MI

Question 1

“new ST segment elevation at the J point in at least two contiguous leads of ≥ 2 mm (0.2 mV)”

Answer 1

in men = STEMI

Question 2

1. ST segment elevation in the anterior leads (V3 and V4) at the J point
2. Reciprocal ST segment depression in the inferior leads (II, III and aVF).

Answer 2

acute anterior wall infarct

occurs when anterior myocardial tissue usually supplied by the left anterior descending coronary artery suffers injury due to lack of blood supply. When an AWMI extends to the septal and lateral regions as well, the culprit lesion is usually more proximal in the LAD or even in the left main coronary artery

Question 3

“new ST segment elevation at the J point in at least two contiguous leads of 1.5 mm (0.15 mV) in leads V2-V3 and/or of ≥ 1 mm (0.1 mV) in other contiguous chest leads or the limb leads.”

Answer 3

1. “new ST segment elevation at the J point in at least two contiguous leads of 1.5 mm (0.15 mV) in women in leads V2-V3 and/or of ≥ 1 mm (0.1 mV) in other contiguous chest leads or the limb leads.”
2. This means:
   
   1. 1 millimeter in any two contiguous leads either
      
      1. V2 or V3 elevation must be 2 mm in men or
      2. V2 or V3: 1.5 mm in women

Question 4

Poor R Wave Progression (PRWP)

Answer 4

AWMI

Question 5

ECG findings of an old anterior wall MI

Answer 5

1. include the loss of anterior forces, leaving Q waves in leads V1 and V2.
2. This is a cause of poor R wave progression, or PRWP.
3. To distinctly say that an old anterior wall MI is present on the ECG, there must be no identifiable R wave in lead V1 — and usually V2, as well. If there is an R wave in V1 or V2, the term poor R wave progression, but not old anterior wall MI, can be used.

Question 8

Answer 8

old AWMI

To distinctly say that an old anterior wall MI is present on the ECG, there must be no identifiable R wave in lead V1 — and usually V2, as well. If there is an R wave in V1 or V2, the term poor R wave progression, but not old anterior wall MI, can be used.

Question 9

Answer 9

inferior wall MI

STE in inferior leads II, III, aVF.
Reciprocal STD in lateral leads I, aVL, V6.

RV infarction typically occurs in the context of inferior STEMI due to RCA occlusion.
These patients are preload sensitive and may have an exaggerated hypotensive response to nitrates.

Answer 10

1. irregularly irregular broad complex tachycardia.
2. Extremely rapid ventricular rates — up to 300 bpm in places (RR intervals as short as 200ms or 1 large square).
3. Beat-to-beat variability in the QRS morphology, with subtle variation in QRS width.
4. Irregularly irregular rhythm is consistent with atrial fibrillation.
5. There is a left bundle branch block morphology to the QRS complexes.
6. However, the ventricular rate is far too rapid for this to be simply AF with LBBB.
7. The rates of 250-300 bpm and the variability in QRS complex morphology indicate the existence of an accessory pathway between the atria and ventricles.
8. Broad complex irregular tachycardia at very rapid rates? -> Suspect AF with WPW!
9. These patients can rapidly become haemodynamically unstable.
10. The options for chemical cardioversion are very limited, favouring DC cardioversion.

Question 11

Atrial Fibrillation: key features

Answer 11

1. Irregularly irregular rhythm.
2. No P waves.
3. Absence of an isoelectric baseline.
4. Variable ventricular rate.
5. QRS complexes usually < 120 ms unless pre-existing bundle branch block, accessory pathway, or rate related aberrant conduction.
6. Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude >0.5mm).
7. Fibrillatory waves may mimic P waves leading to misdiagnosis.

Question 12

Answer 12

1. Severe bradycardia of 36 bpm.
2. Rhythm is difficult to ascertain — appears irregular (?slow AF) although there are some small-voltage P waves seen in V1-2.
3. Broad QRS complexes with an atypical LBBB morphology.
4. Subtle symmetrical peaking (“tenting”) of the T waves in V2-5.
5. The combination of bradycardia, flattening and loss of P waves, QRS broadening and T wave abnormalities is highly suspicious for severe hyperkalaemia. This patient had a potassium of 8.0 in the context of anuric renal failure.
6. Clinical Pearls
   
   1. When you see the combination of…
      
      1. Bradycardia
      2. Blocks — e.g. AV block, bundle branch blocks
      3. Bizarre QRS complexes
   2. ​think HYPERKALEMIA

Question 13

a patient presenting with seizures and hypotension, the combination of…

Answer 13

combination of…

QRS broadening > 100 ms
R’ wave in aVR > 3 mm

… is highly suggestive of poisoning with a sodium-channel blocking agent — e.g. tricyclic antidepressant.

Question 14

Answer 14

1. This ECG demonstrates an anterolateral STEMI
   
   1. ST elevation in V2-6, I and aVL
   2. Reciprocal ST depression in III and aVF
   3. Pathological Q waves in V2-3
   4. Hyperacute T waves in V2-4
2. This pattern of changes in consistent with acute occlusion of the left anterior descending artery.

Question 15

Answer 15

1. There is transient improvement in the ST changes, with development of biphasic T waves in V2-3.
2. This pattern of T wave changes in V2-3 is known as Wellens’ syndrome and indicates reperfusion of a previously occluded LAD artery.
3. The implication of this ECG pattern is that there is an underlying critical LAD stenosis that needs urgent intervention with angiography +/ stenting or CABG.

Question 16

Answer 16

1. biphasic appearance to the ST segments and T waves, with initial negative deflection (= ST segment depression / T wave inversion) followed by a terminal positive deflection (= U wave).
2. combination of…
   
   1. Widespread ST depression / T wave inversion
   2. Prominent U waves
   3. Long QU interval (> 500 ms)
   4. …. is highly suggestive of severe hypokalaemia.
3. This patient had a serum K of 1.7 mmol/L in the context of decompensated Conn’s syndrome (primary aldosteronism).

Question 17

Answer 17

1. Wellen’s Syndrome
2. Biphasic T waves
   
   1. may be seen with
      
      1. myocardial ischaemia (Wellens’ syndrome)
      2. hypokalaemia.
3. The main differentiating factor (apart from the clinical picture) is the direction of the T waves:
   
   1. Wellens’ biphasic T waves go UP then down.
   2. Hypokalaemic T waves go DOWN then up.
4. Below is an image of hypokalemia

Answer 18

1. ECG is an example of hyperacute anterolateral STEMI:
2. There are markedly peaked, asymmetrical T waves (= hyperacute T waves) in V2-5.
3. The associated loss of R wave height (analogous to early Q wave formation) causes the enlarging precordial T waves to tower over the diminishing R waves.
4. There is also some subtle ST elevation in aVL, indicating LAD occlusion proximal to the D1.
5. There are frequent ventricular ectopic beats, which are concerning in this context as they suggest underlying myocardial irritability and a risk of deterioration to malignant ventricular dysrhythmias such as VF or VT.