This document discusses cardiac arrhythmias and their treatment. It defines normal cardiac rhythm and atrial arrhythmias. It describes the cardiac action potential and ECG waves. It explains the differences between pacemaker and non-pacemaker cell action potentials. The document discusses mechanisms of arrhythmias including disorders of impulse formation and conduction. It provides an overview of antiarrhythmic drug classes and mechanisms of action including sodium channel blockade, beta-blockade, and calcium channel blockade.

1. ARRYTHMIAS
Dr Abida Shaheen

2. Normal heartbeat and atrial
arrhythmia
Normal rhythm Atrial arrhythmia
AV septum

3. Cardiac action potential
Phase 1
IV
Phase 2
0 mV
Phase 0 III
I Phase 3
-80mV Phase 4
II

4. ECG (EKG) showing wave
Contraction of
segments ventricles
Contraction Repolarization
of atria of ventricles

5. Cardiac Na+ channels

6. Differences between nonpacemaker and
pacemaker cell action potentials
 PCs - Slow, continuous depolarization during rest
 Continuously moves potential towards threshold for a
new action potential (called a phase 4 depolarization)

7. Mechanisms of Cardiac Arrhythmias
 Result from disorders of impulse
formation, conduction, or both
 Causes of arrhythmias
◦ Cardiac ischemia
◦ Excessive discharge or sensitivity to
autonomic transmitters
◦ Exposure to toxic substances
◦ Unknown etiology

8. Disorders of impulse
formation
 No signal from the pacemaker site
 Development of an ectopic pacemaker
◦ May arise from conduction cells (most are capable of
spontaneous activity)
◦ Usually under control of SA node  if it slows down too
much conduction cells could become dominant
◦ Often a result of other injury (ischemia, hypoxia)
 Development of oscillatory afterdepolariztions
◦ Can initiate spontaneous activity in nonpacemaker tissue
◦ May be result of drugs (digitalis, norepinephrine) used to
treat other cardiopathologies

10. Afterdepolarizations

11. Disorders of impulse conduction
 May result in
◦ Bradycardia (if have AV block)
◦ Tachycardia (if reentrant circuit occurs)
Reentrant
circuit

12. Therapeutic overview
 Na+ channel blockade
 β-adrenergic receptor blockade
 Prolong repolarization
 Ca2+ channel blockade
 Adenosine, Magnesium, Potassium
 Digitalis glycosides

13. Classification of antiarrhythmics
(based on mechanisms of action)
 Class I – blocker’s of fast Na+
channels
◦ Subclass IA
 moderate Phase 0 depression
 Prolong repolarization
 Increased duration of action potential
 Includes
 Quinidine – 1st antiarrhythmic used, treat both atrial
and ventricular arrhythmias, increases refractory period
 Procainamide - increases refractory period but side
effects
 Disopyramide – extended duration of action, used only
for treating ventricular arrthymias

14. Classification of antiarrhythmics
(based on mechanisms of action)
◦ Subclass IB
 Minimal Phase 0 depression
 Decreased action potential duration
 Includes
 Lidocane (also acts as local anesthetic) – blocks Na+
channels mostly in ventricular cells, also good for
digitalis-associated arrhythmias
 Mexiletine - oral lidocaine derivative, similar activity
 Phenytoin – anticonvulsant that also works as
antiarrhythmic similar to lidocane

15. Classification of antiarrhythmics
(based on mechanisms of action)
◦ Subclass IC
 Marked Phase 0 depression
 No effect on action potential duration
 Includes
 Flecainide (initially developed as a local anesthetic)
 Slows conduction in all parts of heart,
 Also inhibits abnormal automaticity
 Propafenone
 Also slows conduction
 Weak β – blocker
 Also some Ca2+ channel blockade