Hyperkalemia ECG Changes: Peaked T Waves to Sine Wave
As potassium rises, the ECG tends to show peaked T waves, then a longer PR and flatter P waves, then a wide QRS, and finally a sine-wave pattern before ventricular fibrillation or asystole. The order is not reliable: many patients with severe hyperkalemia have a near-normal ECG, and some go straight to bradycardia or a wide QRS.
At a glance
- Typical order: tall, narrow, peaked T waves; a longer PR and flatter P waves; a wide QRS; a sine wave.
- The ECG is insensitive: in 90 hospital patients with potassium of 6 mmol/L or more, it could not reliably diagnose hyperkalemia.
- In severe hyperkalemia, bradycardia under 50 bpm, a junctional rhythm and a wide QRS predicted arrhythmia or death within 6 hours. Peaked T waves alone did not.
- Give intravenous calcium at once for any of these changes. It protects the heart within minutes but does not lower potassium.
- Then move potassium into cells with insulin, glucose and a nebulized beta-agonist, and remove it with binders, diuretics or dialysis.
Criteria
Peaked T waves
Tall, narrow, symmetric T waves with a pointed tip, clearest in V2 to V4. The most familiar sign and the least specific.
P wave and PR changes
A longer PR, flatter and wider P waves, then loss of the P wave.
Wide QRS
A broad, often bizarre QRS that can look like bundle branch block or a ventricular rhythm.
Slow rhythms
Sinus bradycardia, AV block, and junctional or slow ventricular rhythms. These predicted short-term adverse events.
Sine wave
The QRS and T waves merge into a smooth, sine-like wave. Cardiac arrest is close.
Other patterns
ST elevation in V1 and V2 that mimics Brugada pattern or STEMI, and pacemakers that fail to capture.
What it looks like
Peaked T waves
Long PR, flat P, peaked T
Wide QRS
Sine wave
How to measure it
- Compare with an old ECG: T waves that have grown taller matter more than their absolute height.
- Check the rate and rhythm first. Bradycardia, a junctional rhythm and AV block are danger signs.
- Measure the QRS. New widening means conduction is affected.
- Look at V2 to V4 for peaked T waves, and at II and V1 for flattening of the P wave.
- Repeat the ECG after treatment and whenever the potassium changes.
Causes
Less excretion
- Acute kidney injury and chronic kidney disease
- ACE inhibitors, ARBs and mineralocorticoid receptor antagonists
- potassium-sparing diuretics
- trimethoprim
- heparin
- calcineurin inhibitors
- hypoaldosteronism
Shift out of cells
- Acidosis
- insulin deficiency and hyperglycemia
- beta-blockers
- digoxin toxicity
- succinylcholine
Release from damaged cells
- Rhabdomyolysis
- tumour lysis
- hemolysis
- burns and crush injury
False high reading
- A hemolysed sample
- a long tourniquet time or fist clenching
- very high platelet or white cell counts
What to do
- Give intravenous calcium for any hyperkalemic ECG change, for example 10 mL of 10% calcium chloride through a large vein or 30 mL of 10% calcium gluconate, following local protocol. Repeat it if the ECG has not improved after 5 to 10 minutes.
- Move potassium into cells: 10 units of regular insulin intravenously with 25 g of glucose, then check the glucose often for several hours. A nebulized beta-agonist such as salbutamol (albuterol) 10 to 20 mg adds to the effect.
- Remove potassium: stop drugs that raise it, give a potassium binder, use a loop diuretic if the kidneys respond, and arrange urgent dialysis for kidney failure or hyperkalemia that does not respond.
- Keep the patient on a cardiac monitor and recheck potassium within 1 to 2 hours. Insulin and beta-agonists wear off within hours, so potassium can rebound.
- Sodium bicarbonate helps mainly when there is metabolic acidosis.
Pitfalls and mimics
- Waiting for ECG changes before treating: severe hyperkalemia can cause arrest without a warning ECG.
- Mixing up peaked T waves and the hyperacute T waves of an early STEMI: compare with the symptoms, an old ECG and the potassium.
- Treating a slow, wide rhythm in a dialysis patient as ventricular tachycardia: think of hyperkalemia first and give calcium.
- Treating a falsely high potassium from a hemolysed sample when the ECG is normal and the result is unexpected: repeat the test quickly, without delaying treatment if the ECG shows changes.
Key studies
Montague 2008, Clin J Am Soc Nephrol
In 90 hospital patients with potassium of 6 mmol/L or more, the ECG was insensitive for hyperkalemia. Changes became more likely as potassium rose, but no T-wave threshold could be set.
Durfey 2017, West J Emerg Med
Of 188 patients with potassium of 6.5 mEq/L or more, 28 (15%) had an adverse event within 6 hours, each after an ECG with at least one hyperkalemic change. QRS widening, bradycardia under 50 bpm and a junctional rhythm raised the risk; peaked T waves did not.
Clase 2020, KDIGO Controversies Conference
Reviews how the body handles potassium and how to manage acute and chronic hyperkalemia in kidney disease.
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Questions clinicians ask
What are the ECG signs of hyperkalemia?
Peaked T waves, a longer PR with flatter P waves, a wide QRS, slow rhythms such as junctional rhythm and AV block, and finally a sine-wave pattern. Not every patient shows them, and they don't always appear in that order.
At what potassium level do ECG changes appear?
There is no reliable threshold. Changes become more likely as potassium rises, but some patients with very high levels have a near-normal ECG, and a rapid rise can cause changes at lower levels.
Can you have hyperkalemia with a normal ECG?
Yes. The ECG misses many cases of hyperkalemia, so a normal tracing does not mean a high potassium is safe. Treat according to the level, the trend and the clinical picture.
Why give calcium in hyperkalemia?
Calcium stabilizes the heart muscle cell membrane and works within minutes, buying time while potassium is shifted into cells and removed. It does not lower the potassium level.
Sources
- Montague BT, Ouellette JR, Buller GK. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol. 2008;3(2):324-330. doi.org/10.2215/CJN.04611007
- Durfey N, Lehnhof B, Bergeson A, et al. Severe hyperkalemia: can the electrocardiogram risk stratify for short-term adverse events? West J Emerg Med. 2017;18(5):963-971. doi.org/10.5811/westjem.2017.6.33033
- Clase CM, Carrero JJ, Ellison DH, et al. Potassium homeostasis and management of dyskalemia in kidney diseases: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int. 2020;97(1):42-61. doi.org/10.1016/j.kint.2019.09.018
- Littmann L, Gibbs MA. Electrocardiographic manifestations of severe hyperkalemia. J Electrocardiol. 2018;51(5):814-817. doi.org/10.1016/j.jelectrocard.2018.06.018
Written in our own words by 2 Minute Medicine's physician editors from the sources listed here. The diagrams are schematic drawings made for 2MM, not patient tracings. This page supports, and does not replace, a full ECG reading and clinical judgment.
For health care professionals. Values are for adults unless a page says otherwise.
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