Fore word

1
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 !!

2
The Objectives

• 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
• 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

3
ECG Resources consulted

• Alan Lindsays 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. Websters Cyber ECG library
• Braunwalds text book of cardiology - 6 ed. 2004
• Goldbergers text book on ECG
• Our personal collection of interesting ECGs

4
ECG Graph Paper
Y- Axis Amplitude in mill volts
X- Axis time in seconds
5
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

6
ECG Complex
P wave PR Interval QRS complex ST segment T
Wave QT Interval RR Interval
7
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

8
Identify the ECG Complex
3
4
5
1
8
2
6
7
9
Identify the ECG Complex
The Wave or Interval
Duration of Boxes

• P wave Atrial contraction 0.12 sec (3)
• PR interval P to begin. of QRS 0.20
  sec (5)
• QRS complex - Ventricular 0.08 sec (2)
• ST segment - Electrical silence Isoelectric
• T wave - repolarization 0.12 sec (3)
• QRS interval Ventricular cont. 0.08 sec (2)
• QT interval - From Q to T end 0.40
  sec (10)
• TP segment - Electrical silence
  0.20 sec (5)

10
Let us Identify the waves
4
7
1
8
6
2
3
5
11
Let us Identify the waves

• P wave Atrial contraction 0.12 sec (3 small
  boxes)
• PR Interval P AV delay 0.20 sec (5 small
  boxes)
• Q wave Septal lt 3 mm, lt 0.04 sec (1 small
  box)
• R wave Ventricular contraction lt 15 mm
• S wave complimentary to R lt 15 mm
• ST segment Isoelectric decides our fate
• T wave ventricular repolarization friend of
  ST
• TP segment ventricular relaxation shortened
  in tachycardia

12
Important Precautions

• 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

13
Normal ECG
14
Normal ECG

• 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 lt 0.08 narrow, Q in V5, V6 lt 0.04, lt 3 mm
• R wave progression from V1 to V6, QT interval lt
  0.4
• Axis normal L1, L3, and aVF all will be
  positive
• ST Isoelectric, T waves ?, Normal T? in aVR,V1, V2

15
Pediatric ECG
16
Pediatric ECG

• This is the ECG of a 6 year old child
• Heart rate is 100 Normal for the age
• See V1 V5 R gtgt 35 Not LVH Normal
• T? in V1, V2, V3 Normal in child
• Base line disturbances in V5, V6 due
  to movement by child

17
Juvenile ECG
18
Be aware of normal ECG

• 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

19
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 lt 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

20
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

21
Pseudo Normalization
T?
Before Chest pain
T?
During Chest pain
T?
Chest pain Relieved
22
Rate Determination
QRS
Next QRS
23
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 43
Eight 1.6 sec 60 1.6 37
T ACHY
NORMA L
BRADY
24
What is the Heart Rate ?
Answer on next slide
25
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

26
What is the Heart Rate ?
Answer on next slide
27
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

28
What is the Heart Rate ?
Answer on next slide
29
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

30
ECG Bipolar Limb Leads

-
-
-
L
R
L
R
F


F
31
ECG Bipolar Limb Leads

• 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

32
ECG Unipolar Limb Leads


R
L

F
Lead aVR
Lead aVL
Lead aVF
33
ECG Unipolar Limb Leads

• 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

34
ECG Chest Leads
35
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

36
Atrial Ectopics
37
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 lt 0.08, not wide

38
Atrial Fibrillation
39
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

40
Look at this ECG
41
Atrial Flutter
Heart rate Rhythm
P wave PR interval QRS
in sec
42
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 lt 0.12 sec
• The P waves have a saw toothed appearance
  called F waves

43
Ventricular Ectopics
44
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 gt 0.12 and their shapes are bizarre

45
Ventricular Tachycardia
46
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 (gt 0.14 ms)
• The QRS is similar to that in ventricular
  ectopics
• Concordance (chest leads all positive or negative)

47
The Six Limb Leads
FRONTAL PLANE
RIGHT
LEFT
INFERIOR
48
The 12 Camera Photography

• 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

49
The Six Chest Leads
TRANSVERSE PLANE
50
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

51
Cardiac Impulse
52
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

53
QRS Axis
NW
NE
SE
SW
54
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

55
Axis Determination
MEET
LEAVE
ALL UPRIGHT
NORMAL
RIGHT LEFT
56
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
57
What is the Axis ?
58
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

59
What is the Axis ?
LEAD 1
LEAD 2
LEAD 3
60
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

61
What is the Axis ?
LEAD 1
aVR
aVL
LEAD 2
aVF
LEAD 3
62
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

63
Atrial Waves
64
Right Atrial Enlargement
65
Right Atrial Enlargement
P wave voltage is 4 boxes or 4 mm
66
Right Atrial Enlargement

