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Fundamental of Electrophysiology
basic science
This is the action potential of
0 1 2 3 4
  • Phase 0: Na +
  • Phase 1: K +
  • Phase 2: Ca 2+
  • Phase 3: K +
  • Phase 4: K +
Phase 0 = QRS,
the rest is for ST-T.
Normal Cardiac Conduction System
Pacemaker vs non-Pacemaker cells
PACEMAKER cells
non-PACEMAKER cells
Properties Pacemaker cells non-Pacemaker cells
Location SA and AV nodes Myocardium, His-Purkinje, bypass tract
Normal resting potential -40 to -65mV -80 to -95mV
Phase 0 current Primarily Calcium Sodium
Conduction velocity Slow: 0.01-0.1 m/s Fast: 0.5-5 m/s
Conduction property Decremental All or None
  • Calcium dependent, slow upstroke and downstroke.
  • Specific current = I or funny current
  • Autonomic nervous system controls the slope and velocity.
re . ACTIVATE
When can an already activated cell be activated again?
Mechanisms of Arrhythmias
Enhance Automaticity

sinus tachycardia | junctional tachycardia | atrial tachycardia | idioventricular rhythm
Reentry

atrial flutter | AVNRT | AVRT | scar VT
Triggered Activity

idiopathic PVC/VT | torsades de pointes | digitalis toxicity
Enhance Automaticity
in normal cells (ie. sinus tachycardia)
in abnormal cells (ie. atrial tachycardia)
REENTRY
can be induced by premature beat.
can be entrained and terminated by rapid pacing or overdrive pacing or ATP.
Long QT | Brady-induced TdP | Hypokalemia | Hypomagnesemia
Calcium overload
Digitalis toxicity | Idiopathic VT
Antiarrhythmic Drugs
Antiarrhythmic Agents
Class I: Sodium Blocker
Class Ia
Quinidine, Ajmaline, Procainamide, Disopyramide

Na+channel association/dissociation rate
intermediate
Class Ib
Lidocaine, Mexiletine, Phenytoin


Na+channel association/dissociation rate
fast
Class Ic
Encainide, Flecainide, Propafenone, Moricizine

Na+channel association/dissociation rate
slow
Class II: Beta-Blockers
bisoprolol, carvedilol, metoprolol, and others -olol.
Class III: Potassium-Blockers
amiodarone, bretylium, dofetilide, ibutilide, sotalol
Class IV: Calcium-Blockers
diltiazem, verapamil
MORE and ABOUT
Antiarrhythmic Agents
  • Ivabradine: block I; slow sinus rate.
  • Digoxin: increase intracellular calcium; increase contractility and decrease heart rate.
  • Adenosine: cause AV block by hyperpolarize cell via adenosine receptor.
  • Except Beta-Blockers, none of AADs save life.
  • In a patient with structural heart disease, class I agents increase mortality. Amiodarone does not (but does not reduce mortality either).
Drugs and Devices
Pacing Increase Threshold
Class Ic,
beta blockers, quinidine
hypoxemia, acidosis, alkalosis, hyperglycemia
Decrease Threshold
Epinephrine, Isoproterenol, Atropine, steroids
Defibrillation Increase Threshold
amiodarone, lidocaine, flecainide,
sildenafil (Viagra), alcohol
Decrease Threshold
sotalol, dofetilide
Prolong QT
Questions and Answers
Q1 Q2 Q3
Q1. A 54-year-old woman with symptomatic paroxysmal AF is admitted to the hospital for sotalol loading. On the third hospital day, a two-channel rhythm strip is recorded (as shown).
Which of the following should you recommend?
  1. Reduce the dose of sotalol by 50%, discharge the patient, and see her in the office the next day.
  2. Refer her for ICD insertion.
  3. Perform immediate electrical defibrillation.
  4. Start IV amiodarone and continue for the duration of five half-lives of sotalol.
  5. Stop sotalol and give IV magnesium.
Show Answer