Pathologic ECG

Adelina Vlad, MD PhD

Basic Interpretation of the ECG

1)

2)
3)
4)

5)
6)

6)
7)

Evaluate calibration
Calculate rate
Determine rhythm
Determine QRS axis
Measure intervals
Analyze the morphology and interrelation of ECG
elements (P, P-Q, Q, QRS, ST, T, QT) in frontal
and in precordial leads
OR
Asses for Hypertrophy
Look for evidence of Infarction

NSR Parameters

Rate
Regularity
P waves
PR interval
QRS duration

60 - 100 bpm
regular
normal
0.12 - 0.20 s
0.04 - 0.12 s

Any deviation from above is sinus tachycardia,

sinus bradycardia or an arrhythmia

Arrhythmia Formation
Arrhythmias can arise from electrophysiological
abnormalities in the:
Sinus node

Atrial cells
AV junction
Ventricular cells
His Purkinje network

Mechanisms Underlying Arrhythmias

Disorders of impulse formation
Automatism
Triggered activity

Disorders of impulse conduction

Partial and complete conduction block
Unidirectional block with reentry
Aberrant (accessory) conduction pathways

SA Node Problems
The SA Node can:
fire too slow (< 60 bpm)
fire too fast (>100 bpm)

Sinus Bradycardia
Sinus Tachycardia

The impulse is conducted normally

Sinus Tachycardia may be an appropriate response to stress

Both are abnormal Sinus Rhythms

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

30 bpm
regular
normal
0.12 s
0.10 s

Interpretation? Sinus Bradycardia

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

130 bpm
regular
normal
0.16 s
0.08 s

Interpretation? Sinus Tachycardia

Sinoatrial Block
Rare
The impulse from the sinus node is blocked before it

enters the atrial muscle

sudden cessation of P wave
the impulse usually originates spontaneously in the
atrioventricular node

Atrial Cell Problems

Atrial cells can:
fire occasionally from a

focus
fire continuously due to

a looping re-entrant
circuit

Premature Atrial
Contractions (PACs)
Atrial Flutter

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

70 bpm
occasionally irreg.
2/7 different contour
0.14 s (except 2/7)
0.08 s

Interpretation? NSR with Premature Atrial

Contractions

Premature Atrial Contractions

Deviation from NSR

These ectopic beats originate in the atria (but not in

the SA node), therefore the contour of the P wave, the

PR interval, and the timing are different than a
normally generated pulse from the SA node
Compensatory pause
Pulse deficit due to a poor ventricular filling during

the extrasystolic cycle

Premature Atrial Contractions

PAC: Excitation of an atrial cell fires a premature impulse

that is conducted normally through the AV node and

ventricles
When an impulse originating anywhere above the ventricles

(SA node, atrial cells, AV node, Bundle of His) is conducted

normally through the ventricles, the QRS will be narrow
(0.04 - 0.12 s)

Mechanisms Underlying Arrhythmias

Disorders of impulse formation
Automatism
Triggered activity

Disorders of impulse conduction

Partial and complete conduction block
Unidirectional block with reentry
Aberrant (accessory) conduction pathways

Enhanced Automaticity
Enhancement of normal automacity
Development of automaticity in plain atrial or ventricular cells
Can arise when
the maximum diastolic potential becomes reduced to -50 mV

and ICa may be operative

at membrane potentials more negative than -70 mV, due to If
Pathophysiologic states: increased catecholamines, electrolyte

disturbances (e.g. hypokalemia), hypoxia or ischemia,

mechanical stretch, drugs (e.g. digitalis)

Triggered Activity
Requires the presence of an action potential
Initiated by afterdepolarizations = depolarizing oscillations

in membrane voltage induced by preceding AP

Early afterdepolarizations (EAD) arise during phases 2
and 3 of AP
Delayed afterdepolarizations (DAD) arise during phase
4 of AP
When the after-depolarization reaches threshold, triggers a

sequence of pacemaker-like action potentials that

generate extrasystoles

EAD
During a prolonged AP (bradicardia, hypokalemia, drugs that

block outward K currents etc.) Ca++ channels recover from

inactivation and can lead to a spontaneous depolarization

DAD
Spontaneous release of Ca++ from SR during Ca++ overload

(digitalis intoxication, injury-related cellular depolarization etc.)

produces a transient inward current, Iti
Iti is a composite current, resulting from
Na+/Ca++ exchange current
non-specific cation current
that are activated by increased intracellular Ca++ concentration
When large enough, Iti can produce a spontaneous AP

DAD

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

Interpretation?

