Transcript ECG by Dr.Sarma for print

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Fore word
Dear Doctor,
This ECG presentation is an attempt to illustrate some of the
fundamentals in ECG interpretation. We have advanced level
courses also on ECG. In addition, we have several educational
resource materials in the form of PowerPoint based CD-Rom
presentations. Also are available several philosophical and
religious works of all time great masters, translated into simple
English and presented as PowerPoint slide shows on CD-Rom.
A list of such materials is appended. Pl. request for your copy of
any of them at a nominal cost of Rs.100/ per CD.
Wishing You a happy learning experience !!
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The Objectives
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To sensitize doctors towards learning ECG
To explain the clinical concepts involved
To illustrate them with diagrams, drawings, tables
To show real life ECG charts and interpret
Differential diagnosis on similar looking ECG changes
Spot light on ECG and Ischemic Heart Disease
Not Included are
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Electrophysiological basis of ECG changes
Details on arrhythmias, conduction disorders
Sensitivity and specificity of different patterns
Atypical presentations, combination of pathologies
Scoring systems and predictive values
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ECG Resources consulted
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Alan Lindsay’s Cyber ECG learning center (on line)
Interactive Electrocardiography by Novartis – CD Rom
Frank H Netter's medical drawings
American Heart Association (AHA) sites
American Heart Lung and Blood Institute (AHLBI) sites
J.G. Webster’s Cyber ECG library
Braunwald’s text book of cardiology - 6 ed. 2004
Goldberger’s text book on ECG
Our personal collection of interesting ECGs
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ECG Graph Paper
Y- Axis Amplitude in mill volts
X- Axis time in seconds
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ECG Graph Paper
 X-Axis represents time - Scale X-Axis – 1 mm = 0.04 sec
 Y-Axis represents voltage - Scale Y-Axis – 1 mm = 0.1 mV
 One big square on X-Axis = 0.2 sec (big box)
 Two big squares on Y-Axis = 1 milli volt (mV)
 Each small square is 0.04 sec (1 mm in size)
 Each big square on the ECG represents 5 small squares
= 0.04 x 5 = 0.2 seconds
 5 such big squares = 0.2 x 5 = 1sec = 25 mm
 One second is 25 mm or 5 big squares
 One minute is 5 x 60 = 300 big squares
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ECG Complex
P wave
PR Interval
QRS complex
ST segment
T Wave
QT Interval
RR Interval
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ECG Complex
 P Wave is Atrial contraction – Normal 0.12 sec
 PR interval is from the beginning of P wave to the
beginning of QRS – Normal up to 0.2 sec
 QRS is Ventricular contraction –Normal 0.08 sec
 ST segment – Normal Isoelectic (electric silence)
 QT Interval – From the beginning of QRS to the end
of T wave – Normal – 0.40 sec
 RR Interval – One Cardiac cycle 0.80 sec
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Identify the ECG Complex
3
4
5
1
8
2
6
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Identify the ECG Complex
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The Wave or Interval
Duration
P wave : Atrial contraction
PR interval – P to begin. of QRS
QRS complex - Ventricular
ST segment - Electrical silence
T wave - repolarization
QRS interval – Ventricular cont.
QT interval - From Q to T end
TP segment - Electrical silence
0.12 sec
0.20 sec
0.08 sec
Isoelectric
0.12 sec
0.08 sec
0.40 sec
0.20 sec
# of Boxes
(3)
(5)
(2)
(3)
(2)
(10)
(5)
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Let us Identify the waves
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1
6
2
3
5
7
8
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Let us Identify the waves
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P wave – Atrial contraction = 0.12 sec (3 small boxes)
PR Interval – P + AV delay = 0.20 sec (5 small boxes)
Q wave – Septal = < 3 mm, < 0.04 sec (1 small box)
R wave – Ventricular contraction < 15 mm
S wave – complimentary to R < 15 mm
ST segment – Isoelectric – decides our fate
T wave – ventricular repolarization – friend of ST
TP segment – ventricular relaxation – shortened in
tachycardia
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Important Precautions
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Correct Lead placement and good contact
Proper earth connection, avoid other gadgets
Deep inspiration record of L3, aVF
Compare serial ECGs if available
Relate the changes to Age, Sex, Clinical history
Consider the co-morbidities that may effect ECG
Make a xerox copy of the record for future use
Interpret systematically to avoid errors
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Normal ECG
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Normal ECG
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Standardization – 10 mm (2 boxes) = 1 mV
Double and half standardization if required
Sinus Rhythm – Each P followed by QRS, R-R constant
P waves – always examine for in L2, V1, L1
QRS positive in L1, L2, L3, aVF and aVL. – Neg in aVR
QRS is < 0.08 narrow, Q in V5, V6 < 0.04, < 3 mm
R wave progression from V1 to V6, QT interval < 0.4
Axis normal – L1, L3, and aVF all will be positive
ST Isoelectric, T waves ↑, Normal T↓ in aVR,V1, V2
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Pediatric ECG
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Pediatric ECG
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This is the ECG of a 6 year old child
Heart rate is 100 – Normal for the age
See V1 + V5 R >> 35 – Not LVH – Normal
T↓ in V1, V2, V3 – Normal in child
Base line disturbances in V5, V6 –
due
to movement by child
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Juvenile ECG
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Be aware of normal ECG
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Normal Resting ECG – cannot exclude disease
Ischemia may be covert – supply / demand equation
Changes of MI take some time to develop in ECG
Mild Ventricular hypertrophy - not detectable in ECG
Some of the ECG abnormalities are non specific
Single ECG cannot give progress – Need serial ECGs
ECG changes not always correlate with Angio results
Paroxysmal events will be missed in single ECG
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Normal Variations in ECG
 May have slight left axis due to rotation of heart
 May have high voltage QRS – simulating LVH
 Mild slurring of QRS but duration < 0.09
 J point depression, early repolarization
 T inversions in V2, V3 and V4 – Juvenile T ↓
 Similarly in women also T↓
 Low voltages in obese women and men
 Non cardiac causes of ECG changes may occur
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Early Repolarization
This ECG has all normal features
The ST-T (J) Junction point is
elevated. T waves are tall, May be inverted in LIII, The ST
segment initial portion is concave. This does not signify Ischemia
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Pseudo Normalization
T↓
Before
Chest pain
T↑
During
Chest pain
T↓
Chest pain
Relieved
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Rate Determination
QRS
Next
QRS
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Rate Determination
No. of Big Boxes
R – R Interval
Rate Cal.
