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ABC of clinical ECG
Magnus Lauritzen
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Goal with this seminar
• Learn a systematic approach for analysing
ECGs:” 5+1”
• Recognize and understand normal ECGs
• Interpret abnormalitets in ryhtm,
conduction or morphology
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Anatomy
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Physiology
• The sinoatrial node (SA node)
contains the fastest
physiological pacemaker cells of
the heart; therefore, they
determine the heart ratedetermine the heart rate
• SA-node initiates depolarization,
first atria, than ventricles by help
of specialized conduction
system
• Repolarization follows
depolarization
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• Depolarization og myocardial cells
causes pos. electrical charges
which can be measured be
electrodes
• Electrical charges moving • Electrical charges moving
towards an electrode causes
positive deflection relative to the
isoelectric line
• Electrical charges moving away
from an electrode causes negative
deflection
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Electrical axis of heart• The electrical heart axis is an
average of all depolarizations
in the heart.
• The depolarization wave
begins in the right atrium and
proceeds to the left and right
ventricle.
• Because the left ventricle wall
is thicker than the right wall,
the arrow indicating the
direction of the depolarization
wave is directed to the left.
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Placements of electrodes
(leads)
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Limb leads (Vertical plane)• Info from limb electrodes
are combined to produce
six limb leads
• Try to look at the leads as
eyes ”looking” at the
heart from different
angles
• Group the leads together
into right, left and inferior-
posterior
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Chest leads (horizontal
plane)
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Normal ECG intervalls• The PQ interval starts at the beginning
of the atrial contraction and ends at the
beginning of the ventricular contraction
(0,12 – 0,20 seconds)
• The QRS duration indicates how fast
the ventricles depolarize (normal < 0,10
seconds)seconds)
• The normal QTc (corrected) interval
indicates how fast the ventricles are
repolarized, becoming ready for a new
cycle. (below 0.45 seconds in men and
below 0,46 in women)
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Normal ECG – ”Sinus
ryhtm”
• A P-wave (atrial contraction) precedes every QRS
complex
• The rhythm is regular, but varies slightly during
respirations
• The rate ranges between 60 and 100 beats per • The rate ranges between 60 and 100 beats per
minute
• The P waves maximum height at 2.5 mm in II
and/or III
• The P wave is positive in I and II, and biphasic in
V1
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Normal ECG
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ArrhytmiasClassifications based on heart rate:
1. Tachycardia (HR > 100 bpm)
2. Bradycardia (HR < 60 bpm)
Classification based on origin of impulse:Classification based on origin of impulse:
1. Supraventricular – ”Narrow QRS complex” (<
0.12 ms)
2. Ventricular - ”Wide QRS complex” (> 0.12 ms)
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Tachyarrhytmias
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An overview of pathological supraventricular arrhythmias and their
origin
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Re-entry mechanism
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Sinustachycardia
Atrial frequency 100 – 180 bpm
Ventricular frequency 100 – 180 bpm
Regularity Regular
Origin Sinus node
P-wave Positive in II, aVF
Effect of Adenosine No (can lead to temporary AV block
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Sinustachycardia
Causes:
• Exercise, anxiety, alcohol, caffeine, drugs
• Fever
•• Hypoxia
• Bleeding
• Anemia
• Hyperthyroidism
• +++++
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Atrial tachycardia
Atrial frequency > 100
Ventricular frequency >100
Regularity Regular
Origin Ectopic foci in atrium (re-entry)
P-wave Negative in I, aVF (different morphology)
Effect of Adenosine / Vagal stimulation Slow down rythm (AV-conduction)
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Atrial fibrillaton (AF)
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Atrial Fibrillation (AF)
Atrial frequency 400-600 bpm
Ventricular frequency 75-175 bpm
Regularity Irregular
Origin Atria (SVT)
P-wave Absent
Effect of Adenosine Reduces heart rate
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Atrial Fibrillation (AF)
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Atrial flutter
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Atrial flutter
Atrial frequency 250-350 bpm
Ventricular frequency 75-150 bpm (3:1 or 2:1 block)
Regularity Regular
Origin Atria (SVT)
P-wave Negative sawtooth in lead II
Effect of Adenosine Temporary reduced AV conduction
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Atrial flutter
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AV-nodal re-entry tachycardia (AVNRT)
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AVNRT
Atrial frequency 180-250 bpm
Ventricular frequency 180-250 bpm
Regularity Regular
Origin AV-node
P-wave Inside or right after QRS-complex
Effect of Adenosine Terminates arrhytmia
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AVNRT
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Atrioventricular Re-entrant
