Hyperkalemia (high serum potassium) is a common and potentially life-threatening disorder of potassium balance. The most common cause is decreased kidney function. It can also be caused by acidosis, cell breakdown, endocrinological disturbances (e.g., hypoaldosteronism, hypocortisolism), and drugs such as potassium-sparing diuretics, angiotensin-converting enzyme (ACE) inhibitors, nonsteroidal antiinflammatory drugs (NSAIDs), and digoxin. Serum potassium (K+) is often falsely elevated due to the method of sampling and levels should be confirmed with repeat testing. To determine the underlying cause of hyperkalemia, it is essential to review the patient's medications, check kidney and endocrine function, and screen for cell lysis (e.g., hemolysis, rhabdomyolysis) and acid-base disorders. Acute increases in serum K+ are very dangerous, as they influence the resting membrane potential and thus the electrical excitability of cells. These changes can lead to life-threatening cardiac arrhythmias. It is, therefore, essential to obtain an ECG to determine the level of cardiotoxicity. Management depends on the severity of the hyperkalemia and includes restriction of dietary K+, as well as medications to bind, shift, or eliminate K+, or to stabilize the cardiac membrane (e.g., calcium gluconate) if necessary. In refractory cases, dialysis may be required. Serum K+ should be monitored closely until it is corrected.
See also “Hypokalemia.”
- Hyperkalemia: Serum potassium level > 5 mEq/L
- Acute hyperkalemia: Abnormal ↑ K+ not known to be chronic
- Chronic hyperkalemia: Recurrent episodic ↑ K+ that require ongoing treatment
- Reduced excretion: acute and 
- Endocrine causes: hypocortisolism, hypoaldosteronism
- Drugs: , ACE inhibitors, angiotensin receptor blockers, NSAIDs, and trimethoprim-sulfamethoxazole 
- GI absorption: increased intake of high-potassium foods (e.g., fresh fruits, dried fruits and legumes, vegetables, nuts, seeds, bran products, milk, and dairy products)
- Type IV renal tubular acidosis
- Release from cells: myolysis, tumor lysis, hemolysis
- Increased intake (high potassium diet, K+ containing IV fluids)
Acidosis → ↑ extracellular H+ → inhibition of the Na+/H+ antiporter → ↓ intracellular Na+ → ↓ sodium gradient inhibits the Na+/K+-ATPase → ↑ extracellular K+ concentration
- Hyperkalemia → ↑ extracellular K+ concentration → ↑ potassium gradient stimulates the Na+/K+-ATPase → ↑ extracellular Na+ → ↑ sodium gradient stimulates the Na+/H+ antiporter → ↑ extracellular H+ → acidosis
- Exceptions: In renal tubular acidosis and acetazolamide toxicity, findings include hypokalemia and metabolic acidosis.
- Insulin deficiency (manifests with hyperglycemia)
- Release from cells: rhabdomyolysis, tumor lysis syndrome, hemolysis
- Acidosis → ↑ extracellular H+ → inhibition of the Na+/H+ antiporter → ↓ intracellular Na+ → ↓ sodium gradient inhibits the Na+/K+-ATPase → ↑ extracellular K+ concentration
- Pseudohyperkalemia: due to the release of potassium from red blood cell lysis
When K+ shifts out of the cell, it's a BAD LOSS! – Beta-blockers, Acidosis, Digoxin, Lysis, hyperOsmolality, high Sugar, Succinylcholine
- Potassium is an important factor in maintaining the resting membrane potential
- ↑ Extracellular K+concentration → resting membrane potential becomes less negative than -90 mV → ↑ excitability
Particularly acute extracellular changes in concentration influence excitability! Chronic changes lead to intracellular compensation!
Symptoms usually occur if serum potassium levels are > 7.0 mEq/L or they change rapidly.
