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 1842- Italian scientist Carlo Matteucci realizes that
electricity is associated with the heart beat
 1876- Irish scientist Marey analyzes the electric
pattern of frog’s heart
 1895 - William Einthoven , credited for the invention
of EKG
 1906 - using the string electrometer EKG,
William Einthoven diagnoses some heart problems
 1924 - the noble prize for physiology or medicine
is given to William Einthoven for his work on
EKG
 1938 -AHA and Cardiac society of great Britan
defined and position of chest leads
 1942- Goldberger increased Wilson’s Unipolar
lead voltage by 50% and made Augmented leads
 2005- successful reduction in time of onset of
chest pain and PTCA by wireless transmission of
ECG on his PDA.
What is an EKG?
•The electrocardiogram (EKG) is a representation
of the electrical events of the cardiac cycle.
•Each event has a distinctive waveform
•the study of waveform can lead to greater insight
into a patient’s cardiac pathophysiology.
With EKGs we can identify
Arrhythmias
Myocardial ischemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances (i.e. hyperkalemia,
hypokalemia)
Drug toxicity (i.e. digoxin and drugs which
prolong the QT interval)
 Contraction of any muscle is associated with
electrical changes called depolarization
 These changes can be detected by electrodes
attached to the surface of the body
 SA Node - Dominant pacemaker with an
intrinsic rate of 60 - 100 beats/minute.
 AV Node - Back-up pacemaker with an
intrinsic rate of 40 - 60 beats/minute.
 Ventricular cells - Back-up pacemaker with an
intrinsic rate of 20 - 45 bpm.
 Standard
calibration
 25 mm/s
 0.1 mV/mm
 Electrical impulse
that travels towards
the electrode
produces an
upright (“positive”)
deflection
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
 P wave - Atrial
depolarization
• T wave - Ventricular
repolarization
• QRS - Ventricular
depolarization
Atrial depolarization
+
delay in AV junction
(AV node/Bundle of
His)
(delay allows time for
the atria to contract
before the ventricles
contract)
 Horizontally
 One small box - 0.04 s
 One large box - 0.20 s
 Vertically
 One large box - 0.5 mV
EKG Leads
which measure the difference in electrical potential
between two points
1. Bipolar Leads: Two different points on the body1. Bipolar Leads: Two different points on the body
2. Unipolar Leads: One point on the body and a virtual2. Unipolar Leads: One point on the body and a virtual
reference point with zero electrical potential, located inreference point with zero electrical potential, located in
the center of the heartthe center of the heart
EKG Leads
The standard EKG has 12 leads:
3 Standard Limb Leads
3 Augmented Limb Leads
6 Precordial Leads
Standard Limb Leads
Standard Limb Leads
Augmented Limb Leads
All Limb Leads
Precordial Leads
Precordial Leads
Arrangement of Leads on the EKG
Anatomic Groups
(Septum)
Anatomic Groups
(Anterior Wall)
Anatomic Groups
(Lateral Wall)
Anatomic Groups
(Inferior Wall)
Anatomic Groups
(Summary)
 Professor Chamberlains 10 rules of normal:-
PR interval should be 120 to 200
milliseconds or 3 to 5 little squares
The width of the QRS complex should not exceed
110 ms, less than 3 little squares
The QRS complex should be dominantly upright in
leads I and II
QRS and T waves tend to have the same
general direction in the limb leads
All waves are negative in lead aVR
The R wave must grow from V1 to at least V4
The S wave must grow from V1 to at least V3
and disappear in V6
The ST segment should start isoelectric
except in V1 and V2 where it may be elevated
The P waves should be upright in I, II, and V2 to V6
There should be no Q wave or only a small q less
than 0.04 seconds in width in I, II, V2 to V6
The T wave must be upright in I, II, V2 to V6
 Always positive in lead I and II
 Always negative in lead aVR
 < 3 small squares in duration
 < 2.5 small squares in
amplitude
 Commonly biphasic in lead V1
 Best seen in leads II
 Tall (> 2.5 mm), pointed P waves (P Pulmonale)
 Notched/bifid (‘M’ shaped) P wave (P
‘mitrale’) in limb leads
P Mitrale
 WPW (Wolff-
Parkinson-White)
Syndrome
 Accessory pathway
(Bundle of Kent)
allows early
activation of the
ventricle (delta
wave and short PR
interval)
 First degree Heart Block
 Non-pathological Q waves may present in I, III,
aVL, V5, and V6
 R wave in lead V6 is smaller than V5
 Depth of the S wave, should not exceed 30 mm
 Pathological Q wave > 2mm deep and > 1mm
wide or > 25% amplitude of the subsequent R
wave
 Sokolow & Lyon Criteria
 S in V1+ R in V5 or V6 > 35 mm
 An R wave of 11 to 13 mm (1.1 to 1.3 mV)
or more in lead aVL is another sign of
LVH
 ST Segment is flat (isoelectric)
 Elevation or depression of ST segment by
1 mm or more
 “J” (Junction) point is the point between
QRS and ST segment
Goldberger AL. Goldberger: Clinical Electrocardiography: A Simplified Approach. 7th
ed: Mosby Elsevier; 2006.
 Normal T wave is asymmetrical, first half
having a gradual slope than the second
 Should be at least 1/8 but less than 2/3 of the
amplitude of the R
 T wave amplitude rarely exceeds 10 mm
 Abnormal T waves are symmetrical, tall,
peaked, biphasic or inverted.
 T wave follows the direction of the QRS
deflection.
1. Total duration of Depolarization and
Repolarization
2. QT interval decreases when heart rate increases
3. For HR = 70 bpm, QT<0.40 sec.
4. QT interval should be 0.35­ 0.45 s,
5. Should not be more than half of the interval
between adjacent R waves (R­R interval).
 U wave related to afterdepolarizations
which follow repolarization
 U waves are small, round, symmetrical and
positive in lead II, with amplitude < 2 mm
 U wave direction is the same as T wave
 More prominent at slow heart rates
Determining the Heart Rate
Rule of 300/1500
10 Second Rule
Rule of 300
Count the number of “big boxes” between two
QRS complexes, and divide this into 300. (smaller
boxes with 1500)
for regular rhythms.
What is the heart rate?
(300 / 6) = 50 bpm
What is the heart rate?
(300 / ~ 4) = ~ 75 bpm
What is the heart rate?
(300 / 1.5) = 200 bpm
The Rule of 300
It may be easiest to memorize the following table:
No of big
boxes
Rate
1 300
2 150
3 100
4 75
5 60
6 50
10 Second Rule
EKGs record 10 seconds of rhythm per page,
Count the number of beats present on the EKG
Multiply by 6
For irregular rhythms.
What is the heart rate?
33 x 6 = 198 bpm
 Calculate the heart rate
The QRS Axis
The QRS axis represents overall direction of the
heart’s electrical activity.
Abnormalities hint at:
Ventricular enlargement
Conduction blocks (i.e. hemiblocks)
The QRS Axis
Normal QRS axis from -30° to
+90°.
-30° to -90° is referred to as a
left axis deviation (LAD)
+90° to +180° is referred to as
a right axis deviation (RAD)
Determining the Axis
The Quadrant Approach
The Equiphasic Approach
Determining the Axis
Predominantly
Positive
Predominantly
Negative
Equiphasic
The Quadrant Approach
1. QRS complex in leads I and aVF
2. determine if they are predominantly positive or negative.
3. The combination should place the axis into one of the 4
quadrants below.
