ECG

Question 1

How to calculate rate?

Answer 1

1 SMALL square (1mm) = 0.04 sec (40ms)
5 SMALL squares (5mm) = 1 LARGE square = 0.2 sec (200ms)
5 LARGE squares = 1 second

calculate bpm by dividing 300 by the number of LARGE squares between each R-R interval

Question 2

What leads correspond to what patterns of infarct (septal, anterior, anteroseptal, anterolateral)?

Answer 2

Septal = V1-2
Anterior = V2-5
Anteroseptal = V1-4
Anterolateral = V3-6, I + aVL
Extensive anterior / anterolateral = V1-6, I + aVL

Question 3

What are the precordial leads?

Answer 3

Septal leads = V1-2
Anterior leads = V3-4
Lateral leads = V5-6

Question 4

Answer 4

Hyperacute Anteroseptal STEMI:

ST elevation and hyperacute T waves in V2-4
ST elevation in I and aVL with reciprocal ST depression in lead III
Q waves are present in the septal leads V1-2
These features indicate a hyperacute anteroseptal STEMI

Question 5

Answer 5

Hyperacute Anterior STEMI:

There is progressive ST elevation and Q wave formation in V2-5
ST elevation is now also present in I and aVL
There is some reciprocal ST depression in lead III

Question 6

Answer 6

Extensive Anterolateral STEMI (acute):

ST elevation in V2-6, I and aVL.
Reciprocal ST depression in III and AVF.

Question 7

Answer 7

Extensive Anterior STEMI (acute):

ST elevation in V1-6 plus I and aVL (most marked in V2-4)
Minimal reciprocal ST depression in III and aVF
Q waves in V1-2, reduced R wave height (a Q-wave equivalent) in V3-4
There is a premature ventricular complex (PVC) with “R on T’ phenomenon at the end of the ECG; this puts the patient at risk for malignant ventricular arrhythmias

Question 8

Answer 8

Extensive anterior MI (“tombstoning” pattern)

Massive ST elevation with “tombstone” morphology is present throughout the precordial (V1-6) and high lateral leads (I, aVL)
This pattern is seen in proximal LAD occlusion and indicates a large territory infarction with a poor LV ejection fraction and high likelihood of cardiogenic shock and death

Question 9

Answer 9

Anterior-inferior STEMI

ST elevation is present throughout the precordial and inferior leads
There are hyperacute T waves, most prominent in V1-3
Q waves are forming in V1-3, as well as leads III and aVF
This pattern is suggestive of occlusion occurring in “type III” or “wraparound” LAD (i.e. one that wraps around the cardiac apex to supply the inferior wall)

Question 10

Answer 10

Atrial fibrillation:

Irregular ventricular response
Coarse fibrillatory waves are visible in V1
“Sagging” ST segment depression is visible in V6, II, III and aVF, suggestive of digoxin effect

Question 11

Answer 11

Atrial fibrillation:

Irregular ventricular response
No evidence of organised atrial activity
Fine fibrillatory waves seen in V1

Question 12

Answer 12

ECG of Benign Early Repolarisation (BER), demonstrating:
1) Generalised concave ST elevation in precordial (V2-6) and limb leads (I, II, III, aVF)
2) J-point notching is evident in the inferior leads (II, III and aVF)
3) ST elevation : T wave ratio < 0.25 in V6

Question 13

Answer 13

Classical (asymmetrical) Hypertrophic Cardiomyopathy:
1) Voltage criteria for LVH in precordial and limb leads
2) Narrow, “dagger-like” Q waves in inferior and lateral leads

Question 14

Answer 14

Classic HCM pattern with asymmetrical septal hypertrophy:

Voltage criteria for left ventricular hypertrophy.
Deep narrow Q waves < 40 ms wide in the lateral leads I, aVL and V5-6.

Question 15

Answer 15

HCM showing features of asymmetrical septal hypertrophy:

Large precordial voltages.
Deep, narrow, septal Q waves most prominent in leads I and aVL; also seen in V5-6.

