10/9/2011
Complex ECGs The ECG & Hyperkalemia William J Brady, MD Department of Emergency Medicine University of Virginia
Hyperkalemia & The ECG Hyperkalemia & The ECG
• Hyperkalemia • Significant variation regarding –Slows impulse formation potassium level & clinical • Ectopic rhythms manifestation –Disrupts conduction – From person to person • Bradycardia – Past exposure • Blocks – Chronicity –Atrioventricular –Intraventricular
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Hyperkalemia & The ECG Hyperkalemia ECG Manifestations • Range of ECG findings • Peaking of T wave – Prominent T waves – Tall, narrow, symmetric – QRS complex widening – Interval prolongation (PR & QT) – Bradycardia / AV block – Ventricular dysrhythmias – Sinoventricular rhythm
Prominent T Wave Hyperkalemia Electrocardiographic Manifestations
• Widening of QRS complex – Disruption of conduction – Widening broad range • Minimal to maximal – Slow to rapid rhythms – Bundle branch block Best seen in the precordial leads mimic
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Widening of QRS Complex Widening of QRS Complex
More pronounced widening
Minimal widening
Bundle Branch Block Mimic Hyperkalemia Electrocardiographic Manifestations • Sinoventricular rhythm
• 52 female ESRD on hemodialysis • “Apparent RBBB” with LAFB • Serum potassium 7.9 • ECG abnormalities normalized with hyperkalemia therapy
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Sinoventricular Rhythm Hyperkalemia Treatment Goals
• Three primary goals • Stabilize the cardiac cell membrane • Transiently shift potassium into the cells • Remove potassium from the body
Slow, very wide QRS complex, absence of P waves
Hyperkalemia Hyperkalemia ECG Guided Management Management • Membrane stabilizer Calcium digoxin exclusion questioned? • Potassium shift Bicarbonate (only if pH <7.35) Glucose / insulin Adrenergic agonists Magnesium • Potassium removal Kayexelate Hemodialysis
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Response to Therapy Wide Complex
Sinoventricular Rhythm Tachycardia …. 15 minutes after therapy Sodium Channel Blocker Poisoning
Sinus Rhythm with Prominent T Waves
Sodium Channel Blocker Toxicity Sodium Channel Blocker Toxicity Broad range of toxins + • Amantadine • Imipramine • Blocks rapid influx of Na • Amitriptyline • Loxapine sodium into cell • Amoxapine • Maprotiline • Carbamazepine • Moricizine • Phase 0 of • Chloroquine • Nortriptyline action • Cocaine • Orphenadrine • Desipramine • Phenothiazines potential • Diltiazem • Procainamide is delayed • Diphenhydramine • Propranolol • Disopyramide • Propafenone • QRS complex • Doxepin • Propoxyphene • Encainide • Thioridazine widens • Flecainide • Quinidine • Hydroxychloroquine • Quinine
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Na+ Channel Blocker Toxicity 1 • What should you do now? M 2 – e Worry and do some thing….any thing, just a some thing. s u 0 Action Potential 3 – Not worry too much and perform serial ECGs. r e – Consider emergent therapy aimed at d myocardial stabilization and intracellular P o potassium shifting. t e + – Ponder the price of hog shares in Oklahoma. n Na Channel Blocker Toxicity t i a ECG l
(mv)
Time (mS)
Sodium Channel Blocker Toxicity TCA Toxicity Electrocardiographic Abnormalities • Multiple agents • CV events leading cause of fatal • Multiple effects outcome • Tricyclic antidepressant agents • ECG ab normaliti es preced e potent sodium channel blocker toxicity –Advance warning of impending end organ toxicity
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TCA Toxicity TCA Toxicity Electrocardiographic Abnormalities Electrocardiographic Abnormalities • Sinus tachycardia • Rightward shift of terminal QRS complex axis – Nonspecific – Specific for TCA / sodium channel blocker toxicity – Multifactorial • Electrocardiographic manifestation • QT interval prolongation – LSLarge S wave ildIin lead I / lRlarge R wave iVin aVr – Nonspecific – Late finding • QRS complex widening – Impending toxicity – Present by 3 6 hours Lead I Lead aVr Deep S wave Prominent R` wave
TCA Toxicity Hydroxychloroquine Ingestion Electrocardiographic Abnormalities over 45 minutes
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TCA / Cocaine Ingestion 38 year-old male 31 year old female Diphenhydramine ingestion Lethargic & tachycardia
Progressive improvement Over 45 minutes Sodium bicarbonate therapy