Rate
One
0.2 sec
60 ÷ 0.2
300
Two
0.4 sec
60 ÷ 0.4
150
Three
0.6 sec
60 ÷ 0.6
100
Four
0.8 sec
60 ÷ 0.8
75
Five
1.0 sec
60 ÷ 1.0
60
Six
1.2 sec
60 ÷ 1.2
50
Seven
1.4 sec
60 ÷ 1.4
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Eight
1.6 sec
60 ÷ 1.6
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T
A
C
H
Y
N
O
R
M
A
L
B
R
A
D
Y
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What is the Heart Rate ?
Answer on next slide
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What is the Heart Rate ?
 To find out the heart rate we need to know
 The R-R interval in terms of # of big squares
 If the R-R intervals are constant
 In this ECG the R-R intervals are constant
 R-R are approximately 3 big squares apart
 So the heart rate is 300 ÷ 3 = 100
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What is the Heart Rate ?
Answer on next slide
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What is the Heart Rate ?
 To find out the heart rate we need to know
 The R-R interval in terms of # of big squares
 If the R-R intervals are constant
 In this ECG the R-R intervals are constant
 R-R are approximately 4.5 big squares apart
 So the heart rate is 300 ÷ 4.5 = 67
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What is the Heart Rate ?
Answer on next slide
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What is the Heart Rate ?
 To find out the heart rate we need to know
 The R-R interval in terms of # of Big Squares
 If the R-R intervals are constant
 In this ECG the R-R intervals are not constant
 R-R are varying from 2 boxes to 3 boxes
 It is an irregular rhythm – Sinus arrhythmia
 Heart rate is 300 ÷ 2 to 3 = 150 to 100 approx
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ECG Bipolar Limb Leads
-
+
R
L
-
-
R
L
+
F
F
+
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ECG Bipolar Limb Leads
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Standard ECG is recorded in 12 leads
Six Limb leads – L1, L2, L3, aVR, aVL, aVF
Six Chest Leads – V1 V2 V3 V4 V5 and V6
L1, L2 and L3 are called bipolar leads
L1 between LA and RA
L2 between LF and RA
L3 between LF and LA
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ECG Unipolar Limb Leads
+
+
R
L
+
Lead aVR
Lead aVL
Lead aVF
F
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ECG Unipolar Limb Leads
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Standard ECG is recorded in 12 leads
Six Limb leads – L1, L2, L3, aVR, aVL, aVF
Six Chest Leads – V1 V2 V3 V4 V5 and V6
aVR, aVL, aVF are called unipolar leads
aVR – from Right Arm Positive
aVL – from Left Arm Positive
aVF – from Left Foot Positive
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ECG Chest Leads
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ECG Chest Leads
Precardial (chest) Lead Position
 V1 Fourth ICS, right sternal border
 V2 Fourth ICS, left sternal border
 V3 Equidistant between V2 and V4
 V4 Fifth ICS, left Mid clavicular Line
 V5 Fifth ICS Left anterior axillary line
 V6 Fifth ICS Left mid axillary line
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Atrial Ectopics
APC
APC
APC
APC
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Atrial Ectopics
 Note the premature (ectopic) beats marked as
 APC (Atrial Premature Contractions)
 These occurred before the next expected QRS
complex (premature)
 Each APC has a P wave preceding the QRS of that
beat – So impulse has originated in the atria
 The QRS duration is normal < 0.08, not wide
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Atrial Fibrillation
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Atrial Fibrillation
 Note ECG changes of Atrial Fibrillation
 The heart rate is irregularly irregular
 The R-R intervals are very different from beat to
beat
 There is narrow QRS tachycardia
 There are no P waves – instead small fibrillary
waves called ‘ f ’ waves are seen
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Look at this ECG
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Atrial Flutter
Heart rate
Rhythm
P wave
PR interval
QRS in sec
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Atrial Flutter
Note ECG changes of Atrial Flutter
The heart rate is regular or variable
Atrial rate is 300 per minute
All P waves are not conducted to ventricles
The R-R intervals very depending on the AV
conduction ratio
 The QRS is narrow – < 0.12 sec
 The P waves have a ‘saw toothed’ appearance
called ‘F’ waves
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Ventricular Ectopics
VPC
VPC
VPC
VPC
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Ventricular Ectopics
 Note the premature (ectopic) beats marked as VPC
(Ventricular Premature Contractions)
 These occurred before the next expected QRS
complex (premature)
 Each VPC has no definite P wave preceding the
QRS of that beat – So impulse has originated in the
ventricles
 The QRS complexes are wide with abnormal
duration of > 0.12 and their shapes are bizarre
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Ventricular Tachycardia
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Ventricular Tachycardia
 A wide QRS tachycardia is VT until proved
 otherwise. Features suggesting VT include
 Evidence of AV dissociation
 Independent P waves (shown by arrows here)
 Beat to beat variability of the QRS morphology
 Very wide complexes (> 0.14 ms)
 The QRS is similar to that in ventricular ectopics
 Concordance (chest leads all positive or negative)
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The Six Limb Leads
FRONTAL PLANE
RIGHT
LEFT
INFERIOR
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The 12 Camera Photography