70 bpm
regular
flutter waves
none
0.06 s
Atrial Flutter

Atrial Flutter

Deviation from NSR

No P waves; instead, flutter waves (note sawtooth

pattern) are formed at a rate of 250 - 350 bpm

Only some impulses conduct through the AV node (usually
every other impulse, resulting in an aprox. 150 ventricular
bpm)
Mechanism: Re-entrant pathway in the atria with every

2nd, 3rd or 4th impulse generating a QRS the others are

blocked in the AV node

Re-entry
A re-entrant pathway

(re-entrant excitation
or circus movement)
Is a wave of
depolarization that
travels in an
endless circle
Occurs when an
action potential
loops and results in
self-perpetuating
impulse formation

Re entrant Excitation
Re-entry has three requirements:

(1) a closed conduction loop,

(2) with unidirectional conduction, provided by a region
of unidirectional block,
(3) a sufficiently slow conduction of action potentials
around the loop (relative to the path length and the action
potential duration)

 Unidirectional block
Partial conduction block in which impulses travel in one

direction, but not in the opposite one

May arise as a result of a local depolarization or may be

due to pathologic changes in functional anatomy

 When the pathway isnt long enough, the head of the re-

entrant impulse bites its own refractory tail, resulting in

extinction of the excitation

Pathway Length APD x Conduction Velocity

APD action potential duration

SHORT PATHWAY

 The impulse can continue to travel around a closed loop,

causing re-entrant excitation if:

the pathway around the circle is long (dilated hearts)
the velocity of conduction decreases (blockage of the
Purkinje system, ischemia, hiperpotasemia etc.)
the refractory period of the muscle is shortened (short
APD) (drugs, such as epinephrine, or after repetitive
electrical stimulation)

Pathway Length > APD x Conduction Velocity

APD action potential duration

Atrial Cell Problems

Atrial cells can also:
fire continuously from

multiple foci
or
fire continuously due to

multiple micro re-entrant

wavelets

Atrial Fibrillation

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

Interpretation?

100 bpm
irregularly irregular
none
none
0.06 s
Atrial Fibrillation

Atrial Fibrillation

Deviation from NSR

No organized atrial depolarization, therefore no normal P

waves; the P waves are replaced by f (fibrillatory) waves

at a rate of 350 - 600 bpm
Atrial activity is chaotic (resulting in an irregularly

irregular rate)

Atrial Fibrillation

Mechanism:
Multiple re-entrant wavelets conducted between the right

and left atria

Impulses are formed in a totally unpredictable fashion;

the AV node allows some of the impulses to pass

through at variable intervals (ventricular rhythm is
irregularly irregular, and the rate about 100 -160 bpm)

 Multiple micro re-entrant wavelets refers

to wandering small areas of activation

which generate fine chaotic impulses
They are generated by transmission of
some of the depolarization waves around
the heart in only some directions but not
other directions
This irregular pattern of impulse travel
causes many circuitous routes for the
impulses to travel
results in an irregular pattern of patchy
refractory areas in the heart
many impulses traveling in all
directions, some dividing and increasing
the number of impulses, whereas others
are blocked by refractory areas

Atrial tissue

AV Junctional Problems
The AV junction can:
fire continuously due to a

looping re-entrant circuit

fire occasionally from a

focus
block impulses coming from

the SA node

Paroxysmal Supraventricular
Tachycardia (PSVT)
Premature Junctional
Contractions
AV Junctional Blocks

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

Interpretation?

