ECG changes Stage of MI Site of injury INFERIOR POSTERIOR LATERAL SEPTAL

1. ECG BASICSECG BASICS
77thth
LectureLecture
ECG Changes in IHD
By
Salah Mabruok Khalaf
South Egypt Cancer Institute
2017
Course of Medical Oncology
Medical Oncology department

2. Coronary artery SuppliesCoronary artery Supplies

3. Lefteft anterioranterior descending arterydescending artery usually supplies
1.the anterior and anterolateral walls of the left ventricle
2.the anterior two-thirds of the septum.
Left circumflexLeft circumflex coronarycoronary artery usually supplies
the posterolateral wall of the left ventricle.
RightRight coronary arterycoronary artery (RCA) supplies
the right ventricle,
the inferior (diaphragmatic) and
true posterior walls of the left ventricle,
the posterior third of the septum.
1.The RCA also supplies SA Node (60%)and the AV nodal
coronary artery in 85-90% of individuals; the remaining is
supplied by a branch of the LCX.

4. J-Point
Junction between end of QRS and beginning of ST
segment; Where QRS stops & makes a sudden
sharp change of direction

5. ST Segment
Segment between J-point and beginning of T wave
Need reference point
Compare to TP segment
DO NOT use PR segment as reference!

6. – ST segment elevation or depression
• More than one millimeter (one small box)
• Present in two anatomically contiguous leads

7. • Infarction – always requires previous ECG for
comparison
• Identifying Injury
(1) Ischemia – inverted T waves (earliest sign) –
symmetrical down- and upslope, opposite direction of
QRS
(2) Acute injury – ST elevation
• Can occur without Q waves: "non Q-wave MI"
• ST depression may indicate "subendocardial
infarction"
(3) Necrosis (non-conductive tissue) – Q-waves
• Significant if more than one small square wide or
greater than 1/3 the amplitude of the QRS
• Remain even after acute infarction is over

8. Q-wave MI
Evolution of typical transmural
MI
A. Normal ECG prior to MI
B. Hyperacute T ± ST elevation
C. Marked ST elevation +
hyperacute T (transmural injury)
D. Pathologic Q waves, less ST
elevation, terminal T wave
inversion (necrosis)
E. Pathologic Q waves, T wave
inversion (necrosis and fibrosis)
F. Pathologic Q waves, upright T
waves (fibrosis)

9. Lateral Wall
• I, aVL, V5, V6
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6
V1 V2
V3
V4
V5
V6

10. Anterior Wall
• V3, V4
– Left anterior chest
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6
V1 V2
V3
V4
V5
V6

11. Septal Wall
• V1, V2
– Along sternal borders
– Look through right
ventricle & see septal
wall
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6
V1 V2
V3
V4
V5
V6

12. I AVR V1 V4
II AVL V2 V5
III AVF V3 V6
Inferior Wall lateral Wall anterior Wall
Septal Wall Posterior Wall

13. Inferior MI Family of Q-wave MI's
includes
1. inferior
2. true posterior
3. right ventricular MI's

14. Inferior MI
• Pathologic Q waves and evolving ST-T changes
in leads II, III, aVF
• Q waves usually largest in lead III, next largest
in lead aVF, and smallest in lead II
• Example #1: frontal plane leads with fully
evolved inferior MI (note Q-waves, residual ST
elevation, and T inversion in II, III, aVF)

15. • Example #2: Old inferior MI (note largest
Q in lead III, next largest in aVF, and
smallest in lead II)

16. True posterior MI
• ECG changes are seen in anterior precordial
leads V1-3, but are the mirror image of an
anteroseptal MI:
1. Increased R wave amplitude and duration (i.e., a
"pathologic R wave" is a mirror image of a
pathologic Q)
2. R/S ratio in V1 or V2 >1 (i.e., prominent anterior
forces)
3. Hyperacute ST-T wave changes: i.e., ST
depression and large, inverted T waves in V1-3
4. Late normalization of ST-T with symmetrical
upright T waves in V1-3
5. Often seen with inferior MI (i.e., "inferoposterior

17. • Example #1: Acute inferoposterior MI (note tall R
waves V1-3, marked ST depression V1-3, ST
elevation in II, III, aVF)

