Merck Manual

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James L. Lewis III

, MD, Brookwood Baptist Health and Saint Vincent’s Ascension Health, Birmingham

Reviewed/Revised Sep 2023
Topic Resources

Hypokalemia is serum potassium concentration < 3.5 mEq/L (< 3.5 mmol/L) caused by a deficit in total body potassium stores or abnormal movement of potassium into cells. The most common cause is excess loss from the kidneys or gastrointestinal tract. Intracellular shifts as well as certain medications can also cause hypokalemia. Clinical features include muscle weakness and polyuria; cardiac hyperexcitability may occur with severe hypokalemia. Diagnosis is by serum measurement. Treatment is giving potassium and managing the cause.

Etiology of Hypokalemia

Hypokalemia can be caused by decreased intake of potassium but is usually caused by excessive losses of potassium in the urine or from the gastrointestinal (GI) tract.

Gastrointestinal tract losses

Abnormal GI potassium losses occur in all of the following:

  • Chronic diarrhea, including chronic laxative abuse and bowel diversion

  • Clay (bentonite) ingestion, which binds potassium and greatly decreases absorption

  • Rarely, villous adenoma of the colon, which causes massive potassium secretion

Protracted vomiting or gastric suction (which removes volume and hydrochloric acid) causes renal potassium losses due to metabolic alkalosis Metabolic Alkalosis Metabolic alkalosis is primary increase in bicarbonate (HCO3) with or without compensatory increase in carbon dioxide partial pressure (Pco2); pH may be high or nearly normal. Common... read more and stimulation of aldosterone due to volume depletion; aldosterone and metabolic alkalosis both cause the kidneys to excrete potassium.

Intracellular shift

The transcellular shift of potassium into cells may also cause hypokalemia. This shift can occur in any of the following:

Familial periodic paralysis Familial Periodic Paralysis Familial periodic paralysis is a rare autosomal dominant condition with considerable variation in penetrance. It is characterized by episodes of flaccid paralysis with loss of deep tendon reflexes... read more is a rare autosomal dominant disorder characterized by transient episodes of profound hypokalemia thought to be due to sudden abnormal shifts of potassium into cells. Episodes frequently involve varying degrees of paralysis. They are typically precipitated by a large carbohydrate meal or strenuous exercise.

Renal potassium losses

Various disorders can increase renal potassium excretion.

Excess mineralocorticoid (ie, aldosterone) effect can directly increase potassium secretion by the distal nephrons and occurs in any of the following:

Hypomagnesemia Hypomagnesemia Hypomagnesemia is serum magnesium concentration < 1.8 mg/dL (< 0.70 mmol/L). Causes include inadequate magnesium intake and absorption or increased excretion due to hypercalcemia or medications... read more is a common correlate of hypokalemia. Much of this correlation is attributable to common causes (ie, diuretics, diarrhea), but hypomagnesemia itself may also result in increased renal potassium losses.


Diuretics are by far the most commonly used medications that cause hypokalemia. Potassium-wasting diuretics that block sodium reabsorption proximal to the distal nephron include

  • Loop diuretics

  • Osmotic diuretics

  • Thiazide diuretics

By inducing diarrhea, laxatives, especially when abused, can cause hypokalemia. Surreptitious use of diuretics or laxatives or both is a frequent cause of persistent hypokalemia, particularly among patients preoccupied with weight loss and among health care professionals with access to prescription medications.

Other medications that can cause hypokalemia include

  • Amphotericin B

  • Antipseudomonal penicillins (eg, carbenicillin)

  • Penicillin in high doses

  • Theophylline (both acute and chronic intoxication)

Symptoms and Signs of Hypokalemia

Mild hypokalemia (serum potassium 3 to 3.5 mEq/L [3 to 3.5 mmol/L]) rarely causes symptoms. Moderate hypokalemia (serum potassium < 3 mEq/L [< 3 mmol/L]) generally causes muscle weakness and may lead to paralysis and respiratory failure.

Persistent hypokalemia can impair renal concentrating ability, causing polyuria with secondary polydipsia.

Diagnosis of Hypokalemia

  • Serum potassium measurement

  • ECG

  • When the mechanism is not evident clinically, measurement of 24-hour urinary potassium excretion and serum magnesium concentration

Hypokalemia (serum potassium < 3.5 mEq/L [< 3.5 mmol/L]) may be found during routine serum electrolyte measurement. It should be suspected in patients with typical changes on an ECG or in those who have muscular symptoms and risk factors. Hypokalemia is confirmed by blood testing.


