advanced ecg interpretation
TRANSCRIPT
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ADVANCED ECGINTERPRETATION
Micelle J. Haydel, M.D.
LSU New Orleans
Emergency Medicine
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Image Sources
My patients
www.ecglibrary.com
The Alan E. Lindsay Ecg Learning Centerhttp://medlib.med.utah.edu/kw/ecg/intro.html
The EKG of the week from NCEMI http://www.ncemi.org
Emergency Medicine Education http://www.emedu.org
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Normal EKG
Axis determination
Blocks
Bundle branch blocks
Nodal blocks
Dysrhythmias
Patterns of Infarction
EKG CASES
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NORMAL EKG
P wave: atrial activity
Q wave: first downwarddeflection from
isoelectric line (t-p) R wave: first upwarddeflection fromisoelectric line
S wave: second
downward deflection
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NORMAL EKG
rS: small upward deflection, and largedownward deflection
Qr: large downward deflection, and small
upward deflection
qRs: small downward deflection, large
upward deflection, and small downward
deflection
Rs: large upward deflection, and small
downward deflection
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AXIS: NORMAL EKG - positive polarity(tall R) in inferior an
lateral leads with increasing positive polarity (r-wave
progression) across the precordium V1-6
AVF
I
II
III
AVL
V1
V2
V3
V4
V5
V6
AVR
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In a normal patient the only leads that should have
negative polarity are AVR and V1-2
AVF
I
II
III
AVL
V1
V2
V3
V4
V5
V6
AVR
---To determine axis: Look at leads I and AVF
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LAD - negative polarity (rS) in AVF
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RAD: negative polarity(rS) in lead I
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Severe RAD, negative polarity(rS) in 1& AVF
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Left axis deviation - negative QRS in lead AVF
Right axis deviation - negative QRS in lead I
Severe Right axis deviation negative QRS inBOTHlead I
and AVF
Quick & Easy AXIS DETERMINATION
AVF
AVF
AVF
AVF
AVF
AVF
I
I
I
I
I
I
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Why do we care about axis determination
in the ER?
Differential Diagnosis
LAD : LBBB, LAFB, Mechanical shift due to ascites or
elevated diaphragm, left atrial hypertrophy
RAD : RBBB, LPFB, right ventricular hypertrophy,dextrocardia, Pulmonary Embolism
Both RAD and LAD can be caused by COPD,Hyperkalemia, MI, WPW
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LAD
Note negativepolarity in
AVF
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RAD
Note negative
polarity (rS) inI
Severe RAD
Note negative
polarity (rS) inI & AVF
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BUNDLE BRANCH BLOCKS
Unifascicular
Right BBB
Left Hemiblocks
Left anterior OR
Left posterior
Bifascicular Left BBB (implies both
hemiblocks present)
Right BBBPLUS
Left anterior
Left posterior
Trifascicular
BifasicularPLUS AV
nodal block
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Right Bundle Branch Block
QRS > 0.12 sec
Predominantly
positive rSR in
V 1-2
Wide slurred S inlead I
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LEFT BUNDLE BRANCH BLOCKLeft bundle branch block
(Both fascicles are
blocked) QRS > 0.12 sec
Deep S in V 1-3
Tall R and RsR in lateral
leads: I, AVL, & V5-6
Left bundle divides into anterior and posterior branches
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Left bundle divides into anterior and posterior branches
Left anterior fascicular
block
Left axis deviation:
negative polarity (rS) of
AVF
rS waves in Inferior leads
Small Q in I (qR)
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Left posterior fascicular block
Right axis deviation
RAD = negativepolarity (rS) ofLead I
Small Q inIII (qR)
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BIFASCICULAR BLOCKS
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BIFASCICULAR BLOCKSRight bundle branch
block associated
with Left posterior
fascicular block --uncommon
RBBB
RADrS I
plus qR III
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SA BLOCK Sinus pause : 1 - 2 second pause
sinus beat resumes
Sinus arrest : > 2 seconds
junctional escape beat intervenes at 40-55 bpm
ventricular escape beat at 20 -40 bpm
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AV-BLOCKS 1st degree - PR > 0.2 sec
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AV-BLOCKS 2nd degree
Mobitz I (Wenckebach) PR increases until a QRS is blocked
dropped
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AV-BLOCKS 2nd degree
Mobitz II - blocked QRS (2:1, 3:1, 4:1) PR interval is fixed and usually normal, then p-waves with
dropped beats
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AV-BLOCKS 3rd degree - disassociation of PP and RR, the PP
intervals and RR intervals are constant.
