3. HISTORY
ā¢ 1842- Italian scientist Carlo Matteucci realizes that
electricity is associated with the heart beat
ā¢ 1876- Irish scientist Marey analyzes the electric
pattern of frogās heart
ā¢ 1895 - William Einthoven , credited for the invention
of EKG
ā¢ 1906 - using the string electrometer EKG,
William Einthoven diagnoses some heart problems
6. What is an EKG?
ā¢The electrocardiogram (EKG) is a representation
of the electrical events of the cardiac cycle.
ā¢Each event has a distinctive waveform
ā¢the study of waveform can lead to greater insight
into a patientās cardiac pathophysiology.
ā¢Electrocardiograph ā is the instrument that
records the electrical activity of the heart
8. 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)
9. Pacemakers of the Heart
ā¢ SA Node - Dominant pacemaker with an
intrinsic rate of 60 - 100 beats/minute.
ā¢ AV Node - Back-up pacemaker with an
intrinsic rate of 40 - 60 beats/minute.
ā¢ Ventricular cells - Back-up pacemaker with
an intrinsic rate of 20 - 45 bpm.
11. The ECG Paper
ā¢ Horizontally
ā One small box - 0.04 s
ā One large box - 0.20 s
ā¢ Vertically
ā One large box - 0.5 mV
12. ā¢ Standard calibration
ā 25 mm/s
ā 0.1 mV/mm
ā¢ Electrical impulse that
travels towards the
electrode produces an
upright (āpositiveā)
deflection
13. EKG Leads
which measure the difference in electrical potential
between two points
1. Bipolar Leads: Two different points on the body
2. Unipolar Leads: One point on the body and a virtual
reference point with zero electrical potential, located in
the center of the heart
14. EKG Leads
The standard EKG has 12 leads:
3 Standard Limb Leads
3 Augmented Limb Leads
6 Precordial Leads
36. P wave
ā¢ Always positive in lead I and II
ā¢ Always negative in lead aVR
ā¢ < 3 small squares in duration
ā¢ < 2.5 small squares in amplitude
ā¢ Commonly biphasic in lead V1
ā¢ Best seen in leads II
40. The PR Interval
Atrial depolarization
+
delay in AV junction
(AV node/Bundle of His)
(delay allows time for
the atria to contract
before the ventricles
contract)
41. Short PR Interval
ā¢ WPW (Wolff-
Parkinson-White)
Syndrome
ā¢ Accessory pathway
(Bundle of Kent) allows
early activation of the
ventricle (delta wave
and short PR interval)
resulting in Atrio
ventricular reentrant
tachycardia.
43. ā¢ can be due to:
ā¢ inferior MI
ā¢ digitalis toxicity
ā¢ hyperkalemia
ā¢ increased vagal tone
ā¢ acute rheumatic fever
ā¢ myocarditis.
44. QRS Complexes
ā¢ Non pathological Q waves may present in I, III, aVL,
V5, and V6
ā¢ R wave in lead V6 is smaller than V5.
ā¢ Depth of the S wave, should not exceed 30 mm
ā¢ Pathological Q wave > 2mm deep and > 1mm wide or
> 25% amplitude of the subsequent R wave
46. Left Ventricular Hypertrophy
ā¢ Sokolow & Lyon Criteria
ā¢ S in V1+ R in V5 or V6 > 35 mm
ā¢ An R wave of 11 to 13 mm (1.1 to 1.3 mV)
or more in lead aVL is another sign of LVH
Sokolow & Lyon Criteria: S (V1) + R(V5 or V6) > 35mm
Cornell Criteria: S (V3) + R (aVL) > 28 mm (men) or > 20 mm (women)
Others: R (aVL) > 13mm
49. RVH- R >S in V1 OR R > 7mm in V1
Rt axis deviation /rt ventricular strain
pattern
50. ST Segment
ā¢ ST Segment is flat (isoelectric)
ā¢ Elevation or depression of ST segment by 1
mm or more
ā¢ āJā (Junction) point is the point between
QRS and ST segment.