The Quadrant Approach
• When LAD is present,
• If the QRS in II is positive, the LAD is non-pathologic or the
axis is normal
• If negative, it is pathologic.
Quadrant Approach: Example 1
Negative in I, positive in aVF  RAD
Quadrant Approach: Example 2
Positive in I, negative in aVF  Predominantly positive in II 
Normal Axis (non-pathologic LAD)
The Equiphasic Approach
1. Most equiphasic QRS complex.
2. Identified Lead lies 90° away from the lead
3. QRS in this second lead is positive or Negative
QRS Axis = -30 degrees
QRS Axis = +90 degrees-KH
Equiphasic Approach
Equiphasic in aVF  Predominantly positive in I  QRS axis ≈ 0°
Thank You
Dr Subroto Mandal, MD, DM, DC
Associate Professor, Cardiology
 Sinus Bradycardia
 Junctional Rhythm
 Sino Atrial Block
 Atrioventricular block
Sinoatrial node
AV node
Bundle of His
Bundle Branches
 Sinus impulses is blocked within the SA junction
 Between SA node and surrounding myocardium
 Abscent of complete Cardiac cycle
 Occures irregularly and unpredictably
 Present :Young athletes, Digitalis, Hypokalemia,
Sick Sinus Syndrome
 First Degree AV Block
 Second Degree AV Block
 Third Degree AV Block
 Delay in the conduction through the conducting
system
 Prolong P-R interval
 All P waves are followed by QRS
 Associated with : AC Rheumati Carditis, Digitalis,
Beta Blocker, excessive vagal tone, ischemia, intrinsic
disease in the AV junction or bundle branch system.
 Intermittent failure of AV conduction
 Impulse blocked by AV node
 Types:
 Mobitz type 1 (Wenckebach Phenomenon)
 Mobitz type 2
The 3 rules of "classic AV Wenckebach"
1. Decreasing RR intervals until pause;
2. Pause is less than preceding 2 RR intervals
3. RR interval after the pause is greater than RR prior to
pause.
Mobitz type 1 (Wenckebach Phenomenon)
•Mobitz type 2
•Usually a sign of bilateral bundle branch disease.
•One of the branches should be completely blocked;
•most likely blocked in the right bundle
•P waves may blocked somewhere in the AV junction, the
His bundle.
•CHB evidenced by the AV dissociation
•A junctional escape rhythm at 45 bpm.
•The PP intervals vary because of ventriculophasic sinus arrhythmia;
3rd degree AV block with a left ventricular escape rhythm,
'B' the right ventricular pacemaker rhythm is shown.
The nonconducted PAC's set up a long pause which
is terminated by ventricular escapes;
Wider QRS morphology of the escape beats
indicating their ventricular origin.
AV Dissociation
AV Dissociation
Due to Accelerated ventricular rhythm
Thank You
Do you think this person is having aDo you think this person is having a
myocardial infarction. If so, where?myocardial infarction. If so, where?
YesYes, this person is having an acute anterior, this person is having an acute anterior
wall myocardial infarction.wall myocardial infarction.
Now, where do you think this person isNow, where do you think this person is
having a myocardial infarction?having a myocardial infarction?
This is an inferior MI. Note the ST elevationThis is an inferior MI. Note the ST elevation
in leads II, III and aVF.in leads II, III and aVF.
How about now?How about now?
This person’s MI involvesThis person’s MI involves bothboth the anteriorthe anterior
wall (Vwall (V22-V-V44) and the lateral wall (V) and the lateral wall (V55-V-V66, I, and, I, and
aVL)!aVL)!
70 bpm• Rate?
• Regularity? regular
flutter waves
0.06 s
• P waves?
• PR interval? none
• QRS duration?
Interpretation? Atrial Flutter
74 148 bpm• Rate?
• Regularity? Regular 
regularNormal  none
0.08 s
• P waves?
• PR interval? 0.16 s  none
• QRS duration?
Interpretation? Paroxysmal Supraventricular
Tachycardia (PSVT)
 Deviation from NSRDeviation from NSR
The heart rate suddenly speeds up,The heart rate suddenly speeds up,
often triggered by a PAC (not seenoften triggered by a PAC (not seen
here) and the P waves are lost.here) and the P waves are lost.
 Ventricular TachycardiaVentricular Tachycardia
 Ventricular FibrillationVentricular Fibrillation
160 bpm• Rate?
• Regularity? regular
none
wide (> 0.12 sec)
• P waves?
• PR interval? none
• QRS duration?
Interpretation? Ventricular Tachycardia
 Deviation from NSRDeviation from NSR
Impulse is originating in the ventriclesImpulse is originating in the ventricles
(no P waves, wide QRS).(no P waves, wide QRS).
none• Rate?
• Regularity? irregularly irreg.
none
wide, if recognizable
• P waves?
• PR interval? none
• QRS duration?
Interpretation? Ventricular Fibrillation
 Deviation from NSRDeviation from NSR
Completely abnormal.Completely abnormal.
Arrhythmias can arise from problems inArrhythmias can arise from problems in
the:the:
• Sinus nodeSinus node
• Atrial cellsAtrial cells
• AV junctionAV junction
• Ventricular cellsVentricular cells
The SA Node can:The SA Node can:
 fire too slowfire too slow
 fire too fastfire too fast Sinus BradycardiaSinus Bradycardia
Sinus TachycardiaSinus Tachycardia
Sinus Tachycardia may be an appropriate
response to stress.
Atrial cells can:Atrial cells can:
 fire occasionallyfire occasionally
from a focusfrom a focus
 fire continuouslyfire continuously
due to a loopingdue to a looping
re-entrant circuitre-entrant circuit
Premature AtrialPremature Atrial
Contractions (PACs)Contractions (PACs)
Atrial FlutterAtrial Flutter
The AV junction can:The AV junction can:
 fire continuouslyfire continuously
due to a looping re-due to a looping re-
entrant circuitentrant circuit
 block impulsesblock impulses
coming from the SAcoming from the SA
NodeNode
ParoxysmalParoxysmal
SupraventricularSupraventricular
TachycardiaTachycardia
AV Junctional BlocksAV Junctional Blocks
30 bpm• Rate?
• Regularity? regular
normal
0.10 s
• P waves?
• PR interval? 0.12 s
• QRS duration?
Interpretation? Sinus Bradycardia
130 bpm• Rate?
• Regularity? regular
normal
0.08 s
• P waves?
• PR interval? 0.16 s
• QRS duration?
Interpretation? Sinus Tachycardia
70 bpm• Rate?
• Regularity? occasionally irreg.
2/7 different contour
0.08 s
• P waves?
• PR interval? 0.14 s (except 2/7)
• QRS duration?
Interpretation? NSR with Premature Atrial
Contractions
 Deviation from NSRDeviation from NSR
These ectopic beats originate in theThese ectopic beats originate in the
atria (but not in the SA node),atria (but not in the SA node),
therefore the contour of the P wave,therefore the contour of the P wave,
the PR interval, and the timing arethe PR interval, and the timing are
different than a normally generateddifferent than a normally generated
pulse from the SA node.pulse from the SA node.
60 bpm• Rate?
• Regularity? occasionally irreg.
none for 7th QRS
0.08 s (7th wide)
• P waves?
• PR interval? 0.14 s
• QRS duration?
Interpretation? Sinus Rhythm with 1 PVC
Normal
Signal moves rapidly
through the ventricles
Abnormal
Signal moves slowly
through the ventricles
 1st Degree AV Block1st Degree AV Block
 2nd Degree AV Block, Type I2nd Degree AV Block, Type I
 2nd Degree AV Block, Type II2nd Degree AV Block, Type II
 3rd Degree AV Block3rd Degree AV Block
60 bpm• Rate?
