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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.

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Drug Induced Arrhythmia

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  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

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