ELECTROCARDIOGRAM

avm
 The Leads
• Leads I, II, III
– are the bipolar limb leads
– Measures the ECG along the frontal planes
• Leads AVR, AVL and AVF
– are the augmented limb leads
• V1-V6
– are the chest or precordial leads
– Measures the ECG along the transverse plane
The Leads
Chest leads
V1: 4th ICS, RPSB

V2: 4th ICS, LPSB

V3: between V2 and V4

V4: 5th ICS, LMCL

V5: 5th ICS, LAAL

V6: 5th ICS, LMAL

• Standardization
– 1mV = 10 mm
• Paper speed 25 mm/sec:
– 1 small box = 0.04 sec
– 1 big box = 0.2 sec
 Ventricular deactivation
(repolarization)

Atrial Activation
(depolarization)

Ventricular Activation
(depolarization)
 RRAHIM
R • Rate

R • Rhythm

A • Axis

H • Hypertrophy/Chamber Enlargement

I • Ischemia/Infarction

M • Miscellaneous
 Measurement of Rate
• Formula 1: 300
# big squares between R-R

• Formula 2: 1500
# small squares between R-R
• For irregular heart rates, get the number of QRS complexes in
a 6-second strip; then multiply by 10
Determination of Heart Rate

Heart rate assessment by “rule of 300”

 Check the Rhythm
1. Regular or irregular?
2. Is there a P wave? Same P wave?
3. Check relation of P wave to QRS.
4. Check PR interval (0.12- 0.20 sec)
Determination of Axis

Normal axis is from -30° to 110°

 Determination of Axis
Lead I Lead AVF
Normal Axis + +
Left axis deviation + -
Right axis deviation - +
Indeterminate Axis - -

• Axis

• If negative in I and positive in aVF (RAD)

= 180 –
Hypertrophy/Chamber Enlargement
Hypertrophy/Chamber Enlargement
 Criteria for Ischemia/Infarction
ISCHEMIA INFARCTION
ST-segment depression ST Elevation:
• At least 1 mm • ≥2mm in ≥ 2 contiguous
T wave inversion chest leads
• >5mm • ≥1mm in ≥ 2 contiguous
limb leads
Significant Q waves:
• ¼ of QRS complex or
• ≥ 0.04 sec (1 sm )
 Wall Involvement
Leads Wall
II, III, avF: Inferior wall
I and avL: High lateral wall
V1, V2: Septal wall
V3, V4: Anterior wall
V5, V6: Lateral wall
Mirror image of V1, V2: Posterior wall
V3R and V4R: RV wall
Significant Q Wave
A. Normal ECG prior to MI

B. Hyperacute T wave changes - increased

T wave amplitude and width; may also
see ST elevation

C. Acute (evolving): Marked ST elevation

with hyperacute T wave changes
(transmural injury)

D. Recent (resolving): Pathologic Q waves,

less ST elevation, terminal T wave
inversion (necrosis)
 
E. Undetermined (healing): Pathologic Q
waves, T wave inversion (necrosis and
fibrosis)

F. Old: Pathologic Q waves, upright T waves

(fibrosis)
 Timing of Myocardial Infarction
Q ST T wave Approx.
Wave Elevation Timing of MI

Hyperacute (-) (-/+) Peaked 0 – 6 hrs

Acute (-/+) (++) (-/+) 6 – 24 hrs

Recent (++) (++) Inverted 24 – 72

hrs
Undetermined (++) (-) Inverted 72 hrs – 6
age wks
Old (++) (-) Upright > 6 wks
• ST depression
in v4-V6

• Note: upsloping
ST depression is
not an ischemic
abnormality
 RRAHIM
Rate • 1500/# small squares between R-R

• P wave (0.12-0.20s); P wave to QRS

Rhythm • Regular/Irregular

Axis

Hypertrophy • SV1 + (RV5 or RV6) > 3.5 mV

• Ischemia: At least 1 mm ST depression; T wave inversion (>5mm)

Ischemia/Infarction • Infarction: ST Elevation: ≥2mm (chest leads); ≥1mm (limb leads);
Significant Q waves
RATE
Determination of Heart Rate

Heart rate assessment by “rule of 300”

 Measurement of Rate
• Formula 1: 300
# big squares between R-R

• Formula 2: 1500
# small squares between R-R
• For irregular heart rates, get the number of QRS complexes in
a 6-second strip; then multiply by 10
 Pacemakers of the Heart
SA NODE Dominant 60-100 bpm
AV Junction Escape 40-60 bpm
SA NODE
Bundle of His
Ventricular Escape 20-40 bpm
Bundle Branch
Purkinje Fiber
 Labeling the ECG
Sinus Tachycardia