RRPP
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PEARLS
Differential diagnosis for slow irregularly irregular rhythm Second Degree heart block : wenckebach
Third Degree heart block
If you see Left Axis Deviation, think about LAFB
If you see Right Axis Deviation, think about LPFB
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TYPES OF DYSRHYTHMIAS
Re-entry (SVT, WPW) Two parallel pathways with different rates and refractory
periods
Something alters the refractory period and the alternative
pathway becomes dominant
This causes a unidirectional conduction block, and a circuitousconduction pathway forms.
PAC
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TYPES OF DYSRHYTHMIAS
Enhanced or Triggered (PACs, PVCs, Afib,MFAT)
Conduction cells act as Pacemaker cells
Conduction cells can be enhanced and become dominant in
the setting of ischemia, sepsis, electrolyte imbalance or
toxins. Some dysrhythmias start with enhanced or triggered
activity, but follow a circuitous pathway seen in re-
entry. (Atrial flutter, Vtach)
A 60 yo with COPD c/o palpitations & SOB. The EKG shows:
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a. Atrial Fibrillation
b. Premature Atrial Complexes
c. Multi-Focal Atrial Tachycardia
d. Paroxismal Atrial Tachycardia with block
MULTIFOCAL ATRIAL TACHYCARDIA (MFAT)
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MULTIFOCAL ATRIAL TACHYCARDIA (MFAT) P waves of at least 3 different shapes
No dominant atrial pacemaker
Rate greater than 100 bpm
Varying PR, RR, and PP intervals Enhanced or triggered automaticity
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MULTIFOCAL ATRIAL TACHYCARDIA (MFAT)
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U OC C C ( ) P waves of at least 3 different shapes
No dominant atrial pacemaker
Rate greater than 100 bpm
Varying PR, RR, and PP intervals
A 56 year old presents with palpitations. EKG shows:
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a. Atrial fibrillation
b. Atrial flutter
c. Left anterior fasicular block
d. RBBB
B. ATRIAL FLUTTER : Rapid, regular flutter (F) waves at 250-3
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p , g ( )per minute (ventricular conduction 1:2, ie ~150bpm)
Sawtooth pattern of F waves in leads 2, 3 and AVF
Little evidence of atrial activity in lead 1
AV conduction variable, QRS typically normal width
Enhanced automaticity leading to circuitous conduction/reentry
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ATRIAL FLUTTER -
TREATMENT Atrial flutter is the most
electrosensitive of all
dysrhythmias therefore
cardioversion is the
treatment of choice for
conversion to sinus rhythm.
Drug of choice forrate
controlis Calcium channel
blockers.
Drug of choice fordiagnostic
purposes is Adenosine (as
long as QRS is narrow
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Atrial flutter with 2:1 conduction is often
confused with SVT
But, look for the sawtooth flutter waves in the inferior leads.
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Same patient after adenosine,
showing prominent flutter waves.
A 46 year old presents with palpitations. EKG shows:At i l fib ill ti
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a. Atrial fibrillation
b. Atrial flutter
c. Left anterior fasicular block
d. RBBB
EKG shows: a. Atrial fibrillation
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Prominent fibrillatory waves in V 1-3 & AVF
Irregular ventricular response, greater than 100 / min
Ventricular rate less than 100 implies AV blockTriggered/enhanced automaticity
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ATRIAL FIBRILLATION - treatment
Cardiovert if unstable Ca Channel Blocker- Drug of
choice for rate control
Beta blocker
Digitalis
ASA alone for afib < 48h
ASA & Anti-coagulate all
others, if unknown or >48h
the longer the patient has been in afib, the less likely you will be able to convert to NSR
Ashmans phenomenonshort runs of wide complex tachycardia
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during rapid atrial fibrillation.
The refractory period is rate-related, and when erratic changes in rate
occur, an impulse conducted during the refractory period will have anaberrant (RBBB) pattern.
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The most common dysrhythmia associated
with digitalis toxicity is:
A. Paroxysmal atrial tachycardia with AV nodal block
B. Premature ventricular contractions
C. Second degree AV nodal blocks
D. Ventricular tachycardia
E. Junctional tachycardia
DIGITALIS TOXICITY
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DIGITALIS TOXICITY -
DYSRHYTHMIAS
Most common : b. PVCs
Most pathognomonic : PAT w/block
Others
AV nodal blocks
sinus bradycardia, pause, SA block
junctional escape beats or tachycardia
Ectopic SVT, V-tach, V-fib
Paroxysmal atrial tachycardia with block is pathognomonic fordigitalis toxicity
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digitalis toxicity.
Note the p waves at a rate > 100 & blocked QRS complexes.(Dont mistake for aflutter with variable conduction or 3rd degree block)
Note the blocked
Impulses!!
