- Potassium is vital for regulating the normal electrical activity of the heart.
- Increased extracellular potassium reduces myocardial excitability, with depression of both pacemaking and conducting tissues.
- Progressively worsening hyperkalaemia leads to suppression of impulse generation by the SA node and reduced conduction by the AV node and His-Purkinje system, resulting in bradycardia and conduction blocks and ultimately cardiac arrest.
- Hyperkalaemia is defined as a potassium level > 5.5 mEq/L
- Moderate hyperkalaemia is a serum potassium > 6.0 mEq/L
- Severe hyperkalaemia is a serum potassium > 7.0 mE/L
Effects of hyperkalaemia on the ECG
Serum potassium > 5.5 mEq/L is associated with repolarization abnormalities:
- Peaked T waves (usually the earliest sign of hyperkalaemia)
Serum potassium > 6.5 mEq/L is associated with progressive paralysis of the atria:
- P wave widens and flattens
- PR segment lengthens
- P waves eventually disappear
Serum potassium > 7.0 mEq/L is associated with conduction abnormalities and bradycardia:
- Prolonged QRS interval with bizarre QRS morphology
- High-grade AV block with slow junctional and ventricular escape rhythms
- Any kind of conduction block (bundle branch blocks, fascicular blocks)
- Sinus bradycardia or slow AF
- Development of a sine wave appearance (a pre-terminal rhythm)
Serum potassium level of > 9.0 mEq/L causes cardiac arrest due to:
- Ventricular fibrillation
- PEA with bizarre, wide complex rhythm
(Warning! In individual patients, the serum potassium level may not correlate closely with the ECG changes. Patients with relatively normal ECGs may still experience sudden hyperkalaemic cardiac arrest.)
ECG manifestations in hyperkalaemia
- Suspect hyperkalaemia in any patient with a new bradyarrhythmia or AV block, especially patients with renal failure, on haemodialysis or taking any combination of ACE inhibitors, potassium-sparing diuretics and potassium supplements.
- For an excellent review of the management of hyperkalaemia, check out this podcast by Scott Weingart.
- Prolonged PR interval.
- Broad, bizarre QRS complexes — these merge with both the preceding P wave and subsequent T wave.
- Peaked T waves.
This patient had a serum K+ of 9.2.
- Broad complex rhythm with atypical LBBB morphology.
- Left axis deviation.
- Absent P waves.
- Huge peaked T waves.
- Sine wave appearance.
This patient had severe hyperkalaemia (K+ 9.0 mEq/L) secondary to rhabdomyolysis.
- Brady WJ, Truwit JD. Critical Decisions in Emergency and Acute Care Electrocardiography
- Hampton, JR. The ECG In Practice, 6e
- Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric, 6e
- Wagner, GS. Marriott’s Practical Electrocardiography 12e
- Chan, TC. ECG in Emergency Medicine and Acute Care
- Wang, K. Atlas of Electrocardiography
- Mattu, A. ECG’s for the Emergency Physician
LITFL Further Reading
- ECG BASICS — Waves, Intervals, Segments and Clinical Interpretation
- ECG A to Z by diagnosis –alphabetical diagnostic approach to the ECG
- ECG CLINICAL CASES — ECG’s placed in clinical context with a challenging Q&A approach
- 100 ECG Quiz — Self-assessment tool for examination practice
- ECG Reference SITES and BOOKS — the best of the rest
- LITFL ECG IMAGE Database — Searchable database of LITFL ECG’s
- ECG and Cardiology Eponymous Syndromes — Cheats guide to eponymous emancipation
- ECG Exam Template — a framework for answering ECG exam questions.