- Cardiac arrhythmias (e.g., atrioventricular block, ventricular fibrillation)
- Muscle weakness, paralysis, paresthesia
- ↓ Deep tendon reflexes
- Nausea, vomiting, diarrhea
All patients require an ECG and routine laboratory studies to confirm the diagnosis and assess the need for urgent treatment. Further diagnostic testing depends on the suspected underlying etiology. Inquire about last renal replacement therapy for patients with ESRD (e.g., screen for missed hemodialysis appointments, adherence to peritoneal dialysis)
Laboratory studies 
- Glucose: If very high, consider spurious hyperkalemia secondary to hyperglycemic crisis.
- Serum electrolytes
- Kidney function tests: often show renal impairment 
- CBC: can show hemolytic anemia or thrombocytosis 
- Liver chemistries: may be abnormal in hemolysis or tumor lysis syndrome
- Blood gases: (venous or arterial): often show metabolic acidosis 
An inverse relationship between serum K+ and pH (e.g., ↓ pH → ↑ K+) has previously been observed in specific types of metabolic acidosis. However, the underlying mechanisms are complex and this association is inconsistent in clinical practice. 
Investigation of underlying causes 
Depending on symptoms and risk factors, further testing may be appropriate, particularly if renal function is normal.
- Creatine kinase: ↑ in rhabdomyolysis
- LDH: ↑ in tumor lysis syndrome or hemolysis
- Renin-angiotensin-aldosterone system
- Cortisol: can be ↓ in primary adrenal insufficiency (see “Endocrine testing for adrenal insufficiency”)
- Urine electrolytes: rarely indicated 
ECG findings in hyperkalemia 
Mild hyperkalemia: 5.5–6.4 mEq/L
- Tall, peaked T waves
- Moderate hyperkalemia: 6.5–8.0 mEq/L
- Severe hyperkalemia: > 8.0 mEq/L
Urgent K+-lowering treatment may be necessary even in the absence of ECG changes.
Risk stratification 
- The risk of hyperkalemic emergency (acute severe elevation requiring urgent lowering) is elevated if any of the following are present:
Less urgent hyperkalemia (typically chronic elevations that can be lowered more slowly) is more likely in the following cases:
- Asymptomatic patient
- Serum K+ = 5.5–6.0 mEq/L
- No high-risk comorbidities
|Therapeutic approach to hyperkalemia |
|Treatment strategy||Acute hyperkalemia ||Chronic hyperkalemia|
|Cardiac membrane stabilization|| |
|Intracellular K+ shifting|
|Enhanced K+ elimination|
|Reduced K+ intake|| |
|Treatment of underlying cause|| |
|Monitoring and disposition|| || |
To remember K+-lowering treatments, think C BIG K Die (if you see a big serum K+, your patient may die!): Calcium salts, Beta-agonists/Bicarbonate, Insulin + Glucose, Kation exchange medication, Dialysis/Diuretics.
Cardiac membrane stabilization 
Calcium salts reduce cardiac irritability.
- Indication: signs of cardiotoxicity (see “ECG changes in hyperkalemia”)
- Considerations 
Calcium salts have no influence on serum K+ levels and therefore should be paired with a K+-lowering agent.
Intracellular potassium shifting 
These drugs should be given in tandem with calcium salts (if calcium is indicated).
- Insulin and glucose
- Inhaled SABAs
Enhanced potassium elimination 
Hemodialysis is the most effective definitive therapy for refractory hyperkalemia. However, it is not a first-line option because of its invasive nature and adverse effects. It is the treatment of choice for patients already receiving regular .
Cation-exchange medications 
- Mechanism of action: These drugs release Na+ or Ca2+ ions in the gut, which are exchanged for K+, thereby enhancing enteral K+ elimination.
- Clinical applications: nonurgent lowering of K+ 
- Gastrointestinal upset
Additional medications 
The following medications are typically reserved to treat refractory hyperkalemia and only in specific circumstances.
- Diuretics: Consider loop diuretics, e.g., furosemide , in patients with volume overload.
- Sodium bicarbonate: : Consider in patients with metabolic acidosis.