74 148 bpm
Regular regular
Normal none
0.16 s none
0.08 s
A-V Nodal Paroxysmal
Tachycardia

PSVT
Deviation from NSR
The heart rate suddenly speeds up ventricular rate 150

220 bpm; the P waves are lost or abnormal

The paroxysm usually ends as suddenly as it began, with
the pacemaker of the heart instantly shifting back to the sinus
node
PSVT: There are several types of PSVT but all originate above

the bifurcation of the His bundle (therefore the QRS is usually

narrow)
Most common: abnormal conduction in the AV node (reentrant
circuit looping in the AV node); P wave absent, covered by the
QRS complex

Atrial Paroxysmal Tachycardia

A PSVT with the abnormal impulse originating in the atria;

the P wave is present, but modified

AV Premature Contractions
Premature contractions fired from the A-V node or the A-V

bundle
The P wave is superimposed onto the QRS-T complex (no P

wave on ECG) because the A-V impulse traveled at the same

time towards atria and ventricles

AV Nodal Blocks
1st Degree AV Block
2nd Degree AV Block, Type I
2nd Degree AV Block, Type II

3rd Degree AV Block

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

Interpretation?

60 bpm
regular
normal
0.36 s
0.08 s
1st Degree AV Block

1st Degree AV Block

Deviation from NSR

PR Interval

> 0.20 s

Each P is followed by a QRS

Etiology: Prolonged conduction delay in the AV node or

bundle of His due to idiopathic fibrosis and sclerosis of the

conduction system, ischemia, drugs (b-blockers, Ca
channel blockers etc), increased vagal tone etc.

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

Interpretation?

50 bpm
regularly irregular
nl, but 4th no QRS
lengthens
0.08 s

2nd Degree AV Block, Type I

2nd Degree AV Block, Mobitz Type I

Deviation from NSR

PR interval progressively lengthens with each beat until the

atrial impulse is completely blocked (P wave not followed by

QRS) Wenckebach phenomenon
R-R intervals > P-P intervals
Each successive atrial impulse encounters a longer and

longer delay in the AV node until one impulse (usually the 3rd
or 4th) fails to be conducted through the AV node

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

75 bpm
regularly irregular
nl, 1 of 5 no QRS
0.14 s
0.08 s

Interpretation? 2nd Degree AV Block, Type II

2nd Degree AV Block, Mobitz Type II

Deviation from NSR

Occasional P waves are completely blocked (P wave not

followed by QRS), usually in a repeating cycle of every 3rd

(3:1 block) or 4th (4:1 block) P wave
Conduction is all or nothing (the PR interval remains

constant)

High-Grade 2nd Degree AV Block

Every 2nd or more P wave is blocked 2 P waves are never

conducted in a row, therefore the distinction between Mobitz

type I and Mobitz type II block is difficult to make

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

Interpretation?

40 bpm
regular
no relation to QRS
none
wide (> 0.12 s)
3rd Degree AV Block

3rd Degree AV Block

Deviation from NSR

The P waves are completely blocked in the AV junction; QRS

complexes originate independently from below the junction

no relationship between P and QRS
The atria and ventricles form impulses independently of each

other (AV dissociation)

Escape rhythms originating
above the bifurcation of the His bundle produce narrow QRS and

a heart rate > 40 bpm

below the bifurcation wide and bizarre QRS, heart rate < 40
bpm

Ventricular Cell Problems

Ventricular cells can:
fire occasionally from 1 or

more foci
fire continuously due to a

Premature Ventricular
Contractions (PVCs)
Ventricular Tachycardia

looping re-entrant circuit

fire continuously from

multiple foci

Ventricular Fibrillation

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

60 bpm
occasionally irreg.
none for 7th QRS
0.14 s
0.08 s (7th wide)

