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1.
2.
3. 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.
9. 9
The 12-Leads
The 12-leads include:
–3 Limb leads
(I, II, III)
–3 Augmented leads
(aVR, aVL, aVF)
1942- Goldberger increased Wilson’s Unipolar
lead voltage by 50%
–6 Precordial leads
(V1- V6)
1938 -AHA and Cardiac society of great Britain
1906 - William Einthoven diagnoses some heart
problems , 1924 - the noble prize
10. 60 – 100 times a minute
40 – 60 times a minute
20 – 40 times a minute
16. ECG RULES
• Professor Chamberlains 10 rules of normal:-
1. PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
2. The width of the QRS complex should not exceed 110 ms, less than 3
little squares
3. The QRS complex should be dominantly upright in leads I and II
4. QRS and T waves tend to have the same general direction in the limb
leads
5. All waves are negative in lead aVR
6. 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
7. The ST segment should start isoelectric
8. The P waves should be upright in I, II, and V2 to V6
9. There should be no Q wave or only a small q less than 0.04 seconds
in width in I, II, V2 to V6
10. The T wave must be upright in I, II, V2 to V6
21. Why “1500 / X”?
• Paper Speed: 25 mm/ sec
• 60 seconds / minute
• 60 X 25 = 1500 mm / minute
• 60 X 5 = 300 big square / minute
• Take 6 sec strip (30 large boxes)
• Count the P/R waves X 10
OR
22. DR/ SHAFEI LASHEEN
Step 1: Calculate Rate when
rhythm is regular
– Find a R wave that lands on a bold line.
– Count the # of large boxes to the next R wave.
– HR = 300/ no large boxes between R-R interval
– Count the # of small boxes to the next R wave
– HR= 1500/ no small boxes between R-R interval
R wave
23. DR/SHAFEI LASHEEN
HR if irregular rhythm
– Count the # of R waves in a 6 second rhythm
strip, then multiply by 10.
– Reminder: all rhythm strips in the Modules are
6 seconds in length.
Interpretation?
9 x 10 = 90 bpm
3 sec 3 sec
24. DR/ SHAFEI LASHEEN
Step 2: Determine rhythm
• Look at the R-R distances (using a caliper or
markings on a pen or paper).
• Regular (are they equidistant apart)? Occasionally
irregular? Regularly irregular? Irregularly
irregular?
Interpretation? Regular
R R
34. True LAD
• So again, if lead I is positive and aVF is
negative, we suspect LAD
• To diagnose true LAD, we examine lead II:
– If lead II is positive, axis = 0° to –30°
– If lead II is negative , axis = –30° to –90°
35. Extreme RAD
• If lead I is negative AND aVF is also
negative – extreme RAD
• Clue: If aVR is positive = extreme RAD
• This is seen with rare situations such as VT or
Pacemakers
• In general we should never have an axis over
here!
44. DR/ SHAFEI LASHEEN
Step 3: Assess the P waves
• Are there P waves?
• Do the P waves all look alike?
• Do the P waves occur at a regular rate?
• Is there one P wave before each QRS?
Interpretation? Normal P waves with 1 P
wave for every QRS
45.
46. PR Interval
Measured from the beginning of the P wave to the
beginning of the Q wave.
Normal PR interval ranges from 0.12 to 0.20 second.
PR interval
47. PR interval
Definition: the time
interval between
beginning of P-wave
to beginning of QRS
complex.
Normal PR interval
3-5mm or 3-5 small
squares on ECG
graph (0.12-0.2 sec)
Abnormalities
1. Short PR interval
• WPW syndrome
2. Long PR interval
• First degree heart
block
53. QRS complex
Normal values
• Duration: < 2.5 mm.
• Morphology:
progression from Short
R and deep S (r/s) in V1
to tall R and short S in
V6 with small Q in V5-6.
Abnormalities:
1. Wide QRS complex
• Bundle branch block.
• Ventricular rhythm.
2. Tall R in V1
• RVH.
• RBBB.
• Posterior MI.
• WPW syndrome.
3. abnormal Q wave
[ > 25% of R wave]
• MI.
• Hypertrophic
cardiomyopathy.
• Normal variant.
54. Small voltage QRS
• Defined as < 5 mm peak-to-peak in all
limb leads or <10 mm in precordial chest
leads.
• causes — pulmonary disease,
hypothyroidism, obesity,
cardiomyopathy.
• Acute causes — pleural and/or
pericardial effusions
62. Abnormal Q waves
• The duration or width of Q waves
becomes more than one small square on
ECG graph.
• The depth of Q wave becomes more than
25% of R wave.
• The above changes comprise pathological
Q wave and happens commonly in
myocardial infarction and septal
hypertrophy.
73. NORMAL ST- SEGMENT
it's isoelectric.
[i.e. at same level of PR
or PQ segment at least
in the beginning]
74. Abnormalities
1. ST elevation:
More than one small
square
• Acute MI.