ECG should be done on patients with moderate to severe hypokalemia. Cardiac effects of hypokalemia are usually minimal until serum potassium concentrations are < 3 mEq/L (< 3 mmol/L). Hypokalemia causes sagging of the ST segment, depression of the T wave, and elevation of the U wave. d As hypokalemia worsens, the T wave becomes progressively smaller and the U wave becomes increasingly larger. Sometimes, a flat or positive T wave merges with a positive U wave, which may be confused with QT prolongation (see figure ). Hypokalemia may cause premature ventricular beats Ventricular Premature Beats (VPB) Ventricular premature beats (VPB) are single ventricular impulses caused by reentry within the ventricle or abnormal automaticity of ventricular cells. They are extremely common in both healthy... read more Ventricular Premature Beats (VPB) and premature atrial contractions Atrial premature beats Various rhythms result from supraventricular foci (usually in the atria). Diagnosis is by electrocardiography. Many are asymptomatic and require no treatment. (See also Overview of Arrhythmias... read more Atrial premature beats , ventricular Ventricular Tachycardia (VT) Ventricular tachycardia is ≥ 3 consecutive ventricular beats at a rate ≥ 120 beats/minute. Symptoms depend on duration and vary from none to palpitations to hemodynamic collapse and death. Diagnosis... read more and supraventricular tachyarrhythmias Reentrant Supraventricular Tachycardias (SVT) Including Wolff-Parkinson-White Syndrome Reentrant supraventricular tachycardias (SVT) involve reentrant pathways with a component above the bifurcation of the His bundle. Patients have sudden episodes of palpitations that begin and... read more , and 2nd- or 3rd-degree atrioventricular block Atrioventricular Block Atrioventricular (AV) block is partial or complete interruption of impulse transmission from the atria to the ventricles. The most common cause is idiopathic fibrosis and sclerosis of the conduction... read more Atrioventricular Block . Such arrhythmias become more severe with increasingly severe hypokalemia; eventually, ventricular fibrillation may occur. Patients with significant preexisting heart disease and patients receiving digoxin are at risk of cardiac conduction abnormalities as a result of even mild hypokalemia.

ECG patterns in hypokalemia

Serum potassium is in mEq/L and mmol/L.

ECG patterns in hypokalemia

Diagnosis of cause

The cause of hypokalemia is usually apparent by history (particularly the medication history); when it is not, further investigation is warranted.

After acidosis and other causes of intracellular potassium shift (increased beta-adrenergic effect, hyperinsulinemia) have been eliminated, 24-hour urinary potassium and serum magnesium concentrations are measured. In hypokalemia, potassium secretion is normally < 15 mEq/L (< 15 mmol/L).

Extrarenal (GI) potassium loss or decreased potassium ingestion is suspected in chronic unexplained hypokalemia when renal potassium secretion is < 15 mEq/L (< 15 mmol/L). Secretion of > 15 mEq/L (> 15 mmol/L). suggests a renal cause for potassium loss.

Unexplained hypokalemia with increased renal potassium secretion and hypertension suggests an aldosterone-secreting tumor or Liddle syndrome. Unexplained hypokalemia with increased renal potassium loss and normal blood pressure suggests Bartter syndrome or Gitelman syndrome, but hypomagnesemia, surreptitious vomiting, and diuretic abuse are more common and should also be considered.

Treatment of Hypokalemia

  • Oral potassium supplements

  • IV potassium supplements for severe hypokalemia or ongoing potassium losses

Many oral potassium supplements are available. Because high single doses can cause GI irritation and occasional bleeding, deficits are usually replaced in divided doses. Liquid potassium chloride given orally elevates concentrations within 1 to 2 hours but has a bitter taste and is tolerated particularly poorly in doses > 25 to 50 mEq (> 25 to 50 mmol). Wax-impregnated potassium chloride preparations are better tolerated. GI bleeding may be even less common with microencapsulated potassium chloride preparations. Several of these preparations contain 8 or 10 mEq/capsule. Because a decrease in serum potassium of 1 mEq/L (1 mmol/L) correlates with about a 200- to 400-mEq (200 to 400 mmol) deficit in total body potassium stores, total deficit can be estimated and replaced over a number of days at 20 to 80 mEq (20 to 80 mmol)/day.