Tachycardia (AVRT)• Also called ”Wolf-Parkinson-White-syndrome” (WPS)
and is a part of ”Preexitation syndromes”
• Caused by an abnormal accessory conduction
pathway between atria and ventriclespathway between atria and ventricles
• Ventricles might be stimulated prematurely, resulting
in an atriventricular re-entry tachycardia
• Can also cause diffuse ECG-changes resembling
ischaemia
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Wolf-Parkinson-White-
Syndrome
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Wolf-Parkinson-White
syndrome
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Ventricular tachycardias
Premature ventricular contractions (PVC)
• Most common of ventriuclar arrhytmias
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Ventricular tachycardia (VT)
• Regular, HR 110-250
Ventricular fibrillation (VF)
• Irregular, HR 400-600 bpm
Torsade de pointes
• Regular, HR 150-300
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Bradyarrhytmias• AV-block 1st degree
• AV-block 2nd degree (Wenckebach and
Mobitz type II)
• AV-block 3rd degree (complete AV-block)
• AV-blocks
• Sick sinus syndrome
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AV-blocks
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• AV-block type 1
• AV-block type 2 – Mobitz I (Wencheback)
• AV-block type 2 – Mobitz II
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• AV-block type III (complete block)
• No relation between P-waves and QRS
complexes
• Atrial rythm 60-100 bpm (or AF)• Atrial rythm 60-100 bpm (or AF)
• Ventricular ryhtm might be nodal,
ventricular or absent
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Conduction system
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Left bundle branch block
(LBBB)• Slowed conduction in left
bundle, causing delayed
depolarization of left ventricle
• QRS > 0,12 sec
• Deep S-waves in V1-V3
• Late R-waves in V5-V6
• ST-segment depression in
lateral leads (I, aVL, V5-V6)
• Always a pathological finding in
patients!
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Right bundle branch block
(RBBB)• Conduction in right bundle
branch is slow, causing late
depolarization of right ventricle
• QRS > 0,12 sec• QRS > 0,12 sec
• rSR (”rabbit ears”) in V1-V2
• Late deep S-waves in lateral
leads (I, aVL, V5-V6)
• Commonly a physiological
finding in patients!
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Myocardial ischemia and infarction
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Evolution of ECG changes in
Myocardial infarction
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Diagnosis of myocardial
infarction• Elevated cardiac enzymes in
blood (Troponin T, C and
CKMB)
AND on of the following:
• Typical symptoms (chest • Typical symptoms (chest
pain > 20 min)
• ECG changes (ST elevation,
ST depression or
pathological Q-waves)
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ECG-changesST-elevation (STEMI)
• Men > 0.2 mV in V2-V3, and/or > 0.1 mV in other leads
• Women > 0.1 mV in two or more leads
ST-depression
•• New horizontal or downsloping ST-depression > 0.05 mV in two contiguous
leads
T-wave inversion
• > 0.1 mV in two contiguous leads
Q-wave (old infarction, develops after hours/days)
New LBBB!!
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Location of ECG-changes
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Location of ECG-changes
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Where is MI located?
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Where is MI located?
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PAUSE!
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How to read ECG”5+1”:
1. Rhytm
2. Rate
3. Conduction (PQ, QRS, QT)3. Conduction (PQ, QRS, QT)
4. Heart axis
5. Morphology (P wave, QRS, ST-segment)
6. Compare current ECG with a previous one
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1. Ryhtm
• Is it sinus ryhtm?
• Regular or irregular?• Regular or irregular?
• Prolonged recording from one lead is used
to provide a rhytm strip (usually lead II)
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2. Heart rate• Determine the time between
two QRS complexes (RR)
• IF paper speed is 25
mm/second, count number of
big squares and divide with 300
(only in regular ryhtm)
• If paperspeed is 50
mm/second, divide with 600
(only in regular ryhtm)
• ”ECG-rulers”
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3. Conduction• The PQ interval starts at the beginning
of the atrial contraction and ends at the
beginning of the ventricular contraction
(0,12 – 0,20 seconds)
• The QRS duration indicates how fast
the ventricles depolarize (normal < 0,10
seconds)seconds)
• The normal QTc (corrected) interval
indicates how fast the ventricles are
repolarized, becoming ready for a new
cycle. (below 0.45 seconds in men and
below 0,46 in women)
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4. Heart axis• Look at lead aVF and I,
should normally be
positive
• Lead II is also postive, • Lead II is also postive,
lead III can be pos. or
neg.
• In normal axis both has
predominant positive
deflections
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5. Morphology
• Normal p wave?
• No pathological Q-waves?
• Prolonged QRS?• Prolonged QRS?
• Normal R-wave progression in V1-V6?
• ST elevation or depression?
• Abnormal T-wave?
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6. Compare to old ECG
• Are the presenting ECG-changes new?
• Remember that new LBBB is treatet as
STEMI..
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For more ECG traces click:
http://ecg.bidmc.harvard.edu/maven/maven
main.asp