• Prinzmetal angina.
• Acute pericarditis.
• Early repolarization
ST depression:
More than one small
square
• Ischemia.
• Ventricular strain.
• BBB.
• Hypokalemia.
• Digoxin effect.
79. QT- interval
Definition: Time interval between beginning of
QRS complex to the end of T wave.
Normally: At normal HR: QT ≤ 11mm (0.44
sec)
Abnormalities:
1. Prolonged QT interval: hypocalcemia and
congenital long QT syndrome.
2. Short QT interval: hypercalcemia.
80. DR/ SHAFEI LASHEEN
QTc interval
@ HR 70 QT< 0.40 sec
@ HR 80 QT< 0.38 sec
@ HR 60 QT< 0.42 sec
< 0.44 s > 0.44 s
Normal Long QT
A prolonged QT can be very dangerous. It may predispose an individual to a type of
ventricular tachycardia called Torsades de Pointes. Causes include drugs, electrolyte
abnormalities, CNS disease, post-MI, and congenital heart disease.
Torsades de Pointes
Long QT
81. EKG Intervals
1. P-wave < 0.110 sec (approximately 3 small boxes)
2. PR interval = beginning of the P-wave to the
beginning of QRS. Normal = 0.120 – 0.200 sec
3. QRS interval = from the first deflection to return to
the baseline. Normal < 0.120 sec
4. QT interval = beginning of the QRS to the END of
the T-wave. Normal < 0.450 sec
82.
83. U Wave
Represents the last phase of
repolarization.
The exact significance is
unknown.
Characteristic of
hypokalemia.
May predispose to
ventricular arrhythmias.
U Wave
85. 1. Every QRS is preceded by a P-wave
2. P-waves appear normal, that is they are of sinus
node origin:
A. Normal Morphology:
1. P-wave duration < 0.12 sec (< 3 boxes)
2. P-wave height < 2.5 mm
B. Normal Axis – upright P-waves in lead II
Sinus Rhythm…or Not!
86. DR/ SHAFEI LASHEEN
Rhythm Summary
• Rate 90-95 bpm
• Regularity regular
• P waves normal
• PR interval 0.12 s
• QRS duration 0.08 s
Interpretation? Normal Sinus Rhythm
87. DR/ SHAFEI LASHEEN
NSR Parameters
• Rate 60 - 100 bpm
• Regularity regular
• P waves normal
• PR interval 0.12 - 0.20 s
• QRS duration 0.04 - 0.12 s
Any deviation from above is sinus Tachycardia,
sinus bradycardia or an arrhythmia
90. What types of pathology can we identify
and study from EKGs?
91. DR/ SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in the:
• Sinus node
• Atrial cells
• AV junction
• Ventricular cells
92. DR/ SHAFEI LASHEEN
SA Node Problems
The SA Node can:
• fire too slow
• fire too fast
SAN diseases
Sinus Arrhythmia
Sinus Bradycardia
Sinus Tachycardia
(Sinus Tachycardia may be an appropriate
response to stress.)
93. DR / SHAFEI LASHEEN
Rhythm #1
30 bpm• Rate?
• Regularity? regular
normal
0.10 s
• P waves?
• PR interval? 0.12 s
• QRS duration?
Interpretation? Sinus Bradycardia
94. DR/ SHAFEI LASHEEN
Rhythm #2
130 bpm• Rate?
• Regularity? regular
normal
0.08 s
• P waves?
• PR interval? 0.16 s
• QRS duration?
Interpretation? Sinus Tachycardia
97. Sick Sinus Syndrome
Sinoatrial block (note the pause
is twice the P-P interval)
Sinus arrest with pause of 4.4 s
before generation and conduction
of a junctional escape beat
Severe sinus bradycardia
99. DR/ SHAFEI LASHEEN
Atrial Cell Problems
• fire occasionally
from a focus
• fire continuously due
to a looping re-
entrant circuit
Premature Atrial
Contractions (PACs)
Atrial Flutter
100. DR/ SHAFEI LASHEEN
Premature Atrial Contractions
• Deviation from NSR
– 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.
101. DR/ SHAFEI LASHEEN
Rhythm #3
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
109. DR/ SHAFEI LASHEEN
AV Junctional Problems
The AV junction can:
• fire continuously
due to a looping re-
entrant circuit
• block impulses
coming from the SA
Node
Paroxysmal
Supraventricular
Tachycardia
AV Junctional Blocks
110. DR/ SHAFEI LASHEEN
Rhythm #7
74 148 bpm• Rate?
• Regularity? Regular regular
Normal none
0.08 s
• P waves?
• PR interval? 0.16 s none
• QRS duration?