• Regularity? regular
normal
0.08 s
• P waves?
• PR interval? 0.36 s
• QRS duration?
Interpretation? 1st Degree AV Block
 Etiology:Etiology: Prolonged conduction delay in theProlonged conduction delay in the
AV node or Bundle of His.AV node or Bundle of His.
50 bpm• Rate?
• Regularity? regularly irregular
nl, but 4th no QRS
0.08 s
• P waves?
• PR interval? lengthens
• QRS duration?
Interpretation? 2nd Degree AV Block, Type I
40 bpm• Rate?
• Regularity? regular
nl, 2 of 3 no QRS
0.08 s
• P waves?
• PR interval? 0.14 s
• QRS duration?
Interpretation? 2nd Degree AV Block, Type II
 Deviation from NSRDeviation from NSR
Occasional P waves are completelyOccasional P waves are completely
blocked (P wave not followed byblocked (P wave not followed by
QRS).QRS).
40 bpm• Rate?
• Regularity? regular
no relation to QRS
wide (> 0.12 s)
• P waves?
• PR interval? none
• QRS duration?
Interpretation? 3rd Degree AV Block
 Deviation from NSRDeviation from NSR
The P waves are completely blocked inThe P waves are completely blocked in
the AV junction; QRS complexesthe AV junction; QRS complexes
originate independently from beloworiginate independently from below
the junction.the junction.
 Atrial FibrillationAtrial Fibrillation
 Atrial FlutterAtrial Flutter
 Paroxysmal SupraventricularParoxysmal Supraventricular
TachycardiaTachycardia
100 bpm• Rate?
• Regularity? irregularly irregular
none
0.06 s
• P waves?
• PR interval? none
• QRS duration?
Interpretation? Atrial Fibrillation
 Deviation from NSRDeviation from NSR
No organized atrial depolarization, soNo organized atrial depolarization, so
no normal P waves (impulses are notno normal P waves (impulses are not
originating from the sinus node).originating from the sinus node).
Atrial activity is chaotic (resulting inAtrial activity is chaotic (resulting in
an irregularly irregular rate).an irregularly irregular rate).
Common, affects 2-4%, up to 5-10% ifCommon, affects 2-4%, up to 5-10% if
> 80 years old> 80 years old
70 bpm• Rate?
• Regularity? regular
flutter waves
0.06 s
• P waves?
• PR interval? none
• QRS duration?
Interpretation? Atrial Flutter
74 148 bpm• Rate?
• Regularity? Regular 
regularNormal  none
0.08 s
• P waves?
• PR interval? 0.16 s  none
• QRS duration?
Interpretation? Paroxysmal Supraventricular
Tachycardia (PSVT)
 Deviation from NSRDeviation from NSR
The heart rate suddenly speeds up,The heart rate suddenly speeds up,
often triggered by a PAC (not seenoften triggered by a PAC (not seen
here) and the P waves are lost.here) and the P waves are lost.
 Ventricular TachycardiaVentricular Tachycardia
 Ventricular FibrillationVentricular Fibrillation
160 bpm• Rate?
• Regularity? regular
none
wide (> 0.12 sec)
• P waves?
• PR interval? none
• QRS duration?
Interpretation? Ventricular Tachycardia
 Deviation from NSRDeviation from NSR
Impulse is originating in the ventriclesImpulse is originating in the ventricles
(no P waves, wide QRS).(no P waves, wide QRS).
none• Rate?
• Regularity? irregularly irreg.
none
wide, if recognizable
• P waves?
• PR interval? none
• QRS duration?
Interpretation? Ventricular Fibrillation
 Deviation from NSRDeviation from NSR
Completely abnormal.Completely abnormal.
To diagnose a myocardial infarction you needTo diagnose a myocardial infarction you need
to go beyond looking at a rhythm strip andto go beyond looking at a rhythm strip and
obtain a 12-Lead ECG.obtain a 12-Lead ECG.
Rhythm
Strip
12-Lead
ECG
Some leads get aSome leads get a
good view of the:good view of the:
Anterior portion
of the heart
Lateral portion
of the heart
Inferior portion
of the heart
One way toOne way to
diagnose andiagnose an
acute MI is toacute MI is to
look forlook for
elevation of theelevation of the
ST segment.ST segment.
Elevation of the STElevation of the ST
segment (greatersegment (greater
than 1 small box) inthan 1 small box) in
2 leads is consistent2 leads is consistent
with a myocardialwith a myocardial
infarction.infarction.
The anterior portion of the heart is best viewedThe anterior portion of the heart is best viewed
using leads Vusing leads V11- V- V44..
If you see changes in leads VIf you see changes in leads V11 - V- V44
that are consistent with athat are consistent with a
myocardial infarction, you canmyocardial infarction, you can
conclude that it is an anterior wallconclude that it is an anterior wall
myocardial infarction.myocardial infarction.
Do you think this person is having aDo you think this person is having a
myocardial infarction. If so, where?myocardial infarction. If so, where?
YesYes, this person is having an acute anterior, this person is having an acute anterior
wall myocardial infarction.wall myocardial infarction.
Now that you know where to look for anNow that you know where to look for an
anterior wall myocardial infarction let’s lookanterior wall myocardial infarction let’s look
at how you would determine if the MIat how you would determine if the MI
involves the lateral wall or the inferior wall ofinvolves the lateral wall or the inferior wall of
the heart.the heart.
First, take a lookFirst, take a look
again at this pictureagain at this picture
of the heart.of the heart.
Anterior portion
of the heart
Lateral portion
of the heart
Inferior portion
of the heart
Second, remember that the 12-leads of the ECG look atSecond, remember that the 12-leads of the ECG look at
different portions of the heart. The limb and augmented leadsdifferent portions of the heart. The limb and augmented leads
“see” electrical activity moving inferiorly (II, III and aVF), to“see” electrical activity moving inferiorly (II, III and aVF), to
the left (I, aVL) and to the right (aVR). Whereas, the precordialthe left (I, aVL) and to the right (aVR). Whereas, the precordial
leads “see” electrical activity in the posterior to anteriorleads “see” electrical activity in the posterior to anterior
direction.direction.
Limb Leads Augmented Leads Precordial Leads
Now, using these 3 diagrams let’s figure where toNow, using these 3 diagrams let’s figure where to
look for a lateral wall and inferior wall MI.look for a lateral wall and inferior wall MI.
Limb Leads Augmented Leads Precordial Leads
Remember the anterior portion of the heart is bestRemember the anterior portion of the heart is best
viewed using leads Vviewed using leads V11- V- V44..
Limb Leads Augmented Leads Precordial Leads
So what leads do you thinkSo what leads do you think
the lateral portion of thethe lateral portion of the
heart is best viewed?heart is best viewed?
Limb Leads Augmented Leads Precordial Leads
Leads I, aVL, and V5- V6
Now how about theNow how about the
inferior portion of theinferior portion of the
heart?heart?
Limb Leads Augmented Leads Precordial Leads
Leads II, III and aVF
Now, where do you think this person isNow, where do you think this person is
having a myocardial infarction?having a myocardial infarction?
This is an inferior MI. Note the ST elevationThis is an inferior MI. Note the ST elevation
in leads II, III and aVF.in leads II, III and aVF.
How about now?How about now?
This person’s MI involvesThis person’s MI involves bothboth the anteriorthe anterior
wall (Vwall (V22-V-V44) and the lateral wall (V) and the lateral wall (V55-V-V66, I, and, I, and
aVL)!aVL)!
