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Killer ECG Patterns

Deadly Diagnoses Not To Miss!!
by

Ed Burns

on 10 April 2014

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Transcript of Killer ECG Patterns

Can you have a look at this ECG?
...and this one!
ECG 2
30-year old with drowsiness
ECG 1
60-year old with shortness of breath
Peaked T waves
Bradycardia (~ 35 bpm)
Sine wave
Broad, bizarre QRS
?HyperK
HyperK may present with sinus arrest or complete heart block
without
other obvious ECG abnormalities.
Tachycardia
Worsening Sodium Channel Blockade
Sodium Channel Blockade
TCAs
Local anaesthetics (incl Cocaine)
Type Ia + Ic antiarrhythmics
Quinine-based antimalarials
Dextropropoxyphene
Propranolol
Na-Channel Blockers
QRS duration > 100ms
Right axis deviation of terminal QRS:
R' wave in aVR > 3mm
Deep S wave in lead I
QRS > 100ms predicts seizures
QRS > 160ms predicts cardiotoxicity
Diagnostic Features
Prognostic Value of ECG
TCAs
Local anaesthetics
Cocaine
Propranolol
Anti-arrhythmics (Ia/Ic)
Anti-malarials
Dextropropoxyphene
Causes
Hyperkalaemia
Regularized AF
Atrial fibrillation
Bidirectional VT
Polymorphic VT
Digoxin Toxicity
Atria = atrial tachycardia, AF, flutter
Junction = accelerated junctional rhythm
Ventricles = VEBs, bigeminy, VT
Atrial tachycardia
+ AV block?
ECG 3
80-year old patient with nausea
Atrial tachycardia
Digoxin toxicity
Giant T-wave inversions

ECG 4
75-year old with atypical chest pain
Electrical alternans
Massive pericardial effusion
ECG 6
40-year old with syncope
Localized changes in V1-2:
Brugada syndrome
ECG 7
30-year old with palpitations
Right axis deviation
Arrhythmogenic Right Ventricular Cardiomyopathy
Hyperkalaemia
ECG Changes in Hyperkalaemia
Peaked T waves
Prolonged PR interval
Flattening and eventual loss of P waves
Widening of QRS
Bradycardias, AV blocks, sinus pauses
Sine wave / PEA / asystole
HyperK!
Bradycardic?
Blocked?
Bizarre?
Hyperkalaemia
? HyperK
Sodium Channel Blockade
Sodium Channel Blockade
Sodium Channel Blockade
Sodium Channel Blockade due to TCA poisoning
Pseudo-Brugada pattern

May mimic hyperkalaemia or VT
P
P
P
P
QRS
QRS
QRS
VEB
VEB
VEB
Increased Automaticity
Digoxin toxicity!
Other Features
Prolonged PR, QT intervals
Atypical RBBB
Brugada-like pattern in V1-2
Following Treatment with HCO3
QRS complexes narrowed
Atrial Tachycardia / Flutter with AV Block
AV Block
1st, 2nd & 3rd degree AV block
Epsilon waves
Arrhythmogenic Right Ventricular Cardiomyopathy
Epsilon waves
Localised QRS widening in V1-3
Paroxysmal RVT
Signs of RV dilatation ("strain")

Diagnostic Features
Epsilon wave
QRS widening V1-3
RV dilation
Fatty infiltration
Arrhythmogenesis
Right Ventricular VT
LBBB morphology
The End!
Broad QRS
R' wave in aVR
Broad QRS > 100ms
Broad QRS > 100ms in lead II
Electrical alternans
Summary
Hyperkalaemia
Sodium channel blockade (TCA)
Digoxin toxicity
Pericardial Effusion
Summary
Raised ICP
Brugada syndrome
ARVC
K 5.5
K 6.5
K 7.0
K 8-9
Bradycardia
P wave flattening
Prolonged PR interval
Peaked T waves
K+ 7.6
Flattening + loss of P waves
QRS prolongation
Peaked T waves
Severe bradycardia
Flattening + loss of P waves
QRS widening
K+ > 8.0
Pacing is futile until the K+ has been corrected.
Low QRS voltage
Tachycardia
? tamponade
Prolonged QT interval
RSR' pattern
Coved ST elevation
T wave inversion
(Type 1 ECG Pattern)
Dominant R wave in V1
RV strain pattern
Inferior axis (+90 degrees)
Prolonged PR, QRS, QT intervals
Positive R' wave in aVR
R' wave in aVR diminished
Brugada-like pattern in V1-2 resolving
R' wave in aVR > 3mm
R wave in aVR > 3mm
Ventricular bigeminy
AV block
AV block
Accelerated junctional escape rhythm
QRS axis rotates 180 degrees with each alternate beat
ECG 5
25-year old with collapse, apparently intoxicated

ECG 5
25-year old with collapse, apparently intoxicated
ECG 6
40-year old with syncope

ECG 7
30-year old with palpitations

More Killer ECG Patterns Not To Miss!!
Hypokalaemia
LMCA occlusion
HOCM
Wellens syndrome
Peri-arrest ECG
Post treatment with IV calcium
Sinus Pauses
Complete AV Block
Then...
Deep S wave in lead I
Atypical RBBB

(35mg/kg doxepin)
Neurogenic Stress Cardiomyopathy (due to SAH)
Widespread deep T wave inversions
Prolonged QTc
Neurogenic Stress Cardiomyopathy (due to SAH)
Widespread T wave inversions
Wellens' syndrome-like appearance in V2
Raised ICP
?SAH
QRS complexes narrowing
Heart rate improving
Anti-arrhythmics (e.g. amiodarone) may be fatal!
S wave in V1
Sagging ST segments in V6 = digoxin
effect
Full transcript