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1. Describe the electrode conventions used to standardize ECG measurements. Know the electrode placements and polarities for the 12-lead ECG and the standard values for pen amplitude calibration and paper speed.
2. Name the parts of a typical bipolar (Lead II) ECG tracing and explain the relationship between each of the waves, intervals, and segments in relation to the electrical state of the heart.
3. Explain why the ECG record looks different in each of the 12 leads.
4. Define mean electrical axis of the heart and give the normal range. Determine the mean electrical axis from knowledge of the magnitude of the QRS complex in the standard frontal limb leads.
5. Describe the roles of altered automaticity, conduction block, and reentry in arrhythmias. Explain the role of refractory period in preventing reentry.
6. Describe electrocardiographic changes associated respectively with myocardial ischemia, injury and necrosis.
Learning objectives
Suggested Reading
• ECG Interpretation made Incredibly Easy, Lippincott
• Dale Dubin, Rapid Interpretation of EKG’s
Website:• http://www.themdsite.com• Costanzo, Physiology, 3rd ed., Ch. 4: Cardiovascular
Physiology, pp. 136-137.
• Boron and Boulpaep, Medical Physiology, 2nd ed., Ch. 21: Cardiac Electrophysiology and the Electrocardiogram Boron & Boulpaep: Medical Physiology, 2nd ed.
3
Fowler, ECG 4
ECG Resources
ECG Learning CenterThe Alan E. Lindsay ECG Learning CenterUniversity of Utah School of Medicine:• http://ecg.utah.edu
An internet ECG library in the United Kingdom:• http://www.ecglibrary.com/ecghome.html
London Ambulance Service (unofficial)Understanding the ECG (EKG):• http://www.lond.ambulance.freeuk.com/ecg/ECG.htm
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5
Electrocardiogram – 12 lead ECG
• The electrocardiogram (ECG or EKG) measures bio-potentials that originate from electrical activity in cardiac muscle (myocardium).
• Electric potentials consist of a repeated sequence of characteristic waveforms which correspond to a heart beat.
• The amplitudes of ECG potentials depend on the amplitude and orientation of electrical activity in cardiac muscle with respect to each recording electrode.
6 frontal leads 6 precordial leads
12 Lead ECG
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
++
+
6
The ECG:• Does NOT provide information on the actual mechanical
functioning of the heart.• CANNOT be used to assess cardiac output, blood pressure or
tissue perfusion.
The ECG DOES provide information on:
1. Rate
2. Disturbances of Rhythm and Conduction
3. Mean electrical axis (MEA)– e.g., the anatomical orientation of cardiac chambers.– e.g., the relative sizes of its chambers such as with
hypertrophy.
4. Infarction– The extent, location, and progression of ischemic damage to
myocardium.
Kinds of information provided by the ECG
Dubin’s Rapid Interpretation of EKG’s, http://www.themdsite.com/
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use this lead for Rate and Rhythm
Lead II
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How depolarization travels through the heart(or, Where do ECG waves, intervals, segments and complex come from?)
Q
RS
P
T wave
Q-T interval
isoelectric line
ventricular muscle action potential
Right side Left side
normally, the QRS is dominated by left ventricular muscle
mass
~200 msec
ST segment
-
+
Lead II
9
Range (s) Events
PR interval 0.12 – 0.20Atrial depolarization and conduction through AV node, Beginning of P wave to beginning of QRS, useful for diagnosing heart blocks
PR segment 0.05 - 0.120Flat baseline indicating transit through AV node, from end of P wave to beginning of ventricular depolarization
J point N/AJ point indicates end of QRS and beginning of ST segment, used to measure the degree of ST elevation or depression
QRS complex 0.08 - 0.10 Ventricular depolarization and atrial repolarization
QT interval 0.40 - 0.43 Ventricular depolarization plus ventricular repolarization
ST segment 0.08 - 0.12Represents the period when the ventricles are depolarized in plateau phase
10 mv
Lead II
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complex
5 mm
0.2 sec
10 mv
Waves, intervals, segments and complex
Rate
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11
Lead IIstart
300150100
7560
between 75 and 60 bpm
each big box = 0.2 seach small box = 0.04 s
1 second
Calculating heart rate
R – R interval
P – P interval
Rhythms
12
Rhythms
13
Arrhythmic complications of acute myocardial infarction (AMI):• About 90% of patients who have an AMI develop
some form of cardiac arrhythmia. • The clinician must be aware of these arrhythmias
and must treat those that require intervention to avoid exacerbation of ischemia and subsequent hemodynamic compromise.