Right atrial enlargementRight atrial enlargement
 Take a look at this ECG. What do you notice aboutTake a look at this ECG. What do you notice about
the P waves?the P waves?
The P waves are tall, especially in leads II, III and avF.
Ouch! They would hurt to sit on!!
Right atrial enlargementRight atrial enlargement
 To diagnose RAE you can use the following criteria:To diagnose RAE you can use the following criteria:
 IIII P > 2.5 mmP > 2.5 mm, or, or
 V1 or V2V1 or V2 P > 1.5 mmP > 1.5 mm
Remember 1 small
box in height = 1 mm
A cause of RAE is RVH from pulmonary hypertension.
> 2 ½ boxes (in height)
> 1 ½ boxes (in height)
Left atrial enlargementLeft atrial enlargement
 Take a look at this ECG. What do you notice aboutTake a look at this ECG. What do you notice about
the P waves?the P waves?
The P waves in lead II are notched and in lead V1 they
have a deep and wide negative component.
Notched
Negative deflection
Left atrial enlargementLeft atrial enlargement
 To diagnose LAE you can use the following criteria:To diagnose LAE you can use the following criteria:
 IIII > 0.04 s (1 box) between notched peaks> 0.04 s (1 box) between notched peaks, or, or
 V1V1 Neg. deflection > 1 box wide x 1 box deepNeg. deflection > 1 box wide x 1 box deep
Normal LAE
A common cause of LAE is LVH from hypertension.
Compare these two 12-lead ECGs. WhatCompare these two 12-lead ECGs. What
stands out as different with the second one?stands out as different with the second one?
Normal Left Ventricular Hypertrophy
Answer: The QRS complexes are very tall
(increased voltage)
 Criteria exists to diagnose LVH using a 12-lead ECG.Criteria exists to diagnose LVH using a 12-lead ECG.
 For example:For example:
 The R wave in V5 or V6 plus the S wave in V1 or V2The R wave in V5 or V6 plus the S wave in V1 or V2
exceeds 35 mm.exceeds 35 mm.
• However, for now, all
you need to know is
that the QRS voltage
increases with LVH.
Right ventricular hypertrophyRight ventricular hypertrophy
 Take a look at this ECG. What do you notice aboutTake a look at this ECG. What do you notice about
the axis and QRS complexes over the rightthe axis and QRS complexes over the right
ventricle (V1, V2)?ventricle (V1, V2)?
There is right axis deviation (negative in I, positive in II) and
there are tall R waves in V1, V2.
Right ventricular hypertrophyRight ventricular hypertrophy
 To diagnose RVH you can use the following criteria:To diagnose RVH you can use the following criteria:
 Right axis deviationRight axis deviation, and, and
 V1V1 R wave > 7mm tallR wave > 7mm tall
A common
cause of RVH
is left heart
failure.
Right ventricular hypertrophyRight ventricular hypertrophy
 Compare the R waves in V1, V2 from a normal ECG and oneCompare the R waves in V1, V2 from a normal ECG and one
from a person with RVH.from a person with RVH.
 Notice the R wave is normally small in V1, V2 because theNotice the R wave is normally small in V1, V2 because the
right ventricle does not have a lot of muscle mass.right ventricle does not have a lot of muscle mass.
 But in the hypertrophied right ventricle the R wave is tall inBut in the hypertrophied right ventricle the R wave is tall in
V1, V2.V1, V2.
Normal RVH
Left ventricular hypertrophyLeft ventricular hypertrophy
 Take a look at this ECG. What do you notice aboutTake a look at this ECG. What do you notice about
the axis and QRS complexes over the left ventriclethe axis and QRS complexes over the left ventricle
(V5, V6) and right ventricle (V1, V2)?(V5, V6) and right ventricle (V1, V2)?
There is left axis deviation (positive in I, negative in II) and there
are tall R waves in V5, V6 and deep S waves in V1, V2.
The deep S waves
seen in the leads over
the right ventricle are
created because the
heart is depolarizing
left, superior and
posterior (away from
leads V1, V2).
Left ventricular hypertrophyLeft ventricular hypertrophy
 To diagnose LVH you can use the followingTo diagnose LVH you can use the following
criteria*:criteria*:
 R in V5 (or V6) + S in V1 (or V2) > 35 mmR in V5 (or V6) + S in V1 (or V2) > 35 mm, or, or
 avLavL R > 13 mmR > 13 mm
A common cause of LVH
is hypertension.
* There are several
other criteria for the
diagnosis of LVH.
S = 13 mm
R = 25 mm
Normal Impulse Conduction
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
So, conduction in theSo, conduction in the
Bundle Branches andBundle Branches and
Purkinje fibers arePurkinje fibers are
seen as the QRSseen as the QRS
complex on the ECG.complex on the ECG.
Therefore, a conduction
block of the Bundle
Branches would be
reflected as a change in
the QRS complex.
Right
BBB
With Bundle Branch Blocks you will see twoWith Bundle Branch Blocks you will see two
changes on the ECG.changes on the ECG.
1.1. QRS complex widensQRS complex widens (> 0.12 sec)(> 0.12 sec)..
2.2. QRS morphology changesQRS morphology changes (varies depending on ECG(varies depending on ECG
lead, and if it is a right vs. left bundle branch block)lead, and if it is a right vs. left bundle branch block)..
What QRS morphology is characteristic?What QRS morphology is characteristic?
V1
For RBBB the wide QRS complex assumes a
unique, virtually diagnostic shape in those
leads overlying the right ventricle (V1 and V2).
“Rabbit Ears”
What QRS morphology is characteristic?What QRS morphology is characteristic?
For LBBB the wide QRS complex assumes a
characteristic change in shape in those leads
opposite the left ventricle (right ventricular
leads - V1 and V2).
Broad,
deep S
waves
Normal
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
ECG BASICS IN DETAIL
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ECG BASICS IN DETAIL

  • 2.  1842- Italian scientist Carlo Matteucci realizes that electricity is associated with the heart beat  1876- Irish scientist Marey analyzes the electric pattern of frog’s heart  1895 - William Einthoven , credited for the invention of EKG  1906 - using the string electrometer EKG, William Einthoven diagnoses some heart problems
  • 3.  1924 - the noble prize for physiology or medicine is given to William Einthoven for his work on EKG  1938 -AHA and Cardiac society of great Britan defined and position of chest leads  1942- Goldberger increased Wilson’s Unipolar lead voltage by 50% and made Augmented leads  2005- successful reduction in time of onset of chest pain and PTCA by wireless transmission of ECG on his PDA.
  • 4.
  • 5.
  • 6. What is an EKG? •The electrocardiogram (EKG) is a representation of the electrical events of the cardiac cycle. •Each event has a distinctive waveform •the study of waveform can lead to greater insight into a patient’s cardiac pathophysiology.
  • 7. With EKGs we can identify Arrhythmias Myocardial ischemia and infarction Pericarditis Chamber hypertrophy Electrolyte disturbances (i.e. hyperkalemia, hypokalemia) Drug toxicity (i.e. digoxin and drugs which prolong the QT interval)
  • 8.  Contraction of any muscle is associated with electrical changes called depolarization  These changes can be detected by electrodes attached to the surface of the body
  • 9.  SA Node - Dominant pacemaker with an intrinsic rate of 60 - 100 beats/minute.  AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute.  Ventricular cells - Back-up pacemaker with an intrinsic rate of 20 - 45 bpm.