Junctional Accelerated Tachycardia

Ventricular Accelerated Tachycardia

0 20 40 60 80 100
RHYTHM
 Rhythm
• Rhythm
– Ensure:
• P wave before every QRS complex
• all the P waves are of the same shape
– Determine if rhythm is regular or irregular
– Measure the PR interval
• Start of P wave to start of QRS wave
• Normal PR interval: 0.12-0.20 sec
 Rhythm
1. Identify the P wave..Sinus?
2. Check relation of P to QRS
3. Check PR interval (0.12- 0.20 sec)
 AV block?
4. Check QRS (<0.12s)
 BBB?
5. Relation of R-R and P-P
 P-P < R-R: complete heart block
 P-P > R-R: AV dissociation
 Rhythm
• Is there a sinus P?
 upright in most leads
 inverted in AVR, biphasic in V1
 3 different Ps in MAT or WP
 absent in AF, junctional /vent rhythm
 buried or after QRS in SVT, 3AVB
 Rhythm: PR Interval (0.12 - 0.20 s)
• Shortened PR
– Pre-excitation syndrome
• WPW
• LGL (Lown-Ganong-Levine)
– AV Junctional Rhythms
with retrograde atrial
activation
– Ectopic atrial rhythms
originating near the AV
node
– Normal variant
• Prolonged PR interval
– First degree AV block
• Intra-atrial conduction delay
(uncommon)
• Slowed conduction in AV node
(most common site)
• Slowed conduction in His
bundle (rare)
• Slowed conduction in bundle
branch
– Second degree AV block
• Type I (Wenckebach)
• Type II (Mobitz)
– AV dissociation
Wolff-Parkinson-White Syndrome
• Note the short PR and the subtle 'delta' wave at
the beginning of the QRS complexes
 1 Degree AV Block
st

• PR intervals > 0.20s

• One-to-one AV conduction
• Tx: none
• This may be caused by:
– drugs, such as digoxin Partial block
at AV node
– excessive vagal tone
– Ischemia
– intrinsic disease in the AV junction or bundle branch
system.
1 Degree AV Block
st
 2 Degree AV Block
nd

Type I Type II
Lesion above the Bundle of His Lesion in the Bundle Branch
PR may prolong prior to dropped beat Fixed PR interval; dropped beat
Responds to pharmacologic tx Does NOT respond well to drugs
Rarely requires pacing REQUIRES pacing
Ventricular rhythm reg/irreg
 3rd Degree AV Block or Complete Heart Block

1. AV dissociation (p waves seen marching through the QRS

complexes)
2. P-P interval is less than R-R interval
3. Idioventricular rhythm
Tx: Pacemaker insertion
3 Degree AV Block
rd
 Measurements
• QRS duration (width of most representative QRS)
– normally: <0.12s
– Differentials:
• QRS duration <0.12s
– Incomplete right or left bundle branch block
– Nonspecific intraventricular conduction delay (IVCD)
– Some cases of left anterior or posterior fascicular block
• QRS duration > 0.12s
– Complete RBBB or LBBB
– Nonspecific IVCD
– Ectopic rhythms originating in the ventricles
Bun
dle
Bra
nch
Blo
ck
 Bundle Branch Block
Complete Left Bundle Branch Block
• QRS duration ≥ 120 msec
• Broad, notched R waves in lateral
precordial leads (V5 and V6) and usually
leads I and aVL
Complete Right Bundle Branch Block
• QRS duration ≥ 120 msec
• Broad, notched R waves (rsr′, rsR′, or
rSR′ patterns) in right precordial leads
(V1 and V2)