Interpretation? Sinus Rhythm with 1 PVC

PVCs

Deviation from NSR

Ectopic beats originate in the ventricles resulting in

wide and bizarre QRS complexes

One or more ventricular cells are depolarizing and the

impulses are abnormally conducting through the

ventricles

Ventricular Conduction

Normal
Signal moves rapidly through
the ventricles

Abnormal
Signal moves slowly through
the ventricles

A
When an impulse originates in a

ventricle, conduction is inefficient

and the QRS is going to be wide
and bizarre (A);
T waves have an opposite
polarity to the net polarity of the
preceding QRS
The origin of the extrasystolic

QRS axis points towards the site

of the abnormal excitation (B)

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

160 bpm
regular
none
none
wide (> 0.12 sec)

Interpretation? Ventricular Tachycardia

Ventricular Tachycardia

Deviation from NSR

Impulse is originating in the ventricles (no P waves, wide

QRS)
> 3 consecutive ventricular beats at a rate > 120 bpm
Can be regular, monomorphic or irregular, polymorphic
Results from a re-entrant pathway looping in a ventricle

(most common cause) or from abnormal foci or pathways

Ventricular tachycardia can sometimes generate enough
cardiac output to produce a pulse; at other times no pulse
can be felt

Rate?
Regularity?
P waves?
PR interval?
QRS duration?

Interpretation?

none
irregularly irreg.
none
none
wide, if recognizable
Ventricular Fibrillation

Ventricular Fibrillation

Deviation from NSR

Completely abnormal, with ultrarapid baseline undulations,

irregular in timing and morphology

Multiple wavelet reentrant electrical activity
Rapid drop in cardiac output and death occurs if not

quickly reversed

Electroshock Debrillation

Basic Interpretation of the ECG

1)

2)
3)
4)

5)
6)

6)
7)

Evaluate calibration
Calculate rate
Determine rhythm
Determine QRS axis
Measure intervals
Analyze the ECG elements (P, P-Q, Q, QRS, ST, T,
QT) and their interrelation in frontal and in
precordial leads
OR
Asses for Hypertrophy
Look for evidence of Infarction

4) Determine QRS Axis

(The Electrical Axis of the Heart)
Is the axis of the mean force during activation,

measured in the frontal plane = mean QRS vector in the

frontal plane
Equals the sum of instantaneous activation vectors
(corresponding to septum, apex, free walls and base
activation)

Normal and Abnormal QRS Axis

The normal QRS axis lies between -30o and +90o.
A QRS axis that falls between
-30o and -90o is abnormal
and called left axis deviation. -150o

-90o
-120o

-60o

-30o

180o

A QRS axis that falls between

+90o and +150o is abnormal 150o
and called right axis
deviation.

0o
30o

120o

90

A QRS axis that falls between +150o and -90o is

abnormal and called superior right axis deviation.

60o

Left Axis Deviation

Left axis deviation in a hypertensive

heart (hypertrophic left ventricle).
Note the slightly prolonged QRS
complex as well.

Left axis deviation caused by left

bundle branch block. Note also
the greatly prolonged QRS complex.

Right Axis Deviation

High-voltage electrocardiogram in
congenital pulmonary valve stenosis with
right ventricular hypertrophy. Superior
right axis deviation and a slightly
prolonged QRS complex also are seen.

Right axis deviation caused by

right bundle branch block.
Note also the greatly prolonged
QRS complex.

5) Calculate Intervals
Intervals refers to the length of the PR and QT intervals

and the width of the QRS complexes

PR interval
< 0.12 s

0.12-0.20 s

> 0.20 s

High catecholamine
states
Wolff-Parkinson-White

Normal

AV nodal blocks

Wolff-Parkinson-White

1st Degree AV Block

Accessory Conduction Pathways

Wolf-Parkinson-White (preexcitation) syndrome

An accessory (aberrant) pathway conducts potential directly

from A to V, providing a short circuit around the delay in the AV

node
Antegrade conduction occurs over both the accessory
pathway and the normal conducting system
The accessory pathway, being faster, depolarizes some of the
V early short PR interval and a delta wave that prolongs
QRS to > 0.1 s

Accessory conduction pathways in cases with WolffParkinson

White syndrome.
K, bundle of Kent; J, bundle of James; M, Mahaim fibres; the
hatched area represents the atrioventricular border.

