1. The ECG and Toxicology Adam Davidson June 4, 2009

2. Toxicologic Window While many toxic ECG changes are non- specific, it can be helpful with the diagnosis in certain cases The ECG often our first clue to a “toxic” patient Easy to get and available before blood work, urine, etc Can be used to guide and monitor therapy

3. Objectives Review cases highlighting ECG changes for some specific overdoses Discuss the ECG as a guide predicting toxicity with TCA overdose Discuss the ECG as a guide for therapy in the TCA overdose

4. Case 1 74 yo M presents with altered mental status Vitals: HR 38, BP 110/55, Afeb, SaO2 97% PMHx: HTN, CHF, Oteoarthritis Meds: Unknown

5. ECG 1:

6. ECG 2:

7. Digoxin ECG changes when “therapeutic” and toxic Classic Toxicity: Increased automaticity with AV block Bi-directional V tach (rare) Dig Effect: T Wave flattening/inversion/biphasic ST scooping (Salvador Dali) QT shortening PR prolongation

8. Dig Toxicity Ectopic Rythms Atrial tach with block Junctional Tach V tach (Uni and bi-directional) Conducction AV blocks Automaticity PVS’s, PAC’s

9. Case 2: 74 yo M presents with collapse and altered mental status Vitals: Afeb, HR 34, BP 84/40, SaO2 97% PMHx: Atrial fibrillation

10. ECG 1:

11. ECG 2:

12. Beta-Blockers ECG Findings Sinus Brady AV blockade Special Cases Propanolol: -Na Channel Blockade (Wide QRS) Sotalol: -K Channel Blockade (Prolonged QT and risk for Torsades)

13. CCB’s At toxic levels the selectivity of the drugs is lost All types will have both cardiac and vascular effects at high doses ECG abnormalities can be delayed b/c of sustained-release tabs

14. CCB’s vs BB’s CCB assoc with hyperglycemia BB assoc with euglycemia or mild hypoglycemia Mental status is often preserved w/ CCB’s

15. Case #2 cont’d What if case #2 had a PMHx of chronic kidney disease instead of A fib?

16. ECG:

17. DDx Hypotension and Bradycardia The Big 4: BB’s CCB’s MI Hyper K

18. Case #3 44 yo F presents confused and tremulous Vitals: Afeb, HR 53, BP 110/65, SaO2 100% REDIS History: mulitple psych visits NeuroExam: hyper-reflexia, clonus, mild ataxia

19. ECG:

20. Lithium Toxicity Acute toxicity associated with GI, Neuro and Cardiac findings ECG: T wave flattening/inversion- present in many patients at “therapeutic levels” Diffuse TWI suggests severe toxicity U Waves Sinus Node Dysfunction- bradycardia and junctional escape rythms Ventricular dysrhythmias are rare

21. Case #4 38 yo M presents after witnessed seizure Vitals: Afeb, HR 112, BP 143/94, SaO2: 99% PMHx: Depression, Insomnia

22. ECG:

23. TCA Overdose Amitriptyline increasing in use for insomnia, migraines, chronic pain Toxic effects are neurologic and cardiac ECG is the #1 test to predict toxicity, guide, and monitor therapy

24. Rick Morris Pimp Question SEVEN!!!! Re-uptake inhibition of Serotonin Re-uptake inhibition of Norepinephrine Na Channel Blockade Alpha blockade Anti-cholinergic Anti-histaminic Anti-GABA How many different receptors/neurotransmitters are affected by TCA’s? Can you name them?

25. ECG Effects of TCA’s Sinus tachycardia Widening of QRS Rightward deviation of terminal 40msec: seen as R wave in AVR and S waves in I and AVL Not specific for toxicity in children QT prolongation RBBB

26. Predicting Toxicity QRS > 120- high risk for seizures QRS > 160- high risk for dysrythmia QRS > 100- generally considered the threshold to start HCO3 therapy AVR R wave >3mm 81% sens, 73% sp for szr or dysrythmia AVR R wave >5mm 50% sens, 97% sp for szr or dysrythmia

27. Sodium Bicarbonate Initial Treatment? How do you prepare a drip? Why does it work? What are your end points of therapy?

28. Thank YOU!!!

29. References ECG in Emergency Medicine and Critical Care Chan, Brady, Harrigan, Ornato, Rosen 2005