Pathologic ECG

Adelina Vlad, MD PhD

Basic Interpretation of the ECG
1) Evaluate calibration
2) Calculate rate
3) Determine rhythm
4) Determine QRS axis
5) Measure intervals
6) Analyze the morphology and interrelation of ECG
elements (P, P-Q, Q, QRS, ST, T, QT) in frontal
and in precordial leads
OR
6) Asses for Hypertrophy
7) Look for evidence of Infarction
 NSR Parameters

Rate 60 - 100 bpm

Regularity regular
P waves normal
PR interval 0.12 - 0.20 s
QRS duration 0.04 - 0.12 s

Any deviation from above is sinus tachycardia,

sinus bradycardia or an arrhythmia
 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) Sinus Bradycardia

fire too fast (>100 bpm) Sinus Tachycardia

The impulse is conducted normally

Sinus Tachycardia may be an appropriate response to stress

Both are abnormal Sinus Rhythms

 Rate? 30 bpm
Regularity? regular
P waves? normal
PR interval? 0.12 s
QRS duration? 0.10 s
Interpretation? Sinus Bradycardia
 Rate? 130 bpm
Regularity? regular
P waves? normal
PR interval? 0.16 s
QRS duration? 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 Premature Atrial

focus Contractions (PACs)

fire continuously due to Atrial Flutter

a looping re-entrant
circuit
 Rate? 70 bpm
Regularity? occasionally irreg.
P waves? 2/7 different contour
PR interval? 0.14 s (except 2/7)
QRS duration? 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? 70 bpm
Regularity? regular
P waves? flutter waves
PR interval? none
QRS duration? 0.06 s
Interpretation? 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
Atrial Fibrillation

fire continuously due to

multiple micro re-entrant
wavelets
 Rate? 100 bpm
Regularity? irregularly irregular
P waves? none
PR interval? none
QRS duration? 0.06 s
Interpretation? 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 Atrial tissue
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
 AV Junctional Problems
The AV junction can:

fire continuously due to a Paroxysmal Supraventricular

looping re-entrant circuit Tachycardia (PSVT)

fire occasionally from a

Premature Junctional
focus
Contractions

block impulses coming from

the SA node AV Junctional Blocks
 Rate? 74 148 bpm
Regularity? Regular regular
P waves? Normal none
PR interval? 0.16 s none
QRS duration? 0.08 s
Interpretation? 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? 60 bpm
Regularity? regular
P waves? normal
PR interval? 0.36 s
QRS duration? 0.08 s
Interpretation? 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? 50 bpm
Regularity? regularly irregular
P waves? nl, but 4th no QRS
PR interval? lengthens
QRS duration? 0.08 s
Interpretation?
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? 75 bpm
Regularity? regularly irregular
P waves? nl, 1 of 5 no QRS
PR interval? 0.14 s
QRS duration? 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? 40 bpm
Regularity? regular
P waves? no relation to QRS
PR interval? none
QRS duration? wide (> 0.12 s)
Interpretation?
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 Premature Ventricular

more foci Contractions (PVCs)

fire continuously due to a Ventricular Tachycardia

looping re-entrant circuit

fire continuously from

multiple foci Ventricular Fibrillation
 Rate? 60 bpm
Regularity? occasionally irreg.
P waves? none for 7th QRS
PR interval? 0.14 s
QRS duration? 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 Abnormal
Signal moves rapidly through Signal moves slowly through
the ventricles 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 B

The origin of the extrasystolic

QRS axis points towards the site
of the abnormal excitation (B)
 Rate? 160 bpm
Regularity? regular
P waves? none
PR interval? none
QRS duration? 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? none
Regularity? irregularly irreg.
P waves? none
PR interval? none
QRS duration? wide, if recognizable
Interpretation? 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) Evaluate calibration
2) Calculate rate
3) Determine rhythm
4) Determine QRS axis
5) Measure intervals
6) Analyze the ECG elements (P, P-Q, Q, QRS, ST, T,
QT) and their interrelation in frontal and in
precordial leads
OR
6) Asses for Hypertrophy
7) 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.
-90o
A QRS axis that falls between -120o -60o
-30o and -90o is abnormal o

and called left axis deviation. -150o -30o

180o 0o
A QRS axis that falls between
+90o and +150o is abnormal 150o 30o
and called right axis
deviation. o
60o
120o o
90

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

abnormal and called superior right axis deviation.
 Left Axis Deviation

Left axis deviation in a hypertensive

heart (hypertrophic left ventricle). Left axis deviation caused by left
Note the slightly prolonged QRS bundle branch block. Note also
complex as well. the greatly prolonged QRS complex.
 Right Axis Deviation

High-voltage electrocardiogram in Right axis deviation caused by

congenital pulmonary valve stenosis with right bundle branch block.
right ventricular hypertrophy. Superior Note also the greatly prolonged
right axis deviation and a slightly QRS complex.
prolonged QRS complex also are seen.
 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 Normal AV nodal blocks
Wolff-Parkinson-White

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? QRS width? QTc interval?

0.16 seconds 0.08 seconds 0.49 seconds
Interpretation of Normal PR and QRS, long QT
intervals?
 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 0.10-0.12 s > 0.12 s

Bundle branch block

Incomplete bundle
Normal PVC
branch block
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,
Leads V1 V4 V5, V6

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 flattened inverted

Appearance
of pathologic
Q-waves
ECG Changes and the Evolving MI

There are two distinct Non-ST Elevation

patterns of ECG
change depending if
the infarction is:

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

normal hours
B. Ischemia from coronary artery occlusion
results in ST elevation and peaked T-waves

C. Infarction from ongoing ischemia results in hours days

marked ST elevation

D/E. Ongoing infarction with appearance of

pathologic Q-waves; T-wave inversion may weeks months
occur

F. Fibrosis (months later) with persistent Q-

waves, but normal ST segment and T- waves 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