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There SIX cameras photographing frontal plane
Lead 1 and aVL are horizontal left sided cameras
Lead 2, aVF, Lead 3 are vertical inferior cameras
aVR is horizontal Rt. sided camera (cavitary lead)
Lateral Leads – L1, aVL, V5 and V6
Inferior Leads – L2, aVF, and L3 leads
Septal Leads – V1 and V2
Anterior Leads – V3 and V4
Anterio-lateral leads – V3, V4, V5, V6, L1 and aVL
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The Six Chest Leads
TRANSVERSE PLANE
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The 12 Camera Photography
 There SIX cameras photographing in transverse or
anterio-posterior plane
 V1 and V2 record events of septum
 V3 and V4 record events of the anterior wall
 V5 and V6 record events of left lateral wall
 To record right side events V2R to V6R are needed
– In dextrocardia, in RV infarction
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Cardiac Impulse
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Cardiac Impulse
 Cardiac impulse originates in the SA node
 Traverses the atria simultaneously – no special
conduction wires in atria – so the delay
 Reaches AV node – the check post – so delay
 Enters bundle of His and branches – through
specialized conducting wires called Purkinje
network - activates both ventricles – quick QRS
 First the septum from L to R, then right ventricle and
then the left ventricle and finally the apex
 Then the ventricles recover for next impulse
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QRS Axis
NW
SW
NE
SE
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QRS Axis
 The QRS electrical (vector) axis can have 4 directions
 Normal Axis - when it is downward and to the left –
southeast quadrant – from -30 to +90 degrees
 Right Axis – when it is downward and to the right –
southwest quadrant – from +90 to 180 degrees
 Left Axis – when it is upward and to the left
–
Northeast quadrant –from -30 to -90 degrees
 Indeterminate Axis – when it is upward & to the right –
Northwest quadrant – from -90 to +180
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Axis Determination
ALL UPRIGHT
NORMAL
MEET
RIGHT
LEAVE
LEFT
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Axis Determination
Axis
LI
LIII or aVF
TIP
Normal
Positive
Positive
Both Up
Right
Negative
Positive
Meet
Left
Positive
Negative
Leave
Indeterminate
Negative
Positive
Meet
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What is the Axis ?
LEAD 1
aVR
LEAD 2
aVL
LEAD 3
aVF
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ECG With Normal Axis
 Note the QRS voltages are positive and
upright in the leads - L1, L2, L3 and aVF
 L2, L3 and aVF tell that it is downward
 L1, aVL tell that it is to the left
 Downward and leftward is Normal Axis
 Normal QRS axis
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What is the Axis ?
LEAD 1
LEAD 2
LEAD 3
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ECG With Right Axis
 Note the QRS voltages are positive and
upright in leads L2, L3
 Negative in Lead 1
 L2, L3 tell that it is downward
 L1 tells that it is not to the left but to right
 Downward and rightward is Right Axis
 See the Right –Meet criterion QRS in
L1 and L3 meet
 Right Axis Deviation - RAD
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What is the Axis ?
LEAD 1
aVR
LEAD 2
aVL
LEAD 3
aVF
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ECG With Left Axis
 Note the QRS voltages are positive and
upright in leads L1and aVL
 Negative in L2, L3 and aVF
 L1, aVL tell that it is leftward
 L2, L3, and aVF tell that it is not down
ward - instead it is upward
 Upward and Leftward is Left Axis
 See the Left - Leave criterion QRS in
L1 and L3 leave each other
 Left Axis Deviation - LAD
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Atrial Waves
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Right Atrial Enlargement
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Right Atrial Enlargement
P wave voltage is 4 boxes or 4 mm
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Right Atrial Enlargement
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Always examine Lead 2 for RAE
Tall Peaked P Waves, Arrow head P waves
Amplitude is 4 mm ( 0.4 mV) - abnormal
Pulmonary Hypertension, Mitral Stenosis
Tricuspid Stenosis, Regurgitation
Pulmonary Valvular Stenosis
Pulmonary Embolism
Atrial Septal Defect with L to R shunt
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Atrial Enlargements
RIGHT ATRIAL ENLARGEMENT
LEFT ATRIAL ENLARGEMENT
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Left Atrial Enlargement
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Left Atrial Enlargement
P wave duration is 4 boxes-0.04 x 4 = 0.16
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Left Atrial Enlargement
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Always examine V 1 and Lead 1 for LAE
Biphasic P Waves, Prolonged P waves
P wave 0.16 sec, ↑ Downward component
Systemic Hypertension, MS and or MR
Aortic Stenosis and Regurgitation
Left ventricular hypertrophy with dysfunction
Atrial Septal Defect with R to L shunt
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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
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Right Ventricular Hypertrophy
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Right Ventricular Hypertrophy
 Tall R in V1 with R >> S, or R/S ratio > 1
 Deep S waves in V4, V5 and V6
 The DD is RVH, Posterior MI, Anti-clock wise
rotation of Heart
 Associated Right Axis Deviation, RAE
 Deep T inversions in V1, V2 and V3
 Absence of Inferior MI
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Is there any hypertrophy ?
