[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [Clinical skills](https://durgical.com/en/clinical-skills/) › [The ECG](https://durgical.com/en/clinical-skills/areas/ecg/) › Hyperkalaemia and other electrolyte changes

# Hyperkalaemia and other electrolyte changes

- ECG tracing

Too much or too little potassium, calcium or magnesium changes the shape of the ECG waves, and high potassium can stop the heart.

Updated Nov 13, 2026

## Key points

- Hyperkalaemia sequence: peaked T, then flat or absent P and long PR, then wide QRS, then sine wave, VF or asystole.
- The ECG correlates poorly with the level: any ECG change is an emergency, and a normal ECG does not make a high potassium safe.
- Stabilise the myocardium with IV calcium when the ECG changes, then shift potassium into cells, then remove it.
- Hypokalaemia: flat or inverted T, ST depression, prominent U waves, apparent long QT (QU), torsades risk.
- Calcium moves the ST segment: hypocalcaemia long ST and long QT; hypercalcaemia short ST and short QT.

On this page

- The basics Key points
- What it is
- How to recognise it
- Why it happens
- Step by step
- Next step
- Memory aid
- Elsewhere in DurgiPedia

- Clinical Electrolytes and their ECG signs
- Differential and pitfalls

- Study Test yourself

- Connections Connections

## What it is

Potassium sets the resting membrane potential of cardiac cells, so a rise in serum potassium changes the ECG in a fairly predictable order, although the link with the measured level is loose and some patients arrest with few warning signs. Hyperkalaemia is usually defined as a potassium above 5.0 to 5.5 mmol/L, and the ECG changes become common as it climbs. First the T waves become tall, narrow-based and peaked, best seen in V2–V4; then the P waves flatten, widen and disappear while the PR interval lengthens; then the QRS widens, conduction blocks and bradycardias appear, and the QRS and T merge into a sine-wave pattern that degenerates into ventricular fibrillation or asystole. Any ECG change of hyperkalaemia is an emergency. The commonest causes are kidney failure, drugs that retain potassium (ACE inhibitors, angiotensin receptor blockers, potassium-sparing diuretics), acidosis such as diabetic ketoacidosis, tissue breakdown (rhabdomyolysis, tumour lysis) and adrenal insufficiency; a haemolysed sample gives a false high value. The other electrolytes leave their own marks. Hypokalaemia flattens or inverts the T waves, depresses the ST segment and brings out U waves, so that the T and U fuse into an apparently long QT, with ectopy and a risk of torsades de pointes. Hypomagnesaemia looks similar and often coexists. Hypocalcaemia lengthens the QT by stretching the ST segment, with a normal T wave, and hypercalcaemia shortens the ST segment and the QT.

## How to recognise it

- Peaked T waves: tall, narrow-based, symmetrical, with a sharp apex, often taller than the R wave in V2–V4.
- P waves: flatten, widen and finally disappear; PR prolongs; a slow junctional or sinoventricular rhythm may follow.
- QRS: widens, often bizarre, with bundle branch block patterns; QRS and T merge into a sine wave as arrest approaches.
- Bradycardia, high-grade AV block, slow idioventricular rhythm, then VF, pulseless electrical activity or asystole.
- Hypokalaemia: T flattening or inversion, ST depression, U waves larger than 1 mm, PR prolongation, ectopy, torsades de pointes.
- Hypomagnesaemia: similar to hypokalaemia, with long QT and torsades; correct both together.
- Hypocalcaemia: long QT from a long, flat ST segment with a normal T. Hypercalcaemia: short ST and short QT; severe cases may show J waves.

## Why it happens

- High extracellular potassium speeds repolarisation (tall, peaked T) and then raises the resting potential, inactivating sodium channels.
- Fewer available sodium channels slow conduction: atria first (P loss), then the ventricles (wide QRS), until the cells cannot depolarise.
- Low potassium slows and prolongs ventricular repolarisation, making U waves prominent and favouring early afterdepolarisations.
- Calcium sets the length of the plateau (phase 2): low calcium lengthens it and the ST segment; high calcium shortens it.

