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)
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