Your SlideShare is downloading. ×
Upcoming SlideShare
Loading in...5

Thanks for flagging this SlideShare!

Oops! An error has occurred.


Saving this for later?

Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime - even offline.

Text the download link to your phone

Standard text messaging rates apply



Published on

Published in: Education, Health & Medicine

1 Like
  • Be the first to comment

No Downloads
Total Views
On Slideshare
From Embeds
Number of Embeds
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

No notes for slide


  • 1. ARRYTHMIAS Dr Abida Shaheen
  • 2. Normal heartbeat and atrial arrhythmiaNormal 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 ofsegments 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 impulseformation  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
  • 9. Afterdepolarizations
  • 10. Disorders of impulse conduction May result in ◦ Bradycardia (if have AV block) ◦ Tachycardia (if reentrant circuit occurs)Reentrantcircuit
  • 11. Therapeutic overview Na+ channel blockade β-adrenergic receptor blockade Prolong repolarization Ca2+ channel blockade Adenosine, Magnesium, Potassium Digitalis glycosides
  • 12. 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
  • 13. 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
  • 14. 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