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Criteria and Causes of LVH
Criteria of RVH
 Tall R in V1 with R >> S, or R/S ratio > 1
 Deep S waves in V4, V5 and V6
 The DD is RVH, Posterior MI, Rotation
 Associated Right Axis Deviation, RAE
 Deep T inversion in V1, V2 and V3
Cause of RVH
 Long standing Mitral Stenosis
 Pulmonary Hypertension of any cause
 VSD or ASD with initial L to R shunt
 Congenital heart with RV over load
 Tricuspid regurgitation, Pulmonary stenosis
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What is in this ECG ?
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ECG OF MS with RVH, RAE
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Classical changes seen are
Right ventricular hypertrophy
Right axis deviation
Right Bundle Branch Block
P – Pulmonale - Right Atrial enlargement
P – Mitrale – Left Atrial enlargement
If Atrial Fibrillation develops – ‘P’ disappears
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Left Ventricular Hypertrophy
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Left Ventricular Hypertrophy
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High QRS voltages in limb leads
R in Lead I + S in Lead III > 25 mm
S in V1 + R in V5 > 35 mm
R in aVL > 11 mm or S V3 + R aVL > 24 ♂, > 20 ♀
Deep symmetric T inversion in V4, V5 & V6
QRS duration > 0.09 sec
Associated Left Axis Deviation, LAE
Cornell Voltage criteria, Estes point scoring
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What is in this ECG ?
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Causes and Criteria of LVH
Causes of LVH
 Pressure overload - Systemic Hypertension, Aortic Stenosis
 Volume overload - AR or MR - dilated cardiomyopathy
 VSD - cause both right & left ventricular volume overload
 Hypertrophic cardiomyopathy – No pressure or volume overload
Criteria of LVH
 High QRS voltages in limb leads
 R in Lead I + S in Lead III > 25 mm or S in V1 + R in V5 > 35 mm
 R in aVL > 11 mm or S V3 + R aVL > 24 ♂, > 20 ♀
 Deep symmetric T inversion in V4, V5 & V6
 QRS duration > 0.09 sec, Associated Left Axis Deviation, LAE
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LVH Types
Pressure Over Load
Volume Over Load
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LVH Types
Pressure Over load
 Like in hypertension, IHD
 LV strain pattern – ST depression with T ↓
in V5, V6, L1 and aVL leads
Volume Over load
 Like in Mitral or Aortic regurgitation
 Shows prominent positive T waves in
V5, V6, L1 and aVL
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Cardiac Conduction
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Causes of Conduction Block
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Clinically normal individual
CAD, Acute MI, Remote MI, Pulmonay embolism
Aortic stenosis, SABE + abscesses in conduction
Cardiac trauma, Hyperkalemia, Rapid heart rates
Lenegre's disease (idiopathic fibrosis of conduction)
Lev's disease (calcification of the cardiac skeleton)
Cardiomyopathy - Dilated and Hypertrophic
Infiltrative Tumor – Chaga’s disease
Myxedema, Amyloidosis, Ventricular hypertrophy
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Complete RBBB
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Complete RBBB
Complete RBBB has a QRS duration > 0.12 sec
R' wave in lead V1 (usually see rSR' complex)
S waves in leads I, aVL, V6, R wave in lead aVR
QRS axis in RBBB is -30 to +90 (Normal)
Incomplete RBBB has a QRS duration of 0.10 to
0.12 sec with the same QRS features as above
 The "normal" ST-T waves in RBBB should be
oriented opposite to the direction of the QRS
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Interpret this ECG
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Complete LBBB
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Complete LBBB
Complete LBBB has a QRS duration > 0.12 sec
Prominent S waves in lead V1, R in L I, aVL, V6
Usually broad, Bizarre R waves are seen, M pattern
Poor R progression from V1 to V3 is common.
The "normal" ST-T waves in LBBB should be
oriented opposite to the direction of the QRS
 Incomplete LBBB looks like LBBB but QRS duration
is 0.10 to 0.12 sec, with less ST-T change.
 This is often a progression of LVH changes.
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Interpret This ECG
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Rate Dependent LBBB
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Rate Dependent LBBB
Complete LBBB is sometimes rate dependent
See the LBBB pattern when the HR is 75 per minute
But, LBBB pattern disappeared when the HR is < 50
Some times the LBBB appears and disappears with out
any change in heart rate. This is called stuttering LBBB.
It signifies underlying Ischemia.
 Appearance of new LBBB in a patient with chest pain is
enough evidence of MI. It presents primary T changes
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Blood Supply of Heart
RCA
LCX
LAD
RCA
LCA
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Blood Supply of Heart
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Heart has four surfaces
Anterior surface – LAD, Left Circumflex (LCx)
Left lateral surface – LCx, partly LAD
Inferior surface – RCA, LAD terminal portion
Posterior surface – RCA, LCx branches
Rt. and Lt. coronary arteries arise from aorta
They are 2.5 mm at origin, 0.5 mm at the end
Coronary arteries fill during diastole
Flow - epicardium to endocardium – poverty/plenty
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Ischemia, Injury & Infarction
1.
Ischemia produces ST segment
depression with
or without T
inversion
Myocardial Injury
2.
Injury causes ST segment
elevation with or without loss of R
wave voltage
Myocardial
Infarction
3.
Infarction causes deep Q waves
with loss of R wave voltage.