 When the accessory pathway conducts in a retrograde direction

can participate in reentrant tachycardia (PSVT)

QTc interval
< 0.44 s

> 0.44 s
Long QT

Normal

Long QT

Torsades de Pointes

A prolonged QT can be very dangerous. It may predispose an

individual to a type of ventricular tachycardia called
Torsades de Pointes. Causes include drugs, electrolyte
abnormalities, CNS disease, post-MI, and congenital heart
disease.

QT = 0.40 s
RR = 0.68 s
Square root of
RR = 0.82
QTc = 0.40/0.82
= 0.49 s

PR interval?
0.16 seconds
Interpretation of
intervals?

QRS width?
0.08 seconds

QTc interval?
0.49 seconds

Normal PR and QRS, long QT

RR
23 boxes

17 boxes

10 boxes

13 boxes

QT

Normal QT

Long QT

QTc = QT/RR
Tip: Instead of calculating the QTc, a quick way to estimate if
the QT interval is long is to use the following rule:
A QT > half of the RR interval is probably long

QRS complex
< 0.10 s

Normal

0.10-0.12 s

> 0.12 s

Incomplete bundle
branch block

Bundle branch block

PVC
Ventricular rhythm

Incomplete bundle branch block

3rd degree AV block with

ventricular escape rhythm

Bundle Branch Blocks

1. QRS complex widens (> 0.12 sec)
2. QRS vector is oriented towards the area with delayed

depolarization
3. QRS morphology changes (varies depending on ECG lead,
and if it is a right vs. left bundle branch block)
4. Intrinsecoid deflection > 0.06 for RBBB and > 0.08 for LBBB
5. T wave inversion appears

 QRS duration: < 0.12 s measured in the lead with the

widest complex
Intrinsecoid deflection:
measures the duration of transmural activation under the
recording electrode of a precordial lead (V1, V2, V5, V6)
measured from the peak of the last R of the complex until
the onset of the QRS complex
Normal values: < 0.035 s in V1, V2 and < 0.045 s in V5, V6

QRS

ID

ID

Right Bundle Branch Block

What QRS morphology is characteristic?
For RBBB the wide QRS complex assumes a unique, virtually
diagnostic shape in those leads overlying the right ventricle (V1
and V2).

V1

Rabbit Ears

 The terminal vector of ventricular depolarization,

corresponding to delayed RV depolarization, is oriented

anteriorly and to the right: rSR in V1 and qRS in V6
T wave in V1 is negative due to the delayed repolarization

of the right ventricular wall (the vector is oriented

posteriorly and to the left)

qRS

Left Bundle Branch Block

Both early and later phases of ventricular depolarization are

altered: both septal and left wall depolarization vectors are

oriented posteriorly and to the left
wide predominantly negative (QS) complexes in V1 and
entirely positive complexes (wide, notched R) in V6
T wave has opposite polarity to the net QRS due to a
repolarization vector oriented anteriorly and to the right

QS

6) Hypertrophy
The ECG can reveal enlargement or hypertrophy of the four
chambers of the heart:
Right atrial enlargement (RAE)

Left atrial enlargement (LAE)

Right ventricular hypertrophy (RVH)
Left ventricular hypertrophy (LVH)

Atrial Enlargement
P wave changes (morphology, axis, amplitude)
Due to
Inlet ventricular valve stenosis (mitral - often, tricuspid -

rare) or insufficiency
Pulmonary hypertension
Congenital heart diseases
Heart failure

Right atrial enlargement

P wave morphology: sharp, tall, symmetric in V1, V2, aVF, II,
III; if biphasic in V1, the positive initial deflection predominates
P wave axis: + 75 - +90
P wave amplitude: II
P > 2.5 mm, or
V1 or V2
P > 1.5 mm
> 1 boxes (in height)

> 2 boxes (in height)

