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.

1. Toxicology and the ECG
Andy Steval 16/03/2016

2. Contents
• Refresher of cardiac 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 Conduction System

4. The Cardiac Conduction System
(
1
.
)

5. The Cardiac Conduction System
Na+
efflux
Na+ influx
Ca2+ influx
K+ efflux

6. The Cardiac Conduction System

7. Specific toxic effects of drugs
on the myocardium

8. • Blockage of sodium
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 of potassium
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 cause bradycardia 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 the ECG 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
• Prolonged PR 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
• Usually caused 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 Degree Heart 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
• QT prolongation 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
• In toxicology, 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
Amantadine Escitalopram 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. Management of specific
cardiotoxic drugs

24. Resus-RSI-DEAD
• Resuscitation
• Risk assessment
• Supportive care
• Investigations
• Decontamination
• Enhanced Elimination
• Antidotes
• Disposition

25. Beta-blocker overdose
• Usually present 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
Evidence largely 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
May cause 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
May present 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 a step-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 CNX Anatomy 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/