• 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

67
Atrial Enlargements
RIGHT ATRIAL ENLARGEMENT LEFT
ATRIAL ENLARGEMENT
68
Left Atrial Enlargement
69
Left Atrial Enlargement
P wave duration is 4 boxes-0.04 x 4 0.16
70
Left Atrial Enlargement

• 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

71
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

72
Right Ventricular Hypertrophy
73
Right Ventricular Hypertrophy

• Tall R in V1 with R gtgt S, or R/S ratio gt 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

74
Is there any hypertrophy ?
75
Criteria and Causes of LVH

• Criteria of RVH
• Tall R in V1 with R gtgt S, or R/S ratio gt 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

76
What is in this ECG ?
77
ECG OF MS with RVH, RAE

• 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

78
Left Ventricular Hypertrophy
79
Left Ventricular Hypertrophy

• High QRS voltages in limb leads
• R in Lead I S in Lead III gt 25 mm
• S in V1 R in V5 gt 35 mm
• R in aVL gt 11 mm or S V3 R aVL gt 24 ?, gt 20 ?
• Deep symmetric T inversion in V4, V5 V6
• QRS duration gt 0.09 sec
• Associated Left Axis Deviation, LAE
• Cornell Voltage criteria, Estes point scoring

80
What is in this ECG ?
81
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 gt 25 mm or S in V1
  R in V5 gt 35 mm
• R in aVL gt 11 mm or S V3 R aVL gt 24 ?, gt 20 ?
• Deep symmetric T inversion in V4, V5 V6
• QRS duration gt 0.09 sec, Associated Left Axis
  Deviation, LAE

82
LVH Types
Volume Over Load
Pressure Over Load
83
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

84
Cardiac Conduction
85
Causes of Conduction Block

• 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 Chagas disease
• Myxedema, Amyloidosis, Ventricular hypertrophy

86
Complete RBBB
87
Complete RBBB

• Complete RBBB has a QRS duration gt 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

88
Interpret this ECG
89
Complete LBBB
90
Complete LBBB

• Complete LBBB has a QRS duration gt 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.

91
Interpret This ECG
92
Rate Dependent LBBB
93
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 lt 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

94
Blood Supply of Heart
RCA
LCX
LAD
RCA
LCA
95
Blood Supply of Heart

• 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

96
Ischemia, Injury Infarction

1. Ischemia produces ST segment depression with
   or without T inversion
2. Injury causes ST segment elevation with or
   without loss of R wave voltage
3. Infarction causes deep Q waves with loss of R
   wave voltage.

97
Ischemia and Infarction
TRANSMURAL Injury ST Elevation
98
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
99
Types of Angina
CHRONIC STABLE ANGINA
100
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 ?

101
Micro Vascular Angina
102
Micro Vascular Angina

• 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

103
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

104
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

105
T wave inversion
106
T Wave Inversion

• Deep symmetric inverted T waves
• In more than 2 precardial leads
• 85 of the patients with such T wave?had gt 75
  stenosis of the coronary artery
• T wave ?are significantly associated with MI or
  death during follow up

107
Acute Coronary Syndromes
Minor Plaque Disruption
Occlusive Thrombus
Non-Occlusive Thrombus
Non-Vulnerable Atherosclerotic Plaque
Vulnerable Atherosclerotic Plaque
Myocardial Infarction or Sudden Cardiac Death
Asymptomatic Unstable Angina or Non-Q-MI
Major Plaque Disruption
Occlusive Thrombus
108
ACUTE CORONARY SYNDROMES
No ST Elevation
ST Elevation
NSTEMI
Unstable Angina
NQMI QWMI Myocardial Infarction
109
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
110
Pathogenesis of ACS
Platelet rupture
Platelet Adhesion
Platelet Activation

• Sequence of events
• Plaque Rupture
• Platelet Adhesion
• Platelet Activation
• Platelet Aggregation
• Thrombotic Occlusion