When hypokalemia is severe (eg, with ECG changes or severe symptoms), is unresponsive to oral therapy, or occurs in hospitalized patients who are taking digoxin or who have significant heart disease or ongoing losses, potassium must be replaced IV. Because potassium solutions can irritate peripheral veins, the concentration should not exceed 40 mEq/L (40 mmol/L). The rate of correction of hypokalemia is limited because of the lag in potassium movement from the extracellular space into cells. Routine infusion rates should not exceed 10 mEq (10 mmol)/hour.

In hypokalemia-induced arrhythmia, IV potassium chloride must be given more rapidly, usually through a central vein or using multiple peripheral veins simultaneously. Infusion of 40 mEq (40 mmol) potassium chloride/hour can be undertaken but only with continuous cardiac monitoring and hourly serum potassium determinations. Dextrose or glucose solutions used for dilution are avoided because elevation in the serum insulin concentrations could result in transient worsening of hypokalemia.

Even when potassium deficits are severe, it is rarely necessary to give > 100 to 120 mEq (> 100 to 120 mmol) of potassium in a 24-hour period unless potassium loss is ongoing. In potassium deficit with high serum potassium concentration, as in diabetic ketoacidosis, IV potassium is deferred until the serum potassium starts to fall. When hypokalemia occurs with hypomagnesemia Treatment Hypomagnesemia is serum magnesium concentration < 1.8 mg/dL (< 0.70 mmol/L). Causes include inadequate magnesium intake and absorption or increased excretion due to hypercalcemia or medications... read more , both the potassium and magnesium deficiencies must be corrected to stop ongoing renal potassium wasting.

Prevention of Hypokalemia

Routine potassium replacement is not necessary in most patients receiving diuretics. However, serum potassium should be monitored during diuretic use when risk of hypokalemia or of its complications is high. Risk is high in

  • Patients with decreased left ventricular function

  • Patients taking digoxin

  • Patients with diabetes (in whom insulin concentrations can fluctuate)

  • Patients with asthma who are taking beta 2-agonists

Triamterene 100 mg orally once a day or spironolactone 25 mg orally 4 times a day does not increase potassium excretion and may be useful in patients who become hypokalemic but must use diuretics. When hypokalemia develops, potassium supplementation, usually with oral potassium chloride, is indicated.

Key Points

  • Hypokalemia can be caused by decreased intake of potassium or shift of extracellular potassium into cells, but it is usually caused by excessive losses of potassium in the urine or from the gastrointestinal tract.

  • Clinical signs include muscle weakness, cramping, fasciculations, paralytic ileus, and when hypokalemia is severe, hypoventilation, and hypotension.

  • ECG changes typically occur when serum potassium is < 3 mEq/L (< 3 mmol/L), and include ST segment sagging, T wave depression, and U wave elevation. With marked hypokalemia, the T wave becomes progressively smaller and the U wave becomes increasingly larger.

  • Hypokalemia may cause premature ventricular and atrial contractions, ventricular and atrial tachyarrhythmias, and 2nd- or 3rd-degree atrioventricular block; eventually, ventricular fibrillation may occur.

  • Replace potassium orally, giving 20 to 80 mEq (20 to 80 mmol)/day unless patients have ECG changes or severe symptoms.

  • For hypokalemic arrhythmia, give IV potassium chloride through a central vein at a maximum of 40 mEq (40 mmol)/hour and only with continuous cardiac monitoring; routine IV infusion should be no more than 10 mEq (10 mmol)/hour.

Drugs Mentioned In This Article

Drug Name Select Trade
Amphocin, Fungizone
Elixophyllin, Quibron T, Quibron T/SR, Respbid, Slo-Bid, Slo-Phyllin, Theo X, Theo-24, Theo-Bid Duracap, TheoCap, Theochron, Theo-Dur, Theo-Dur Sprinkle , Theolair, Theolair SR, Theovent LA, T-Phyl, Uni-Dur, Uniphyl
Digitek , Lanoxicaps, Lanoxin, Lanoxin Pediatric
Cena K , ED-K+10, Epiklor, K Plus, K Plus Care, K-10 , K-8, Kaon-CL, Kay Ciel , K-Dur, K-Lor, Klor-Con, Klor-Con M10, Klor-Con M15, Klor-Con M20, Klotrix, K-Lyte CL, K-Sol , K-Tab, Micro-K, Micro-K Extencaps, POKONZA, PROAMP, Rum-K, Slow-K, Tri-K
Advocate Glucose SOS, BD Glucose, Dex4 Glucose, Glutol , Glutose 15 , Glutose 45 , Glutose 5
Aldactone, CAROSPIR
NOTE: This is the Professional Version. CONSUMERS: View Consumer Version
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