Myocardial
Ischemia
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Ischemia and Infarction
TRANSMURAL Injury ST
Elevation
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Ischemic Heart Disease (IHD)
Blood supply
Sub-endocardial
Transmural
Ischemia
Transient loss
Stable
Angina
Variant
Angina
Infarction
Persistent loss
NSTEMI
ACS
STEMI
ACS
ST Segment
Depressed
Elevated
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Types of Angina
CHRONIC STABLE ANGINA
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Types of Angina
 Chronic Stable Angina – Dynamic occlusion +
Micro vascular dysfunction – Progressive
 Micro vascular Angina – No flow limiting
stenosis – Angio normal – less severe IHD
 Unstable Angina – Dynamic occlusion + Micro
vascular dysfunction + Active Thromb
 Prinzemetal Angina – Occlusive spasm, No
Micro vascular dys, No thrombus – ST ↑
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Micro Vascular Angina
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Micro Vascular Angina
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Normal Coronary blood flow by angiogram
No significant CAD in epicardial blood vessels
Cardiac micro circulation is at fault
Poor collateral connections – younger age
More common in women – Syndrome X
ECG or TMT show ST - T changes repeatedly
Patient will be symptomatic for IHD
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ST Segment Depression
1. Upward sloping depression of ST segment is not indicative of IHD
2. It is called J point depression or sagging ST seg
3. Downward slopping or Horizontal depression of ST segment
leading to T↓is significant of IHD
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Lateral Wall Ischemia
 Note the classical ischemic ST
depressions
 ST ↓ are seen in V4,V5,V6 –
lateral wall
 His ST segments retuned to
base line after sublingual
nitroglycerine
 His pain is precipitated by effort
 Notice the tachycardia – heart
rate = 140
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T wave inversion
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T Wave Inversion
 Deep symmetric inverted T waves
 In more than 2 precardial leads
 85% of the patients with such T
wave↓had > 75% stenosis of the
coronary artery
 T wave ↓are significantly
associated with MI or death during
follow up
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Acute Coronary Syndromes
Minor
Plaque
Disruption
Non-Occlusive
Thrombus
Occlusive
Thrombus
Non-Vulnerable
Vulnerable
Atherosclerotic Atherosclerotic
Plaque
Plaque
Myocardial
Infarction or
Sudden
Cardiac Death
Asymptomatic
Unstable Angina
or Non-Q-MI
Major Plaque
Disruption
Occlusive
Thrombus
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ACUTE CORONARY SYNDROMES
No ST Elevation
ST Elevation
NSTEMI
Unstable Angina
NQMI
QWMI
Myocardial Infarction
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The Plaque – Clinical Effects
Nature of the Plaque
Clinical Presentation
Picture
Stable Plaque
Silent or Stable Angina
Vulnerable Plaque
Stable Angina
A
Minor Plaque Disruption
Unstable Angina
B
Major Plaque Rupture
USA / NSTEMI
C
Non Occlusive Thrombus
NSTEMI or STEMI
D
Occlusive Thrombus
STEMI or Sudden Death
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Pathogenesis of ACS
Platelet
rupture
Platelet
Adhesion
Sequence of events
• Plaque Rupture
• Platelet Adhesion
• Platelet Activation
• Platelet Aggregation
• Thrombotic Occlusion
Platelet
Activation
Platelet
Aggregation
Anti-platelet drugs
Thrombotic
Occlusion
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Plaque Rupture, Thrombosis, and Microembolization
Quiescent plaque
Process
Lipid core
Vulnerable plaque
TF  Clotting Cascade
Inflammation
Collagen 
platelet
activation
Foam Cells
Macrophages Metalloproteinases
Plaque rupture
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Marker
Plaque formation
Cholesterol
LDL, LP (a), HCy
Inflammation
Multiple factors
? Infection
C-Reactive Protein
sICAM
Interleukin 6, TNFa,
sCD-40 ligand, SAA
Plaque Rupture
? Macrophages
Metalloproteinases
MDA Modified LDL,
MMP-9, sICAM,
Thrombosis
Platelet Activation
Thrombin
D-dimer, Neopterin
Complement,
Fibrinogen, Troponin,
CRP, CD40L
Platelet-thrombin micro-emboli
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Thrombus Formation and ACS
Plaque Disruption/Fissure/Erosion
Thrombus Formation
Old
Terminology:
New
Terminology:
UA
NQMI
Non-ST-Segment Elevation Acute Coronary
Syndrome (ACS)
STE-MI
QMI
ST-Segment
Elevation
Acute
Coronary
Syndrome
(ACS)
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Management of ACS
IHD type
Drug Rx.
Hep. /LMH
ICU Care
Lytic Rx
P PTCA
Stable
Angina
A+B
No
No
No
No
Unstable
Angina
A+B+C
Heparin
No / Yes
No
No
NSTEMI
A+B+C+G
LMH
YES
No
No
STEMI or
QWMI
A+B+C+G
LMH
YES
YES
YES
A = Aspirin, B = Beta-blocker, C = Clopidogrel, G = GPIIb/IIIa Inhibitor
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New Markers of CHD
1. Markers of Plaque formation (Stable
Plaque) LDLc, LP(a),Homocysteine
2. Markers of Inflammation
(Vulnerable Plaque)
HS CRP – High Sensitivity C Reactive
Protein
sICAM – Soluble Intercellular Adhesion
Molecule
IL 6 – Interleukin 6
TNFα- Tumor Necrosis Factor Alpha
SAA – Serum Amyloid Alpha
sCD 40 – serum CD 40 Ligand
3. Markers of Plaque Rupture
MDA Modified LDL – Oxidized LDL
MMP-9 – Matrix Metallo Proteinase
sICAM – Soluble Intercellular
Adhesion Molecule
4. Markers of Thrombosis
D-dimer, Complement
Neopterin, Fibrinogen
Troponins, CRP, CD 40 L
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Lipid Profile Report
LIPID TYPE
LIPOPROTEIN
Remarks
Treatment
TC = 250
HDL = 30
Abnormal
Exercise
LDL = 170
Abnormal
STATINS
VLDL = 50
Abnormal
Diet
VLDL = 235
Abnormal
FIBRATE
Chylomicron= 85
Abnormal
Diet
TG = 350
We have 2 types of fats in our body – the cholesterol and the triglyceride
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CHD Risk Factors
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Diabetes Mellitus – FBG > 110, PPBG > 140
Hypertension – SBP > 140, DBP > 90
Dyslipidemia – LDL > 100, TG > 150, HDL < 50
Overweight – BMI > 25, Waist girth > 34 ♀ 38 ♂
Micro-albuminuria > 20 mg / L or GFR < 60 ml / min.