• Small or absent initial r waves in right • Wide and deep S waves in left
precordial leads (V1 and V2) followed by precordial leads (V5 and V6)
deep S waves
• Absent septal q waves in left-sided
leads
• Prolonged intrinsicoid deflection (>60
msec) in V5 and V6[*}
• LBBB
– QRS duration >0.12s
– monophasic R waves in I and V6
– terminal QRS forces oriented leftwards and posterior
– The ST-T waves oriented opposite to the terminal QRS forces
• RBBB
– QRS duration >0.12s
– rSR' in V1
– terminal QRS forces oriented rightwards and anterior
– ST-T waves oriented opposite to the terminal QRS forces
 Fascicular Blocks
Left Anterior Fascicular Block
• Frontal plane mean QRS axis of -45 to -
90 degrees with rS patterns in leads II,
III, and aVF and a qR pattern in lead
aVL
• QRS duration <120 msec
Left Posterior Fascicular Block
• Frontal plane mean QRS axis >120
degrees
• RS pattern in leads I and aVL with qR
patterns in inferior leads
• QRS duration < 120 msec
• Exclusion of other factors causing right
axis deviation (e.g., right ventricular
overload patterns, lateral infarction)
Fascicular Blocks
Atrial Mechanism
 Premature Atrial Complex

P’ waves: premature, flattened, or notched

P’RI: varies from 0.12-0.20s
QRS: <0.12 sec but may be prolonged
QRS rate: usually normal, but may depend on underlying rhythm
QRS rhythm: irregular due to PACs
 Atrial Flutter

P’ waves: usually saw-tooth, >250/min

P’RI: not measurable
QRS: usually <0.12s
QRS rate: usually 60-100/min
QRS rhythm: regular to irregular
 Atrial Fibrillation

P’ waves: unable to identify

P’RI: not measurable
QRS: ≤0.12s
QRS rate: 60-100/min when controlled
QRS rhythm: irregularly irregular
Multifocal Atrial Tachycardia
 Supraventricular Tachycardia

P’ waves: atrial P waves are different from the

sinus P waves; maybe buried in the QRS (AVNRT); P
waves follows the QRS (CMT by an accessory
pathway)
P’RI: usually not measurable
QRS: < 0.12s
QRS rate: 150-250 bpm
QRS rhythm: regular
Paroxysmal Supraventricular Tachycardia
Junctional Mechanism
 Junctional Mechanism
• Sinus node failure  AV junction takes over
• P prime (P’) – any P wave that originates from other
than the SA node

– P’ wave: none
– P’RI: < 0.12 sec
– QRS: < 0.12 sec
– QRS rate: at least 40-60bpm
– QRS rhythm: regular
 Junctional Escape Beat

P’ waves: none
P’RI: < 0.12s
QRS: usually <0.10s
QRS rate:
QRS rhythm:
 Junctional Rhythm

P’ waves: (-) or none

P’RI: <0.12 sec
QRS: <0.12 sec
QRS rate: 40-60 bpm
QRS rhythm: regular to slightly irregular
 Accelerated Junctional Rhythm

P’ waves: (-) or none

P’RI: <0.12 sec
QRS: <0.12 sec
QRS rate: 60-100 bpm
QRS rhythm: regular
 Premature Junctional Complex

P’ waves: (-) or none

P’RI: <0.12 sec
QRS: <0.12 sec
QRS rate:
QRS rhythm:
Ventricular Mechanisms
Premature Ventricular Complex

Left ventricular impulse

Right ventricular impulse

Variations in PVCs
Variations in PVCs
 Variations in PVCs

• Bigeminy: every other beat is a PVC

 Variations in PVCs

• Trigeminy: every 3rd beat is a PVC

Variations in PVCs
 Ventricular Tachycardia

P’ waves: may be present or absent, if present

they have no set relationship to the QRS
complex
P’RI: none
QRS: <0.12 sec
QRS Rate: 100-250 bpm
QRS Rhythm: regular
Ventricular Tachycardia
Intermittent V-Tach
Polymorphic V-tach: Torsade de Pointes

P’ waves: may be present or absent, if present

they have no set relationship to the QRS
complex
P’RI: none
QRS: > 0.12 sec; gradual alteration in the
amplitude and direction of the QRS
QRS Rate: 150-250 bpm
QRS Rhythm: irregular or regular
 Ventricular Fibrillation


  


P’ waves: not discernible

P’RI: not discernible
QRS: not discernible
QRS Rate: cannot be determined
QRS Rhythm: rapid and chaotic with no pattern of regularity
Ventricular Escape: Idioventricular Rhythm

P’ waves: absent
P’RI: none
QRS: >0.12s
QRS Rate: 20-40 bpm
QRS Rhythm: regular
Idioventricular Rhythm: Agonal rhythm
 Accelerated Idioventricular Rhythm

P’ waves: absent
P’RI: none
QRS: >0.12s
QRS Rate: 40-100 bpm
QRS Rhythm: regular
 Asystole