52. T wave
ā¢ Normal T wave is asymmetrical, first half having a
gradual slope than the second
ā¢ Should be at least 1/8 but less than 2/3 of the
amplitude of the R
ā¢ T wave amplitude rarely exceeds 10 mm
ā¢ Abnormal T waves are symmetrical, tall, peaked,
biphasic or inverted.
ā¢ T wave follows the direction of the QRS deflection.
53. IT waves Inversion are seen in the following conditions:
ā¢ Normal finding in children
ā¢ Persistent juvenile T wave pattern
ā¢ Myocardial ischaemia and infarction
ā¢ Bundle branch block
ā¢ Ventricular hypertrophy (āstrainā patterns)
ā¢ Pulmonary embolism
ā¢ Hypertrophic cardiomyopathy
ā¢ Raised intracranial pressure
T wave inversion in lead III is a normal variant. New T-
wave inversion (compared with prior ECGs) is always
abnormal. Pathological T wave inversion is usually
symmetrical and deep (>3mm).
54. Ā» Biphasic T waves- wellens type 2 syndrome
Ā» Camel hump T waves- severe
hypokalaemia(U waves) and sinus
tachycardia (hidden p waves )
55. QT interval
1. Total duration of Depolarization and
Repolarization of ventricles.
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).
Examples of Long QT syndromes- Jervell and Lange
-nielsen syndrome and Romano Ward syndrome
57. To calculate the heart rate-corrected QT interval QTc. Bazett's formula is used
Calculation of QT interval
ā¢Use lead II. Use lead V5 alternatively if lead II cannot be read.
ā¢Draw a line through the baseline (preferably the PR segment)
ā¢Draw a tangent against the steepest part of the end of the T wave. If the T wave has
two positive deflections, the taller deflection should be chosen. If the T wave is
biphasic, the end of the taller deflection should be chosen.
ā¢The QT interval starts at the beginning of the QRS interval and ends where the
tangent and baseline cross.
ā¢If the QRS duration exceeds 120ms the amount surpassing ,120ms should be
deducted from the QT interval (i.e. QT=QT-(QRS width-120ms) )
58. U wave
ā¢ U wave related to after depolarizations which
follow repolarization
ā¢ U waves are small, round, symmetrical and
positive in lead II, with amplitude < 2 mm
ā¢ U wave direction is the same as T wave
ā¢ More prominent at slow heart rates
59. U-WAVE
Prominent U waves are most often seen in hypokalemia, but may be present
in hypercalcemia, thyrotoxicosis, or exposure to digitalis,epinephrine, and Class 1A and
3 antiarrhythmics, as well as in congenital long QT syndrome, and in the setting of intracranial
hemorrhage.
An inverted U wave may represent myocardial ischemia or left ventricular volume overload
The U wave is a wave on an electrocardiogram that is not always seen. It is typically small,
and, by definition, follows the T wave. U waves are thought to represent repolarization of
the papillary muscles or Purkinje fibers
Normal U waves are small, round and symmetrical and positive in lead II. It is the same
direction as T wave in that lead.
62. Rule of 300
For Regular rhythms-
Count the number of ābig boxesā between two
QRS complexes, and divide this into 300. (smaller
boxes with 1500)
68. The QRS Axis
The QRS axis represents overall direction of the
heartās electrical activity.
Abnormalities hint at:
Ventricular enlargement
Conduction blocks (i.e. hemiblocks)
69. The QRS Axis
Normal QRS axis from -30Ā° to
+90Ā°.
-30Ā° to -90Ā° is referred to as a
left axis deviation (LAD)
+90Ā° to +180Ā° is referred to as
a right axis deviation (RAD)
72. 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.
