Hypokalemia– Causes, Symptoms, Diagnosis, Treatment and Ongoing care



Hypokalemia is defined as a serum potassium concentration <3.5 mEq/L (normal range: 3.5–5.0 mEq/L).


Predominant sex: Male = Female


  • Commonly encountered electrolyte abnormality in clinical practice (1)[B],(2)
  • Found in >20% of hospitalized patients (when defined as potassium <3.6 mEq/L)
  • Higher incidence in individuals with eating disorders from 5–20% (3):
  • >10% of inpatients with alcoholism
  • Higher incidence in patients with AIDS (4,5)
  • Associated risk after bariatric surgery

Risk Factors


Some rare familial disorders cause hypokalemia:

  • Familial hypokalemic periodic paralysis: Hypokalemia after high-carbohydrate or high-sodium meal or after exercise
  • Congenital adrenogenital syndromes
  • Liddle syndrome: Increases K+ secretion
  • Familial interstitial nephritis

General Prevention

When initiating a diuretic, especially loop and thiazide diuretics, patients should be advised to increase their dietary potassium intake (see Diet).


  • Most common causes:
  • Decreased intake: Deficient diet in alcoholics and elderly, anorexia nervosa
  • Gastrointestinal loss: Vomiting, diarrhea, nasogastric tubes, laxative abuse, fistulas, villous adenoma, ureterosigmoidostomy, malabsorption, chemotherapy, radiation enteropathy, bulimia
  • Intracellular shift of potassium: Metabolic alkalosis, insulin excess, β-adrenergic catecholamine excess (acute stress, B2 agonists), hypokalemic periodic paralysis, intoxications (theophylline, caffeine, barium, toluene)
  • Renal potassium loss:
    • Drugs: Diuretics (especially loop and thiazides), amphotericin B, aminoglycosides (6,5,7,8)
    • Mineralocorticoid-excess states: Primary hyperaldosteronism, secondary hyperaldosteronism (congestive heart failure [CHF], cirrhosis, nephrotic syndrome, malignant hypertension, renin-producing tumors), renovascular hypertension, Bartter syndrome, Gitelman syndrome, congenital adrenogenital syndromes, exogenous mineralocorticoids (glycyrrhizic acid in licorice, carbenoxolone, steroids in nasal sprays), Liddle syndrome, vasculitis
  • Glucocorticoid-excess states: Cushing syndrome, exogenous steroids, ectopic adrenocorticotrophic hormone (ACTH) production, II B hydroxysteroid dehydrogenase deficiency
  • Renal tubular acidosis (type I and II):
    • Leukemia
    • Magnesium depletion
    • Thyrotoxic hypokalemic paralysis
  • Osmotic diuresis (e.g., poorly controlled diabetes)

Commonly Associated Conditions

Acute gastrointestinal (GI) illnesses with severe vomiting or diarrhea

Nutrition and Metabolism Disorders, laxative abuse, dietary potassium, malignant hypertension, high carbohydrate, anorexia nervosa, nephrotic syndrome,


  • Patients with hypokalemia often have no symptoms, especially if the hypokalemia is mild (serum potassium 3.0–3.5 mEq/L).
  • Neuromuscular (most prominent manifestations):
    • Skeletal muscle weakness (proximal > distal muscles, lower limbs > upper) may range from mild weakness to total paralysis, including respiratory muscles; may lead to rhabdomyolysis and/or respiratory arrest in severe cases.
    • Smooth-muscle involvement may lead to GI hypomotility, producing ileus and constipation (1)[B].
  • Cardiovascular:
    • Ventricular arrhythmias; higher risk if underlying CHF, left ventricular failure (LVF), cardiac ischemia
    • Hypotension
    • Cardiac arrest
  • Renal: Polyuria, polydipsia, nocturia owing to impaired concentrating ability, myoglobinuria
  • Metabolic: Hyperglycemia

