1 / 38

Drug Induced Arrhythmia

Drug Induced Arrhythmia. Dr. SH TSUI 15 June 2005. ECG Disturbances in Poisoned Patients. Fast rate Slow rate Abnormal rhythm/pattern Focus: Underlying mechanism and patho-physiology. Cardiovascular Physiology . Electrolyte movement and action potential.

joann
Download Presentation

Drug Induced Arrhythmia

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Drug Induced Arrhythmia Dr. SH TSUI 15 June 2005

  2. ECG Disturbances in Poisoned Patients • Fast rate • Slow rate • Abnormal rhythm/pattern Focus: Underlying mechanism and patho-physiology

  3. Cardiovascular Physiology • Electrolyte movement and action potential

  4. Action potential of different cardiac muscle cells

  5. Normal Depolarization

  6. Normal Repolarization

  7. Cardiovascular Toxicity Mediated by affecting: • Calcium channel • Sodium channel • Potassium channel • Na-K-ATPase Pump • Electrolyte disturbances • Autonomic nervous system

  8. Adrenergic receptors

  9. Drug Induced Tachycardia 1 Enhanced SYM tone • Response to increases substrate requirement • Tissue hypoxia • Hypoglycaemia • Increased centrally mediated psychomotor activity CO Salicylates All stimulants

  10. Drug Induced Tachycardia 1 Enhanced SYM tone 2. SYM stimulation • Direct central activation • Direct peripheral Withdrawal Cocaine Amphetamine Theophylline

  11. Drug Induced Tachycardia 2 Reflexive Response • Response to contractility • Response to vasodilatation • Response to hypovolaemia TCA Salicylates

  12. Drug Induced Tachycardia 3 Parasympathetic antagonism • Antagonism of Ach receptors on the myocardium •  Release of Ach from the nerve terminal

  13. Drug Induced Tachycardia 4 Enhanced myocardial sensitization •  sensitivity to catecholamines • Predispose to tachycardia and arrhthymia Halogenated Hydrocarbon

  14. F: A: S: T: Free base or other forms of cocaine Anticholinergics, Antihistamines, Amphetamines, Antipsychotics Sympathomimetics, Solvent abuse Theophylline Mnemonics

  15. Drug Induced Bradycardia 1 Altered autonomic tone • Enhanced cholinergic tone • Increased central PARA tone • Cholinesterase inhibition Central Myocardial muscarinic Ach receptors Organophosphates

  16. Drug Induced Bradycardia 1 Altered autonomic tone • Altered SYM tone 1. 2. Clonidine/Imidazolines 3. Depletion of circulating catecholamines Sedative-hypnotic Central α2 agonism  SYM output

  17. Drug Induced Bradycardia 1 Reflex response • Baroreceptor reflex response to HT PPA

  18. Drug Induced Bradycardia 2 Toxicity on conduction and pacemakers • Mediated by affecting: • Na/K ATPase pump • Sodium channel • ß1 Adrenergic receptor • Potassium channel • Calcium channel

  19. Calcium Channel Blockers • Inhibits SA and AV nodal conduction resulting in bradycardia and heart block

  20. CCB Toxicity: Treatments • Atropine • Calcium • Catecholamines • Insulin • Glucagon • Phosphodiesterase inhibitor

  21. ß Blockers Toxicity • Decrease SA node function • Impaired AV conduction • Prolonged QRS (Membrane stabilizing activities) • Prolonged QT intervals (K channel Blockade)

  22. ß Blockers Toxicity: Treatment • Atropine • Glucagon • Calcium • Insulin • Catecholamines • Phosphodiesterase inhibitor

  23. P: A: C: E: D: Propranolol(ß-blockers), Poppies Anticholinesterase, Aconitine Clonidine, CCB, Ciguatera Ethanol or other alcohols Digoxin Mnemonics

  24. Arrhythmia Underlying mechanisms • Increased automaticity • Re-entry • Triggered automaticity • Delayed after depolarization • Early after depolarization

  25. Automaticity: Digoxin • Excessive elevation of the intracellular calcium elevates the resting potential • Producing increased automaticity

  26. Re-entry: Anti-dysrhythmic agents

  27. TCA Terminal right axis deviation • RBB is preferentially affected • Appearance of right ventricular force at the late phase of QRS

  28. Predictive Values QRS duration • Seizures: 0% if <100ms, 30% if >100ms • Ventricular dysrhythmias: 0% if <160ms, 50% if >160ms Boehnert M, N Eng J Med 1985 313;474-479

  29. Predictive Values • Amplitude of terminal R wave in aVR: RaVR3mm predicts seizures and dysrhythmia Liebelt EL Ann Emerg Med 1995;26:195-201 • Terminal R-axis deviation, prolonged QTc, sinus tachycardia: specific and sensitive for TCA OD Wolfe TR Ann Emerg Med 1989;18:348-351

  30. TCA: tachyarrhythmia VT Mechanisms • Non-uniform conduction slowing  Re-entry • Precipitated by hypoxia, tissue ischaemia and metabolic acidosis Sinus tachycardia plus aberrancy is more common

  31. Delayed After-depolarization • Normal depolarization is followed by an oscillation during phase 4 • Occurs with  intracellular Ca • E.g. Cardiac glycoside toxicity

  32. Digoxin Toxicity: Risks of treatment • Pacing: DAD amplitude • Overdrive supression: Useless in dysrhythmias due to automaticity • DC version: Risk of inducing VF/VT • Treatment choices: Atropine, Lignocaine, Phenytoin, Amiodarone *Digoxin antibody

  33. Early After-depolarization • Occurs during the downslope of phase 3 of the action potential • Occurs when cardiac action potential is markedly prolonged ( QTc)

  34. Drugs that cause QT prolongation

  35. Aconitine Toxicity •  Na influx through Na channel • Delay the final phase of repolarization and promote premature excitation • Expect Na channel blockers to be effective • Amiodarone, flecainide, procainamide have been reported to be successful in terminating ventricular dysrhthymias

  36. Treatment of Drug-induced ventricular dysrhythmias • NaHCO3 if widened QRS • Lignocaine for prolonged QT • Mg, DC version, Overdrive pacing for Torsades de pointes, correct e-

  37. Toxin Induced SVT • Usually mediated by sympathomimetic activity of drugs • Cardioversion • Adenosine: may not be effective for methylxanthines toxicity • CCB and ß-blockers: risks • Toxin removal

  38. Conclusion • Understanding the underlying patho-physiology of toxin induced arrhythmias improves our diagnosis and treatment of such problems

More Related