Sodium Channel Blocker Toxicity Management • Supportive care – ABCs Wolff Parkinson White • Early intubation Syndrome • SdiSodium bicarb onat e therapy –Bolus Dysrhythmias –Infusion
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WPW Syndrome The Accessory Pathway The ECG in Normal Sinus Rhythm
The Classic Triad -- Shortened PR interval -- Delta wave -- Widened QRS complex
Dysrhythmias Encountered Arrhythmias in WPW Syndrome Atrial fibrillation • 20 to 25% arrhythmias Arrhythmias Encountered in WPW Syndrome • Potentially malignant • Loss of AVN “rate control” • Irregular & very rapid rates AV Reciprocating Tachycardia Atrial Fibrillation Sudden Death • Wide QRS –exaggerated Delta ~ 70% ~ 25% <5% wave • Bizarre morphologies Narrow Complex Tachycardia Broad Complex Tachycardia • Occasional narrow QRS ~ 90% ~ 10% Orthodromic Antidromic
Narrow QRS Wide QRS Regular Regular
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Wide Complex Tachycardia Arrhythmias Atrial Fibrillation Narrow Complex Tachycardia • AVRT (AV re entrant tachycardia) • Orthodromic tachycardia • 65% of WPW dysrhythmias • AV conduction is antegrade • Rapid, regular • Narrow QRS complex • Indistinguishable from “typical” PSVT (AVNRT)
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Narrow Complex Tachycardia AVRT / Orthodromic Tachycardia
Arrhythmias Wide Complex Tachycardia • AVRT (AV re-entrant tachycardia) • Antidromic tachycardia • Rare - 5% • AV con duc tion i s ret rograd e • Malignant • Wide QRS – exaggerated Delta wave • Difficult to distinguish from VT
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Wide Complex Tachycardia AVRT / Antidromic Tachycardia WPW Syndrome Dysrhythmia Management
• Dependent on ECG & clinical situation • Unstable – electrical therapy • Stable – QRS complex – narrow vs wide – Regularity
WPW Syndrome Dysrhythmia Management WPW Syndrome Dysrhythmia Management Tachycardia • Narrow QRS complex QRS Width • Unstable – electrical • Stable -- standard therapy for NCT Wide Narrow – Adenosine – Beta- or calcium channel blocker Regular Irregular – +/- Procainamide – Electrical conversion Antidromic Atrial Fibrillation Orthodromic
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WPW Syndrome Dysrhythmia Management
• Wide QRS complex Left Bundle Branch Block – Regular – Irregular AMI • Unstable – electrical • Stable – Procainamide – Avoid AVN blocking agents – Electrical conversion
Left Bundle Branch Block Left Bundle Branch Block
Patients with LBBB pattern: Characteristics of LBBB If new QRS > 0.12 sec Candidates for fibrinolysis Mainly negative QS High risk for CHB, cardiogenic shock, & death or rS in lead V If old 1 Monophasic R wave in leads V , I & aVl Have significant, pre-existing LV dysfunction 6 High risk for death ST segment characteristics defined by the Rule of Appropriate May benefit significantly from acute Discordance revascularization therapies Leads w/ QS or rS complexes -- ST elevation Yet less often receive it Leads w/ large monophasic R wave -- ST depression
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Concordance / Discordance Appropriate Discordance QRS complex ST segment / T wave Expected ST Segment Relationshships
B “Normal”
A Discordance major, terminal portion of QRS complex (“A”) & ST segment / T wave (“B”) A opposite sides of baseline B
NEJM 1996; 334(8):481-487
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Concordance LBBB with Electrocardiographic AMI
Concordance LBBB with Electrocardiographic AMI
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“Excessive” Discordance LBBB with Electrocardiographic AMI
Evolving AMI with LBB 0850 And what about RBBB?
0903
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• May also hinder ECG diagnosis – Not due to electrophysiologic issues – Resulting from interpretative errors
• Age of RBBB – Chronicity not an issue for fibrinolysis – ECG can be interpreted – consider ST segments – Marker for poor outcome
• NRMI 2 registry – RBBB pattern in approximately 6% of AMI patients – Less often received fibrinolysis – Increased poor outcome [64% increased odds ratio of death] • Worse than LBBB!
RBBB with Anterior Wall STEMI RBBB with Anterior Wall STEMI
0037
0129
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William J. Brady, M.D. [email protected] THE END
THANKS
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