  • 10.  Standard calibration  25 mm/s  0.1 mV/mm  Electrical impulse that travels towards the electrode produces an upright (“positive”) deflection
  • 11. Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers
  • 12.  P wave - Atrial depolarization • T wave - Ventricular repolarization • QRS - Ventricular depolarization
  • 13. Atrial depolarization + delay in AV junction (AV node/Bundle of His) (delay allows time for the atria to contract before the ventricles contract)
  • 14.
  • 15.  Horizontally  One small box - 0.04 s  One large box - 0.20 s  Vertically  One large box - 0.5 mV
  • 16. EKG Leads which measure the difference in electrical potential between two points 1. Bipolar Leads: Two different points on the body1. Bipolar Leads: Two different points on the body 2. Unipolar Leads: One point on the body and a virtual2. Unipolar Leads: One point on the body and a virtual reference point with zero electrical potential, located inreference point with zero electrical potential, located in the center of the heartthe center of the heart
  • 17. EKG Leads The standard EKG has 12 leads: 3 Standard Limb Leads 3 Augmented Limb Leads 6 Precordial Leads
  • 24.
  • 25. Arrangement of Leads on the EKG
  • 31.  Professor Chamberlains 10 rules of normal:-
  • 32. PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
  • 33. The width of the QRS complex should not exceed 110 ms, less than 3 little squares
  • 34. The QRS complex should be dominantly upright in leads I and II
  • 35. QRS and T waves tend to have the same general direction in the limb leads
  • 36. All waves are negative in lead aVR
  • 37. The R wave must grow from V1 to at least V4 The S wave must grow from V1 to at least V3 and disappear in V6
  • 38. The ST segment should start isoelectric except in V1 and V2 where it may be elevated
  • 39. The P waves should be upright in I, II, and V2 to V6
  • 40. There should be no Q wave or only a small q less than 0.04 seconds in width in I, II, V2 to V6
  • 41. The T wave must be upright in I, II, V2 to V6
  • 42.  Always positive in lead I and II  Always negative in lead aVR  < 3 small squares in duration  < 2.5 small squares in amplitude  Commonly biphasic in lead V1  Best seen in leads II
  • 43.  Tall (> 2.5 mm), pointed P waves (P Pulmonale)
  • 44.  Notched/bifid (‘M’ shaped) P wave (P ‘mitrale’) in limb leads
  • 46.  WPW (Wolff- Parkinson-White) Syndrome  Accessory pathway (Bundle of Kent) allows early activation of the ventricle (delta wave and short PR interval)
  • 47.  First degree Heart Block
  • 48.  Non-pathological Q waves may present in I, III, aVL, V5, and V6  R wave in lead V6 is smaller than V5  Depth of the S wave, should not exceed 30 mm  Pathological Q wave > 2mm deep and > 1mm wide or > 25% amplitude of the subsequent R wave
  • 49.
  • 50.
  • 51.
  • 52.  Sokolow & Lyon Criteria  S in V1+ R in V5 or V6 > 35 mm  An R wave of 11 to 13 mm (1.1 to 1.3 mV) or more in lead aVL is another sign of LVH
  • 53.
  • 54.  ST Segment is flat (isoelectric)  Elevation or depression of ST segment by 1 mm or more  “J” (Junction) point is the point between QRS and ST segment
  • 55. Goldberger AL. Goldberger: Clinical Electrocardiography: A Simplified Approach. 7th ed: Mosby Elsevier; 2006.
  • 56.  Normal T wave is asymmetrical, first half having a gradual slope than the second  Should be at least 1/8 but less than 2/3 of the amplitude of the R  T wave amplitude rarely exceeds 10 mm  Abnormal T waves are symmetrical, tall, peaked, biphasic or inverted.  T wave follows the direction of the QRS deflection.
  • 57.
  • 58. 1. Total duration of Depolarization and Repolarization 2. QT interval decreases when heart rate increases 3. For HR = 70 bpm, QT<0.40 sec. 4. QT interval should be 0.35­ 0.45 s, 5. Should not be more than half of the interval between adjacent R waves (R­R interval).
  • 59.
  • 60.  U wave related to afterdepolarizations which follow repolarization  U waves are small, round, symmetrical and positive in lead II, with amplitude < 2 mm  U wave direction is the same as T wave  More prominent at slow heart rates
  • 61. Determining the Heart Rate Rule of 300/1500 10 Second Rule
  • 62. Rule of 300 Count the number of “big boxes” between two QRS complexes, and divide this into 300. (smaller boxes with 1500) for regular rhythms.
  • 63. What is the heart rate? (300 / 6) = 50 bpm
  • 64. What is the heart rate? (300 / ~ 4) = ~ 75 bpm
  • 65. What is the heart rate? (300 / 1.5) = 200 bpm
  • 66. The Rule of 300 It may be easiest to memorize the following table: No of big boxes Rate 1 300 2 150 3 100 4 75 5 60 6 50
  • 67. 10 Second Rule EKGs record 10 seconds of rhythm per page, Count the number of beats present on the EKG Multiply by 6 For irregular rhythms.
  • 68. What is the heart rate? 33 x 6 = 198 bpm
  • 69.
  • 70.  Calculate the heart rate
  • 71. The QRS Axis The QRS axis represents overall direction of the heart’s electrical activity. Abnormalities hint at: Ventricular enlargement Conduction blocks (i.e. hemiblocks)
  • 72. The QRS Axis Normal QRS axis from -30° to +90°. -30° to -90° is referred to as a left axis deviation (LAD) +90° to +180° is referred to as a right axis deviation (RAD)
  • 73. Determining the Axis The Quadrant Approach The Equiphasic Approach
  • 75. The Quadrant Approach 1. QRS complex in leads I and aVF 2. determine if they are predominantly positive or negative. 3. The combination should place the axis into one of the 4 quadrants below.
  • 76. The Quadrant Approach • When LAD is present, • If the QRS in II is positive, the LAD is non-pathologic or the axis is normal • If negative, it is pathologic.
  • 77. Quadrant Approach: Example 1 Negative in I, positive in aVF  RAD
  • 78. Quadrant Approach: Example 2 Positive in I, negative in aVF  Predominantly positive in II  Normal Axis (non-pathologic LAD)
  • 79. The Equiphasic Approach 1. Most equiphasic QRS complex. 2. Identified Lead lies 90° away from the lead 3. QRS in this second lead is positive or Negative
  • 80. QRS Axis = -30 degrees
  • 81. QRS Axis = +90 degrees-KH
  • 82.
  • 83. Equiphasic Approach Equiphasic in aVF  Predominantly positive in I  QRS axis ≈ 0°
  • 85. Dr Subroto Mandal, MD, DM, DC Associate Professor, Cardiology
  • 86.  Sinus Bradycardia  Junctional Rhythm  Sino Atrial Block  Atrioventricular block
  • 87. Sinoatrial node AV node Bundle of His Bundle Branches
  • 88.
  • 89.
  • 90.  Sinus impulses is blocked within the SA junction  Between SA node and surrounding myocardium  Abscent of complete Cardiac cycle  Occures irregularly and unpredictably  Present :Young athletes, Digitalis, Hypokalemia, Sick Sinus Syndrome
  • 91.  First Degree AV Block  Second Degree AV Block  Third Degree AV Block
  • 92.  Delay in the conduction through the conducting system  Prolong P-R interval  All P waves are followed by QRS  Associated with : AC Rheumati Carditis, Digitalis, Beta Blocker, excessive vagal tone, ischemia, intrinsic disease in the AV junction or bundle branch system.
