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Physiology · Cardiovascular

The ECG in potassium and calcium disorders !

  • Measurement
  • Exam priority: medium

Potassium and calcium reshape the cardiac action potential, and it shows in the T wave, the QRS and the QT interval.

Updated 2026-11-01

See it in 3D: Left ventricle

What it is

Extracellular potassium sets the resting potential and the speed of repolarization, so its disorders change the T wave and the QRS and can stop the heart. Calcium acts on the length of the plateau (phase 2), which on the ECG is the ST segment: it mainly changes the QT length.

How it works, step by step

  1. More K⁺ outside shrinks the gradient: the resting potential becomes less negative.
  2. At that partly depolarized potential Na⁺ channels inactivate: phase 0 is slower and the QRS widens.
  3. Hyperkalemia also raises the conductance of repolarizing K⁺ channels: phase 3 is faster and the T wave turns tall and peaked.
  4. Less K⁺ outside lowers that conductance: repolarization lengthens, the T flattens and a U wave appears.
  5. Extracellular calcium sets how long the plateau lasts: low calcium prolongs phase 2 (long QT); high calcium shortens it (short QT).

Electrocardiogram: a normal beat in lead II

Electrocardiogram: a normal beat in lead II: 75 /min Lead II · 25 mm/s · 10 mm/mVPRQSTUPRSTQRSQTRhythm strip · 75 /minRR 0.80 s = 4 big boxes → 300 / 4 = 75 /min

HR 75 /minRR 0.80 sPR 0.16 sQRS 0.09 sQT 0.37 sQTc 0.41 s

Tap a wave (P, QRS, T, U), an interval (PR, ST, QT) or the RR.

  • ECG trace (lead II)
  • Small box: 0.04 s · 0.1 mV
  • Big box: 0.20 s · 0.5 mV
  • Selected part
Illustrative trace drawn by Durgical from smoothed waves (not a real recording); durations and amplitudes are approximate. Not for reading a clinical ECG.

Action potential

Action potential: Ventricular myocyte 0100200300400−100−80−60−40−200+20+40Time (ms)Membrane potential (mV)Rest −80 mVThreshold −70 mVARPRRPPhase 4Phase 0Phase 1Phase 2Phase 3

Rest −80 mVThreshold −70 mVPeak +15 mVDuration ≈ 240 ms

Hyperkalemia: with more K⁺ outside the cell the K⁺ gradient falls and the resting potential becomes less negative (closer to threshold). The sustained depolarization inactivates some Na⁺ channels: the upstroke is slower and lower (in the heart, a wide QRS) and the myocyte repolarizes sooner (peaked T wave). Excitability first rises, then falls (weakness, arrhythmias).

Tap a phase (the pills above or its band) or a refractory period (ARP, RRP) at the base of the plot.

  • Mainly Na⁺
  • Mainly K⁺
  • Mainly Ca²⁺
  • Rest
  • Threshold
  • ARP: absolute refractory period
  • RRP: relative refractory period
  • Curve at normal K⁺
Compare the action potential at normal and high K⁺: see how the resting level and phase 0 change.

Plasma reference values (adult)

ParameterValueNote
Potassium3.5–5.0 mEq/Lranges vary by laboratory
Total calcium8.5–10.2 mg/dLcorrect for albumin
Ionized calcium≈1.1–1.3 mmol/L
Normal QTc< 450 ms men; < 460–470 ms womenapprox.

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

What changes on the ECG and why

DisorderECGWhy
HyperkalemiaPeaked T, long PR, flat P, wide QRS, sine waveLess negative rest inactivates Na⁺ channels; faster repolarization
HypokalemiaFlat T, U wave, ST depression, long QUSlow repolarization and more automaticity
HypercalcemiaShort ST and QTShorter plateau
HypocalcemiaLong ST and QTLonger plateau

Clinical notes

  • Hyperkalemia with ECG changes is an emergency: intravenous calcium stabilizes the membrane without lowering potassium.
  • Hypokalemia and hypomagnesemia prolong repolarization and favor torsades de pointes.
  • In chronic kidney disease hyperkalemia is one of the causes of sudden death.

Test yourself

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

Why does severe hyperkalemia widen the QRS?

Resting potential becomes less negative, Na⁺ channels inactivate and phase 0 rises more slowly: ventricular conduction slows.

Which ECG wave typically appears in hypokalemia, and what extra risk does it add for a patient on digoxin?

The U wave (with a flat T); hypokalemia potentiates digoxin toxicity because both compete at the Na⁺/K⁺-ATPase.

Why does calcium change the QT interval but barely the T wave or the QRS?

Calcium acts on the plateau (phase 2), which matches the ST segment; changing its length lengthens or shortens the QT.

Why is intravenous calcium given in hyperkalemia with ECG changes if it does not lower potassium?

It restores the gap between resting potential and threshold, stabilizes the membrane and protects against arrhythmias while other measures lower potassium.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 19.2 Cardiac Muscle and Electrical Activity (OpenStax (Rice University), 2022); High potassium level: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Low blood potassium: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Hypercalcemia: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 13). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.