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Phases of cardiac action potential cycle

• Phase 0 : It is the rapid depolarisation of the cell membrane that is associated with fast inflow of sodium ions through channels that are selectively permeable to ions.

• Phase 1: It is a short initial period of rapid depolarisation brought about mainly by an outflow of potassium.

• Phase 2: It is a period when there is delay in repolarisation caused mainly by slow movement of calcium ions from the exterior into cells through channels that are selectively permeable to these ions.

• Phase 3: Second period of rapid repolarisation during which potassium ions move out of the cells.

• Phase 4: Begins with fully repolarised state. For cells that discharge automatically potassium ions then progressively move back into cells ; sodium & calcium move out of the cell. This will lead to gradual negativity until a threshold potential is reached , which allows rapid depolarisation to occur and cycle is repeated.

During phase 1 & 2 the cell is absolute refractory state , but during phase 3 is relatively refractory

Cardiac arrhythmia are mainly produced by

• • Increased automaticity

  • Re entry

  • Trigerred activity

  • Reduced automaticity or blocked or abnormally slow conduction cause bradyarrythmias.





Vaughan-Williams Classification

Class I

• Class IA :

  • Block Sodium channel and prolong action potential. Eg :Qunidine, procainamide & Disopyramide

  • This class includes drug that reduce (Vmax ) rate of action potential upstroke (Phase 0) & prolongs action potential duration.

  • Their kinetics of onset & offset in blocking Na+ channels are of intermediate rapidity (25 sec) compared class Ib & class Ic.

• Class IB :

  • Block sodium channel and shortens action potential.Eg: Lidocaine, Mexiletine, Phenytoin.

  • Their kinetics of onset & offset in blocking sodium channel are rapid < 500msec.

• Class IC : Block sodium channel with no effect on action potential. Eg :Flecainide, Propafenone

Class II

• Beta adrenoreceptor antagonist Eg: Metoprolol, esmolol, propranolol

Class III

• They predominantly blocks potassium channels and prolongs action potential Eg: Amiodarone, sotalol

Class IV

• Slow Calcium channel blockers. Eg: Verapamil, diltiazem

Other : Atropine, Adenosine, Magnesium, Digoxin , Isoprenaline

What is after depolarisation ?

• Spontaneous depolarisation requiring a preceding imulse are called afterdepolarisation.

• If afterdepolarisation originate during phase 2 or 3 of the monophasic action potential they are classified as early afterdepolarisation. Drug induced torsade de pointe is an example. Prolongation of repolarisation by inhibiting the potassium channel will result in lengthening of QT Interval precipitating early after depolarisation. Sotalol, quinidine, dofetilide and procainamide

• Afterdepolarisation originating from phase 4 of MAP are classified as delayed afterdepolarisation. Digoxin induced arrythmia is an example.