P’ waves: not discernible

P’RI: not discernible
QRS: not discernible
QRS Rate: cannot be determined
QRS Rhythm: not discernible
 Pulseless Electrical Activity

• Absence of detectable pulse and the presence of some

type of electrical activity
THANK YOU!
AXIS
Determination of Axis

Hexaxial System
Determination of Axis

Normal axis is from -30° to 110°

 Determination of Axis
Lead I Lead AVF
Normal Axis + +
Left axis deviation + -
Right axis deviation - +
Indeterminate Axis - -

• Axis

• If negative in I and positive in aVF (RAD)

= 180 –
 Differential Diagnoses…
• Left Axis Deviation: • Right Axis Deviation:
– Left ventricular
hypertrophy
– Short, fat individuals
– Inferior wall infarction
– LBBB
– Left anterior fascicular
block
– Wolff Parkinson White
syndrome
– Right ventricular
hypertrophy
– Lateral wall infarction
– Pulmonary embolism
– Thin, tall individuals
– Left posterior fascicular
block
– Wolff Parkinson White
syndrome
Vector Analysis
 Vector Analysis
• First find the isoelectric lead if there is one;
– the lead with equal forces in the positive and negative
direction
– often this is the lead with the smallest QRS.

• The QRS axis is perpendicular to that lead's

orientation.

• Since there are two perpendiculars to each isoelectric

lead, chose the perpendicular that best fits the
direction of the other ECG leads.
 Vector Analysis
• If there is no isoelectric lead
– Look for two leads that are nearly isoelectric, and these
are always 30o apart.
– Find the perpendiculars for each lead
– Choose an approximate QRS axis within the 30o range.

• Occasionally if each of the 6 frontal plane leads is

small and/or isoelectric
– The axis cannot be determined and is called
indeterminate.
– This is a normal variant.
CHAMBER ENLARGEMENT
 Right Atrial Enlargement
(p pulmonale)
• Any of the following:
– In lead V1: tall initial component of p wave which
is >/= 2 mm wide (0.08 sec) and >/= 2 mm tall
– In any lead: P wave >/= 2.5 mm tall
• tall P waves in Lead II
 Left Atrial Enlargement
(p mitrale)
• Any of the following:
– In lead V1: wide terminal component of p wave
which is >/= 1 mm wide (0.04 sec) and >/= 1 mm
deep
– In any lead: P wave wider than 0.12 sec (>3 small
squares) or
– with a >/= 1mm notched in the middle
 Biatrial Enlargement
Features of both RAE and LAE in same ECG
– P wave in lead II >2.5 mm tall and >0.12s in
duration
– In V1, P wave diphasic with initial positive
component ≥ 2mm tall and terminal negative
component ≥ 1mm depp and ≥0.04 sec duration
 Criteria for LVH
Parameter Criteria
Sokolow-Lyon index • SV1 + (RV5 or RV6) > 3.5 mV
• RaVL > 1.1 mV
Romhilt-Estes point • Any limb lead R wave or S wave ≥2.0 mV (3)
score system (points) • or SV1 or SV2 ≥ 3.0 mV (3)
• or RV5 to RV6 ≥ 3.0 mV (3)
• ST-T wave abnormality (no digitalis therapy) (3)
• ST-T wave abnormality (digitalis therapy) (1)
• Left atrial abnormality (3)
• Left axis deviation ≤ -30 degrees (2)
• QRS duration >90 msec (1)
• Intrinsicoid deflection in V5 or V6 > 50 msec (1)
Cornell voltage criteria
• SV3 + SaVL ≥ 2.8 mV (for men)
• SV3 + SaVL ≥ 2.0 mV (for women)
Cornell voltage- • QRS duration × Cornell voltage >2436
duration measurement • QRS duration × sum of voltages in all leads >17,472
 Left Ventricular Hypertrophy
• Romhilt and Estes criteria
– Amplitude (any) – 3 points
• Largest R/S in limb leads > 20mm
• S wave in V1/V2 ≥ 30 mm
• R wave in V5/V6 ≥ 30 mm
– ST-T segment changes typical of LV strain
• Without digitalis – 3 points
• With digitalis – 1 point
– LAE (terminal negativity of P in V1, depth ≥ 1 mm, duration ≥ 0.04 sec) – 3 points
– LAD – 2 points
– QRS duration ≥ 0.09 sec, < 0.12 sec – 2 points
– Intrinsicoid deflection in V5 and V6 ≥ 0.05 sec – 1 point
• Interpretation:
– Possible = 3 points
– Probable = 4 points
– Definite ≥ 5 points
 Differentials for LVH
• Hypertension
• Aortic stenosis
• Aortic insufficiency
• Cardiomyopathy
• Initial compensating mechanism in obesity,
smoking, dyslipidemia, obstructive sleep
apnea, DM
 Criteria for RVH
Criterion Sensitivity (%) Specificity (%)
R in V1 ≥ 0.7 mV <10 —
QR in V1 <10 —
R/S in V1 > 1 with R > 0.5 mV <25 89
R/S in V5 or V6 < 1 <10 —
S in V5 or V6 > 0.7 mV <17 93
R in V5 or V6 ≥ 0.4 mV with S in V1 ≥ 0.2 mV <10 —
Right axis deviation ≥ + 90 degrees <14 99
S1Q3 pattern <11 93
S1S2S3 pattern <10 —
P pulmonale <11 97
 Right Ventricular Hypertrophy
• Right axis deviation (>/= 110 deg), with any of
the following:
– Lead V1: R wave > S wave
– Deep S wave in leads V5 and V6: R/S ratio less
than 1 in leads V5 and V6
– ST depression and T wave inversion in V1-V3
 Right Ventricular Hypertrophy
• If QRS duration <0.12 sec, any of the ff:
– Right axis deviation (>90 degrees) in presence of
disease capable of causing RVH
– R in aVR > 5 mm, or
– R in aVR > Q in aVR
• Any one of the following in lead V1:  
– R/S ratio > 1 and negative T wave
– R > 6 mm, or S < 2mm, or rSR' with R' >10 mm
 Differentials for RVH
• Normal in young adults and children
• COPD
• RBBB
• True posterior infarction
• WPW syndrome
 Biventricular Hypertrophy
– In the presence of LAE + any one of the
following suggests this diagnosis:  
• R/S ratio in V5 or V6 < 1
• S in V5 or V6 > 6 mm
• RAD (>90 degrees)
– Other suggestive ECG findings
• Criteria for LVH and RVH both met
• LVH criteria met and RAD or RAE present
ISCHEMIA AND INFARCTION
 Wall Involvement
1. Transmural
– extends through the myocardial wall from endocardial
to epicardial surfaces