A cause of RAE is RVH from pulmonary hypertension (P pulmonale)

Left atrial enlargement

The P waves are broad (> 0.12 s) and often notched in lead I,
aVL, V5, V6 ; in lead V1 they have a deep and wide negative
component
In lead II, > 0.04 s (1 box) between notched peaks, or
In V1, neg. deflection > 1 box wide x 1 box deep
P wave axis: left deviation

Normal
Notched

Negative deflection

A common cause of LAE is Mi stenosis

Ventricular Hypertrophy
Due to a pressure or volume load
ECG abnormalities
High voltage R, S waves
QRS axis deviation
Increased intrinsecoid deflection
T-wave inversions

Left Ventricular Hypertrophy

Left Ventricular Hypertrophy

Normal
The QRS complexes are
very tall in the right panel
(increased voltage)

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized by tall QRS
complexes?
As the heart muscle wall thickens there is an increase in
electrical forces moving through the myocardium resulting
in increased QRS voltage.

LVH

Increased QRS voltage

ECHOcardiogram

Left ventricular hypertrophy

Take a look at this ECG. What do you notice about the

axis and QRS complexes in leads V5, V6 and V1, V2?

The deep S waves seen

in the leads over the right
ventricle and the tall R
waves in the left leads
are created because the
heart is depolarizing left,
superior and posterior
(away from leads V1, V2,
toward leads V5, V6)

There is left axis deviation and there are tall R waves in V5,
V6 and deep S waves in V1, V2

 QRS amplitude = algebraic sum of the amplitudes of

the component waves

> 1 mV in one precordial lead, > 0.5 mV in a standard

lead
The amplitude of R and S waves it is used for the

diagnosis of left ventricular hypertrophy:

Sokolow-Lyon index: Sv1+ (Rv5 or Rv6) > 3.5 mV
Cornell voltage criteria: Sv3 + SaVL 2.8 mV for men,

2.0 for women

or of right ventricular hypertrophy:

Rv1 > 0.7 mV, SV5 or V6 > 0.7 mV etc.

Left ventricular hypertrophy, diagnostic criteria:

Most characteristic: increased QRS amplitude - R waves in left

leads (I, aVL, V5, V6) and S waves in the right leads (V1, V2)
are oversized (and sometimes notched)
Sokolow-Lyon index: SV1 + (RV5 or RV6) > 3.5 mV,
RaVL > 1.1 mV
Cornell voltage criteria: SV3 + SaVL > 2.8 mV and > 2.0 mV
QRS duration > 0.11 s, ID > 0.05 s in V5, V6
QRS axis horizontal or with a left deviation
ST depression and T inversion in leads with a tall R

S = 13 mm

R = 25 mm

A common cause of LVH

is systemic hypertension.

A 63 years old man has longstanding, uncontrolled

hypertension. Is there evidence of heart disease from his
hypertension?

Yes, there is left axis deviation (positive in I, negative in II),

left atrial enlargement (> 1 x 1 boxes in V1) and LVH (R in
V5 = 27 + S in V2 = 10 > 35 mm).

Right Ventricular Hypertrophy

Right axis deviation, tall R waves in V1, V2, T-wave

inversions; P pulmonale can be observed as well

Right ventricular hypertrophy

Tall R in aVR, V1, V2 (R/S>1) and deep

S in I, aVL, V5 (V6):
R in V1 > 0.7 mV, S in V5, V6 > 0.7 mV
RV1 + SV5 > 1,05 mV
ID > 0.03 s in V1,2
Right QRS axis deviation
T-wave inversions

Normal

RVH

R waves in V1, V2 from a normal ECG and from a person with RVH

7) Look for Evidence of Infarction

ECG findings depend on
The nature of the process
Reversible ischemia
Irreversible - infarction

The duration: acute/ chronic

The extent:
Transmural
Subendocardial

Localization: anterior, inferoposterior

ECG can identify other underlying abnormalities:

ventricular hypertropy, conduction defects etc.