A 23 yo male with c/o palpitations, EKG shows:
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a. Atrial fibrillation
b. MFAT
c. SVT
d. PAT with block
His EKG shows c. SVT or AV nodal reentry tachycardia with
i & Q S
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rapid, regular rate, absent p waves & narrow QRS complexes
AV nodal Re-entry tachycardia/SVT
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AV
SA
y yTwo parallel pathways with different
rates and refractory periods
Something alters the refractory
period and the alternative pathway
becomes dominant
This causes a unidirectional
conduction block, and a circuitous
conduction pathway forms.
AV nodal Re-entry tachycardia/SVT
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AV
SA
y y
The circuitous impulse is
typically transmitted anterograde(forward) over the relatively
slow AV nodal fibers, limiting
the rate to 200bpm.
WHATS THE BIGDEAL???
Treat by blocking the AV node
and allowing the normal
pacemaker to resume.
Adenosine
Ca channel blocker
Beta blocker
SVT with Aberrancy (rate-related block)
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AV
SA
SVT with aberrancy is a
supraventricular
tachycardia with a wide-
complex QRS due to a rate-
related bundle branch
block.
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44yo with complaint of palpitations and shortness of breath, ekg shows:
a. SVT with aberrancy
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b. Ashmans phenomenon
c. WPW
d. V-tach
C. The EKG is WPW w/ retrograde conduction causing wide QRS.
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Because the etiology of a wide complex tachydysrhythmia is often
unknown in the ER, treat with amiodarone, procainamide, lidocaine
or cardioversion. (avoid procainamide in TCA OD or prolonged qt toursades)
Pre-Excitation Syndromes-
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Pre-Excitation Syndromes-
WPW & LGL Accessory pathway connects atria to the ventricles,
bypassing the AV node
Wolff-Parkinson-White: short PR (< 0.12 s), Delta
wave (slurred upstroke QRS), slight wide QRS
>0.10s, and frequently a psuedoinfarction pattern
in the inferior leads and RBBB pattern.
Lown-Ganong-Levine: short PR (< 0.12 s), NO
Delta wave, normal QRS & episodes of
tachydysrhythmias
LGLWPW
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Delta waves, short pr interval, wide QRS
The underlying ECG in WPW is a fusion of the accessory pathway
(delta wave) and normal pathway of the QRS. During tachy-
dysrhythmias, the electrical impulse follows only the accessory
pathway in a circuitous fashion.
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Accessory Pathways-WPW
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AV
SA
If narrow QRS d/tforward conduction,
treat as SVT
(Adenosine)
Wide QRS b/c retrograde conduction10%
Accessory Pathways-WPW
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AV
SA
Wide QRS if
retrograde conduction
Amiodarone and procainamide affect the
forward and retrograde pathways as well as
the ventricles and are safe in wide-complextachydysrhythmias.
(Caveat: Procainamide and Amiodarone not to be used in
Toursades)
Adenosine, Ca channel blockers, B blockers and digitalis
block the forward conduction, not the retrograde
conduction. In a wide complex WPW (retrograde
impulses) most AV nodal blockers stop only anterogradeconduction and can allow the rate of retrograde conduction
to speed up and deteriorate into Vfib! This is seen in wide
complex WPW with Afib or Aflutter.
Evaluation of Re-entry
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y
Tachycardias - QRS Width
Wide or Narrow
If the QRS is narrow, it MUST have atrial origin and conduct
through the AV node in a forward manner.
If the QRS is wide, more than 0.12 seconds, consider :
Bypass tract (WPW) with retrograde conduction
SVT with aberrancy (rate-related bundle branch block)
Junctional origin
Ventricular origin
Re-entry Tachycardias -
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Treatment Modalities
Based on hemodynamic stability & QRS widthUnstable : synchronized cardioversion
Stable :
Narrow complexvagal maneuvers, adenosine,
calcium channel blockers or beta blockers Wide complexAmiodarone, Lidocaine or
Procainamide to treat both anterograde and
retrograde impulses and ventricular
dysrhythmias
Beware: it is very difficulty to tell the difference between the wide-
complex tachy-dysrhythmias. It is safer to treat as presumed V-tach.
