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10/9/2011

ComplexECGs TheECG&
Hyperkalemia
WilliamJBrady,MD
DepartmentofEmergencyMedicine
UniversityofVirginia

wjbrady@virginia.edu

Hyperkalemia&TheECG Hyperkalemia&TheECG
• Hyperkalemia • Significantvariationregarding
–Slowsimpulseformation potassiumlevel&clinical
• Ectopicrhythms
Ectopic rhythms manifestation
–Disruptsconduction – Frompersontoperson
• Bradycardia – Pastexposure
• Blocks – Chronicity
–Atrioventricular
–Intraventricular

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Hyperkalemia&TheECG Hyperkalemia
ECGManifestations
• RangeofECGfindings
• PeakingofTwave
– ProminentTwaves
– Tall,narrow,symmetric
– QRScomplexwidening
– Intervalprolongation(PR&QT)
– Bradycardia/AVblock
– Ventriculardysrhythmias
– Sinoventricularrhythm

ProminentTWave Hyperkalemia
ElectrocardiographicManifestations

• WideningofQRS
complex
– Disruptionofconduction
Disruption of conduction
– Widening broadrange
• Minimaltomaximal
– Slowtorapidrhythms
– Bundlebranchblock
Best seen in the precordial leads
mimic

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WideningofQRSComplex WideningofQRSComplex

More pronounced
widening

Minimal widening

BundleBranchBlockMimic Hyperkalemia
ElectrocardiographicManifestations
• Sinoventricularrhythm

• 52femaleESRDonhemodialysis
• “ApparentRBBB”withLAFB
• Serumpotassium7.9
• ECGabnormalitiesnormalizedwithhyperkalemia
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
ECGGuidedManagement
Management
• Membranestabilizer
Calcium digoxinexclusionquestioned?
• Potassiumshift
Potassium shift
Bicarbonate(onlyifpH<7.35) Glucose/insulin
Adrenergicagonists Magnesium
• Potassiumremoval
Kayexelate Hemodialysis

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Response to Therapy

WideComplex
Sinoventricular Rhythm Tachycardia
…. 15 minutes after therapy SodiumChannelBlocker
Poisoning

Sinus Rhythm with Prominent T Waves

SodiumChannelBlockerToxicity SodiumChannelBlockerToxicity
Broadrangeoftoxins
• Amantadine • Imipramine • Blocksrapidinfluxof Na+
• Amitriptyline • Loxapine sodiumintocell
• Amoxapine • Maprotiline
• Carbamazepine • Moricizine • Phase0of
• Chloroquine • Nortriptyline
• Cocaine • Orphenadrine
action
action
• Desipramine • Phenothiazines potential
• Diltiazem • Procainamide isdelayed
• Diphenhydramine • Propranolol
• Disopyramide • Propafenone • QRScomplex
• Doxepin • Propoxyphene
• Encainide • Thioridazine
widens
• Flecainide • Quinidine
• Hydroxychloroquine • Quinine

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Na+ Channel Blocker Toxicity


1
• Whatshouldyoudonow? M
2
– Worryanddosomething….anything,just e
a
something. s
u 0 Action Potential 3
– NotworrytoomuchandperformserialECGs. r
e
– Consideremergenttherapyaimedat d

myocardial stabilization and intracellular


myocardialstabilizationandintracellular P
o
potassiumshifting. t
e
– PonderthepriceofhogsharesinOklahoma. n Na+ Channel Blocker Toxicity
t
i
a ECG
l

(mv)

Time (mS)

SodiumChannelBlockerToxicity TCAToxicity
ElectrocardiographicAbnormalities
• Multipleagents • CVevents leadingcauseoffatal
• Multipleeffects outcome
• Tricyclicantidepressantagents
Tricyclic antidepressant agents • ECGabnormalitiesprecede
ECG b liti d
potentsodiumchannelblocker toxicity
–Advancewarningofimpending
endorgantoxicity

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TCAToxicity TCAToxicity
ElectrocardiographicAbnormalities ElectrocardiographicAbnormalities
• Sinustachycardia
• RightwardshiftofterminalQRScomplexaxis
– Nonspecific
– SpecificforTCA/sodiumchannelblockertoxicity
– Multifactorial
• Electrocardiographicmanifestation
• QTintervalprolongation
QT interval prolongation – LLargeSwaveinleadI/
S i l d I / llargeRwaveinaVr
R i V
– Nonspecific
– Latefinding
• QRScomplexwidening
– Impendingtoxicity
– Presentby3 6hours Lead I
Deep S wave
Lead aVr
Prominent R` wave