Question 16

Answer 16

LBBB
Broad notched R waves are best appreciated in leads aVL and I here. There is absence of Q waves in leads V5-6.

QRS duration ≥ 120ms
Dominant S wave in V1
Broad monophasic R wave in lateral leads (I, aVL, V5-6)
Absence of Q waves in lateral leads
Prolonged R wave peak time > 60ms in leads V5-6

Question 17

Answer 17

LBBB
QRS duration ≥ 120ms
Dominant S wave in V1
Broad monophasic R wave in lateral leads (I, aVL, V5-6)
Absence of Q waves in lateral leads
Prolonged R wave peak time > 60ms in leads V5-6

Question 18

Answer 18

Acute Pericarditis:

Widespread concave ST elevation and PR depression is present throughout the precordial (V2-6) and limb leads (I, II, aVL, aVF).
There is reciprocal ST depression and PR elevation in aVR.

Question 19

Answer 19

Acute Pericarditis:

Sinus tachycardia
Widespread concave STE and PR depression (I, II, III, aVF, V4-6)
Reciprocal ST depression and PR elevation in V1 and aVR
Spodick’s sign best visualised in lead II

Question 20

Answer 20

Massive bilateral pulmonary embolus

Sinus tachycardia
RBBB
T-wave inversions in the right precordial leads (V1-3) as well as lead III

Question 21

Answer 21

Massive bilateral pulmonary embolus

RBBB
Extreme right axis deviation (+180 degrees)
S1 Q3 T3
T-wave inversions in V1-4 and lead III
Clockwise rotation with persistent S wave in V6

Question 22

Answer 22

RBBB: Right Bundle Branch Block
V1: RSR’ pattern in V1, with (appropriate) discordant T wave changes
V6: Widened, slurred S wave in V6

Question 23

Answer 23

Isolated RBBB.

Typical RSR’ pattern in V1-2
Widened S waves again demonstrated in lateral leads, especially V4-6
Appropriate discordance in leads V1-2

Question 24

Answer 24

LBBB: Left Bundle Branch Block
V1: Dominant S wave
V6: broad, notched (‘M’-shaped) R wave

Question 25

Answer 25

Inferior STEMI: ST elevation in II, III and aVF. Q-wave formation in III and aVF. Reciprocal ST depression and T wave inversion in aVL ST elevation in lead II = lead III and absent reciprocal change in lead I (isoelectric ST segment) suggests a left circumflex artery occlusion

Question 26

Answer 26

Inferior STEMI: The concave ST elevation in II, III and aVF may be mistaken for pericarditis. However, the fact that the ST elevation is localised to the inferior leads with reciprocal changes in aVL confirms that this is an inferior STEMI.

Question 27

Answer 27

Anterior STEMI There is progressive ST elevation and Q wave formation in V2-5 ST elevation is now also present in I and aVL There is some reciprocal ST depression in lead III

Question 28

Answer 28

SVT Slow-Fast (Typical) AVNRT: Narrow complex tachycardia at ~ 150 bpm No visible P waves There are pseudo R’ waves in V1-2

Question 29

Answer 29

VF

Question 30

Answer 30

Sinus rhythm with a very short PR interval (< 120 ms) Broad QRS complexes with a slurred upstroke to the QRS complex — the delta wave Dominant R wave in V1 suggests a left-sided AP, and is sometimes referred to as “Type A” WPW Tall R waves and inverted T waves in V1-3 mimicking right ventricular hypertrophy (RVH) — these changes are due to WPW and do not indicate underlying RVH Negative delta wave in aVL simulating the Q waves of lateral infarction — this is referred to as the “pseudo-infarction” pattern

Question 31

Answer 31

WPW Another example of a left-sided AP (type A WPW), with dominant R wave in V1 and right precordial T-wave inversions simulating RVH.

Question 32

Answer 32

normal ECG

Question 33

Answer 33

normal ECG