Hyperkalemia
Peaked T waves, the earliest sign
Hyperkalemia
criticalRising potassium changes the ECG in a set order: peaked T waves, then a long PR and a fading P, then a wide QRS, a sine wave and ventricular fibrillation.
On the trace
The tracing above is K⁺ 6, the earliest form; the Variant control beside the title steps up through the rest. Turn on the Normal switch under the tracing to draw the same heart at a normal potassium in grey behind it: at this level almost all the difference is in the T waves.
- Look at the T in V2 to V4.
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Tall and narrow: 9.0 mm in V3, against 4.9 mm at a normal potassium. In V3 it is as tall as the QRS itself, in V2 and V4 about 60% of it. Half the QRS's height or more is the peaked-T criterion. - Look at the T in II, III and aVF.
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Taller than normal (3.7 mm in II, against 2.3) and symmetric: it rises as fast as it falls, where a normal T rises slowly. Tap a lead and choose T in the box that opens: it gives the T's height as a share of the QRS. - Look at the ST segment.
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Level at the J point in every lead, and short: by 60 ms after the J point the T is already rising, 0.8 mm up in V3. - Measure the QRS and the QT.
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QRS 105 ms: not yet wide. QT 347 ms, QTc 374 ms: not long. - Measure the PR.
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211 ms, just past the 200 ms limit: the first sign of the slowing to come in the atria and the AV node. - Check the rhythm.
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Sinus, 75 per minute, every P conducted.
How to recognise it
The changes come in order. Each row is the form of that name beside the title.
| Serum K⁺ | What appears | On this tracing |
|---|---|---|
| 5.5 to 6.5 | Peaked T: tall, narrow, symmetric, at least half the QRS's height, best seen in II, III and V2 to V4. The ST shortens | K⁺ 6: T 9.0 mm in V3, 103% of the QRS |
| 6.5 to 7.5 | The P flattens and widens; the PR lengthens past 200 ms; the QRS starts to widen | K⁺ 7: PR 267 ms, P 1.0 mm in II, QRS 114 ms |
| 7 to 9 | The P disappears; the QRS widens past 120 ms; the rate slows | K⁺ 8: no P, QRS 131 ms, 59 per minute |
| Around 9 to 10 | The QRS merges with the T: the sine wave | Sine wave: one broad wave per beat |
| 10 to 12 | Ventricular fibrillation or asystole | VF |
Mechanism
Potassium sets the resting potential. More of it outside the cell makes the inside less negative, and a cell resting nearer its threshold has fewer sodium channels ready to open. Each beat therefore starts with a weaker upstroke and spreads more slowly.
At the same time, the potassium channels that end the action potential conduct more when potassium is high. Repolarisation finishes sooner and faster, and in step across the ventricle: a short, steep, symmetric T.
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Background
Hyperkalaemia is a serum potassium above 5.0 mmol/L (the same number in mEq/L), and it is one of the few blood results the ECG can warn of before the laboratory does. The levels on this page are a guide, not a rule: how fast the potassium rose matters as much as how high it is, and a patient can arrest at a level that looked safe on paper.
Why the atria go first
Atrial muscle rests nearer its threshold than ventricular muscle and has fewer sodium channels to spare, so it loses its conduction first. The P fades and then vanishes, usually between 7 and 9 mmol/L.
No P, but still sinus
The sinus node and the internodal pathways are more resistant than ordinary atrial muscle. Once the P has gone, the sinus node can still reach the AV node and drive the ventricles, with no visible atrial activity: a sinoventricular rhythm. It looks like a junctional or ventricular rhythm, and it is not one.
The wide QRS
Ventricular conduction slows everywhere at once rather than in one bundle, so the QRS widens as a whole. V1 often looks like left bundle branch block and I and V6 like right bundle branch block, with broad, slurred S waves: a combination that on its own should suggest hyperkalaemia.
The QT
The QT does not lengthen, because the action potential shortens as the QRS widens. A long QT alongside these changes suggests low calcium as well, common in kidney failure.
The sine wave
Once the QRS is wide enough, repolarisation of the earliest ventricle begins before the last has depolarised. There is no ST segment left, and the QRS runs smoothly into the T.
Clinical impact
A normal ECG does not make a high potassium safe, but an abnormal one makes any high level an emergency. The progression can skip stages, from peaked T waves straight to a wide QRS, a severe bradycardia or an arrest.
Management
Protect the heart first: intravenous calcium
For any ECG change of hyperkalaemia. It lowers no potassium, but restores the cells' margin within minutes, for 30 to 60 minutes. Repeat it if the ECG does not improve.
Move potassium into the cells
Insulin with glucose, and nebulised salbutamol: within 15 to 30 minutes, for a few hours. Watch the glucose afterwards.
Remove it from the body
Potassium binders, stopping the drugs that raise it, and haemodialysis when the kidneys cannot, or when the level is severe or rising.
Monitor until it is down
Continuous ECG and repeat levels: an ECG that improves after calcium can worsen again as it wears off.
Differential
Broad-based, bulky and often asymmetric, confined to one coronary territory, and usually with ST changes or reciprocal depression. Peaked T waves of hyperkalaemia are narrow and symmetric, and appear across territories.
Common in young men and in early repolarisation, largest in V2 to V4. Broad-based and asymmetric, with a normal P, PR and QRS.
The sine wave is often mistaken for VT. A slow, very wide, smooth complex with no sharp deflection, in a patient with kidney failure, is hyperkalaemia until proved otherwise. Antiarrhythmics can precipitate arrest; calcium is the treatment.
Tricyclics and class I drugs also widen the QRS and slow conduction, but with a terminal R in aVR, a fast rate and no peaked T.
References
- Clinical Practice Guidelines: Treatment of Acute Hyperkalaemia in Adults — UK Kidney Association, 2023
- ECG frequency changes in potassium disorders: a narrative review — American Journal of Cardiovascular Disease, 2022
- European Resuscitation Council Guidelines 2021: Cardiac arrest in special circumstances — Resuscitation, 2021