http://emedicine.medscape.com/article/164924-overview#aw2aab6b3
ECG strips to recognize
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• Sinus rhythms
• Sinus Arrhythmia
• Sinus Bradycardia
• Sinus Tachycardia
• Sinus arrest or pause
• Nonsinus atrial rhythm
• Premature atrial contraction (PAC)
• Wandering pacemaker
• Atrial tachycardia
• Atrial flutter
• Atrial fibrillation
• Junctional arrhythmia
• Wolff-Parkinson-White syndrome (WPW)
• Premature junctional contraction (PJC)
• Junctional escape rhythm
• Ventricular arrhythmias
• Premature ventricular contraction (PVC)
• Idioventricular rhythm
• Ventricular tachycardia
• Torsades de pointes
• Ventricular fibrillation
• Asystole
• Atrioventricular blocks
• First degree AV block
• Second degree block
• Mobitz Type I (Wenckebach)
• Mobitz Type II
• Third degree block
Sinus rhythms
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• occurs with increased vagal tone
http://www.bem.fi/book/
• physiological response to physical exercise or stress, but may also result from congestive heart failure
Sinus Rhythm: origin in SA node
Sinus rhythm 60 to 100 bpm
Sinus tachycardia > 100 bpm
Sinus bradycardia < 60 bpm
∆ 300 150 100 75 60 50
∆ 300 150 100 75 60 50
Sinus arrhythmia
Fowler, ECG 16
http://www.bem.fi/book/19/19.htm
• This arrhythmia is so common in young people that it is not considered heart disease.
• One origin for the sinus arrhythmia may be the vagus nerve which mediates respiration as well as heart rhythm.
• The nerve is active during respiration and, through its effect on the sinus node, causes an increase in heart rate during inspiration and a decrease during expiration.
• The effect is particularly pronounced in children.
Nonsinus atrial rhythm – wandering pacemaker
Fowler, ECG 17
• Occurs when multiple areas (ectopic foci) within the atrium generate consecutive action potentials that are all conducted to the ventricles.
• Irregular rhythm
• Rate < 100bpm
• If Rate > 100 bpm then it is called Multifocal Atrial Tachycardia (MAT)
• The origin of the atrial contraction may also vary or wander. Consequently, the P-waves will vary in polarity, and the PR-interval will also vary.
http://www.bem.fi/book/19/19.htm
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Paroxysmal atrial tachycardia (PAT)• “Circus movement reentry” - when the P-
waves are a result of a reentrant activation in the atria.
• Abnormal P-waves difficult to see.• Rate between 160 and 220/min. • The P-wave is regularly followed by a normal
QRS-complex. • The isoelectric baseline is apparent between
T and next P-wave.
Atrial flutter• The isoelectric interval between the end of T
and beginning of P disappears.• Origin is circus reentrant atrial pathway. • Rate between 220 and 300/min. • The AV-node and, thereafter, the ventricles
are generally activated by every second or every third atrial impulse (2:1 or 3:1 heart block).
Atrial fibrillation• Activation in the atria is fully irregular and
chaotic, producing irregular fluctuations in the baseline.
• A consequence is that the ventricular rate is rapid and irregular, though the QRS contour is usually normal.
Nonsinus atrial rhythm
http://www.bem.fi/book/19/19.htm
Junctional arrhythmia
19
• Arising from the atrioventricular (AV) junction as an automatic tachycardia or as an escape mechanism during periods of significant bradycardia with rates slower than the intrinsic junctional pacemaker.
• Rate: 40-60 bpm (intrinsic junctional pacemaker)• Rhythm: Regular• P Wave: Inverted, absent or after QRS• PR interval <.12 seconds• QRS <.12 seconds
inverted P wave narrow QRS
Ventricular arrhythmias
20
Ventricular tachycardia
• Activation of the ventricular muscle at a high rate (over 120/min)
• AV dissociation
• Bizarre and wide QRS-complexes
• Ventricular automaticity limit overcome by multiple foci.
• Often a consequence of ischemia and myocardial infarction.
Ventricular fibrillation
• Coarse irregular undulations without QRS-complexes.