## Step by step

- Look at the T waves in V2–V4 — tall, narrow, symmetrical peaks are the first sign of high potassium.
- Check P waves and PR — loss of P waves and a long PR mean atrial conduction is failing.
- Measure QRS width — a QRS over 120 ms in hyperkalaemia is a pre-arrest sign.
- Note rate and rhythm — bradycardia, block or a sine wave need treatment within minutes.
- Look for U waves, ST depression and a long QT — they point to low potassium, magnesium or calcium.
- Match the tracing to the electrolyte panel and the drugs — the ECG tells urgency; the sample confirms the cause.

## Electrolytes and their ECG signs

| Disorder | Main ECG signs | Danger |
| --- | --- | --- |
| Hyperkalaemia | Peaked T, flat or absent P, long PR, wide QRS, sine wave | Bradycardia, block, VF, asystole |
| Hypokalaemia | Flat or inverted T, ST depression, U waves, apparent long QT | Ectopy, torsades de pointes, VF |
| Hypomagnesaemia | Similar to hypokalaemia, long QT | Torsades de pointes |
| Hypocalcaemia | Long QT from a long ST segment, normal T | Torsades (rare), laryngospasm, seizures |
| Hypercalcaemia | Short ST and short QT; J waves if severe | Bradyarrhythmias (rare) |

## Differential and pitfalls

- Pseudohyperkalaemia: haemolysis, a tight tourniquet, fist clenching or high platelet or white counts; the ECG is normal. Repeat the sample, but treat if the ECG changes.
- Peaked T waves of hyperkalaemia versus hyperacute T waves of early STEMI: hyperacute T waves are broad-based and regional.
- Wide QRS of hyperkalaemia may mimic ventricular tachycardia, bundle branch block or a STEMI (pseudo-infarction pattern).
- Benign tall T waves in young people and in LVH are broad and asymmetrical, not narrow and peaked.
- Pitfall: a U wave counted as part of the T in hypokalaemia overestimates the QT; measure the QT where the T ends.
- Pitfall: digoxin toxicity with hyperkalaemia; stop digoxin and seek specialist advice.

## Next step

- ECG changes of hyperkalaemia: continuous monitoring, call a senior and give IV calcium (gluconate or chloride) as the protocol sets; repeat the ECG after it.
- Shift potassium into cells with insulin plus glucose and inhaled salbutamol as protocol sets; check glucose afterwards to catch hypoglycaemia.
- Remove potassium: binders, loop diuretics if the kidneys work, and dialysis for kidney failure or refractory cases (call nephrology).
- Stop potassium supplements and drugs that retain potassium; treat the cause (acidosis, rhabdomyolysis, adrenal insufficiency).
- Low potassium or magnesium with a long QT: replace both as the protocol sets and stop QT-prolonging drugs; repeat the ECG and electrolytes.

## Memory aid

Rising potassium: «T up, P out, QRS wide, sine and stop».

## Test yourself

Think of the answer, then tap the question to see it.

## A man on dialysis has tall, narrow, peaked T waves in V2–V4, no visible P waves and a QRS of 160 ms at 40 bpm. What is the tracing and what comes first?

Severe hyperkalaemia with loss of P waves, wide QRS and bradycardia, close to a sine wave. First: monitoring, a senior and IV calcium to stabilise the myocardium, then shift and remove potassium.

## Why does a normal ECG not rule out dangerous hyperkalaemia?

The ECG correlates poorly with the potassium level; some patients go straight to arrhythmia or arrest. The level, the trend and the cause also decide treatment.

## What does hypokalaemia look like on the ECG?

Flattened or inverted T waves, ST depression and prominent U waves, which fuse with the T to give an apparently long QT, with ectopy and a risk of torsades de pointes.

## How does hypocalcaemia change the QT interval, and which segment lengthens?

It prolongs the QT by lengthening the ST segment, while the T wave itself stays normal. Hypercalcaemia does the opposite and shortens the ST and QT.

