You ought to have a good idea of the sheer depth of information you can gain from an ECG. Pathologies affecting the heart also create characteristic signs in the trace that are useful in clincial diagnosis.

MI

The ECG pathology evolves through 3 stages:

  1. 1. T-wave peaking followed by T-wave inversion
  2. 2. ST segment elevation
  3. 3. Appearance of new pathological Q-waves

Pathological Q-waves

These are Q-waves exceeding 0.04s (one small square) and 2mV (2 small squares). They are created by infarcted or dead tissue, which is electrically inert – forming an electrical ‘hole' or ‘window' with all the electrical activity moves away from this point, so any lead sitting over it records a large pathological Q wave (remember that if the vector of the electrical activity is away from the lead, it records a negative wave) of septal and ventricular depolarisation moving away.

ST Deviation

Due to area of injured tissue surrounding the ‘hole' which is electronegative – may also be caused by pericarditis (in this case, the ST deviation occurs in all leads).

T-waves

Due to ischaemia.

Infarct

Artery involved
Visible in leads

Anterior

Left coronary, anterior descending branch

V1-V6 (Q in V3-V6, T in V4-V6)

Lateral

Left circumflex coronary

I, aVL, V5, V6

Anterolateral

 

Q: I, II, aVL, V5, V6
ST : V2-V6

Inferior

Right coronary

II, III, aVF (Q in III, aVF, ST in aVL and V6)

Posterior

Right coronary

Reciprocal changes in V1 (ST depression, tall R-waves)

 

pulmonary embolism

  • Large S-wave in lead I
  • Deep Q-wave in lead II
  • Inverted T-wave in lead III

(S1, Q3, T3)
Patients will also demonstrate a pattern of right heart strain and right axis deviation.

Metabolic abnormalities

Hyperkalaemia

•  Tall, tented T-waves
•  Widened QRS
•  Prolonged PR
•  Arrhythmias

Hypokalaemia

•  Small T-waves
•  Prominent U-waves (occur after T-wave)
•  ST depression
•  Arrythmias

Hypercalcaemia

•  Short QT interval

Hypocalcaemia

•  long QT
•  Small T-waves