Emergency: requires immediate attention
Hyperkalemia
Alerts and Notices
Synopsis

Signs and symptoms include muscle weakness, paralysis, hypothermia, and cardiac abnormalities (irregular conduction and arrhythmias).
ECG changes of hyperkalemia do not reliably correlate with potassium levels, but mild elevation (5.5-6.5 mmol/L) may cause peaked T waves, shortened QT interval, and ST-segment depression.
At higher levels of potassium (< 8.0 mmol/L), the ECG may demonstrate peaked T waves, PR prolongation with decreased P waves, and widening QRS. At potassium levels > 8.0 mmol/L, P waves may be absent, with progressively widening QRS, and intravesicular / fascicular / bundle branch block development, progressing to a sine wave pattern, followed by ventricular fibrillation or asystole. It is important to note that approximately 50% of patients do not have ECG changes even with serum potassium > 6.0 mmol/L, however. Still, the absolute level of serum potassium is important in predicting morbidity and mortality, along with the rate at which it is reached and how long the patient remains hyperkalemic.
Pseudohyperkalemia can be caused by improper blood drawing techniques, hemolysis, tourniquet use, and clenched fists.
In addition to acquired hyperkalemia, hyperkalemic periodic paralysis is an autosomal dominant inherited disorder that causes fluctuating potassium levels and episodic muscle weakness when potassium levels are high.
Codes
ICD10CM:E87.5 – Hyperkalemia
SNOMEDCT:
14140009 – Hyperkalemia
Look For
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Diagnostic Pearls
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Differential Diagnosis & Pitfalls
Causes of hyperkalemia:Increased potassium release from cells
- Pseudohyperkalemia – serum potassium is 0.5 mmol/L > plasma potassium
- Metabolic acidosis
- Hypertonicity / hyperglycemia
- Beta blockers
- Exercise
- Hyperkalemic periodic paralysis
- Tissue injury (eg, rhabdomyolysis, trauma / surgery, tumor lysis)
- Excess consumption of potassium-rich foods (banana, potatoes, melons, citrus, avocados)
- Salt substitutes (common in patients with CKD)
- Oliguric renal failure
- Acute or chronic kidney disease
- Hyporeninemic hypoaldosteronism
- Type 4 renal tubular acidosis
- Drugs – angiotensin inhibitors, NSAIDs, calcineurin inhibitors (cyclosporine, tacrolimus), heparin, potassium-sparing diuretics
- Mineralocorticoid deficiency or resistance
- Cortical collecting tubule defect
Best Tests
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Management Pearls
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Therapy
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Drug Reaction Data
Below is a list of drugs with literature evidence indicating an adverse association with this diagnosis. The list is continually updated through ongoing research and new medication approvals. Click on Citations to sort by number of citations or click on Medication to sort the medications alphabetically.Subscription Required
References
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Last Reviewed:05/08/2019
Last Updated:05/13/2019
Last Updated:05/13/2019