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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.
See also “.”
- 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 becomes 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. 
Consider confirming abnormal serum potassium levels with a repeat blood draw.
ECG findings in hypokalemia 
- Mild to moderate hypokalemia
- Moderate to severe hypokalemia
Identification of underlying etiology
- Review the patient's history and medication list to help identify potential causes of hypokalemia.
- 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 further details on , treatment goals, warnings, and adverse effects.
Severe hypokalemia (< 2.5 mEq/L) and/or high risk of recurrent severe hypokalemia
- KCl: IV repletion PLUS oral repletion if tolerated 
- Rate of repletion should not exceed 10–20 mEq/hour through a peripheral IV. 
- Higher doses (up to 40 mEq/hour) must be administered through a central line.
- Order continuous cardiac monitoring for IV potassium infusions over 10 mEq/hour.
- Check potassium levels every 2–4 hours or after a maximum of 60 mEq (combined total from oral and IV sources) has been repleted.
- Consider admission to ICU, continuous cardiac monitoring, and central line placement.
- KCl: IV repletion PLUS oral repletion if tolerated 
Moderate hypokalemia (2.5–2.9 mEq/L)
- KCl: Oral repletion is preferred unless the patient is unable to tolerate PO, has severe symptoms, or has . 
- Disposition is usually determined by treatment of the underlying disorder.
Mild hypokalemia (3.0–3.5 mEq/L) with easily reversible cause
- Prioritize treatment of the underlying condition (e.g., GI fluid losses).
- Consider oral supplementation, e.g., KCl
- Consider increasing dietary potassium intake. 
- Patients can usually be discharged after stabilization.
High concentrations of IV potassium can cause local venous irritation and potentially lead to cardiac arrhythmias. Limit the rate of infusion according to the type of IV access and place patients on a continuous cardiac monitor.
Correction of hypokalemia is a common cause of hyperkalemia in hospitalized patients; monitor K+ levels frequently in patients receiving potassium repletion. 
In patients with hypokalemia, avoid solutions containing dextrose, which can increase insulin secretion and worsen hypokalemia. 
Treatment of underlying condition
- Review medications that may be affecting potassium balance, e.g., β2 agonists, laxatives.
- Diuretic-induced hypokalemia (e.g., loop diuretics or thiazides) 
- Start oral or IV magnesium for patients with hypomagnesemia.
- Treat and provide for .
- Consider aggressive potassium repletion for conditions at high risk of relapsing or refractory hypokalemia, e.g., , high-dose insulin therapy, .
- Consider specialist consult (e.g., nephrology, endocrinology, dietician) as directed by the suspected underlying etiology.
- One-Minute Telegram 62-2022-1/3: K+ may be more than OK at making bad rhythms go away
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