Male Sex up to age 55 yrs – Equal after 55
Smoking, Alcohol, sedentary life, couch potatoes
Family H/o premature CAD – 1º blood relative < 50
Presence of LVH by Echo or ECG
Emerging new risk factors – HCy, LP(a)
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Complications of Acute MI
Extension / Ischemia
Expansion / Aneurysm
Mechanical
Arrhythmia
Pericarditis
Acute MI
Heart Failure
RV Infarct
Mural Thrombus
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Which BP Drug to Choose ?
1. HT + DM
ACEi, ARB
2. HT + IHD
ACEi, Perindopril + BB (Meto, Carva)
3. HT + MRD
ACEi + / or Methyl dopa (MD)
4. HT + CHF
ARB, ACEi, Diuretics, No CCB
5. HT + Pregnancy
MD or CCB (Amlo) No ACEi
6. HT + Asthma, COPD
No beta blockers, Alpha blockers OK
7. HT + Tachycardia
No CCBs, Give BB
8. HT + Dyslipidemia
No Diuretics- give ACEi, ARB, CCB
9. HT in elderly, ISH
Indapamide, Diuretics, CCB
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What is in this ECG
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Unstable Angina
 Presence of one or more of the three features,
 Crescendo Angina- more severe, prolonged,
or frequent. Decrease in exercise capacity
 New onset (1 month) & brought on by minimal
exertion. Not relieved by Nitrates
 Angina at rest as well as with minimal
exertion. There are 3 classes – 1 to 3
 This may progress to NSTEMI or STEMI
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Look at This ECG
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Prinzemetal Angina
 Transient ST-segment elevation during chest pain
due to coronary vasospasm – variant angina
 ECG with ST ↑. Becomes normal soon, No Q wave
 Intermittent chest pain
 often repetitive, usually at rest, early morning
 Other vasospasms - syncope, Raynaud’s, migraine
 βblockers contraindicated. CCB, α blockers Rx.
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Interpret this ECG
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NSTEMI
Non ST ↑ MI or NSTEMI, Non Q MI
 Or also called sub-endocardial Infarction
 Non transmural, restricted to the sub-endocardial region
- there will be no ST ↑ or Q waves
 ST depressions in anterio-lateral & inferior leads
 Prolonged chest pain, autonomic symptoms like nausea,
vomiting, diaphoresis
 Persistent ST-segment ↓even after resolution of pain
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What are these ECGs
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STEMI and QWMI
STEMI and QWMI
 ST ↑ signifies severe transmural myocardial injury – This is
early stage before death of the muscle tissue – the infarction
 Q waves signify muscle death – They appear late in the
sequence of MI and remain for a long time
 Presence of either is an indication for thrombolysis
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Evolution of Acute MI
A – Normal ST segment and T waves
B – ST mild ↑ and prominent T waves
C – Marked ST ↑ + merging upright T
D – ST elevation reduced, T↓,Q starts
E – Deep Q waves, ST segment returning to
baseline, T wave is inverted
F – ST became normal, T Upright, Only Q+
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Critical Narrowing of LAD
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Holter & TMT in CAD
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Holter & TMT in CAD
 Holter is an ambulatory ECG, BP monitor
 Look at the Stress Test – Deep ST ↓
 The Holter recordings show the changing patterns in
ST segments and Heart rate during different activities
 Worst ST changes during vigorous physical activity
like playing tennis
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Normal Q waves
Notice the small
Normal Q in Lead I
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Normal Q Waves
 The normal Q wave in lead I is due to septal
depolarization
 It is small in amplitude – less than 25% of the
succeeding R wave, or less than 3 mm
 Its duration is < 0.04 sec or one small box
 It is seen in L1 and some times in V5, V6
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Pathological Q wave
Notice the deep & wide
Infarction Q in Lead I
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Pathological Q wave
 The pathological Q wave of infarction in the
respective leads is due to dead muscle
 It is deep in amplitude – more than 25% of
the succeeding R wave, or more than 4 mm
 Its duration is > 0.04 sec or > 1 small box
 It is seen in Leads facing the infarcted
muscle mass
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Q wave of Cardiomyopathy
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Q Wave of Cardiomyopathy
 In idiopathic hypertrophic cardiomyopathy the septal
Q wave in lead 1 is deep and prolonged because of
excessive septal thickness. Similar to MI Q wave,
but
 There will be marked LVH evidence and
 The R wave amplitude is very tall unlike in infarction
– where R waves are reduced
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Serial ECG changes of MI
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Serial ECG Changes of MI
 Normal ECG does not exclude MI or IHD
 First few hours of MI – Hyper acute T with ST
segment elevation starting
 Drop in R wave voltage and ST elevation
 Significant Q, R wave none, ST ↑, T↓
 No R, Marked Q, ST baseline, T↓
 Small R starts, Q remains, ST normal, T↓
 In some Q waves disappear, R improves,
ECG becomes nearly normal.
