle, coronary sinus ostia), muscle of the tricuspid and mitral annuli, and distal AV node cells may undergo gradual phase 4 depolarisation, The SA node discharge normally exceeds that of these pacemakers, so that they are kept from reaching threshold potential. This is termed "overdrive suppression" of automaticity. The mechanisms for automaticity in latent pacemakers are probably similar to those for SA node cells and Purkinje fibres, with the actual mechanism most dependent on fibre MDP. Compared with the SA node, latent pacemakers are not as subject to the influence of neurotransmitters and the autonomic nervous system.

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Responses

  • samlad
    What is diastolic depolarisation?
    7 years ago
  • sarama
    What is low diastolic depolarisation phase?
    2 years ago

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