2. Nontransmural
– clinical evidence of myocardial damage without
consistent ECG changes

3. Endocardial/Epicardial
– refers to the innermost and outermost surfaces of the
myocardium
 Wall Involvement
Leads Wall
II, III, avF: Inferior wall
I and avL: High lateral wall
V1, V2: Septal wall
V3, V4: Anterior wall
V5, V6: Lateral wall
Mirror image of V1, V2: Posterior wall
V3R and V4R: RV wall
Wall Involvement
 Criteria for Ischemia
1. At least 1 mm ST-segment depression
2. Symmetrically or deeply inverted T waves
3. Abnormally tall T waves
4. Normalization of abnormal T waves
5. Prolongation of the QT interval
6. Others: Arrhythmias, BBB, AV blocks, or
electrical alternans
• ST depression
in v4-V6

• Note: upsloping
ST depression is
not an ischemic
abnormality
 Differential Diagnosis ST Depression
• Digitalis effect
• Hypokalemia
• LVH with strain (V5-V6)
• RVH with strain (V1-V2)
• NSTEMI
• Mitral valve prolapse (some cases)
• CNS disease
• Secondary ST segment changes with IV conduction
abnormalities (e.g., RBBB, LBBB, WPW, etc)
 Differentials of ST Depression
Normal variants or artifacts:  
• Pseudo-ST-depression (wandering baseline due to poor
skin-electrode contact)  
• Physiologic J-junctional depression with sinus
tachycardia (most likely due to atrial repolarization)
• Hyperventilation-induced ST segment depression
 Criteria for Infarction
ST elevation:
– ≥2mm in ≥ 2 contiguous chest leads
– ≥1mm in ≥ 2 contiguous limb leads
Significant Q waves: ¼ of QRS complex or ≥ 0.04 sec (1 sm )
– Not significant if…
 in AVR
 in lead III or V1 alone
 in V1-V3 if associated with LBBB
– Pathologic if…
 > 0.04 seconds duration
 > 25% of the R wave amplitude
Significant Q Wave
 Ischemia and Infarction
In presence of bundle branch blocks
• RBBB:
– usual MI criteria
• LBBB:
– diminishing R wave forces in chest leads (reverse R wave progression),
or
– Q waves at V5, V6, I, aVL (any 2)
– Notching of the downstroke/upstroke of the S wave in precordial
leads before QRS changes from a predominate S wave complex to a
predominate R wave complex
– rSR' complex in leads I, V5 or V6
– RS complex in V5-6 rather than the usual monophasic R waves seen in
uncomplicated LBBB
– "Primary" ST-T wave changes (i.e., ST-T changes in the same direction
as the QRS complex rather than the usual "secondary" ST-T changes
seen in uncomplicated LBBB
A. Normal ECG prior to MI