TCAToxicity HydroxychloroquineIngestion
ElectrocardiographicAbnormalities over45minutes

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TCA/CocaineIngestion 38 year-old male


31yearoldfemale Diphenhydramine ingestion
Lethargic & tachycardia

Progressive improvement
Over 45 minutes
Sodium bicarbonate therapy

SodiumChannelBlockerToxicity
Management
• Supportivecare– ABCs WolffParkinsonWhite
• Earlyintubation Syndrome
• Sodiumbicarbonatetherapy
S di bi b t th
–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
• 20to25%arrhythmias
Arrhythmias Encountered in WPW Syndrome • Potentiallymalignant
• LossofAVN“ratecontrol”
• Irregular&veryrapidrates
AV Reciprocating Tachycardia Atrial Fibrillation Sudden Death
• Wide QRS –exaggerated
WideQRS exaggeratedDelta
Delta
~ 70% ~ 25% < 5%
wave
• Bizarremorphologies
Narrow Complex Tachycardia Broad Complex Tachycardia • OccasionalnarrowQRS
~ 90% ~ 10%
Orthodromic Antidromic

Narrow QRS Wide QRS


Regular Regular

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Wide Complex Tachycardia Arrhythmias


Atrial Fibrillation Narrow Complex Tachycardia
• AVRT(AVreentranttachycardia)
• Orthodromictachycardia
• 65%ofWPWdysrhythmias
• AVconductionisantegrade
• Rapid,regular
• NarrowQRScomplex
• Indistinguishablefrom“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 conduction
d ti is
i retrograde
t d
• 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
QRSWidth
• 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 LeftBundleBranchBlock


– Regular
– Irregular AMI
• Unstable – electrical
• Stable
– Procainamide
– Avoid AVN blocking agents
– Electrical conversion

LeftBundleBranchBlock LeftBundle
BranchBlock
ƒ Patients with LBBB pattern: ƒ Characteristics of LBBB
ƒ If new ƒ QRS > 0.12 sec
 Candidates for fibrinolysis ƒ Mainly negative QS
 High risk for CHB, cardiogenic shock, & death or rS in lead V1
ƒ If old
ƒ Monophasic R wave in leads V6, I & aVl
 Have significant, pre-existing LV dysfunction
ƒ ST segment characteristics defined by the Rule of Appropriate
 High risk for death
ƒ May benefit significantly from acute Discordance
revascularization therapies ƒ Leads w/ QS or rS complexes -- ST elevation
ƒ Yet less often receive it ƒ Leads w/ large monophasic R wave -- ST depression

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Concordance/Discordance AppropriateDiscordance
QRScomplex STsegment/Twave ExpectedSTSegmentRelationshships

B
ƒ “Normal”

ƒ Discordance  major,terminal
A

portionofQRScomplex(“A”)&
STsegment/Twave(“B”)
A
oppositesidesofbaseline B

NEJM 1996; 334(8):481-487

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Concordance
LBBBwithElectrocardiographicAMI

Concordance
LBBBwithElectrocardiographicAMI

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“Excessive”Discordance
LBBBwithElectrocardiographicAMI

EvolvingAMIwithLBB
0850
Andwhatabout
RBBB?
0903

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• MayalsohinderECGdiagnosis
– Notduetoelectrophysiologic issues
– Resultingfrominterpretativeerrors

• AgeofRBBB
– Chronicity notanissueforfibrinolysis
not an issue for fibrinolysis
– ECGcanbeinterpreted– considerSTsegments
– Markerforpooroutcome

• NRMI2registry
– RBBBpatterninapproximately6%ofAMIpatients
– Lessoftenreceivedfibrinolysis
– Increasedpooroutcome[64%increasedoddsratioofdeath]
• WorsethanLBBB!

RBBBwithAnteriorWallSTEMI
RBBBwithAnteriorWallSTEMI

0037

0129

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William J. Brady, M.D.


wjbrady@virginia.edu
THE END

THANKS

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