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The ECG and Toxicology. Adam Davidson June 4, 2009. 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
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The ECG and Toxicology Adam Davidson June 4, 2009
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
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
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
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
Dig Toxicity • Ectopic Rythms • Atrial tach with block • Junctional Tach • V tach (Uni and bi-directional) • Conducction • AV blocks • Automaticity • PVS’s, PAC’s
Case 2: • 74 yo M presents with collapse and altered mental status • Vitals: Afeb, HR 34, BP 84/40, SaO2 97% • PMHx: Atrial fibrillation
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)
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
CCB’s vs BB’s • CCB assoc with hyperglycemia • BB assoc with euglycemia or mild hypoglycemia • Mental status is often preserved w/ CCB’s
Case #2 cont’d • What if case #2 had a PMHx of chronic kidney disease instead of A fib?
DDx Hypotension and Bradycardia • The Big 4: • BB’s • CCB’s • MI • Hyper K
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
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
Case #4 • 38 yo M presents after witnessed seizure • Vitals: Afeb, HR 112, BP 143/94, SaO2: 99% • PMHx: Depression, Insomnia
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
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?
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
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
Sodium Bicarbonate • Initial Treatment? • How do you prepare a drip? • Why does it work? • What are your end points of therapy?
References • ECG in Emergency Medicine and Critical Care • Chan, Brady, Harrigan, Ornato, Rosen • 2005