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Blood Supply - MI - Leads
ANTERIOR
LAD
V1, V2, V3, V4
LATERAL
INFERIOR
LAD or LCx
RCA
RCA + LCx
L2, L3, aVF
V1, V2 Mirror
V5, V6, L1, aVL
POSTERIOR
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What are the Investigations ?
 Resting 12 Lead ECG, Chest X-Ray
 Tread Mill Test (TMT) – Provocative stress tests
 Troponins (bed side), LDH, CPK isoenzymes
 Echocardiography and Doppler
 Calcium scoring and CT angiography
 Exercise Echo, Dobutamine challenge echocardiography
 Perfusion – Stress Thalium, Sistemibi, Dipyridamole
 3D Coronary Cartography (CCG), PET scan
 Coronary Angiography (Gold Standard)
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Acute Anterior MI
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Acute Anterior Wall MI
 Due to occlusion of the proximal LAD
 Significant Q waves, ST elevation and T
inversions in Leads V2, V3 and V4
 Q waves and T inversion in L1
 If only V1 and V2 show the changes it is
called septal MI
 Associated with abnormal conduction
 Septal perforation with acquired VSD
is a rare complication
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Very Striking
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Hyper Acute MI
 Note the hyper acute elevation of ST
 The R wave is continuing with ST and the
complexes are looking rectangular
 Some times tall and peaked T waves in the
precardial leads may be the only evidence
of impending infarct
 Sudden appearance LBBB indicates MI
 MI in Dextro-cardia – right sided leads are
to be recorded
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What is striking ?
 Note the ST↑in V1, V2, V3
 T↓ in V1 to V5
 R wave voltages of all lateral
leads well preserved
 No ST ↑in the Lateral leads
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Acute Anterio-Lateral MI
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Acute Anterio-lateral MI
 Due to occlusion of the marginal branch or
the main trunk of Left Circumflex artery
 Or due to occlusion of the diagonal branch
of Left anterior descending artery
 Significant Q waves, ST elevation and T
inversions in Lead 1, aVL, V5 and V6
 This is the most common form of MI
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Severe Chest Pain – Why ?
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Acute Anterio-lateral MI
 Note the marked ST elevations in chest leads
V2 to V5 and also ST↑ in L1 & aVL
 T inversions have not appeared as yet
 R wave voltages have dropped markedly in
V3, V4, V5 and V6
 Small R in L1 and aVL.
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What changes we see ?
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Acute Anterio-lateral MI
 Note the marked ST elevations in chest
leads V2 to V5, also ST↑ in L1 & aVL
 T inversions have not appeared as yet
 R wave voltages have merged with ST ↑
markedly in V3, V4, V5 and V6
 In addition complimentary St ↓in L2, L3
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Why Acute changes disappeared ?
r TPA
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Thrombolysed Anterio-lateral MI
 Note the ST elevations in chest leads V2 to V5
are returned toward baseline
 Deep T ↓have appeared in all leads
 R wave voltages have improved in V2 to V5
 No residual Q waves seen
 This patient was thrombolysed within 2 hours
and MI has become stable – Golden period
 Thrombolytics – UK, SK, TPA, r-TPA
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Guess How Old is this MI !
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Stable Anterio-lateral MI
 The coved ST↑ in chest leads V2 to V5
almost returned to baseline
 T↓are becoming less marked in all leads
 R wave voltages improved well in V4 to V5
 No residual Q waves seen
 This ECG is 4 weeks after the Acute MI
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Acute Inferior wall MI
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Acute Inferior wall MI
 Due to occlusion of the right coronary artery
 Significant Q waves, ST elevation and T
inversions in Lead II, Lead III, aVF,
 This is the associated with arrhythmias
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Which wall MI ?
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Acute Inferior wall MI
 Note the ST elevations in Inferior leadsnamely L2, L3 and aVF
 T inversions yet to appear
 aVL lead shows complimentary ST↓and
T inversion
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What is striking ?
Acute Inf Post
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Acute Inferior wall MI
 Note the ST elevations in Inferior leadsnamely L2, L3 and aVF
 Hyper acute T waves merging with ST
 V1, V2, aVL lead shows rsR’ pattern with
ST↓and T inversion – Inferior MI
 Associated RBBB also is present –
QRS is wide > 0.12 sec
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Where are the ST ↑ ?
Inf Lysed
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Inferior Wall MI - Thrombolysed
 A case of inferior wall MI
 Thrombolysed with in 2 hours
 ST segments returned to base line
 Deep T inversions signify residual ischemia
 This patient became stable
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What Can We Infer ?
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Old Inferior wall MI
 This is months after the acute event
 Patient suffered inferior MI
 Residual QS waves in L3 and aVF
 T inversions in L3 and aVF
 ST segments are isoelectric
 L3 t inversion became normal
 Chest leads R wave voltages are good
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Acute True Posterior MI
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Acute True Posterior MI
 Due to occlusion of the distal Left circumflex
artery or posterior descending or distal right
coronary artery
 Mirror image changes or reciprocal changes
in the anterior precardial leads
 Lead V1 shows unusually tall R wave (it is
the mirror image of deep Q)
 V1 R/S > 1, Differential Diagnosis - RVH
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Decipher V1, V2, V3
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Acute True Posterior MI
 V2, V3 show tall R waves, Even V1 shows R
 V2, V3, V1 leads R/s ratio is >> 1
 These R waves are the mirrored MI – Qs
 These leads show deep ST depression
 This ST↓is in fact the mirrored ST↑of MI
 The same leads show sharp T waves
 These are the mirrored T inversions of MI
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Identify the Double wall MI
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Inferio-Posterior MI
 V1, V2 show tall R waves
 V1, V2 leads R/s ratio is >> 1
 These R waves are the mirrored MI – Qs
 This ST↓ is in fact the mirrored ST ↑ of MI
 The T ↓are the mirrored T inversions of MI
 L2, L3 and aVF show gross ST ↑ - Inferior MI
 V4R, V5R show ST elevations – RV – MI too.
