ISCHEMIA AND MYOCARDIAL INFARCTION

Asist. Univ. Dr. Mihaela Popescu

Catedra de Cardiologie Spitalul Universitar
de Urgenta Elias
 The ischemic action potential
Reduced depolarization
Reduced repolarization
Reduced duration and amplitude

Ischemic AP
Normal AP
Systole = ST
Diastole Diastole= TP
QRS complex= phase 0

and 1

ST Segment = phase 2

T wave= phase 3

TQ Interval = phase 4
 Ischemia
Decreased myocardial perfussion reversible
Ischemic cardiomyocite- early repolarization(+)
Subendocardial ischemia negative T waves
Transmural ischemia positive, sharp, symmetrical
T waves
 The difference in potential between normal
and ischemic areas small current= injury
current
K ions flow from the positive toward the
negative
In systole (ST ) the ischemic region is more
negative- current from normal to ischemic
In diastole ( TP ) - the ischemic region is
more positive- current from ischemic to
normal
ST- current from normal to ischemic
TP current from ischemic to normal

ST
TP
sistolic injury current diastolic injury current
sistolic injury current diastolic injury current
sistolic injury current diastolic injury current
 Miocardial infarction
Persistent ischemia cells lose viability= necrosis
ST elevation myocardial infarction
Non ST elevation myocardial infarction
One way to
diagnose an
acute MI is to
look for
elevation of the
ST segment.

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 ST segment elevation over area of damage
ST depression in leads opposite infarction
Pathological Q waves
Reduced R waves
Inverted T waves
 Occurs in the early stages
R
Occurs in the leads facing the
ST infarction
Slight ST elevation may be normal in
P V1 or V2

Q
 Only diagnostic change of myocardial
R infarction
ST At least 0.04 seconds in duration
Depth of more than 25% of ensuing R
P wave

T
Q
 Late change
R Occurs as ST elevation is
returning to normal
ST Apparent in many leads
P

T
Q
 R
R R
ST ST
T

P P P

T
QS Q
Q

1 minute after onset 1 hour or so after onset A few hours after onset

ST T
P P ST
P

T T
Q Q Q

A day or so after onset Later changes A few months after AMI

CATEGORY
Occlusion location ECG at admission
1. LAD -proximal Before the first septal ST in DI, aVL, V1-V6 and
perforating artery fascicular block or bundle
branch block
2. LAD - medium After the first septal ST in DI, aVL, V1-V6
perforating artery, before
the great diagonal artery
3. LAD - distal or After the great diagonal ST in V1-V4 or ST in DI,
Diagonal artery artery or first diagonal aVL, V5-V6
4. Inferior Proximal RCA or CX ST in DII, DIII, aVF and
moderate MI (RV, any or all of the
posterior, lateral) following:
a) V1, V3R, V4R
b) V5-V6
c) R>S in V1-V2
5.Small inferior Distal RCA or CX, or CX ST only in DII, DIII, aVF
MI branches
Anterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left
coronary
artery
Inferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right
coronary
artery
Lateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

distal LAD or the diagonala/ circumflex

 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right or circumflex
artery
 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right or circumflex
artery
I aVR V1 V4

ANT
LATERAL POST
ANT
II aVL V2 SEPTAL
V5

ANT
V3 V6 LAT
III aVF
INFERIOR
Now, where do you think this person is having
a myocardial infarction?
This is an inferior MI. Note the ST elevation in
leads II, III and aVF.

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Do you think this person is having a
myocardial infarction. If so, where?

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Yes, this person is having an acute anterior
wall myocardial infarction.

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How about now?

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

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May indicate the
localization of the
occlusion in a certain
artery
Q wave duration of more than
0.04 seconds
Q wave depth of more than 25%
of ensuing r wave
ST elevation in leads facing
infarct (or depression in
opposite leads)
Deep T wave inversion overlying
and adjacent to infarct
Cardiac arrhythmias
Prinzmetal Angina
Pericarditis
Early repolarization
Brugada Sdr.
Osborne wave
frozen ST elevation
ventricular aneurism
 Anteroseptal
aneurism
Osborne wave
Osborne wave

Brugada
syndrome

Normal Sdr. Brugada

Anterior wall MI Left bundle branch block

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

 Sgarbossa criteria (for MI with LBBB)

ST > 1mm in leads with positive QRS -5 points

ST > 1 mm in V1-V3 -3 points
ST > 5 mm in leads with negative QRS -2 points

For a score of more than 3 specifficity

>90% for detecting AMI associated with LBBB or
pace-maker rhythm.

