The ECG and Toxicology
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Transcript of The ECG and Toxicology
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The ECG and Toxicology
Adam DavidsonJune 4, 2009
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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
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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
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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
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ECG 1:
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ECG 2:
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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
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Dig Toxicity Ectopic Rythms
Atrial tach with block Junctional Tach V tach (Uni and bi-directional)
Conducction AV blocks
Automaticity PVS’s, PAC’s
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Case 2:
74 yo M presents with collapse and altered mental status
Vitals: Afeb, HR 34, BP 84/40, SaO2 97%
PMHx: Atrial fibrillation
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ECG 1:
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ECG 2:
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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)
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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
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CCB’s vs BB’s
CCB assoc with hyperglycemia BB assoc with euglycemia or mild
hypoglycemia Mental status is often preserved w/
CCB’s
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Case #2 cont’d
What if case #2 had a PMHx of chronic kidney disease instead of A fib?
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ECG:
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DDx Hypotension and Bradycardia
The Big 4: BB’s CCB’s MI Hyper K
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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
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ECG:
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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
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Case #4
38 yo M presents after witnessed seizure
Vitals: Afeb, HR 112, BP 143/94, SaO2: 99%
PMHx: Depression, Insomnia
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ECG:
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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
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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?
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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
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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
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Sodium Bicarbonate
Initial Treatment? How do you prepare a drip? Why does it work? What are your end points of
therapy?
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Thank YOU!!!
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References
ECG in Emergency Medicine and Critical Care
Chan, Brady, Harrigan, Ornato, Rosen
2005