[Add to my cards (4)](https://durgical.app/estudiar/?add=/en/clinical-skills/hyperkalaemia-and-other-electrolyte-changes/)

## Elsewhere in DurgiPedia

- [The ECG in potassium and calcium disorders](https://durgical.com/en/physiology/the-ecg-in-potassium-and-calcium-disorders/)
- [Potassium balance](https://durgical.com/en/physiology/potassium-balance/)
- [The ventricular action potential](https://durgical.com/en/physiology/the-ventricular-action-potential/)
- [ECG basics: waves, intervals and leads](https://durgical.com/en/physiology/ecg-basics-waves-intervals-and-leads/)

## Connections

## Related 9

- [Electrolytes, urea and creatinine](https://durgical.com/en/clinical-skills/electrolytes-urea-and-creatinine/)
- [The long QT interval](https://durgical.com/en/clinical-skills/the-long-qt-interval/)
- [Reading an ECG step by step](https://durgical.com/en/clinical-skills/reading-an-ecg-step-by-step/)
- [Right and left bundle branch block and fascicular blocks](https://durgical.com/en/clinical-skills/right-and-left-bundle-branch-block-and-fascicular-blocks/)
- [AV blocks: first, second (Mobitz I and II) and third degree](https://durgical.com/en/clinical-skills/av-blocks-first-second-and-third-degree/)
- [Broad-complex tachycardia, VF and the arrest rhythms](https://durgical.com/en/clinical-skills/broad-complex-tachycardia-vf-and-the-arrest-rhythms/)
- [The ECG in pulmonary embolism, hypothermia and digoxin effect](https://durgical.com/en/clinical-skills/the-ecg-in-pulmonary-embolism-hypothermia-and-digoxin-effect/)
- [Arterial blood gas: worked cases for the station](https://durgical.com/en/clinical-skills/arterial-blood-gas-worked-cases-for-the-station/)
- [Transcutaneous pacing](https://durgical.com/en/clinical-skills/transcutaneous-pacing/)

## Related conditions 10

- [Hyperkalaemia](https://durgical.com/en/conditions/hyperkalaemia/)
- [Hypokalaemia](https://durgical.com/en/conditions/hypokalaemia/)
- [Hypocalcaemia](https://durgical.com/en/conditions/hypocalcaemia/)
- [Hypercalcaemia](https://durgical.com/en/conditions/hypercalcaemia/)
- [Hypomagnesaemia](https://durgical.com/en/conditions/hypomagnesaemia/)
- [Acute kidney injury](https://durgical.com/en/conditions/acute-kidney-injury/)
- [Chronic kidney disease](https://durgical.com/en/conditions/chronic-kidney-disease/)
- [Diabetic ketoacidosis](https://durgical.com/en/conditions/diabetic-ketoacidosis/)
- [Rhabdomyolysis](https://durgical.com/en/conditions/rhabdomyolysis/)
- [Tumour lysis syndrome](https://durgical.com/en/conditions/tumour-lysis-syndrome/)

## In Pharmacology 8

- [Calcium gluconate](https://durgical.com/en/pharmacology/calcium-gluconate/)
- [Calcium chloride](https://durgical.com/en/pharmacology/calcium-chloride/)
- [Insulins](https://durgical.com/en/pharmacology/classes/insulins/)
- [Salbutamol](https://durgical.com/en/pharmacology/salbutamol/)
- [Potassium binders](https://durgical.com/en/pharmacology/classes/potassium-binders/)
- [Loop diuretics](https://durgical.com/en/pharmacology/classes/loop-diuretics/)
- [Magnesium sulfate](https://durgical.com/en/pharmacology/magnesium-sulfate/)
- [Potassium chloride](https://durgical.com/en/pharmacology/potassium-chloride/)

[← All clinical skills](https://durgical.com/en/clinical-skills/)

Educational content; it does not replace supervised hands-on training, your institution's protocols or a prescriber's order. A procedure is learnt with a teacher and done only once you are trained to do it.

Sources: [Hyperkalemia](https://www.ncbi.nlm.nih.gov/books/NBK470284/) (StatPearls (NCBI Bookshelf), 2025).

## **Spotted a mistake?** We are always improving for the community. Tell us what is wrong and our team will review it. Report a mistake

Representative model, for educational purposes only.

---
Source: https://durgical.com/en/clinical-skills/hyperkalaemia-and-other-electrolyte-changes/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/clinical-skills/hyperkalaemia-and-other-electrolyte-changes/