Criteria to detect old MI with LBBB

Q wave in at least two of DI, aVL, V5, V6
Regression of the R wave from V1 to V4
Incisure on the S wave in V3-V5 Cabrera sign
MI ST elevation Reciprocal ST
depression

Anterior V1-V6 (slow progression II, III, aVF

of the R wave)

Lateral DI, aVL, V5, V6 V1-V3

Inferior II, III, aVF DI, aVL, possibly in

the anterior leads

Posterior Abnormally high R waves V1-V3

in V1- V3, ST elevation
in V7-V9
ATRIAL ENLARGEMENT

VENTRICULAR
HYPERTROPHY
 Criteria

P wave height in II 2.5mm

Positive component of biphasic P
wave in V1 1 small box in
area
Sharp wave
Vertical axis +75 - +90
Also called pulmonar p wave
Best seen in DII, DIII, aVF
Causes of Right Atrial Enlargement

Valve disease
Tricuspid stenosis
Tricuspid regurgitation

Pulmonary hypertension
COPD
Pulmonary embolism
Sleep apneea

Congenital disease
Pulmonary stenosis
Fallot Tetralogy

Tranzitory conditions
Acute pulmonary embolism
Status astmaticus

NB: Associated usualy eith RV hypertrophy, exception- Tricusp

Criteria

P wave duration in II 120ms

Bifid p wave
Also called mitral p wave
Negative component of biphasic P wave
in V1 1 small box in area
Best seen in DI, aVL, V5, V6
Valve disease

Mitral stenosis
Mitral regurgitation

Low LV compliance

Systemic hypertension
Obstructive cardiomyopathy
Aortic stenosis
Aortic regurgitation
Amiloidosis
 Criteria for both
V1: large biphasic wave
Positive component > 1,5 mm
Negative component >1 mm, >0.04s
DII:
P wave > 2.5 mm
P wave > 0,12 sec
 LV overload causes:
Volume overload : Mi /Ao regurgitation,
Pressure overload : Hypertension, Ao stenosis,
Coarctation of the Aorta, Hypertrophic
cardiomyopathy

LV overload effect:
Volume overload cavity dilation
Pressure overload hypertrophy
 Sokolow Lyon index: R (V5/V6) + S (V1/V2) > 3.5 mV
(4.5 mV la copil)
Cornell index: R (aVL) + S (V3) > 2.8 mV (B), 2 mV (F)

Criterion Points
Amplitude (any of the following: 3
Largest R or S wave in any limb lead 20mm
S in V1 or V2 30mm
Romhilt
Estes R in V5 or V6 30mm
score ST depressions or T wave inversions in lateral 3
precordial leads, I, and/or aVL

Left atrial enlargement 3

Left axis deviation 2

QRS duration 90 ms 1

Intrinsicoid deflection in V5 or V6 50 ms 1
4 points Probable LVH ;5 points Definite LVH
 Etiology:
Volume overload VSD, Fallot (left-right shunt)
Pressure overload
primary pulmonary artery hypertension
secondary pulmonary artery hypertension
(emphysema, TB, bilateral bronchyectasis, pulmonary
fibrosis, Mitral stenosis)
Effects:
Tall R in V1, V2 + deep S in V5, V6
Clockwise rotation, toward the anterior of the RV +
posterior rotation of the apex
 3 patternS
1. no right ventricle conduction disturbances
2. incomplete RBBB
3. complete RBBB
 Sokolow Lyon
R in V1 + S in V5/ V6>1.1mV

Other criteria:
1) axis deviation> 90
2) R V1 > 7 mm
3) R/S V1 >1
4) pulmonary P wave
5) S/R V6 >1
6) Intrinsicoid deflection V1 > 0.035 sec.
7) RBBB- like aspect
 SV1 + RV5(or V6) >35 mm (Sokolov index) +
right axis deviation
SV6 >7 mm (without RBBB)
Best sign= combination of RVH pattern with
LA enlargement (p >=120 ms)
S/R>1 in V5/V6 + LA enlargement
SV6 >7 mm + LA enlargement
QRS axis >+90 + LA enlargement (with RBBB)