• Cause of fibrillation is the establishment of multiple reentry loops usually involving diseased heart muscle.
• The contraction of the ventricular muscle is irregular and is ineffective at pumping blood. The lack of blood circulation leads to almost immediate loss of consciousness and death within minutes.
• Fibrillation progresses to Asystole
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Ventricular arrhythmias – Torsade de pointes
21
• Polymorphic ventricular tachycardia with a characteristic illusion of a twisting of the QRS complex around the isoelectric baseline.
• Hemodynamically unstable and causes a sudden drop in arterial blood pressure, leading to dizziness and syncope.
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Premature ventricular contraction (PVC)
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• Caused by an ectopic cardiac pacemaker located in the ventricle
• Also called ventricular premature beat (VPB) or extrasystole
• QRS-complex has a very abnormal form and lasts longer than 0.1 s.
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Coming up:
• Conduction block and Reentrant excitation
• Sinus Arrest (aka sinus pause) resulting in Escape rhythms
• Atrioventricular (AV) conduction blocks
• Wolf-Parkinson-White syndrome (WPW)
Disorders of activation sequence
Fowler, ECG 24
Reentry
• Reentry (bottom panel) can occur if branch 2, for example, has a unidirectional block.
• In such a block, impulses can travel retrograde (from branch 3 into branch 2) but not orthograde.
• An action potential will travel down the branch 1, into the common distal path (branch 3), and then travel retrograde through the unidirectional block in branch 2 (blue line).
• Within the block (gray area), the conduction velocity is reduced because of depolarization.
• When the action potential exits the block, if it finds the tissue excitable, then the action potential will continue by traveling down (i.e., reenter) the branch 1
http://cvphysiology.com/Arrhythmias/A008c.htm
Sinus Arrest (aka sinus pause) resulting in Escape rhythms
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Escape rhythm is determined by automaticity of ectopic
focus.
Atrial escape rhythm rate: 60-100 bpm
Junctional escape rhythmrate: 40-60 bpm
Ventricular escape rhythm rate: 15-40 bpm
Atrioventricular (AV) conduction blocks
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10 AV block• When the P-wave always
precedes the QRS-complex and PR-interval > 0.2 s.
20 AV block• Mobitz Type I (Wenckebach) -
PR interval progressively increases until failure of conduction occurs.
• Mobitz Type II – PR interval remains fairly constant until conduction fails.
30 AV block or complete hear block
• No relationship between the P-wave and the QRS-complex.
• Note there are two rates.
Wolff-Parkinson-White (WPW) syndrome
• The accessory pathway, Kent bundle, is an abnormal "bridge" of tissue that allows the heart's electrical impulse to bypass the AV node and to travel in a circular pattern from the ventricles to the atria.
• Delta wave is a slurring and slow rise of the initial upstroke of QRS complex.
Fowler, ECG 27http://www.mayoclinic.org/wolff-parkinson-white/enlargeimage2572.html
Q&A
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a) sinus arrhythmia
b) sinus bradycardia
c) sinus tachycardia
d) atrial fibrillation
e) atrial flutter
http://afib.utorontoeit.com/clinicalevaluation.html
What does strip show?
Mean Electrical Axis (MEA)
29
Mean Electrical Axis (MEA)
30
• The MEA tells us the net direction the depolarization or repolarization is heading.
• When the atria (or ventricles) undergo depolarization, the wave of depolarization that spreads across the muscle mass occurs in many different directions simultaneously.
• If a snapshot of electrical activity could be taken at a given instant, each individual wave of depolarization can be represented as a vector.
• The mean electrical axis (MEA) represents the sum of all of the individual vectors at a given instant in time.
• Einthoven’s triangle is an equilateral triangle, with heart at the center, used to determine the MEA.
• The MEA of the QRS complex is right-to-left and downward on Einthoven’s triangle.
http://www.cvphysiology.com/Arrhythmias/A015.htm
Calculation of the MEA requires some additional background associated with the leads of the electrocardiogram:
– ‘Rules of the ECG’– Frontal hexaxial reference system (6 lead ECG)– Four-quadrant method of determining MEA
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Mean Electrical Axis (MEA)
‘Rules of the ECG’
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• Wave of depolarization traveling towards a positive electrode = an upward deflection on the ECG.