73. The Quadrant Approach
1. When LAD is present,
2. If the QRS in II is positive, the LAD is non-pathologic or the
axis is normal
3. If negative, it is pathologic.
75. Quadrant Approach: Example 2
Positive in I, negative in aVF ā Predominantly positive in II ā
Normal Axis (non-pathologic LAD)
76. The Equiphasic Approach
1. Most equiphasic QRS complex.
2. Identified Lead lies 90Ā° away from the lead
3. QRS in this second lead is positive or Negative
80. SA Node Problems
The SA Node can:
ā¢ fire too slow
ā¢ fire too fast Sinus Bradycardia
Sinus Tachycardia
Sinus Tachycardia may be an appropriate
response to stress.
81. Atrial Cell Problems
Atrial cells can:
ā¢ fire occasionally
from a focus
ā¢ fire continuously
due to a looping re-
entrant circuit
Premature Atrial Contractions
(PACs)
Atrial Flutter
82. AV Junctional Problems
The AV junction can:
ā¢ fire continuously due
to a looping re-
entrant circuit
ā¢ block impulses
coming from the SA
Node
Paroxysmal
Supraventricular
Tachycardia
AV Junctional Blocks
83. Rhythm #1
30 bpmā¢ Rate?
ā¢ Regularity? regular
normal
0.10 s
ā¢ P waves?
ā¢ PR interval? 0.12 s
ā¢ QRS duration?
Interpretation? Sinus Bradycardia
85. Rhythm #2
130 bpmā¢ Rate?
ā¢ Regularity? regular
normal
0.08 s
ā¢ P waves?
ā¢ PR interval? 0.16 s
ā¢ QRS duration?
Interpretation? Sinus Tachycardia
86. Rhythm #3
70 bpmā¢ Rate?
ā¢ Regularity? occasionally irreg.
2/7 different contour
0.08 s
ā¢ P waves?
ā¢ PR interval? 0.14 s (except 2/7)
ā¢ QRS duration?
Interpretation? NSR with Premature Atrial
Contractions
87. Premature Atrial Contractions
ā¢ Deviation from NSR
ā These ectopic beats originate in the atria
(but not in the SA node), therefore the
contour of the P wave, the PR interval, and
the timing are different than a normally
generated pulse from the SA node.
88. Rhythm #4
60 bpmā¢ Rate?
ā¢ Regularity? occasionally irreg.
none for 7th QRS
0.08 s (7th wide)
ā¢ P waves?
ā¢ PR interval? 0.14 s
ā¢ QRS duration?
Interpretation? Sinus Rhythm with 1 PVC
89. RHYTHM
Junctional Premature Beat
Arises from an irritable focus at the AV junction. The P wave associated with atrial
depolarization in this instance is usually buried inside the QRS complex and not
visible. If p is visible, it is -ve in lead II and +ve in lead aVR and it it may occur before
or after QRS.
92. Atrial Fibrillation
ā¢ Deviation from NSR
ā No organized atrial depolarization, so no
normal P waves (impulses are not originating
from the sinus node).
ā Atrial activity is chaotic (resulting in an
irregularly irregular rate).
ā Common, affects 2-4%, up to 5-10% if > 80
years old
102. SA Block
ā¢ Sinus impulses is blocked within the SA junction
ā¢ Between SA node and surrounding myocardium
ā¢ Abscent of complete Cardiac cycle
ā¢ Occures irregularly and unpredictably
ā¢ Present :Young athletes, Digitalis, Hypokalemia, Sick
Sinus Syndrome
103. Rhythm #10
60 bpmā¢ Rate?
ā¢ Regularity? regular
normal
0.08 s
ā¢ P waves?
ā¢ PR interval? 0.36 s
ā¢ QRS duration?
Interpretation? 1st Degree AV Block
104. 1st Degree AV Block
ā¢ Etiology: Prolonged conduction delay in the AV
node or Bundle of His.
105. First Degree AV Block
ā¢ Delay in the conduction through the conducting system
ā¢ Prolong P-R interval
ā¢ All P waves are followed by QRS
ā¢ Associated with : AC Rheumatic Carditis, Digitalis, Beta
Blocker, excessive vagal tone, ischemia, intrinsic disease in
the AV junction or bundle branch system.