Diagnostic Tests & Interpretation

  • Electrocardiogram (ECG) (9)[B]:
    • Hypokalemia increases the myocyte resting potential, which increases the refractory period; this can lead to arrhythmias.
    • Flattening or inversion of T waves
    • Increased prominence of U waves (small positive deflection after T wave, best seen in V2 and V3)
    • Depression of ST segment
    • Ventricular ectopia
  • Workup for cause:
    • Excessive renal potassium loss: Urinary potassium is >20 mEq/d in presence of hypokalemia
    • In patient with excessive renal potassium loss and hypertension, plasma renin and aldosterone levels should be determined to differentiate adrenal from nonadrenal causes of hyperaldosteronism.
    • If hypertension is absent and patient is acidotic, renal tubular acidosis should be considered.
    • If hypertension is absent and serum pH is normal to alkalotic, high urine chloride (>10 mEq/d [>10 mmol/d]) suggests hypokalemia secondary to diuretics or Bartter syndrome; low urine chloride (<10 mEq/d [<10 mmol/d]) suggests vomiting as probable cause.


  • Serum potassium <3.5 mEq/L (<3.5 mmol/L)
  • Drugs that may alter lab results: Diuretics
  • Disorders that may alter lab results: Leukemia and other conditions with high white blood cells (WBC)


Computed tomography (CT) scan of adrenal glands if evidence of mineralocorticoid excess

Pathological Findings

In severe hypokalemia, necrosis of cardiac and skeletal muscle

Differential Diagnosis

  • Spurious hypokalemia: Occurs when blood with high WBC count (>100,000/mm3) is allowed to stand at room temperature (WBCs extract potassium from plasma)
  • Thyrotoxicosis (10)



  • Nonemergent conditions (serum potassium >2.5 mEq/L [>2.5 mmol/L], no cardiac manifestations):
    • Oral therapy preferred; 40–120 mEq/d (40–120 mmol/d) in divided doses usually adequate
    • IV potassium should be given only when oral administration is not feasible (e.g., vomiting, postoperative state). Rate should not exceed 10 mEq/hour, and concentration should not exceed 40 mEq/L. Up to 40 mEq in 100 mL over 1 hour can be safely given through a central venous line. Patient’s cardiac rhythm should be closely monitored.
    • Potassium chloride is suitable for all forms of hypokalemia.
    • Other potassium salts may be indicated if coexisting disorder is present: Potassium bicarbonate or bicarbonate precursor (gluconate, acetate, or citrate) in metabolic acidosis or phosphate in phosphate deficiency.
  • Emergent situations (serum potassium <2.5 mEq/L [<2.5 mmol/L], arrhythmias): IV replacement:
    • Rate of administration should not exceed 20 mEq/h (20 mmol/h); maximum recommended concentration, 60 mEq/L (60 mmol/L) of saline for peripheral administration. Administration through central venous lines may allow for greater concentrations.
  • Check serum magnesium and replace if needed; cannot adequately replace potassium in setting of low magnesium.
  • Precautions:
    • Any form of potassium replacement carries risk of hyperkalemia.
    • Serum potassium should be checked more frequently in groups at higher risk: Elderly, diabetic patients, and patients with renal insufficiency.
    • Patients receiving digitalis and patients with diabetic ketoacidosis in whom intracellular shift in potassium is expected after insulin therapy is initiated must have more aggressive replacement.
  • Significant possible interactions: Concomitant administration of potassium-sparing diuretics (spironolactone, triamterene, amiloride, angiotensin-converting enzyme [ACE] inhibitors) magnifies risk of hyperkalemia.

Additional Treatment

General Measures

  • For asymptomatic patients treated with oral replacement, outpatient follow-up is sufficient.
  • Patients with cardiac manifestations require intravenous replacement with cardiac monitoring in an intensive care setting.

Geriatric Considerations

May need to correct magnesium depletion

Ongoing Care

Follow-Up Recommendations

Patient Monitoring

  • Patients receiving IV therapy should have cardiac monitoring and serum potassium level checked frequently (q4–6h).
  • Patients requiring potassium supplements should have serum potassium studied at intervals dictated by clinical judgment and patient compliance.


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Mild hypokalemia (potassium 3.0–3.5 mEq/L [3.0–3.5 mmol/L]) not caused by gastrointestinal (GI) losses: Dietary supplementation may be sufficient; potassium-rich foods include oranges, bananas, cantaloupes, prunes, raisins, dried beans, dried apricots, and squash.

