- Clinical science
Hypokalemia (low serum potassium) is a common electrolyte disorder that is typically caused by potassium loss (e.g., due to diarrhea, vomiting, or diuretic medication). Mild hypokalemia may be asymptomatic or cause mild nonspecific symptoms such as nausea, muscle weakness, and fatigue. Severe deficiency can cause cardiac arrhythmias and death. Treatment consists of oral or IV supplementation in conjunction with treatment of the underlying cause. In concurrent hypomagnesemia, which may lead to refractory hypokalemia, the simultaneous repletion of magnesium and potassium is necessary.
- Serum potassium (K+) level < 3.5 mEq/L 
- Severe hypokalemia: K+ level < 2.5 mEq/L
Hypokalemia is most often caused by renal or gastrointestinal potassium loss. Other electrolyte imbalances (e.g., hypomagnesemia), alkalosis, and several medications can also have an impact on potassium homeostasis.
|Etiology of hypokalemia |
|Renal loss|| |
|Intracellular shift|| |
- Potassium is an important factor in maintaining the resting membrane potential.
- ↓ Extracellular K+ concentration → ↑ resting membrane potential (more negative than -90 mV) → ↓ excitability 
Alkalosis can impact potassium balance via intracellular shifts and vice versa.
- Alkalosis → ↓ extracellular H+ → stimulation of the Na+/H+ antiporter (transfers H+ out of the cells in exchange for Na+) → ↑ intracellular Na+ → ↑ sodium gradient stimulates the Na+/K+-ATPase (transfers K+ into the cells in exchange for Na+) → ↓ extracellular K+ concentration
- Hypokalemia → ↓ extracellular K+ concentration → ↓ potassium gradient inhibits the Na+/K+-ATPase → ↓ extracellular Na+ → ↓ sodium gradient inhibits the Na+/H+ antiporter → ↓ extracellular H+ → alkalosis
- Exception: In renal tubular acidosis, findings include hypokalemia and metabolic acidosis!
K+ acts like H+: Hypokalemia leads to alkalosis and vice versa!
Particularly acute extracellular changes in concentration influence excitability! Chronic changes lead to intracellular compensation!
Hypomagnesemia can impact potassium balance via the following mechanisms of increased renal loss: 
- Magnesium serves as a cofactor in Na+/K+-ATPases → hypomagnesemia disrupts the Na+/K+-ATPase in the basolateral membrane of the proximal convoluted loop of Henle → ↓ Na+ reabsorption → ↑ luminal Na+ → ↑ Na+ reabsorption and ↑ K+ secretion by the principal cells distally
- Apical ROMK channels in principal cells are inhibited by intracellular magnesium. With low levels of magnesium available, the ROMK channels are not inhibited, resulting in increased K+ secretion.
Hypomagnesemia can lead to refractory hypokalemia!
Patients may be asymptomatic, particularly if the deficiency is mild. Symptoms usually occur if serum K+ levels are < 3.0 mEq/L and/or decrease rapidly. 
- Cardiovascular manifestations
- Neuromuscular manifestations
- Gastrointestinal manifestations
- Other manifestations
- Electrolytes and kidney function
- Blood gas (venous or arterial): : may show metabolic alkalosis
Urinary potassium: Consider measuring to narrow down underlying etiology 
- Spot urine: rapid assessment, indicated in urgent cases , less reliable than 24-hour collections
- 24-hour urine collection: less practical, indicated for chronic cases and uncertain diagnoses, more accurate than spot urine
- Renal loss; : spot urine > 15–20 mEq/L (24 hour collection > 15 mEq/L) 
- Extrarenal loss; : spot urine < 15–20 mEq/L (24 hour collection < 15 mEq/L) 
Consider confirming abnormal serum potassium levels with a repeat blood draw.
- Indication: all patients
- Mild to moderate hypokalemia
- Moderate to severe hypokalemia
Identification of underlying etiology
- If the etiology is still unclear, further testing can help determine the underlying etiology.
- Imaging is not routinely required but may be necessary if certain underlying etiologies are suspected. 
|Evaluation of underlying etiology in hypokalemia |
|Type of potassium loss||Clinical features||Recommended tests||Findings and interpretation|
|Extrarenal losses|| || || |
|Renal loss|| |
| || || |
Most patients require potassium chloride (KCl) repletion, management of concurrent electrolyte abnormalities (see electrolyte repletion), and treatment of the underlying cause. See for detailed , treatment goals, warnings and adverse effects.
Severe hypokalemia (< 2.5 mEq/L) and/or high risk of recurrent severe hypokalemia
- KCl: High-dose IV repletion
- Consider admission to ICU, continuous cardiac monitoring, and central line placement.
Moderate hypokalemia (2.5–2.9 mEq/L)
- KCl: Oral or IV repletion may be used.
- Disposition usually determined by treatment of underlying disorder
Mild hypokalemia with easily reversible cause (3.0–3.5 mEq/L)
- Prioritize treatment of the underlying condition (e.g., GI fluid losses).
- Consider oral supplementation.
- Consider increasing dietary potassium intake. 
- Patients can usually be discharged after stabilization.
IV potassium may cause local irritation and lead to cardiac arrhythmias. Therefore, it should always be administered slowly (max. rate of 10 mEq/hour via a peripheral line or 40 mEq/hour via a central line)
Treatment of underlying condition
- Diuretic-induced hypokalemia (e.g., loop diuretics or thiazides) 
- Oral or IV magnesium for patients with hypomagnesemia
- For other underlying conditions, see .
Potassium supplementation will be ineffective if concurrent hypomagnesemia is left untreated (see ).