106. Rhythm #11
50 bpmā¢ Rate?
ā¢ Regularity? regularly irregular
nl, but 4th no QRS
0.08 s
ā¢ P waves?
ā¢ PR interval? lengthens
ā¢ QRS duration?
Interpretation? 2nd Degree AV Block, Type I
107. 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)
108. Rhythm #12
40 bpmā¢ Rate?
ā¢ Regularity? regular
nl, 2 of 3 no QRS
0.08 s
ā¢ P waves?
ā¢ PR interval? 0.14 s
ā¢ QRS duration?
Interpretation? 2nd Degree AV Block, Type II
109. 2nd Degree AV Block, Type II
ā¢ Deviation from NSR
ā Occasional P waves are completely blocked
(P wave not followed by QRS).
110. ā¢Mobitz type 2
ā¢Usually a sign of bilateral bundle branch disease.
ā¢One of the branches should be completely blocked;
ā¢most likely blocked in the right bundle
ā¢P waves may blocked somewhere in the AV junction, the
His bundle.
111. Rhythm #13
40 bpmā¢ Rate?
ā¢ Regularity? regular
no relation to QRS
wide (> 0.12 s)
ā¢ P waves?
ā¢ PR interval? none
ā¢ QRS duration?
Interpretation? 3rd Degree AV Block
112. 3rd Degree AV Block
ā¢ Deviation from NSR
ā The P waves are completely blocked in the
AV junction; QRS complexes originate
independently from below the junction.
113. Third Degree Heart Block
ā¢CHB evidenced by the AV dissociation
ā¢A junctional escape rhythm at 45 bpm.
ā¢The PP intervals vary because of ventriculophasic sinus arrhythmia;
114. Third Degree Heart Block
3rd degree AV block with a left ventricular escape rhythm,
'B' the right ventricular pacemaker rhythm is shown.
115. RHYTHM
Atrial Escape
a cardiac dysrhythmia occurring when sustained suppression of sinus impulse
formation causes other atrial foci to act as cardiac pacemakers. Rate= 60-80bpm,
p wave of atrial escape has abnormal axis and different from the p wave in the
sinus beat. However QRS complexes look exactly the same.
116. RHYTHM
Junctional Escape
Depolarization initiated in the atrioventricular junction when one or more
impulses from the sinus node are ineffective or nonexistent. Rate: 40-60 bpm,
Rhythm: Irregular in single junctional escape complex; regular in junctional escape
rhythm, P waves: Depends on the site of the ectopic focus. They will be inverted,
and may appear before or after the QRS complex, or they may be absent, hidden
by the QRS. QRS is usually normal
118. RHYTHM
Torsades de Pointes
literally meaning twisting of points, is a distinctive form of polymorphic
ventricular tachycardia characterized by a gradual change in the amplitude
and twisting of the QRS complexes around the isoelectric line. Rate cannot be
determined.
119. RHYTHM
Asystole
a state of no cardiac electrical activity, hence no contractions of the myocardium
and no cardiac output or blood flow.
Rate, rhythm, p and QRS are absent
120. RHYTHM
Artificial pacemaker
Sharp, thin spike. Rate depends on pacemaker, p wave maybe
absent or present
Ventricular paced rhythm shows wide ventricular pacemaker
spikes
121. RHYTHM
Asystole
a state of no cardiac electrical activity, hence no contractions of the myocardium
and no cardiac output or blood flow.
Rate, rhythm, p and QRS are absent
127. Diagnosing a MI
To diagnose a myocardial infarction you need to
go beyond looking at a rhythm strip and obtain
a 12-Lead ECG.
Rhythm
Strip
12-Lead
ECG
128. ST Elevation (cont)
Elevation of the ST
segment (greater
than 1 small box) in
2 leads is consistent
with a myocardial
infarction.