7) Look for Evidence of Infarction

When analyzing a 12-lead ECG for evidence of an infarction

one looks for the following:

Abnormal Q waves
ST elevation or depression
Peaked, flat or inverted T waves

ST elevation (or depression) in at least two leads is the

earliest and most consistent ECG finding during AMI
There are ST elevation (Q-wave) and non-ST elevation
(non-Q wave) MIs

ST Elevation
Elevation of the ST
segment in at least 2
leads is consistent with a
myocardial infarction
Because blood flow is
regional, the area of
infarction are also
regional specific ECG
leads can provide the
best view of the infarcted
area

Views of the Heart

Some leads get a good view of the:

Lateral portion
of the heart
Anterior portion
of the heart

Leads I, aVL,
V5, V6

Leads V1 V4

Inferior portion
of the heart

Leads II, III, aVF

Anterior Wall MI
Can be recognized if there are changes in leads V1 - V4
that are consistent with a myocardial infarction

Inferior Wall MI
ST segment is elevated in leads II, III and aVF

Anterolateral MI
This persons MI involves both the anterior wall (V2-V4)
and the lateral wall (V5-V6, I, and aVL)!

ST Elevation and non-ST Elevation MIs

When myocardial blood supply is abruptly reduced or cut

off to a region of the heart, a sequence of injurious events

occur beginning with ischemia (inadequate tissue
perfusion), followed by necrosis (infarction), and eventual
fibrosis (scarring) if the blood supply is not restored in an
appropriate period of time.
The ECG changes over time with each of these events

 Mild ischemia increases K+ outflow

shortens APD
affected areas are repolarized before the rest of the
myocardium
changes of repolarization vector leading to T wave
abnormalities

 Severe, acute ischemia can reduce the resting membrane

potential, shorten APD and decrease the slope and amplitude of

phase 0 voltage gradient between normal and ischemic area
current flows = diastolic and systolic injury currents

 Transmural ischemia: overall ST vector shifts toward epicardial

layers ST elevation, tall T waves in the overlying leads

Subendocardial ischemia: overall ST vector shifts toward the

inner layer and the ventricular cavity ST segment depression

in the overlying leads

 Necrosis decreased R amplitude or pathologic Q waves

genesis due to loss of electric activity in the infarcted area

ECG Changes
Ways the ECG can change include:
ST elevation &
depression

T-waves

peaked
Appearance
of pathologic
Q-waves

flattened

inverted

ECG Changes and the Evolving MI

There are two distinct
patterns of ECG
change depending if
the infarction is:

Non-ST Elevation

ST Elevation

ST Elevation (Transmural or Epicardial MI)

Non-ST Elevation (Subendocardial or non-Q-wave)

ST Elevation Infarction
Diagram depicting an evolving infarction:
A. Normal ECG prior to MI
B. Ischemia from coronary artery occlusion
results in ST elevation and peaked T-waves
C. Infarction from ongoing ischemia results in
marked ST elevation

D/E. Ongoing infarction with appearance of

pathologic Q-waves; T-wave inversion may
occur
F. Fibrosis (months later) with persistent Qwaves, but normal ST segment and T- waves

normal

hours

hours

days

weeks

months

of the clinical onset of an MI

ST Elevation Infarction
ECG of an inferior MI:
Look at the
inferior leads
(II, III, aVF)
What ECG
changes do
you see?
ST elevation
and Q-waves

Extra credit:
What is the
rhythm? Atrial fibrillation (irregularly irregular with narrow QRS)!

Non-ST Elevation Infarction

The ECG changes seen with a non-ST elevation infarction are:

Before injury Normal ECG

Ischemia

ST depression & T-wave inversion

Infarction

ST depression & T-wave inversion

Fibrosis

ST returns to baseline, but T-wave

inversion persists

Non-ST Elevation Infarction

Heres an ECG of an evolving non-ST elevation MI:
Note the ST
depression
and T-wave
inversion in
leads V2-V6.

Question:
What area of
the heart is
infarcting?

Anterolateral