ECG Changes in Electrolyte Disturbances and Drugs
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Direct answer
ECG changes in electrolyte disturbances and drugs follow recognisable patterns that can be read from the tracing before a patient develops an arrhythmia. Hyperkalaemia produces tall peaked T waves first and then PR prolongation and QRS widening, while hypokalaemia flattens T waves and produces prominent U waves. Hypocalcaemia prolongs the QT by lengthening the ST segment, hypercalcaemia shortens it, digoxin causes scooped ST depression with a short QT, and quinidine prolongs the QT and QRS.
What you must remember
- Hyperkalaemia: peaked T waves appear first, followed by P wave flattening, PR prolongation, QRS widening and eventually a sine-wave pattern.
- Hypokalaemia: flattened T waves, ST depression and prominent U waves, which can merge with the T wave and make the QT look prolonged.
- Hypocalcaemia: a prolonged QT from a lengthened ST segment, with a risk of ventricular arrhythmia.
- Hypercalcaemia: a shortened QT, mainly from a short ST segment.
- Digoxin: scooped, reverse-tick ST depression with a shortened QT, and bradyarrhythmias, AV block or ventricular ectopy in toxicity.
- Quinidine and class IA drugs: prolonged QRS and QT intervals, with a risk of torsades de pointes.
- Urgent treatment: calcium gluconate protects the myocardium in hyperkalaemia with ECG change, and digoxin toxicity is treated with specific Fab antibody fragments.
- Torsades: IV magnesium sulphate is the drug of choice, and the offending drug is stopped.
Reading the tracing before blaming the drug
A 66-year-old woman on digoxin and a loop diuretic presents with nausea and a heart rate of 48 per minute. Her ECG shows scooped ST segments and a short QT, and her potassium is low.
| Disturbance or drug | Classic ECG feature | Practical link |
|---|---|---|
| Hyperkalaemia | Peaked T, PR prolongation, QRS widening | Calcium gluconate and potassium lowering |
| Hypokalaemia | Flat T, ST depression, prominent U | Potassium replacement and magnesium check |
| Hypercalcaemia | Shortened QT from a short ST segment | Correct calcium and review drugs |
| Hypocalcaemia | Prolonged QT from a long ST segment | IV calcium replacement |
| Digoxin toxicity | Scooped ST, short QT, bradycardia | Specific Fab antibodies |
| Quinidine or class IA drugs | Prolonged QRS and QT | Stop the drug, IV magnesium for torsades |
Hypokalaemia makes digoxin toxicity more likely, so this patient needs her potassium checked before the digoxin level is interpreted. Scooped ST segments can mimic ischaemia, and the short QT is the clue that the change is drug-related.
Where the exam tries to catch you
Electrolyte and drug questions reward reading the pattern before naming the cause.
- Trap: Waiting for QRS widening before acting in hyperkalaemia. Correct: Peaked T waves are the earliest change, and calcium gluconate is given when hyperkalaemia is suspected with ECG change.
- Trap: Assuming every long QT is caused by a drug. Correct: Hypocalcaemia and hypokalaemia prolong or distort the QT, so electrolytes are checked before blaming the drug alone.
- Trap: Reading digoxin's scooped ST depression as ischaemia. Correct: Scooped ST depression with a short QT is a characteristic drug effect and occurs without ischaemia.
- Trap: Treating torsades with a class IA or class III agent. Correct: IV magnesium sulphate is first-line, and QT-prolonging drugs are stopped.
Frequently asked questions
Which ECG change appears first in hyperkalaemia?
Peaked T waves are the earliest ECG change in hyperkalaemia, and they are tall, narrow and symmetrical. Later changes include P wave flattening, PR prolongation and QRS widening, which show that potassium is dangerously high.
Why do prominent U waves appear in hypokalaemia?
Prominent U waves in hypokalaemia are thought to reflect delayed repolarisation in the Purkinje fibres and mid-myocardium. They can fuse with the T wave and make the QT interval look prolonged, so the examiner expects the candidate to correct the potassium.
How does hypercalcaemia change the QT interval?
Hypercalcaemia shortens the QT interval, mainly by shortening the ST segment. A short QT alongside other features of calcium excess points to hypercalcaemia rather than the long QT seen in hypocalcaemia.
How is digoxin toxicity with bradyarrhythmia treated?
Digoxin toxicity is treated with specific Fab antibody fragments that bind the drug, along with correction of electrolyte abnormalities. Atropine or temporary pacing may be needed for bradyarrhythmia, depending on the clinical picture.