Adelina Vlad, MD PhD

Pathologic ECG

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)

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

30 bpm • Rate?

• Regularity? regular

normal

0.10 s

• P waves?

• PR interval? 0.12 s

• QRS duration?

Interpretation? Sinus Bradycardia

130 bpm • Rate?

• Regularity? regular

normal

0.08 s

• P waves?

• PR interval? 0.16 s

• QRS duration?

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

70 bpm • Rate?

• Regularity? occasionally irreg.

2/7 different contour

0.08 s

• P waves?

• PR interval? 0.14 s (except 2/7)

• QRS duration?

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

70 bpm • Rate?

• Regularity? regular

flutter waves

0.06 s

• P waves?

• PR interval? none

• QRS duration?

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 isn’t 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

100 bpm • Rate?

• Regularity? irregularly irregular

none

0.06 s

• P waves?

• PR interval? none

• QRS duration?

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)

Atrial tissue 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

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

74 148 bpm • Rate?

• Regularity? Regular regular

Normal none

0.08 s

• P waves?

• PR interval? 0.16 s none

• QRS duration?

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

A PSVT with the abnormal impulse originating in the atria;

the P wave is present, but modified

Atrial Paroxysmal Tachycardia

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 Premature Contractions

AV Nodal Blocks

1st Degree AV Block

2nd Degree AV Block, Type I

2nd Degree AV Block, Type II

3rd Degree AV Block

60 bpm • Rate?

• Regularity? regular

normal

0.08 s

• P waves?

• PR interval? 0.36 s

• QRS duration?

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.

50 bpm • Rate?

• Regularity? regularly irregular

nl, but 4th no QRS

0.08 s

• P waves?

• PR interval? lengthens

• QRS duration?

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

75 bpm • Rate?

• Regularity? regularly irregular

nl, 1 of 5 no QRS

0.08 s

• P waves?

• PR interval? 0.14 s

• QRS duration?

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

40 bpm • Rate?

• Regularity? regular

no relation to QRS

wide (> 0.12 s)

• P waves?

• PR interval? none

• QRS duration?

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

more foci

fire continuously due to a

looping re-entrant circuit

fire continuously from

multiple foci

Premature Ventricular

Contractions (PVCs)

Ventricular Tachycardia

Ventricular Fibrillation

60 bpm • Rate?

• Regularity? occasionally irreg.

none for 7th QRS

0.08 s (7th wide)

• P waves?

• PR interval? 0.14 s

• QRS duration?

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

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)

A

B

160 bpm • Rate?

• Regularity? regular

none

wide (> 0.12 sec)

• P waves?

• PR interval? none

• QRS duration?

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

none • Rate?

• Regularity? irregularly irreg.

none

wide, if recognizable

• P waves?

• PR interval? none

• QRS duration?

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 Defibrillation

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)

0o

30o

-30o

60o

-60o

-90o

-120o

90o 120o

150o

180o

-150o

Normal and Abnormal QRS Axis

The normal QRS axis lies between -30o and +90o.

o

o

A QRS axis that falls between

-30o and -90o is abnormal

and called left axis deviation.

A QRS axis that falls between

+90o and +150o is abnormal

and called right axis

deviation.

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).

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

Right axis deviation caused by

right bundle branch block.

Note also the greatly prolonged

QRS complex.

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.

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

5) Calculate Intervals

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

Accessory conduction pathways in cases with Wolff–Parkinson–

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)

http://upload.wikimedia.org/wikipedia/commons/a/a5/Wolff-Parkinson-White_syndrome_12_lead_EKG.png

QTc interval

< 0.44 s > 0.44 s

Normal Long QT

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.

Torsades de Pointes

Long QT

PR interval? QRS width? QTc interval?

0.08 seconds 0.16 seconds 0.49 seconds

QT = 0.40 s

RR = 0.68 s

Square root of

RR = 0.82

QTc = 0.40/0.82

= 0.49 s

Interpretation of

intervals?

Normal PR and QRS, 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

Normal QT Long QT

QT

RR

10 boxes

23 boxes 17 boxes

13 boxes

QRS complex

< 0.10 s 0.10-0.12 s > 0.12 s

Normal Incomplete bundle

branch block

Bundle branch block

PVC

Ventricular rhythm

3rd degree AV block with

ventricular escape rhythm

Incomplete bundle branch block

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

Bundle Branch Blocks

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

ID ID QRS

Right Bundle Branch Block

What QRS morphology is characteristic?

V1

For RBBB the wide QRS complex assumes a unique, virtually

diagnostic shape in those leads overlying the right ventricle (V1

and V2).

“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

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

Left Bundle Branch Block

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

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

> 2 ½ boxes (in height)

> 1 ½ boxes (in height)

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

A common cause of LAE is Mi stenosis

Notched

Negative deflection

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

Normal

Left Ventricular Hypertrophy

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?

LVH ECHOcardiogram Increased QRS voltage

As the heart muscle wall thickens there is an increase in

electrical forces moving through the myocardium resulting

in increased QRS voltage.

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?

There is left axis deviation and there are tall R waves in V5,

V6 and deep S waves in 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)

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

A common cause of LVH

is systemic hypertension.

S = 13 mm

R = 25 mm

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

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

7) Look for Evidence of Infarction

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:

Anterior portion

of the heart

Lateral portion

of the heart

Inferior portion

of the heart Leads II, III, aVF

Leads I, aVL,

V5, V6 Leads V1 – V4

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 person’s 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:

Appearance

of pathologic

Q-waves

ST elevation &

depression

T-waves

peaked flattened inverted

ECG Changes and the Evolving MI

There are two distinct

patterns of ECG

change depending if

the infarction is:

–ST Elevation (Transmural or Epicardial MI)

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

Non-ST Elevation

ST Elevation

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 Q- waves, but normal ST segment and T- waves

ST Elevation Infarction

Diagram depicting an evolving infarction:

hours

hours days

weeks months

normal

… 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

ST depression & T-wave inversion

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

Before injury Normal ECG

ST depression & T-wave inversion

ST returns to baseline, but T-wave

inversion persists

Ischemia

Infarction

Fibrosis

Non-ST Elevation Infarction

Here’s 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