129. Anterior MI
Remember the anterior portion of the heart is best
viewed using leads V1- V4.
Limb Leads Augmented Leads Precordial Leads
130. Lateral MI
So what leads do you think
the lateral portion of the
heart is best viewed?
Limb Leads Augmented Leads Precordial Leads
Leads I, aVL, and V5- V6
131. Inferior MI
Now how about the inferior
portion of the heart?
Limb Leads Augmented Leads Precordial Leads
Leads II, III and aVF
135. Right atrial enlargement
ā To diagnose RAE you can use the following criteria:
ā¢ II P > 2.5 mm, or
ā¢ V1 or V2 P > 1.5 mm
Remember 1 small box
in height = 1 mm
A cause of RAE is RVH from pulmonary hypertension.
> 2 Ā½ boxes (in height)
> 1 Ā½ boxes (in height)
136. Left atrial enlargement
ā To diagnose LAE you can use the following criteria:
ā¢ II > 0.04 s (1 box) between notched peaks, or
ā¢ V1 Neg. deflection > 1 box wide x 1 box deep
Normal LAE
A common cause of LAE is LVH from hypertension.
137. Right ventricular hypertrophy
ā To diagnose RVH you can use the following criteria:
ā¢ Right axis deviation, and
ā¢ V1 R wave > 7mm tall
A common
cause of RVH
is left heart
failure.
138. Right ventricular hypertrophy
ā Compare the R waves in V1, V2 from a normal ECG and one from a
person with RVH.
ā Notice the R wave is normally small in V1, V2 because the right ventricle
does not have a lot of muscle mass.
ā But in the hypertrophied right ventricle the R wave is tall in V1, V2.
Normal RVH
139. Left ventricular hypertrophy
ā To diagnose LVH you can use the following criteria*:
ā¢ R in V5 (or V6) + S in V1 (or V2) > 35 mm, or
ā¢ avL R > 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
142. Bundle Branch Blocks
With Bundle Branch Blocks you will see two changes on
the ECG.
1. QRS complex widens (> 0.12 sec).
2. QRS morphology changes (varies depending on ECG lead,
and if it is a right vs. left bundle branch block).
143. Right Bundle Branch Blocks
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).
āRabbit Earsā
144. Left Bundle Branch Blocks
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
149. Narrow and tall peaked T wave (A) is an early sign
PR interval becomes longer
P wave loses its amplitude and may disappear
QRS complex widens (B)
When hyperkalemia is very severe, the widened QRS complexes merge with their corresponding T
waves and the resultant ECG looks like a series of sine waves (C).
If untreated, the heart arrests in asystole
T wave becomes flattened together with appearance of a prominent U wave.
The ST segment may become depressed and the T wave inverted.
these additional changes are not related to the degree of hypokalemia.
HYPERKALAEMIA
HYPOKALAEMIA
153. Usually, signs are not obvious
Hypercalcemia is associated with short QT interval (A) and
Hypocalcemia with long QT interval (B).
Interval shortening or lengthening is mainly in the ST segment.
HYPERCALCEMIA/HYPOCALCEMIA
155. ACUTE PERICARDITIS
ā¢ stage 1 ā widespread STE and PR
depression with reciprocal changes in aVR
(occurs the first two weeks)
ā¢ Stage 2 ā normalization of ST changes;
generalized T wave flattening (1 to 3 weeks)
ā¢ Stage 3ā Flattened T waves become
inverted (3 to several weeks)
ā¢ Stage 4 ā ECG returns to normal (several
weeks onwards)
158. PULMONARY EMBOLISM
Tachycardia and incomplete RBBB differentiated PE from no PE.
SIQIIITIII = deep S wave in lead I, pathological Q wave in lead III, and inverted T wave in
lead III.
The ECG is often abnormal in PE, but findings are not sensitive, not specific
Any cause of acute cor pulmonale can cause the S1Q3T3 finding on the ECG.
