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Toxicology and the ECG
This document discusses toxicology and ECG interpretation in poisoned patients. It provides an overview of the cardiac conduction system and how specific drugs can affect it. Drugs that block sodium channels can cause a wide QRS complex, while potassium channel blockers prolong the QT interval and increase risk of Torsades de Pointes. A systematic approach to ECG interpretation is outlined, examining rate, rhythms, intervals, and morphology. Management strategies are presented for various cardiotoxic drugs like beta blockers, calcium channel blockers, sodium channel blockers, and cardiac glycosides.
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Toxicology and the ECG
- 1. Toxicology and theECG Andy Steval 16/03/2016
- 2. Contents • Refresher ofcardiac physiology • Specific toxic effects of drugs on the myocardium • Approach to ECG interpretation in the toxic patient • Management of specific cardiotoxic drugs
- 3. The Cardiac ConductionSystem
- 4. The Cardiac ConductionSystem ( 1 . )
- 5. The Cardiac ConductionSystem Na+ efflux Na+ influx Ca2+ influx K+ efflux
- 6. The Cardiac ConductionSystem
- 7. Specific toxic effectsof drugs on the myocardium
- 8. • Blockage ofsodium channels results in increased slope of phase 0 • This results in a wide QRS and altered morphology • Often a positive R wave in AvR and RBBB ( 2 . )
- 9. • Blockage ofpotassium channels results in lengthening of phase 2 and 3 • This gives rises to a long QT and the potential for Torsades de Pointes
- 10. Beta-Blockade • Beta-blockers causebradycardia through blockage of B1 receptors • This reduces levels of cAMP and intracellular calcium • Slope of pre-potential (phase 4) is reduced • Often cause AV conduction disturbance (increased PR interval /heart block) and bradycardia Beta-blocked Normal
- 11. Calcium Channel Blockade •Calcum Channel blockers cause bradycardia through impaired influx of calcium • Slope of phase 0 is decreased • Often cause AV conduction disturbance and bradycardia
- 12. Approach to theECG in a poisoned patient • Rate/Rhythm • PR interval • QRS interval and morphology • QT interval • ST Segments
- 13. Rate/Rhythm • Bradycardia –Suggests poisoning with: • Calcium channel/beta blockers/Digoxin (AV block) • Opioids/Ethanol • Organophosphates • Lithium • Tachycardia – suggests poisoning with: • Sympathomimetics e.g. methamphetamine • Anticholinergics e.g. antidepressants, antipsychotics • Group 1a and 1c antiarrhythmics, TCAs • Enhanced automaticity – suggests digoxin/sympathomimetic toxicity
- 14. • Ventricular bigeminy •AF, irregular rhythm • Frequent ectopics Digoxin Overdose (3.)
- 15. PR Interval • ProlongedPR interval may indicate Calcium channel blockade, beta blockade or digoxin toxicity. • Other drugs include Opioids, clonidine, sedative-hypnotics • All of these may increase vagal tone or antagonise sympathetic system • May present with purely 1st degree block or progress to complete heart block.
- 16. • Junctional Bradycardia •No P-waves. • Rate 30, regular Verapamil overdose
- 17. QRS Interval • Usuallycaused by drugs that block sodium channels e.g. TCA’s, Class 1A anti-arrhythmics, carbamazepine • QRS of over 100ms in young individuals in considered abnormal • Right bundle branch is preferentially blocked, leading to prominent R wave in AVR and RBBB.