Platelet Aggregation
Thrombotic Occlusion
Anti-platelet drugs
111
ACS PathophysiologyPlaque Rupture, Thrombosis,
and Microembolization
Marker CholesterolLDL, LP (a), HCy C-Reactive
ProteinsICAM Interleukin 6, TNFa, sCD-40 ligand,
SAA MDA Modified LDL, MMP-9, sICAM, D-dimer,
Neopterin Complement, Fibrinogen, Troponin, CRP,
CD40L
Quiescent plaque
Process Plaque formation InflammationMultiple
factors ? Infection Plaque Rupture ?
Macrophages Metalloproteinases ThrombosisPlatele
t ActivationThrombin
Lipid core
Vulnerable plaque
TF ? Clotting Cascade
Inflammation
Collagen ? platelet activation
Foam Cells
Macrophages
Metalloproteinases
Platelet-thrombin micro-emboli
Plaque rupture
112
QMI
113
Management of ACS
IHD type Drug Rx. Hep. /LMH ICU Care Lytic Rx P PTCA
Stable Angina AB No No No No
Unstable Angina ABC Heparin No / Yes No No
NSTEMI ABCG LMH YES No No
STEMI or QWMI ABCG LMH YES YES YES
A Aspirin, B Beta-blocker, C Clopidogrel, G
GPIIb/IIIa Inhibitor
114
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
• TNFa- 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
115
Lipid Profile Report
LIPID TYPE LIPOPROTEIN Remarks Treatment
TC 250 HDL 30 Abnormal Exercise
LDL 170 Abnormal STATINS
VLDL 50 Abnormal Diet
TG 350 VLDL 235 Abnormal FIBRATE
Chylomicron 85 Abnormal Diet
We have 2 types of fats in our body the
cholesterol and the triglyceride
116
CHD Risk Factors

• Diabetes Mellitus FBG gt 110, PPBG gt 140
• Hypertension SBP gt 140, DBP gt 90
• Dyslipidemia LDL gt 100, TG gt 150, HDL lt 50
• Overweight BMI gt 25, Waist girth gt 34 ? 38 ?
• Micro-albuminuria gt 20 mg / L or GFR lt 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 lt 50
• Presence of LVH by Echo or ECG
• Emerging new risk factors HCy, LP(a)

117
Complications of Acute MI
Arrhythmia
118
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

119
What is in this ECG
120
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

121
Look at This ECG
122
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, Raynauds, migraine
• ßblockers contraindicated. CCB, a blockers Rx.

123
Interpret this ECG
124
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

125
What are these ECGs
126
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

127
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

128
Critical Narrowing of LAD
129
Holter TMT in CAD
130
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

131
Normal Q waves
Notice the small Normal Q in Lead I
132
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 lt 0.04 sec or one small box
• It is seen in L1 and some times in V5, V6

133
Pathological Q wave
Notice the deep wide Infarction Q in Lead I
134
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 gt 0.04 sec or gt 1 small box
• It is seen in Leads facing the infarcted muscle
  mass

135
Q wave of Cardiomyopathy
136
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

137
Serial ECG changes of MI
138
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.

139
Blood Supply - MI - Leads
ANTERIOR LATERAL
INFERIOR POSTERIOR
LAD LAD or LCx
RCA RCA LCx
V1, V2, V3, V4 V5, V6, L1, aVL
L2, L3, aVF V1, V2 Mirror
140
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)

141
Acute Anterior MI
142
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

143
Very Striking
144
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

145
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

146
Acute Anterio-Lateral MI
147
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

148
Severe Chest Pain Why ?
149
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.

150
What changes we see ?
151
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

152
Why Acute changes disappeared ?
r TPA
153
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

154
Guess How Old is this MI !
155
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

156
Acute Inferior wall MI
157
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

158
Which wall MI ?
159
Acute Inferior wall MI

• Note the ST elevations in Inferior leads- namely
  L2, L3 and aVF
• T inversions yet to appear
• aVL lead shows complimentary ST?and T inversion

160
What is striking ?
Acute Inf Post
161
Acute Inferior wall MI

• Note the ST elevations in Inferior leads- namely
  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
  gt 0.12 sec

162
Where are the ST ? ?
Inf Lysed
163
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

164
What Can We Infer ?
165
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

166
Acute True Posterior MI
167
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 gt 1, Differential Diagnosis - RVH

168
Decipher V1, V2, V3
169
Acute True Posterior MI

• V2, V3 show tall R waves, Even V1 shows R
• V2, V3, V1 leads R/s ratio is gtgt 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

170
Identify the Double wall MI
171
Inferio-Posterior MI

• V1, V2 show tall R waves
• V1, V2 leads R/s ratio is gtgt 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.

172
New or Old What MI ?
173
Old Inferio-Posterior MI

• V2 shows residual R waves of Posterior MI
• V2 lead R/s ratio is gt 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

174
Look at the Right Chest Leads
R
R
R
R
R
R
175
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

176
Will Right Ventricular MI occur ?
177
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

178
Electrical Alternans
179
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

180
Ventricular Bigeminy
181
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

182
Myxedema
Heart rate Rhythm
P wave PR interval QRS in sec
50
183
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

184
S.A.H. ECG changes
185
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

186
Hyperkalemia
187
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

188
Hypokalemia
189
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

190
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

191
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

192
AC Interference

• 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

193
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

194
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.