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:
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)