- 18. • Regular Tachycardia •Broad QRS • Terminal R wave in AvR > 3mm • RBBB TCA Overdose
- 19. • 1st DegreeHeart Block • Broad QRS complex • Positive R wave in AvR Flecanide overdose (Also seen in propranolol overdose but patient would be more bradycardic )
- 20. QT Interval • QTprolongation usually caused by potassium blocking agents as previously discussed • Measure from the beginning of the QRS to the end of the T- wave
- 21. QT Interval • Intoxicology, the absolute QT is a better predictor of Torsades risk then the corrected QT (QTc) • Therefore, it is best to use the QT nomogram to predict risk • Drugs that cause tachycardia (e.g. Quetiapine) are less likely to cause Torsades than drugs causing bradycardia
- 22. Albuterol Erythromycin* Phentermine AmantadineEscitalopram Phenylephrine Amiodarone* Fenfluramine Phenylpropanolamine Amitriptyline Flecainide Procainamide* Dextroamphetamine Fluconazole Protriptyline Amphetamine Fluoxetine Pseudoephedrine Arsenic trioxide* Fosphenytoin Quetiapine Astemizole * Gatifloxacin Quinidine* Atomoxetine Gemifloxacin Risperidone Azithromycin Haloperidol* Ritodrine Chloral hydrate Ibutilide* Ritonavir Chloroquine* Imipramine Salmeterol Chlorpromazine* Isoproterenol Sertindole Ciprofloxacin Itraconazole Sertraline Cisapride* Ketoconazole Sotalol* Citalopram Levalbuterol Sparfloxacin* Clarithromycin*Levofloxacin Tacrolimus Clomipramine Lithium Tamoxifen Clozapine Methadone * Telithromycin Cocaine Methylphenidate Terbutaline Desipramine Mexiletine Terfenadine* Dexmethylphenidate Midodrine Thioridazine* Diphenhydramine Moxifloxacin Tizanidine Dobutamine Nicardipine Trazodone Domperidone * NorepinephrineTrimethoprim-Sulfa Dopamine Nortriptyline Trimipramine Doxepin Ofloxacin Vardenafil Droperidol * Ondansetron Venlafaxine Ephedrine Paroxetine Ziprasidone Epinephrine Pentamidine* Some drugs that prolong QT
- 23.
- 24. Resus-RSI-DEAD • Resuscitation • Riskassessment • Supportive care • Investigations • Decontamination • Enhanced Elimination • Antidotes • Disposition
- 25. Beta-blocker overdose • Usuallypresent with bradycardia, varying AV block. • Special consideration to propranolol (sodium channel blocking effects) and sotalol (K+ channel blocking effects) • Hypotension: Fluid resuscitation, vasopressors • Bradycardia: Atropine, beta-agonists e.g. isoprenaline infusion • Specific antidotes: High dose insulin euglycaemic therapy. Glucagon infusion (inferior to HIET)
- 26. Calcium Channel blockade •Usually present with bradycardia, varying AV block, myocardial depression, hyperglycaemia • Hypotension: Fluid resuscitation, cardiac inotropes, vasopressors, ECMO • Bradycardia: Atropine, pacing • Specific antidotes: Calcium gluconate bolus, High dose insulin euglycaemic therapy.
- 27. Sodium Channel Blockade/QRS widening Evidencelargely derived from TCA poisoning • Sodium Bicarbonate therapy: (Repeat bolus +- infusion) 1. Increases sodium load within cardiac cells to help reverse blockade 2. Causes serum alkalisation which may help remove drug by increased protein binding • Hyperventilation • Aim to correct PH to 7.5-7.55
- 28. Drug-induced QT prolongation Maycause life-threatening arrhythmias e.g. Torsades De Pointes. Onset Proceeded by U-waves, Ventricular ectopics, Runs of VT. • Magnesium sulphate bolus/infusion • Electrolyte correction • DC Cardioversion if life-threatening arrhythmia develops
- 29. Bidirectional VT • Regular,broad complex tachycardia • 180 degree alterational of QRS axis every beat
- 30. Cardiac glycoside toxicity Maypresent with variable ECG changes: Increased automaticity, AV blockade, Arrhythmia, Bidirectional VT Toxicity can be acute or chronic • Mild toxicity • Mild symptoms without serious ECG changes • Supportive care, cardiac monitoring • Severe toxicity: Digoxin-specific Fab
- 31. Summary • Use astep-wise approach when interpreting the toxicological ECG do avoid missing subtle changes. • Manage using the R-RSI-DEAD mnemonic • Don’t forget standard ABC resuscitation when dealing with the cardiotoxic patient
- 32. References 1. OpenStax CNXAnatomy and physiology http://cnx.org/contents/FPtK1zmh@6.27:MCgS6S0t@3/Cardiac-Muscle-and- Electrical- 1. Utility of the Electrocardiogram in Drug Overdose and Poisoning: Theoretical Considerations and Clinical Implications Christopher Yates1, Alex F Manini. Curr Cardiol Rev. 2012 May; 8(2): 137–151. 2. Life in the Fast Lane: http://lifeinthefastlane.com/ecg-library/basics/