Patient Education

  • Instructions for diet
  • If potassium supplementation necessary, stress need for compliance


  • Associated with higher morbidity and mortality due to cardiac arrhythmias
  • Ease of correction of hypokalemia and need for prolonged treatment rests on primary cause; if it can be eliminated (e.g., resolution of diarrhea, discontinuation of diuretics, removal of adrenal tumor), hypokalemia can be expected to resolve and no further treatment is indicated.


  • Hyperkalemia can occur in the course of treatment (2).
  • Increased risk of digoxin toxicity (1)[A]


1. Schaefer TJ, Wolford RW. Disorders of potassium. Emerg Med Clin North Am. 2005;23:723–47, viii–ix.

2. Crop MJ, Hoorn EJ, Lindemans J, et al. Hypokalaemia and subsequent hyperkalaemia in hospitalized patients. Nephrol Dial Transplant. 2007.

3. Miller KK, Grinspoon SK, Ciampa J, et al. Medical findings in outpatients with anorexia nervosa. Arch Intern Med. 2005;165:561–6.

4. Peter SA. Electrolyte disorders and renal dysfunction in acquired immunodeficiency syndrome patients. J Natl Med Assoc. 1991;83:889–91.

5. Cirino CM, Kan VL. Hypokalemia in HIV patients on tenofovir. AIDS. 2006;20:1671–3.

6. Ben Salem C, Hmouda H, Bouraoui K. Drug-Induced Hypokalaemia. Curr Drug Saf. 2009;4:55–61.

7. Ernst ME, Moser M et al. Use of diuretics in patients with hypertension. N Engl J Med. 2009;361:2153–64.

8. Cowtan T et al. Thiazide diuretics. N Engl J Med. 2010;362:659; author reply 660.

9. Webster A, Brady W, Morris F. Recognising signs of danger: ECG changes resulting from an abnormal serum potassium concentration. Emerg Med J. 2002;19:74–7.

10. Barahona MJ, Vinagre I, Sojo L, et al. Thyrotoxic Periodic Paralysis: A Case Report and Literature Review. Clin Med Res. 2009.

Additional Reading

Chan KE, Lazarus JM, Hakim RM et al. Digoxin Associates with Mortality in ESRD. Journal of the American Society of Nephrology: JASN. 2010

12. Facchini M, Sala L, Malfatto G, et al. Low-K+ dependent QT prolongation and risk for ventricular arrhythmia in anorexia nervosa. Int J Cardiol. 2006;106:170–6.

13. Fisher M. Treatment of eating disorders in children, adolescents, and young adults. Pediatr Rev. 2006;27:5–16.

14. Gennari FJ. Disorders of potassium homeostasis. Hypokalemia and hyperkalemia. Crit Care Clin. 2002;18:273–88, vi.

15. Jones E. Hypokalemia. N Engl J Med. 2004;350:1156.

16. Osadchii OE et al. Mechanisms of hypokalemia-induced ventricular arrhythmogenicity. Fundamental & clinical pharmacology. 2010

17. Vacca V. Hypokalemia. Nursing. 2009;39:64.

18. Zietse R, Zoutendijk R, Hoorn EJ. Fluid, electrolyte and acid-base disorders associated with antibiotic therapy. Nat Rev Nephrol. 2009;5:193–202.

See Also (Topic, Algorithm, Electronic Media Element)


Algorithm: Hypokalemia



276.8 Hypopotassemia


43339004 Hypokalemia (disorder)

Clinical Pearls

  • In patients without heart disease, a low potassium level will rarely cause cardiac disturbances. In an otherwise healthy patient, gentle repletion using oral potassium or an increase in potassium-rich foods should be adequate.
  • In patients with cardiac ischemia, heart failure, or left ventricular hypertrophy, even mild-to-moderate hypokalemia can cause arrhythmias. These patients should receive potassium repletion as well as cardiac monitoring.
  • To safely prevent hypokalemia in diabetic and renal insufficiency patients, the safest way is to ensure adequate dietary potassium intake with foods rich in potassium, including spinach, tomatoes, broccoli, squash, potatoes, bananas, cantaloupe, and oranges. Avoid potassium-sparing diuretics, if possible.
  • Uncorrected hypomagnesemia can hinder the correction of hypokalemia. Check magnesium levels and replete as nec

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