B. Hyperacute T wave changes - increased

T wave amplitude and width; may also
see ST elevation

C. Acute (evolving): Marked ST elevation

with hyperacute T wave changes
(transmural injury)

D. Recent (resolving): Pathologic Q waves,

less ST elevation, terminal T wave
inversion (necrosis)
 
E. Undetermined (healing): Pathologic Q
waves, T wave inversion (necrosis and
fibrosis)

F. Old: Pathologic Q waves, upright T waves

(fibrosis)
 Differential of ST Elevation
• Acute myocardial infarction
• Acute pericarditis
• Early repolarization changes
• Ventricular aneurysm
• Severe LV wall hypokinesia
• Variant (Prinzmetal) angina
 Differentials for ST Elevation
Ischemic Heart Disease
– usually convex upwards, or straightened
– Acute transmural injury
– Persistent ST elevation after acute MI suggests
ventricular aneurysm
– ST elevation may also be seen as a manifestation
of Prinzmetal's angina
– ST elevation during exercise testing suggests
extremely tight coronary artery stenosis or spasm
(transmural ischemia)
 Differentials for ST Elevation
Acute Pericarditis
– Concave upwards ST elevation in most leads
except aVR
– No reciprocal ST segment depression (except in
aVR)
– Unlike "early repolarization", T waves are usually
low amplitude, and heart rate is usually increased.
– May see PR segment depression, a manifestation
of atrial injury
 Differentials for ST Elevation
Normal Variant "Early Repolarization"
– usually concave upwards, ending with
symmetrical, large, upright T waves
– high take off of the ST segment in leads V4-6;
– ST elevation in V2-3 is generally seen in most
normal ECG’s
– ST elevation in V2-6 is concave upwards
 Differentials for ST Elevation
Other Causes 
– LVH (in right precordial leads with large S-waves)
– LBBB (in right precordial leads with large S-waves)
– Advanced hyperkalemia
– Hypothermia (prominent J-waves or Osborne
waves)
 Pseudoinfarcts
– WPW preexcitation (negative delta wave may mimic
pathologic Q waves)
– IHSS (septal hypertrophy may make normal septal Q
waves "fatter" thereby mimicking pathologic Q waves)
– LVH (may have QS pattern or poor R wave progression
in leads V1-3)
– RVH (tall R waves in V1 or V2 may mimic true
posterior MI)
– Complete or incomplete LBBB (QS waves or poor R
wave progression in leads V1-3)
 Pseudoinfarcts
– Pneumothorax (loss of right precordial R waves)
– Pulmonary emphysema and cor pulmonale (loss of
R waves V1-3 and/or inferior Q waves with right axis
deviation)
– Left anterior fascicular block (may see small q-waves
in anterior chest leads)
– Acute pericarditis (the ST segment elevation may
mimic acute transmural injury)
– CNS disease (may mimic non-Q wave MI by causing
diffuse ST-T wave changes)
 Waveform Analysis
• The specificity of ST-T and U wave abnormalities is
provided more by the clinical circumstances in
which the ECG changes are found than by the
particular changes themselves.
• Thus the term, nonspecific ST-T wave abnormalities,
is frequently used when the clinical data are not
available to correlate with the ECG findings.
• This does not mean that the ECG changes are
unimportant!
 Waveform Analysis
• Factors affecting the ST-T and U wave configuration
– "Primary" ST-T Wave Abnormalities
• independent of changes in ventricular activation and that
may be the result of global or segmental pathologic
processes that affect ventricular repolarization  
• Drug effects (e.g., digoxin, quinidine, etc)
• Electrolyte abnormalities (e.g., hypokalemia)
• Ischemia, infarction, inflammation, etc
• Neurogenic effects (e.g., subarrachnoid hemorrhage
causing long QT)
 Waveform Analysis
– "Secondary" ST-T Wave changes
• are normal ST-T wave changes solely due to alterations
in the sequence of ventricular activation
• ST-T changes seen in bundle branch blocks
– (ST-T polarity is opposite to the major or terminal
deflection of the QRS)
• ST-T changes seen in fascicular block
• ST-T changes seen in nonspecific IVCD
• ST-T changes seen in WPW preexcitation
• ST-T changes in PVCs, ventricular arrhythmias, and
ventricular paced beats
  Inferior MI
•  Pathologic Q waves and evolving ST-T changes in
leads II, III, aVF