18. • Example #2: Old inferoposterior MI (note
tall R in V1-3, upright T waves and inferior
Q waves)

19. • Example #3: Old posterolateral MI (precordial
leads): note tall R waves and upright T's in V1-3,
and loss of R in V6

20. Right Ventricular MI
• (only seen with proximal right coronary occlusion; i.e., with inferior
family MI's)
• ECG findings usually require additional leads on right chest (V1R to
V6R, analogous to the left chest leads)
• ST elevation, >1mm, in right chest leads, especially V4R (see
below)

21. Anterior Family of Q-wave MI's
• Anteroseptal MI
• Q, QS, or qrS complexes in leads V1-V3 (V4)
• Evolving ST-T changes
• Example: Fully evolved anteroseptal MI (note QS waves
in V1-2, qrS complex in V3, plus ST-T wave changes)

22. • Anterolateral MI
• similar changes, but usually V1 is spared; V4-6
involved
• Example: Acute anterior or anterolateral MI (note
Q's V2-6 plus hyperacute ST-T changes)

23. High Lateral MI
Typical MI features seen in leads I and/or aVL
Example: note Q-wave, slight ST elevation, and T inversion in lead
aVL
(Note also the slight U-wave inversion in leads II, III, aVF, V4-6, a
strong marker for coronary disease)

24. MI with Bundle Branch Block
1- MI + RBBB
• Usually easy to recognize because Q waves and ST-T changes
are not altered by the RBBB
• Example #1: Inferior MI + RBBB (note Q's in II, III, aVF and rSR'
in lead V1)

25. • Example #2: Anteroseptal MI with RBBB (note Q's in
leads V1-V3, terminal R wave in V1, fat S wave in V6)

26. 2- MI + LBBB
• Often a difficult ECG diagnosis because in LBBB the
right ventricle is activated first and left ventricular
infarct Q waves may not appear at the beginning of
the QRS complex (unless the septum is involved).
• Suggested ECG features, not all of which are
specific for MI include:
1- Q waves of any size in two or more of leads I, aVL,
V5, or V6 (See below: one of the most reliable signs
and probably indicates septal infarction, because the
septum is activated early from the right ventricular
side in LBBB)

27. • Notching of the downstroke of the S wave in precordial
leads to the right of the transition zone (i.e., before QRS
changes from a predominate S wave complex to a
predominate R wave complex); this may be a Q-wave
equivalent.
Notching of the upstroke of the S wave in precordial
leads to the right of the transition zone (another Q-wave
equivalent).
rSR' complex in leads I, V5 or V6 (the S is a Q-wave
equivalent occurring in the middle of the QRS complex)
RS complex in V5-6 rather than the usual monophasic R
waves seen in uncomplicated LBBB; (the S is a Q-wave
equivalent).
"Primary" ST-T wave changes (i.e., ST-T changes in the
same direction as the QRS complex rather than the
usual "secondary" ST-T changes seen in uncomplicated

28. • Non-Q Wave MI
• Recognized by evolving ST-T changes over
time without the formation of pathologic Q
waves (in a patient with typical chest pain
symptoms and/or elevation in myocardial-
specific enzymes)
Although it is tempting to localize the non-Q
MI by the particular leads showing ST-T
changes, this is probably only valid for the ST
segment elevation pattern

29. • Evolving ST-T changes may include any of the following
patterns:
• Convex downward ST segment depression only (common)
Convex upwards or straight ST segment elevation only
(uncommon)
Symmetrical T wave inversion only (common)
Combinations of above changes
Example: Anterolateral ST-T wave changes

30. • The Pseudoinfarcts
• These are ECG conditions that mimic myocardial infarction either by
simulating pathologic Q or QS waves or mimicking the typical ST-T
changes of acute MI.
• WPW preexcitation (negative delta wave may mimic pathologic Q
waves)
IHSS (septal hypertrophy may make normal septal Q waves "fatter"
thereby mimicking pathologic Q waves)
LVH (may have QS pattern or poor R wave progression in leads V1-3)
RVH (tall R waves in V1 or V2 may mimic true posterior MI)
Complete or incomplete LBBB (QS waves or poor R wave progression
in leads V1-3)