Interpretation? Paroxysmal Supraventricular
Tachycardia (PSVT)
112. Junctional Premature Beat
• single ectopic beat that originates in the AV node
or
• Bundle of His area of the condunction system
• – Retrograde P waves immediately preceding the
QRS
• – Retrograde P waves immediately following the
QRS
• – Absent P waves (buried in the QRS)
116. DR/ SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells can:
• fire occasionally
from 1 or more foci
• fire continuously
from multiple foci
• fire continuously
due to a looping re-
entrant circuit
Premature Ventricular
Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
117. DR/ SHAFEI LASHEEN
Ventricular Conduction
Normal
Signal moves rapidly
through the ventricles
Abnormal
Signal moves slowly
through the ventricles
136. Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR
interval
2nd Degree, Mobitz Type I
Progressive PR interval
prolongation
2nd Degree, Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
137. DR/ SHAFEI LASHEEN
60 bpm• Rate?
• Regularity? regular
normal
0.08 s
• P waves?
• PR interval? 0.36 s
• QRS duration?
Interpretation? 1st Degree AV Block
138. Second Degree AV Block
• Mobitz type I or Winckebach
• Mobitz type II
139. DR/ SHAFEI LASHEEN
Rhythm #11
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
140. DR/ SHAFEI LASHEEN
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
141. Third Degree AV Block
(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60
BPM
Two independent pacemakers
142. Third Degree AV Block
(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
143.
144. DR/ SHAFEI LASHEEN
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
150. DR/ SHAFEI LASHEEN
ECG Changes & the Evolving MI
There are two
distinct patterns of
ECG change
depending if the
infarction is:
–ST Elevation (Transmural or Q-wave), or
–Non-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
151. DR/ SHAFEI LASHEE
ECG Changes
Ways the ECG can change include:
Appearance
of pathologic
Q-waves
T-waves
peaked flattened inverted
ST elevation &
depression
154. Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TST
R
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
T
ST
R
P
Q
T
155. DR/ SHAFEI LASHEEN
Views of the Heart
Some leads get a
good view of the:
Anterior portion
of the heart
Lateral portion
of the heart
Inferior portion
of the heart
167. AWMI (pardee’s sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was
described by Pardee in 1920 and has been called the “Pardee’s sign”
168. DR/ SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST
segment (greater
than 1 small box)
in 2 leads is
consistent with a
myocardial
infarction.
169. What part of the heart is affected ?
I, aVL, V5 and V6
Lateral wall of left ventricle
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
188. DR/ SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression & T-wave inversion
The ECG changes seen with a non-ST elevation infarction are:
Before injury Normal ECG
ST depression & T-wave inversion
ST returns to baseline, but T-wave
inversion persists
Ischemia
Infarction
Fibrosis
190. DR/ SHAFEI LASHEEN
Non-ST Elevation Infarction
Here’s an ECG of an evolving non-ST elevation MI:
Note the ST
depression and
T-wave
inversion in
leads V2-V6.
Question:
What area of
the heart is
infarcting?
Anterolateral
193. DR/ SHAFEI LASHEEN
Hypertrophy
In this step of the 12-lead ECG analysis, we use the ECG to
determine if any of the 4 chambers of the heart are enlarged or
hypertrophied. We want to determine if there are any of the
following:
– Right atrial enlargement (RAE)
– Left atrial enlargement (LAE)
– Right ventricular hypertrophy (RVH)
– Left ventricular hypertrophy (LVH)
196. DR/ SHAFEI LASHEEN
– To diagnose RAE you can use the following criteria:
• II P > 2.5 mm, or
• V1 or V2 P > 1.5 mm
Right atrial enlargement
197. DR/ SHAFEI LASHEEN
Left atrial enlargement
– To diagnose LAE you can use the following criteria:
• II > 0.04 s (1 box) between notched peaks, or
• V1 Neg. deflection > 1 box wide x 1 box deep
198.
199. 199
199
Ventricular Hypertrophy
• Ventricular Muscle
Hypertrophy
• QRS voltages in V1 and V6, L
1 and aVL
• We may have to record to ½
standardization
• T wave changes opposite to
QRS direction
• Associated Axis shifts
• Associated Atrial hypertrophy
201. DR// SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS
complexes?
LVH ECHOcardiogram
Increased QRS voltage
As the heart muscle wall thickens there is an increase in
electrical forces moving through the myocardium resulting
in increased QRS voltage.
202. Criteria for LVH
• Sokolow-Lyon
– S v1+R v5/v6>35mm
– R I+S III>25mm
– R avl>11mm
• Cornell
– S v3+R avl >28 (men)
>20 (women)
• Romhilt-Estes
– LV strain 3
– LAE 3
– LAD 2
– QRS duration 1
– R v5/v6>3 3
– Sv1/v2>3 3
– Largest R or S>2 3
5 or more points suggests LVH
208. DR / SHAFEI LASHEE
Right Bundle Branch Blocks
What QRS morphology is characteristic?
For RBBB the wide QRS complex assumes a
unique, virtually diagnostic shape in those
leads overlying the right ventricle (V1 and V2).
210. DR/SHAFEI LASHEEN
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).