• Wave of depolarization traveling away from a positive electrode = a downward deflection on the ECG
• Wave of depolarization traveling perpendicular to a positive electrode line = biphasic wave.
• Wave of repolarization traveling away from a positive electrode = an upward deflection on the ECG
• Wave of repolarization traveling towards a positive electrode = a downward deflection.
depolarization wave
repolarization wave
direction depolarization
direction repolarization
33
Frontal hexaxial reference system (6 lead ECG)
+
Right Left
++
+
+
++
major direction of ventricular
depolarization
Lead I Lead II Lead III
aVR aVL aVF
• Leads I, II, III are bipolar limb leads• aVR, aVL and aVF are augmented unipolar limb leads
LR
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Frontal hexaxial reference system (6 lead ECG)
++
+
+
+
++
• The hexaxial reference system is diagram based on the first six (frontal) leads of the 12 lead ECG.
• It is used to help determine the heart's mean electrical axis in the frontal plane.
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Four-quadrant method of determining MEA using Lead I and aVF
Normal range ~ -300 to +900
+-
+
-
Ventricular hypertrophy
36
LVH RVH
+ aVF
+ I
-
-
Right Left
LVH = Left axis deviation RVH = Right axis deviation
R L
37
12 lead ECG - adding the 6 precordial leads
V1
V4
V3V2
V5
V6
• Anterior surface of heart: V1 - V4
• Lateral surface of heart: V5 - V6
RV
Interventricular septum
LV
+
+ +
+++
Note R wave progression through V1
- V6
• 12 lead ECG adds 6 precordial chest leads.
• The six precordial leads record the bio-electric potentials in a cross sectional plane.
Fowler, ECG
Right anterior
Left lateral
Bundle Branch Blocks
38
• Delay in left ventricle activation
• Delay in right ventricle activation• A helpful hint for recalling an RBBB is “rabbit
ears.” The QRS complex can resemble rabbit ears in V1 and V2. There are two peaks of the R wave (R and R').
“rabbit ears” of RBBB
Summary of QRS amplitudes in 12 lead ECG
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Lead I
aVR
V1
V4
Lead 2
aVL
V2
V5
Lead 3
aVF
V3
V6
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Myocardial Infarction
• Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, results from the partial interruption of blood supply to a part of the heart.
• Most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque.
41
An ‘heart attack’ evolves over time and space
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Classic ECG signs are:1. T-wave inversion
• occurs at onset• indicates myocardial ischemia• reversible
2. Elevated ST segment • indicates myocardial injury• reversible
3 Large Q wave• occurs after hours to days• indicates irreversible death (necrosis)
“Tombstone” ST elevation
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Major cardiac territories and their corresponding coronary artery supplyLocation ECG changes Coronary artery
Anterior V2-V4 Left main coronary artery or LAD (“widow maker”)
Inferior II, III, aVF Right coronary, circumflex
Lateral I, aVL, V5-V6 Circumflex, diagonal
Typically, ECG changes are confined to the leads that 'face' the infarction
http://www.med.umich.edu/lrc/baliga/case01/03A-T.html
Inferior wall
Anterior wall
Lateral wall
http://www.madsci.com/manu/ekg_mi.htm
Blueprints Clinical Cases in Emergency Medicine
Fowler, ECG 43
Electrocardiography - Key concepts
1. The 12 lead ECG is composed of I, II, III, avR, aVL, aVF and precordial leads V1 – V6.
2. Each of these leads has a different ‘view’ of cardiac bio-potentials as described by the ‘Rules of the ECG’.
3. The ECG is a repeated sequence of waves, segments and intervals that reflect the myocardial electrical state during each heart beat.
4. The mean electrical axis (MEA) tells us the net direction of depolarization or repolarization through myocardium. A mean electrical axis can be calculated from any ECG waveform but is most often done with the QRS where shifts in the axis can indicate pathological changes in the relative thickness of ventricular muscle masses.
5. In general, arrhythmias can arise from one of 4 mechanisms: abnormal SA pacemaker function, ectopic focus (originating from some point other than the SA node), conduction system blocks, and abnormal conduction pathways.
6. Classic ECG signs of a heart attack are: inverted T wave indicating myocardial ischemia and occurring at onset; elevated ST segment indicating myocardial injury, and a large Q wave indicating irreversible death (necrosis), occurring within hours to days.
Fowler, ECG 44
THE END