31. • Pneumothorax (loss of right precordial R waves)
Pulmonary emphysema and cor pulmonale (loss of
R waves V1-3 and/or inferior Q waves with right axis
deviation)
Left anterior fascicular block (may see small q-waves
in anterior chest leads)
Acute pericarditis (the ST segment elevation may
mimic acute transmural injury)
Central nervous system disease (may mimic non-Q
wave MI by causing diffuse ST-T wave changes)

32. • Miscellaneous Abnormalities of the QRS Complex:
• The differential diagnosis of these QRS abnormalities depend on other ECG findings as well as
clinical patient information
Poor R Wave Progression - defined as loss of, or no R waves in leads V1-3 (R £2mm):
• Normal variant (if the rest of the ECG is normal)
LVH (look for voltage criteria and ST-T changes of LV "strain")
Complete or incomplete LBBB (increased QRS duration)
Left anterior fascicular block (should see LAD in frontal plane)
Anterior or anteroseptal MI
Emphysema and COPD (look for R/S ratio in V5-6 <1)
Diffuse infiltrative or myopathic processes
WPW preexcitation (look for delta waves, short PR)
•

33. • Prominent Anterior Forces - defined as R/S ration >1
in V1 or V2
• Normal variant (if rest of the ECG is normal)
True posterior MI (look for evidence of inferior MI)
RVH (should see RAD in frontal plane and/or P-
pulmonale)
Complete or incomplete RBBB (look for rSR' in V1)
WPW preexcitation (look for delta waves, short PR)

34. • Effects of Other Medical Conditions
on EKG
• Pulmonary Embolism
– prominent S wave in I
– Q wave in III
– inverted T waves in III and V1 through
V4
– ST depression in II
– acute incomplete RBBB
– RAD with rightward rotation

35. • Electrolyte Disturbances
• hyperkalemia
– wide flat P – P disappears entirely with severe
hyperkalemia
– wide QRS
– peaked T wave
• hypokalemia
– flat T wave
– U wave (after T wave; represents Purkinje cell
repolarization) – prominent with severe hypokalemia
– can cause torsades des pointes if extreme
• hypercalcemia – shortened QT interval
• hypocalcemia – prolonged QT interval

36. • Drugs
• Digitalis
– therapeutic – ST slopes below baseline, inverted T
waves, shortened QT
– excessive – blocks: SA block, paroxysmal atrial
tachycardia (PAT) with block, AV block (can be 3rd
degree)
– toxic – atrial fibrillation, junctional or ventricular
tachycardia, frequent PVC's, ventricular fibrillation
• Quinidine (blocks potassium channels)
– wide notched P wave
– wide QRS
– very deep ST
– U wave
– long QT interval

37. • Pericarditis
• flat or concave downward ST segment
elevation in leads where QRS is mainly
negative (right chest leads – V1 to V3)
• elevated ST segment with T wave off
baseline in leads where QRS is mainly
positive (lateral/inferior limb leads – aVL, I,
II, aVF, III)
• COPD
• all waves of minimal amplitude; often
leads to RVH with RAD; MAT in some

38. • Effect of Cardiac Syndromes on EKG
• Wolff-Parkinson-White Syndrome – caused by accessory
bundle of Kent that bypasses the AV node to allow
ventricular pre-excitation
– delta wave with apparently shortened PR interval
– can cause tachycardia through three mechanisms:
• (1) rapid conduction of rapid atrial beats (PSVT, atrial flutter, or
atrial fibrillation)
• (2) automaticity foci within the bundle
• (3) re-entry of ventricular depolarization
• Lown-Ganong-Levine Syndrome – caused by James bundle
(extention of the anterior internodal tract) that bypasses the
AV node directly to the bundle of His
– no PR delay (so PR interval is minimal)
– QRS immediately responds to any atrial tachyarrythmias, so
(for example) atrial flutter produces a rapid QRS response

39. • Brugada Syndrome – familial dysfunction of Na+
channels
• characterized by RBBB with ST elevation
(downsloping) in V1 through V3
• can cause deadly arrythmias leading to sudden
cardiac death with no apparent structural heart
disease (responsible for half of all cases)
• Wellen's Syndrome – stenosis of LAD
• causes marked T-wave inversion in V2 and V3
• Long QT Syndrome – QT interval more than 1/2
the cardiac cycle
• predisposed to ventricular arrythmias