  • 93.  Intermittent failure of AV conduction  Impulse blocked by AV node  Types:  Mobitz type 1 (Wenckebach Phenomenon)  Mobitz type 2
  • 94. The 3 rules of "classic AV Wenckebach" 1. Decreasing RR intervals until pause; 2. Pause is less than preceding 2 RR intervals 3. RR interval after the pause is greater than RR prior to pause. Mobitz type 1 (Wenckebach Phenomenon)
  • 95.
  • 96. •Mobitz type 2 •Usually a sign of bilateral bundle branch disease. •One of the branches should be completely blocked; •most likely blocked in the right bundle •P waves may blocked somewhere in the AV junction, the His bundle.
  • 97. •CHB evidenced by the AV dissociation •A junctional escape rhythm at 45 bpm. •The PP intervals vary because of ventriculophasic sinus arrhythmia;
  • 98. 3rd degree AV block with a left ventricular escape rhythm, 'B' the right ventricular pacemaker rhythm is shown.
  • 99. The nonconducted PAC's set up a long pause which is terminated by ventricular escapes; Wider QRS morphology of the escape beats indicating their ventricular origin. AV Dissociation
  • 100. AV Dissociation Due to Accelerated ventricular rhythm
  • 102. Do you think this person is having aDo you think this person is having a myocardial infarction. If so, where?myocardial infarction. If so, where?
  • 103. YesYes, this person is having an acute anterior, this person is having an acute anterior wall myocardial infarction.wall myocardial infarction.
  • 104. Now, where do you think this person isNow, where do you think this person is having a myocardial infarction?having a myocardial infarction?
  • 105. This is an inferior MI. Note the ST elevationThis is an inferior MI. Note the ST elevation in leads II, III and aVF.in leads II, III and aVF.
  • 106. How about now?How about now?
  • 107. This person’s MI involvesThis person’s MI involves bothboth the anteriorthe anterior wall (Vwall (V22-V-V44) and the lateral wall (V) and the lateral wall (V55-V-V66, I, and, I, and aVL)!aVL)!
  • 108. 70 bpm• Rate? • Regularity? regular flutter waves 0.06 s • P waves? • PR interval? none • QRS duration? Interpretation? Atrial Flutter
  • 109. 74 148 bpm• Rate? • Regularity? Regular  regularNormal  none 0.08 s • P waves? • PR interval? 0.16 s  none • QRS duration? Interpretation? Paroxysmal Supraventricular Tachycardia (PSVT)
  • 110.  Deviation from NSRDeviation from NSR The heart rate suddenly speeds up,The heart rate suddenly speeds up, often triggered by a PAC (not seenoften triggered by a PAC (not seen here) and the P waves are lost.here) and the P waves are lost.
  • 111.  Ventricular TachycardiaVentricular Tachycardia  Ventricular FibrillationVentricular Fibrillation
  • 112. 160 bpm• Rate? • Regularity? regular none wide (> 0.12 sec) • P waves? • PR interval? none • QRS duration? Interpretation? Ventricular Tachycardia
  • 113.  Deviation from NSRDeviation from NSR Impulse is originating in the ventriclesImpulse is originating in the ventricles (no P waves, wide QRS).(no P waves, wide QRS).
  • 114. none• Rate? • Regularity? irregularly irreg. none wide, if recognizable • P waves? • PR interval? none • QRS duration? Interpretation? Ventricular Fibrillation
  • 115.  Deviation from NSRDeviation from NSR Completely abnormal.Completely abnormal.
  • 116. Arrhythmias can arise from problems inArrhythmias can arise from problems in the:the: • Sinus nodeSinus node • Atrial cellsAtrial cells • AV junctionAV junction • Ventricular cellsVentricular cells
  • 117. The SA Node can:The SA Node can:  fire too slowfire too slow  fire too fastfire too fast Sinus BradycardiaSinus Bradycardia Sinus TachycardiaSinus Tachycardia Sinus Tachycardia may be an appropriate response to stress.
  • 118. Atrial cells can:Atrial cells can:  fire occasionallyfire occasionally from a focusfrom a focus  fire continuouslyfire continuously due to a loopingdue to a looping re-entrant circuitre-entrant circuit Premature AtrialPremature Atrial Contractions (PACs)Contractions (PACs) Atrial FlutterAtrial Flutter
  • 119. The AV junction can:The AV junction can:  fire continuouslyfire continuously due to a looping re-due to a looping re- entrant circuitentrant circuit  block impulsesblock impulses coming from the SAcoming from the SA NodeNode ParoxysmalParoxysmal SupraventricularSupraventricular TachycardiaTachycardia AV Junctional BlocksAV Junctional Blocks
  • 120. 30 bpm• Rate? • Regularity? regular normal 0.10 s • P waves? • PR interval? 0.12 s • QRS duration? Interpretation? Sinus Bradycardia
  • 121. 130 bpm• Rate? • Regularity? regular normal 0.08 s • P waves? • PR interval? 0.16 s • QRS duration? Interpretation? Sinus Tachycardia
  • 122. 70 bpm• Rate? • Regularity? occasionally irreg. 2/7 different contour 0.08 s • P waves? • PR interval? 0.14 s (except 2/7) • QRS duration? Interpretation? NSR with Premature Atrial Contractions
  • 123.  Deviation from NSRDeviation from NSR These ectopic beats originate in theThese ectopic beats originate in the atria (but not in the SA node),atria (but not in the SA node), therefore the contour of the P wave,therefore the contour of the P wave, the PR interval, and the timing arethe PR interval, and the timing are different than a normally generateddifferent than a normally generated pulse from the SA node.pulse from the SA node.
  • 124. 60 bpm• Rate? • Regularity? occasionally irreg. none for 7th QRS 0.08 s (7th wide) • P waves? • PR interval? 0.14 s • QRS duration? Interpretation? Sinus Rhythm with 1 PVC
  • 125. Normal Signal moves rapidly through the ventricles Abnormal Signal moves slowly through the ventricles
  • 126.  1st Degree AV Block1st Degree AV Block  2nd Degree AV Block, Type I2nd Degree AV Block, Type I  2nd Degree AV Block, Type II2nd Degree AV Block, Type II  3rd Degree AV Block3rd Degree AV Block
  • 127. 60 bpm• Rate? • Regularity? regular normal 0.08 s • P waves? • PR interval? 0.36 s • QRS duration? Interpretation? 1st Degree AV Block
  • 128.  Etiology:Etiology: Prolonged conduction delay in theProlonged conduction delay in the AV node or Bundle of His.AV node or Bundle of His.
  • 129. 50 bpm• Rate? • Regularity? regularly irregular nl, but 4th no QRS 0.08 s • P waves? • PR interval? lengthens • QRS duration? Interpretation? 2nd Degree AV Block, Type I
  • 130. 40 bpm• Rate? • Regularity? regular nl, 2 of 3 no QRS 0.08 s • P waves? • PR interval? 0.14 s • QRS duration? Interpretation? 2nd Degree AV Block, Type II
  • 131.  Deviation from NSRDeviation from NSR Occasional P waves are completelyOccasional P waves are completely blocked (P wave not followed byblocked (P wave not followed by QRS).QRS).
  • 132. 40 bpm• Rate? • Regularity? regular no relation to QRS wide (> 0.12 s) • P waves? • PR interval? none • QRS duration? Interpretation? 3rd Degree AV Block
  • 133.  Deviation from NSRDeviation from NSR The P waves are completely blocked inThe P waves are completely blocked in the AV junction; QRS complexesthe AV junction; QRS complexes originate independently from beloworiginate independently from below the junction.the junction.
