ECG Flashcards
How to calculate rate?
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
What leads correspond to what patterns of infarct (septal, anterior, anteroseptal, anterolateral)?
Septal = V1-2
Anterior = V2-5
Anteroseptal = V1-4
Anterolateral = V3-6, I + aVL
Extensive anterior / anterolateral = V1-6, I + aVL
What are the precordial leads?
Septal leads = V1-2
Anterior leads = V3-4
Lateral leads = V5-6
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
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
Extensive Anterolateral STEMI (acute):
ST elevation in V2-6, I and aVL.
Reciprocal ST depression in III and AVF.
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
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
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)
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
Atrial fibrillation:
Irregular ventricular response
No evidence of organised atrial activity
Fine fibrillatory waves seen in V1
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
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
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.
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.
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
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
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.
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
Massive bilateral pulmonary embolus
Sinus tachycardia
RBBB
T-wave inversions in the right precordial leads (V1-3) as well as lead III
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
RBBB: Right Bundle Branch Block
V1: RSR’ pattern in V1, with (appropriate) discordant T wave changes
V6: Widened, slurred S wave in V6
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
LBBB: Left Bundle Branch Block
V1: Dominant S wave
V6: broad, notched (‘M’-shaped) R wave
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
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.
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
SVT
Slow-Fast (Typical) AVNRT:
Narrow complex tachycardia at ~ 150 bpm
No visible P waves
There are pseudo R’ waves in V1-2
VF
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
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.
normal ECG
normal ECG