• Q waves usually largest in lead III, next largest in lead

aVF, and smallest in lead II

Example #1: frontal plane leads with fully evolved

inferior MI (note Q-waves, residual ST elevation, and
T inversion in II, III, aVF)
• Example #2: Old inferior MI (note largest Q
in lead III, next largest in aVF, and smallest
in lead II)
 True Posterior MI
ECG changes:
• anterior precordial leads V1-3, but are the mirror image of an
anteroseptal MI:  
• Increased R wave amplitude and duration (i.e., a "pathologic R
wave" is a mirror image of a pathologic Q)
• R/S ratio in V1 or V2 >1 (i.e., prominent anterior forces)
• Hyperacute ST-T wave changes: i.e., ST depression and large,
inverted T waves in V1-3
• Late normalization of ST-T with symmetrical upright T waves in
V1-3
• Often seen with inferior MI (i.e., "inferoposterior MI")
Example #1: Acute inferoposterior MI (note tall R waves V1-3,
marked ST depression V1-3, ST elevation in II, III, aVF)
Example #2: Old inferoposterior MI (note tall R in V1-3,
upright T waves and inferior Q waves)
Example #3: Old posterolateral MI (precordial leads): note tall R
waves and upright T's in V1-3, and loss of R in V6
 Right Ventricular MI
• Right Ventricular MI (only seen with proximal
right coronary occlusion; i.e., with inferior
family MI's)  
• ECG findings usually require additional leads
on right chest (V1R to V6R, analogous to the
left chest leads)
• ST elevation, >1mm, in right chest leads,
especially V4R
 Anteroseptal MI  
• Q, QS, or qrS complexes in leads V1-V3 (V4)

• Evolving ST-T changes

Example: Fully evolved anteroseptal MI (note

QS waves in V1-2, qrS complex in V3, plus ST-T
wave changes)
 Anterior MI
• (similar changes, but usually V1 is spared; if
V4-6 involved call it anterolateral")  
• Example: Acute anterior or anterolateral MI
(note Q's V2-6 plus hyperacute ST-T changes)
 High Lateral MI
• typical MI features seen in leads I and/or aVL  
• Example: note Q-wave, slight ST elevation, and T inversion in lead aVL
• (Note also the slight U-wave inversion in leads II, III, aVF, V4-6, a strong marker for coronary disease)
 MI with Bundle Branch Block
• MI + Right Bundle Branch Block
• Usually easy to recognize because Q waves
and ST-T changes are not altered by the RBBB
• Example #1: Inferior MI + RBBB (note Q's in II, III, aVF and rSR' in lead V1)
• Example #2: Anteroseptal MI with RBBB (note Q's in leads V1-V3, terminal R
wave in V1, fat S wave in V6)
 MI + Left Bundle Branch Block
•  Often a difficult ECG diagnosis because in
LBBB the right ventricle is activated first and
left ventricular infarct Q waves may not
appear at the beginning of the QRS complex
(unless the septum is involved).
• Suggested ECG features, not all of which are
specific for MI include:  
 Q waves of any size in two or more of leads
I, aVL, V5, or V6 (probably indicates septal
infarction, because the septum is activated
early from the right ventricular side in LBBB)
• Reversal of the usual R wave progression in
precordial leads

