The ECG and Toxicology

Adam DavidsonJune 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

ECG 1:

ECG 2:

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

ECG 1:

ECG 2:

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?

ECG:

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

ECG:

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

ECG:

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?

Thank YOU!!!

References

ECG in Emergency Medicine and Critical Care

Chan, Brady, Harrigan, Ornato, Rosen

2005