ECG

Normal ranges

PR - 0.12-20

QRS - 0.06-0.10

QT ~ 0.4

 

Changes in ECG in infarction

Initial change

Abnormally rapid repolarisation
* Due to accelerated K+ channel opening

--> ST segment elevation

Few minutes later

RMP decreases
Due to loss of intracellular K+

--> TQ segment depression (seen as ST segment elevation)

30 minutes later

Infarcted fibres begin to depolarise more slowly

--> ST segment elevation

Changes in ECG in electrolyte disturbance

High potassium (Hyperkalaemia)

Initial change:

• Tall peaked T waves

Later (??> 8meq/L):

• Shortening of QT interval
• Prolongation of PR interval
• P-wave flattening/Loss of P wave
  * Due to paralysis of atria
• Widening of QRS
• RMP decreases
• Ventricular arrhythmia
• Conduction blocks

Eventually heart stops in diastole

NB:

[UTD]

Progressive slowing of impulses

Low potassium (Hypokalaemia)

Early:

• Prolongation of PR interval
• Prominent U wave

Late:

• If T and U wave merge, the apparent QT interval is prolonged, but true QT interval is of normal duration
• Occasional late T wave inversion on precordial leads
• ST segment depression

NB:

[UTD]

• Decreased T wave amplitude
• Increased U wave amplitude
• P wave can become larger.
• PR increase slightly
• When severe, QRS duration may increase, marked ST segment depression, T wave inversion
• Hypokalemia is a particularly important risk factor that can promote digitalis-induced arrhythmia at any level of digoxin

High calcium (Hypercalcaemia)

• Enhanced contractility
• Heart relaxes less
• Eventually arrest in systole (calcium rigour)

But clinically rarely high enough to affect heart.

Low calcium (Hypocalcaemia)

• Prolongation of ST segment

Then

• Prolongation of QT interval
  (which may also be produced by TCA or phenothiazine)