• Notching of the downstroke of the S wave in

precordial leads to the right of the transition zone
(i.e., before QRS changes from a predominate S wave
complex to a predominate R wave complex); this may
be a Q-wave equivalent.
• Notching of the upstroke of the S wave in
precordial leads to the right of the transition
zone (another Q-wave equivalent).
• rSR' complex in leads I, V5 or V6 (the S is a Q-
wave equivalent occurring in the middle of the
QRS complex)
• RS complex in V5-6 rather than the usual monophasic
R waves seen in uncomplicated LBBB; (the S is a Q-
wave equivalent).
• "Primary" ST-T wave changes (i.e., ST-T changes in
the same direction as the QRS complex rather than
the usual "secondary" ST-T changes seen in
uncomplicated LBBB); these changes may reflect an
acute, evolving MI.
MISCELLANEOUS
 T Wave
• most labile wave in the ECG
• changes may be the result of many cardiac
and non-cardiac conditions
• normal T wave is usually in the same direction
as the QRS except in the right precordial leads
• normal T wave is asymmetric with the first half
moving more slowly than the second half
 T Wave
• normal T wave is always upright in leads I, II, V3-6, and always
inverted in lead aVR.
• other leads are variable depending on the direction of the
QRS and the age of the patient.
 Differentials for T Wave Inversion
– Q wave and non-Q wave MI
– Myocardial ischemia
– Subacute or old pericarditis
– Myocarditis
– Myocardial contusion (from trauma)
– CNS disease causing long QT interval (especially SAH)
– Idiopathic apical hypertrophy (a rare form of hypertrophic
cardiomyopathy)
– Mitral valve prolapse
– Digoxin effect
– RVH and LVH with "strain" pattern
 U Wave
• origin is still in question
• most authorities correlate the U wave with
electrophysiologic events called "afterdepolarizations" in
the ventricles.
– afterdepolarizations can be the source of arrhythmias caused by
"triggered automaticity" including torsade de pointes.
• has the same polarity as the T wave
• is usually less than one-third the amplitude of the T wave
• usually best seen in the right precordial leads especially
V2 and V3
• normal U wave is asymmetric with the ascending limb
moving more rapidly than the descending limb (just the
opposite of the normal T wave).
 Differentials for Upright U Waves
– Sinus bradycardia accentuates the U wave
– Hypokalemia (remember the triad of ST segment
depression, low amplitude T waves, and prominent
U waves)
– Quinidine and other type 1A antiarrhythmics
– CNS disease with long QT intervals (often the T and
U fuse to form a giant "T-U fusion wave")
– LVH
– Mitral valve prolapse
– Hyperthyroidism
 Differentials for Negative U Waves
• Ischemic heart disease (often indicating left main or LAD
disease)  
• Myocardial infarction (in leads with pathologic Q waves)
• During episode of acute ischemia (angina or exercise-
induced ischemia)
• Post extrasystolic in patients with coronary heart disease
• During coronary artery spasm (Prinzmetal's angina)
• Nonischemic causes  Some cases of LVH or RVH (usually
in leads with prominent R waves)
• Some patients with LQTS
 Hypokalemia
• ECG may be normal
• Prominent U waves
– (as tall or taller than the T wave at leads II and V3)
• Flattened or inverted T waves
• ST depression
• Fusion of T and U waves
• Prolonged QRS
 Hyperkalemia
• Hyperkalemia:
– In chest leads, T waves > 10 mm in most leads
– In limb leads, T waves > 5 mm in most leads
 Differentials for Peaked T Waves

• Myocardial ischemia
• Hyperacute myocardial infarction
• Hyperkalemia
• Normal variant in young athletes
 Hypocalcemia
• Prolonged QT interval (longer than half of the
RR interval by eyeballing)
• If tachycardic or bradycardic, get the QTc using
Basset’s formula
 Hypercalcemia
• Shortened QT interval
 Digitalis Effect
• Prolonged PR interval
• Scooping of the ST segment
• Short QT interval
 QRS Electrical Alternans
• Height of QRS varies from beat to beat
• Differentials:
– Cardiac tamponade
– Large pericardial effusion
– Low cardiac output
– COPD
– Tension pneumothorax
 Poor R Wave Progression
• Height of the R wave in V1-V3 is <3 mm
• Exceptions:
– LVH
– LBBB
– WPW
– Anteroseptal wall MI
– Low Voltage Complexes
• Differentials:
– Normal variant
– Old anteroseptal wall MI; LVH; LBBB
 Low Voltage QRS Complexes
• The amplitude of the entire QRS complex in
– < 5 mm in Limb leads
– <10mm in Chest leads
• Differentials:
– Normal elderly patients
– Obese or edematous patient
– Cardiac tamponade
– Large pericardial effusion
– Pneumothorax
– Hypothyroidism
– Dilated cardiomyopathy
 Artifacts
• ARTIFACTS
– EKG deflections caused by influences other than the heart’s
electrical activity
• CAUSES:
– electrical interference
– muscle tremors
– metal objects
– loose electrodes
– ground hum
– varies with respiration
Artifacts