  • 134.  Atrial FibrillationAtrial Fibrillation  Atrial FlutterAtrial Flutter  Paroxysmal SupraventricularParoxysmal Supraventricular TachycardiaTachycardia
  • 135. 100 bpm• Rate? • Regularity? irregularly irregular none 0.06 s • P waves? • PR interval? none • QRS duration? Interpretation? Atrial Fibrillation
  • 136.  Deviation from NSRDeviation from NSR No organized atrial depolarization, soNo organized atrial depolarization, so no normal P waves (impulses are notno normal P waves (impulses are not originating from the sinus node).originating from the sinus node). Atrial activity is chaotic (resulting inAtrial activity is chaotic (resulting in an irregularly irregular rate).an irregularly irregular rate). Common, affects 2-4%, up to 5-10% ifCommon, affects 2-4%, up to 5-10% if > 80 years old> 80 years old
  • 137. 70 bpm• Rate? • Regularity? regular flutter waves 0.06 s • P waves? • PR interval? none • QRS duration? Interpretation? Atrial Flutter
  • 138. 74 148 bpm• Rate? • Regularity? Regular  regularNormal  none 0.08 s • P waves? • PR interval? 0.16 s  none • QRS duration? Interpretation? Paroxysmal Supraventricular Tachycardia (PSVT)
  • 139.  Deviation from NSRDeviation from NSR The heart rate suddenly speeds up,The heart rate suddenly speeds up, often triggered by a PAC (not seenoften triggered by a PAC (not seen here) and the P waves are lost.here) and the P waves are lost.
  • 140.  Ventricular TachycardiaVentricular Tachycardia  Ventricular FibrillationVentricular Fibrillation
  • 141. 160 bpm• Rate? • Regularity? regular none wide (> 0.12 sec) • P waves? • PR interval? none • QRS duration? Interpretation? Ventricular Tachycardia
  • 142.  Deviation from NSRDeviation from NSR Impulse is originating in the ventriclesImpulse is originating in the ventricles (no P waves, wide QRS).(no P waves, wide QRS).
  • 143. none• Rate? • Regularity? irregularly irreg. none wide, if recognizable • P waves? • PR interval? none • QRS duration? Interpretation? Ventricular Fibrillation
  • 144.  Deviation from NSRDeviation from NSR Completely abnormal.Completely abnormal.
  • 145. To diagnose a myocardial infarction you needTo diagnose a myocardial infarction you need to go beyond looking at a rhythm strip andto go beyond looking at a rhythm strip and obtain a 12-Lead ECG.obtain a 12-Lead ECG. Rhythm Strip 12-Lead ECG
  • 146. Some leads get aSome leads get a good view of the:good view of the: Anterior portion of the heart Lateral portion of the heart Inferior portion of the heart
  • 147. One way toOne way to diagnose andiagnose an acute MI is toacute MI is to look forlook for elevation of theelevation of the ST segment.ST segment.
  • 148. Elevation of the STElevation of the ST segment (greatersegment (greater than 1 small box) inthan 1 small box) in 2 leads is consistent2 leads is consistent with a myocardialwith a myocardial infarction.infarction.
  • 149. The anterior portion of the heart is best viewedThe anterior portion of the heart is best viewed using leads Vusing leads V11- V- V44..
  • 150. If you see changes in leads VIf you see changes in leads V11 - V- V44 that are consistent with athat are consistent with a myocardial infarction, you canmyocardial infarction, you can conclude that it is an anterior wallconclude that it is an anterior wall myocardial infarction.myocardial infarction.
  • 151. Do you think this person is having aDo you think this person is having a myocardial infarction. If so, where?myocardial infarction. If so, where?
  • 152. YesYes, this person is having an acute anterior, this person is having an acute anterior wall myocardial infarction.wall myocardial infarction.
  • 153. Now that you know where to look for anNow that you know where to look for an anterior wall myocardial infarction let’s lookanterior wall myocardial infarction let’s look at how you would determine if the MIat how you would determine if the MI involves the lateral wall or the inferior wall ofinvolves the lateral wall or the inferior wall of the heart.the heart.
  • 154. First, take a lookFirst, take a look again at this pictureagain at this picture of the heart.of the heart. Anterior portion of the heart Lateral portion of the heart Inferior portion of the heart
  • 155. Second, remember that the 12-leads of the ECG look atSecond, remember that the 12-leads of the ECG look at different portions of the heart. The limb and augmented leadsdifferent portions of the heart. The limb and augmented leads “see” electrical activity moving inferiorly (II, III and aVF), to“see” electrical activity moving inferiorly (II, III and aVF), to the left (I, aVL) and to the right (aVR). Whereas, the precordialthe left (I, aVL) and to the right (aVR). Whereas, the precordial leads “see” electrical activity in the posterior to anteriorleads “see” electrical activity in the posterior to anterior direction.direction. Limb Leads Augmented Leads Precordial Leads
  • 156. Now, using these 3 diagrams let’s figure where toNow, using these 3 diagrams let’s figure where to look for a lateral wall and inferior wall MI.look for a lateral wall and inferior wall MI. Limb Leads Augmented Leads Precordial Leads
  • 157. Remember the anterior portion of the heart is bestRemember the anterior portion of the heart is best viewed using leads Vviewed using leads V11- V- V44.. Limb Leads Augmented Leads Precordial Leads
  • 158. So what leads do you thinkSo what leads do you think the lateral portion of thethe lateral portion of the heart is best viewed?heart is best viewed? Limb Leads Augmented Leads Precordial Leads Leads I, aVL, and V5- V6
  • 159. Now how about theNow how about the inferior portion of theinferior portion of the heart?heart? Limb Leads Augmented Leads Precordial Leads Leads II, III and aVF
  • 160. Now, where do you think this person isNow, where do you think this person is having a myocardial infarction?having a myocardial infarction?
  • 161. This is an inferior MI. Note the ST elevationThis is an inferior MI. Note the ST elevation in leads II, III and aVF.in leads II, III and aVF.
  • 162. How about now?How about now?
  • 163. This person’s MI involvesThis person’s MI involves bothboth the anteriorthe anterior wall (Vwall (V22-V-V44) and the lateral wall (V) and the lateral wall (V55-V-V66, I, and, I, and aVL)!aVL)!
  • 164.
  • 165. Right atrial enlargementRight atrial enlargement  Take a look at this ECG. What do you notice aboutTake a look at this ECG. What do you notice about the P waves?the P waves? The P waves are tall, especially in leads II, III and avF. Ouch! They would hurt to sit on!!
  • 166. Right atrial enlargementRight atrial enlargement  To diagnose RAE you can use the following criteria:To diagnose RAE you can use the following criteria:  IIII P > 2.5 mmP > 2.5 mm, or, or  V1 or V2V1 or V2 P > 1.5 mmP > 1.5 mm Remember 1 small box in height = 1 mm A cause of RAE is RVH from pulmonary hypertension. > 2 ½ boxes (in height) > 1 ½ boxes (in height)
  • 167. Left atrial enlargementLeft atrial enlargement  Take a look at this ECG. What do you notice aboutTake a look at this ECG. What do you notice about the P waves?the P waves? The P waves in lead II are notched and in lead V1 they have a deep and wide negative component. Notched Negative deflection
  • 168. Left atrial enlargementLeft atrial enlargement  To diagnose LAE you can use the following criteria:To diagnose LAE you can use the following criteria:  IIII > 0.04 s (1 box) between notched peaks> 0.04 s (1 box) between notched peaks, or, or  V1V1 Neg. deflection > 1 box wide x 1 box deepNeg. deflection > 1 box wide x 1 box deep Normal LAE A common cause of LAE is LVH from hypertension.