PEARLS
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PEARLS
Wide complex QRS tachydysrhythmias of unknownetiologyuse amiodorone, procainamide, lidocaine
Differential diagnosis for rapid, irregularly
irregular rhythm
MFAT Atrial Fib
Atrial flutter with variable conduction
SVT at 150 or 300, consider Atrial flutter
DYSRHYTHMIAS OF
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VENTRICULAR ORIGIN
Idioventricular rhythms
Ventricular Tachycardia
Ventricular Fibrillation
Torsades de pointes
VENTRICULAR
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DYSRHYTHMIAS - Etiology
V Tach, V Fib & Idioventricular rhythms
typically caused by an ischemic focus whichallows a rapid reentry dysrhythmia
Torsades de pointes - caused by a prolongedQT interval
Brugada syndromesodium ion channel-
apathy
IDIOVENTRICULARRHYTHMS
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RHYTHMS Mechanism : re-entry with unidirectional block due to myocardial
ischemia
QRS width > 0.12 sec and rate 40 - 140
T waves typically have opposite polarity to QRS
Treatment :
Controversial, tends to be self-limited
Supportive care & close observation
VENTRICULARTACHYCARDIA
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TACHYCARDIA Mechanism : re-entry with unidirectional block due to
myocardial ischemia (Monomorphic)
QRS width > 0.12 sec and rate > 140 bpm
T waves have opposite polarity to QRS
Treatment :
Stable : Amiodarone, Procainamide, Sotolol, Lidocaine, Mag
Unstable : Unsynchronized defibrillation plus meds
VENTRICULARFIBRILLATION
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Chaotic ventricular depolarization with loss of
organized QRS complexes
Life-threatening
Immediate loss of consciousness
Loss of blood pressure & death
Treatment : immediate unsynchronizeddefibrillation at 200, 300, then 360 joules (if
Biphasic use dose or 150j)
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Brugada Syndrome: Look for ST elevation V1-3
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g y
part of the syncope or palpitation work-up
immediate cardiology referral for ICD placement
CARDIOVERSION PEARLS
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CARDIOVERSION PEARLS
Atrial flutter is the most electro-responsive dysrhythmia
10-50 joules ~ treatment of choice
SVT and STABLE ventricular tachycardia often respond to
50 joules
Atrial and Ventricular FIBRILLATION require 100 joules
or more
Biphasic defibrillators use half the joules or 150j
TORSADES DE POINTES V-tach due to prolonged QT interval, in which the QRS axis
alternates between positive and negative (Polymorphic)
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alternates between positive and negative (Polymorphic)
Often self-limited, but may deteriorate into ventricular
fibrillation
Treatment of Choice : Magnesium Overdrive pacing & Isoproterenol can be used to speed the heart and
decrease QT interval
Avoid procainamide and amiodarone, as can worsen QT prolongatio If refractory, defibrillate
QUESTION ~ All of the following
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cause Torsades de pointes, except:
A. Hypomagnesemia
B. Tricyclic antidepressant overdose
C. Procainamide
D. Hyperkalemia
E. Quinidine
CAUSES OF PROLONGED
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QT INTERVAL
Hypo -Mg, -Ca, -K,
Type Ia antidysrhythmics - quinidine,procainamide
Tricyclic antidepressant overdose
drug reactions-EES, antihistamines,antifungals
d is incorrect, hyperkalemia does not causeprolonged QT
Prolonged qt interval
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Shortened qt: hypercalcemia
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HyperkalemiaPeaked T waves ( > 1/3 QRS)Prolonged PR interval Widening of QRS
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Sine Wave
U waves in Hypokalemia
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Potassium 3.5mEq/L
Potassium 3mEq/L
Potassium 2mEq/L
Potassium 1mEq/L
Osborne J wave in hypothermia: notching at
end of a slurred downstroke of QRS
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end of a slurred downstroke of QRS
Tricyclic Antidepressant Overdose
tall r in AVR
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tall r in AVR
slurring of the terminal portion ofthe rS in AVR
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Inferior Wall MIST segment
l ti i II III & VF
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elevation in II, III & aVF
Anterior Wall MIST segment elevation
i V2 4
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in V2-4
Septal MIST segment elevation V1-2
Lateral Wall MIST segment elevation in V5-6
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g
and/or I & aVL
Posterior Wall MI- Tall R in V1 & ST segment
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g
depression in V1-2
Pericarditis
diffuse ST segment elevation & PR depression,
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d use S seg e t e evat o & dep ess o ,
with PR elevation in AVR
EKG PEARLS
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When you see a normal looking EKG on a test, start
looking for:
Hyperkalemia :Peaked T waves
Hypokalemia : U waves
Hypomagnesimia : Prolonged QT
Hypercalcemia: Shortened QT
WPW : short PR, slurring of upstroke qrs
Hypothermia : Osborne J waves (notched downstroke QRS; reversedelta waves)
TCA overdose : stach, widening QRS, slurring of theterminal rS in aVR
Axis deviation & Hemiblocks : LAFB, LPFB
EKG PEARLS
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Usefulness of aVR & V1
Tall R wave in V1
RBBB
WPW
Posterior wall MI
Severe RV strain: PE, pneumothorax, severe COPD
aVR is normally flipped/negative polarity
slurring terminal rS in TCA OD
PR elevation in pericarditis
Diffuse ST elevation: think pericarditis
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