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Arrythmia

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  • 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