  • 169.
  • 170. Compare these two 12-lead ECGs. WhatCompare these two 12-lead ECGs. What stands out as different with the second one?stands out as different with the second one? Normal Left Ventricular Hypertrophy Answer: The QRS complexes are very tall (increased voltage)
  • 171.  Criteria exists to diagnose LVH using a 12-lead ECG.Criteria exists to diagnose LVH using a 12-lead ECG.  For example:For example:  The R wave in V5 or V6 plus the S wave in V1 or V2The R wave in V5 or V6 plus the S wave in V1 or V2 exceeds 35 mm.exceeds 35 mm. • However, for now, all you need to know is that the QRS voltage increases with LVH.
  • 172. Right ventricular hypertrophyRight ventricular hypertrophy  Take a look at this ECG. What do you notice aboutTake a look at this ECG. What do you notice about the axis and QRS complexes over the rightthe axis and QRS complexes over the right ventricle (V1, V2)?ventricle (V1, V2)? There is right axis deviation (negative in I, positive in II) and there are tall R waves in V1, V2.
  • 173. Right ventricular hypertrophyRight ventricular hypertrophy  To diagnose RVH you can use the following criteria:To diagnose RVH you can use the following criteria:  Right axis deviationRight axis deviation, and, and  V1V1 R wave > 7mm tallR wave > 7mm tall A common cause of RVH is left heart failure.
  • 174. Right ventricular hypertrophyRight ventricular hypertrophy  Compare the R waves in V1, V2 from a normal ECG and oneCompare the R waves in V1, V2 from a normal ECG and one from a person with RVH.from a person with RVH.  Notice the R wave is normally small in V1, V2 because theNotice the R wave is normally small in V1, V2 because the right ventricle does not have a lot of muscle mass.right ventricle does not have a lot of muscle mass.  But in the hypertrophied right ventricle the R wave is tall inBut in the hypertrophied right ventricle the R wave is tall in V1, V2.V1, V2. Normal RVH
  • 175. Left ventricular hypertrophyLeft ventricular hypertrophy  Take a look at this ECG. What do you notice aboutTake a look at this ECG. What do you notice about the axis and QRS complexes over the left ventriclethe axis and QRS complexes over the left ventricle (V5, V6) and right ventricle (V1, V2)?(V5, V6) and right ventricle (V1, V2)? There is left axis deviation (positive in I, negative in II) and there are tall R waves in V5, V6 and deep S waves in V1, V2. The deep S waves seen in the leads over the right ventricle are created because the heart is depolarizing left, superior and posterior (away from leads V1, V2).
  • 176. Left ventricular hypertrophyLeft ventricular hypertrophy  To diagnose LVH you can use the followingTo diagnose LVH you can use the following criteria*:criteria*:  R in V5 (or V6) + S in V1 (or V2) > 35 mmR in V5 (or V6) + S in V1 (or V2) > 35 mm, or, or  avLavL R > 13 mmR > 13 mm A common cause of LVH is hypertension. * There are several other criteria for the diagnosis of LVH. S = 13 mm R = 25 mm
  • 177.
  • 178. Normal Impulse Conduction Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers
  • 179. So, conduction in theSo, conduction in the Bundle Branches andBundle Branches and Purkinje fibers arePurkinje fibers are seen as the QRSseen as the QRS complex on the ECG.complex on the ECG. Therefore, a conduction block of the Bundle Branches would be reflected as a change in the QRS complex. Right BBB
  • 180. With Bundle Branch Blocks you will see twoWith Bundle Branch Blocks you will see two changes on the ECG.changes on the ECG. 1.1. QRS complex widensQRS complex widens (> 0.12 sec)(> 0.12 sec).. 2.2. QRS morphology changesQRS morphology changes (varies depending on ECG(varies depending on ECG lead, and if it is a right vs. left bundle branch block)lead, and if it is a right vs. left bundle branch block)..
  • 181.
  • 182. What QRS morphology is characteristic?What QRS morphology is characteristic? V1 For RBBB the wide QRS complex assumes a unique, virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2). “Rabbit Ears”
  • 183.
  • 184.
  • 185. What QRS morphology is characteristic?What QRS morphology is characteristic? For LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2). Broad, deep S waves Normal

Editor's Notes

  1. Atrial depolarisation Electrically both atria act almost as one. They have relatively little muscle and generate a single, small P wave. P wave amplitude rarely exceeds two and a half small squares (0.25 mV). The duration of the P wave should not exceed three small squares (0.12 s). The wave of depolarisation is directed inferiorly and towards the left, and thus the P wave tends to be upright in leads I and II and inverted in lead aVR. Sinus P waves are usually most prominently seen in leads II and V1. A negative P wave in lead I may be due to incorrect recording of the electrocardiogram (that is, with transposition of the left and right arm electrodes), dextrocardia, or abnormal atrial rhythms. Normal P waves may have a slight notch, particularly in the precordial (chest) leads. Bifid P waves result from slight asynchrony between right and left atrial depolarisation. A pronounced notch with a peak­to­peak interval of &amp;gt; 1 mm (0.04 s) is usually pathological, and is seen in association with a left atrial abnormality—for example, in mitral stenosis.
  2. The R wave in lead V6 is smaller than the R wave in V5, since the V6 electrode is further from the left ventricle. The depth of the S wave, generally, should not exceed 30 mm in a normal individual (although &amp;gt; 30 mm are occasionally recorded in normal young male adults) In another website it is also shown that small q wave seen in leads III and aVF Normal q-waves reflect normal septal activation (beginning on the LV septum); they are narrow (&amp;lt;0.04s duration) and small (&amp;lt;25% the amplitude of the R wave). They are often seen in leads I and aVL when the QRS axis is to the left of +60o, and in leads II, III, aVF when the QRS axis is to the right of +60o. Septal q waves should not be confused with the pathologic Q waves of myocardial infarction (http://medstat.med.utah.edu/kw/ecg/ecg_outline/Lesson3/index.html)
  3. Sokolow + Lyon (Am Heart J, 1949;37:161) S V1+ R V5 or V6 &amp;gt; 35 mm Cornell criteria (Circulation, 1987;3: 565-72) SV3 + R avl &amp;gt; 28 mm in men SV3 + R avl &amp;gt; 20 mm in women Framingham criteria (Circulation,1990; 81:815-820) R avl &amp;gt; 11mm, R V4-6 &amp;gt; 25mm S V1-3 &amp;gt; 25 mm S V1 or V2 + R V5 or V6 &amp;gt; 35 mm R I + S III &amp;gt; 25 mm Romhilt + Estes (Am Heart J, 1986:75:752-58) Point score system
  4. ST segment depression is always an abnormal finding, although often nonspecific (http://medstat.med.utah.edu/kw/ecg/ecg_outline/Lesson3/index.html)
  5. As a general rule, T wave amplitude corresponds with the amplitude of the preceding R wave, though the tallest T waves are seen in leads V3 and V4. Tall T waves may be seen in acute myocardial ischaemia and are a feature of hyperkalaemia.
  6. Poor Man&amp;apos;s Guide to upper limits of QT: For HR = 70 bpm, QT&amp;lt;0.40 sec; for every 10 bpm increase above 70 subtract 0.02 sec, and for every 10 bpm decrease below 70 add 0.02 sec. For example: QT &amp;lt; 0.38 @ 80 bpm QT &amp;lt; 0.42 @ 60 bpm