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New or Old – What MI ?
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Old Inferio-Posterior MI
 V2 shows residual R waves of Posterior MI
 V2 lead R/s ratio is > 1
 The R waves are the mirrored old Qs of MI
 This ST↓ is no longer seen – stabilized MI
 L3 & aVF show deep QS of old Inferior MI
 The T ↓in L3, aVF signify old inferior MI
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Look at the Right Chest Leads
R
R
R
R
R
R
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Dextrocardia and MI
 Note the ECG carefully – It is an eye opener
 55 years ♀ is sent for ECG by another doctor
 She has dextrocardia of which she is unaware
 She has typical clinical features of acute MI
 Routine chest leads placed on left chest
showed no evidence of MI at all
 ECG with chest leads on the right chest –
V2R to V6R - typical acute anterio-septal MI
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Will Right Ventricular MI occur ?
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Right Ventricular MI
 Note the ECG carefully – It is an eye opener
 65 yrs ♂ has typical clinical features of acute MI
 Routine chest leads placed on left chest showed
no MI - but limb leads showed acute Inferior MI
 ECG with chest leads on the right chest – V2R
to V6R show typical changes of acute MI of the
Right Ventricle. RV MI is associated with Inferior
wall MI
 His serum troponins were very high
 Angio showed 95% block of the RCA
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Electrical Alternans
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Electrical Alternans
 Note the typical ECG changes
 Every alternate QRS complex has a small
and a large amplitude but of sinus origin
 The heart rate is 110 per minute
 There are P waves preceding all QRS
waves
 This is a feature of pericardial effusion
with cardiac tamponade
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Ventricular Bigeminy
Normal
VPC
Normal
VPC
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Ventricular Bigeminy
 Note this typical ECG of bigeminy
 Each normal sinus originated ventricular
complex with narrow QRS is followed by a
 Premature beat with wide and bizarre looking
QRS of ventricular origin
 Similarly Trigeminy, Quadrigeminy
 These ectopics signify heart failure
 In this ECG there are features of Inferior MI
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Myxedema
Heart rate
50
Rhythm
P wave
PR interval
QRS in sec
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Myxedema
 Note the ECG changes
 Bradycardia – HR of 55 per minute
 Low voltages of all complexes
 Less than 5 mm Limb leads
 Less than 8 mm chest leads
 DD of low voltage complexes
 Pericardial effusion, Constrictive pericarditis
 Severe Emphysema
 Pneumothorax or left sided pleural effusion
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S.A.H. ECG changes
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S.A.H – ECG changes
 Striking ECG changes of Non Cardiac origin
 Incredible deep and symmetric T Inversions
 In young person with massive Sub Arachnoid
Haemorrhage
 He has no cardiac disease
 Presumably due to autonomic dysfunction
 Intense Head ache, Has very high B.P
 Lumbar Puncture clinches the issue
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Hyperkalemia
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Hyperkalemia
 This is a 58 yr old man's with CRF
 Serum K was 7.6 m mol/L. (Normal upto 4.2)
 Hyperkalaemia ECG changes are
 Small or absent P waves
 Atrial fibrillation (not in this ECG)
 Wide QRS
 Shortened or absent ST segment
 Wide, tall and tented T waves
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Hypokalemia
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Hypokalemia
 This 22 year lady had prolonged vomiting
 Her serum K was 1.8 mmol/L.
 Normal 3.2 to 4.2
 Hypokalaemia ECG changes are
 Small or absent T waves or inverted T
 Prominent U waves (see pointer)
 T wave is the tent house of K
 More K – tall T, less K flat or inverted T
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Wandering base line
 In non co-operative child
 Excessive movements of limbs
 Movement disorders of CNS
 Not properly earthed machine
 Additional wet ground earth
helps
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Muscle Tremor
 Limb movements cause baseline fluctuations
 Tense muscles cause tremor of baseline
 Hairy chest interferes with proper contact of chest
leads – better to shave the area if needed.
 Reassurance, starting recording a few minutes after
the leads are placed – reduce muscle tension
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AC Interference
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Any electrical gadgets in the same line may interfere
Like Mixie, Motor, Musical tube lights etc
Proper earthing is essential
Dedicated direct line for ECG power point
Use battery mode, Artifacts are quite misleading
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Our Other Resources
 We have also an advanced course on ECG
 We have several other educative CMEs prepared
 Please refer to the list at the beginning of this book
 We have several religious and philosophical texts
sung, translated and made as PowerPoint slides
 Please request what ever you want
 CME talk can also be given if you intimate ahead
 The charge of Rs.100/- per CD is nominal and to
cover the incidental costs only
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THIS IS NOT THE END
 This only a beginning and certainly not the end
 We look forward for more learning experiences
 Please write to us what you felt about this ECG
 Contact address and phone are in the beginning
Thank YOU and
With Warm Regards,
Dr.Sarma.