Guide — Electrolytes
Electrolyte Disorders: Clinical Overview
Comprehensive review of the five major electrolyte disorders — sodium, potassium, calcium, magnesium, and phosphate — covering causes, clinical manifestations, treatment approaches, and nursing priorities for bedside practice and NCLEX.
14 min read · Electrolytes
Educational use only. Laboratory reference ranges and treatment thresholds vary by institution. Always follow facility protocols and provider orders. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
Overview
Electrolytes are electrically charged minerals dissolved in body fluids. They maintain fluid balance, acid-base balance, nerve conduction, and muscle function. Imbalances frequently coexist — correcting one without addressing others can prevent recovery or worsen the clinical picture.
- Sodium governs water distribution between compartments — hypo/hypernatremia = water imbalance, not salt intake alone
- Potassium is the primary intracellular cation — small serum changes reflect large total-body shifts; ECG changes are the key safety concern
- Calcium is protein-bound — always correlate with albumin; ionized Ca is the functional fraction
- Magnesium is required to correct potassium and calcium — hypomagnesemia must be treated first
- Phosphate inversely correlates with calcium — renal failure is the most common cause of hyperphosphatemia
Sodium (Na⁺)
Normal: 135–145 mEq/L| Hyponatremia (< 135 mEq/L) | Hypernatremia (> 145 mEq/L) |
|---|---|
| Causes | |
| Excess free water (SIADH, psychogenic polydipsia), diuretics (thiazides), heart failure, cirrhosis, nephrotic syndrome, adrenal insufficiency | Inadequate water intake, diabetes insipidus, excessive sodium intake, excessive free water loss (fever, diarrhea, burns) |
| Signs & Symptoms | |
| Headache, nausea, confusion, seizures, coma (severe); neurological symptoms dominate | Thirst, dry mucous membranes, agitation, confusion, seizures, coma |
| Treatment | |
| Fluid restriction for SIADH; isotonic saline for volume depletion; 3% saline ONLY for severe symptomatic — correct ≤ 10–12 mEq/L per 24 hours to prevent osmotic demyelination syndrome | Identify and treat cause; free water replacement (oral or D5W IV); correct slowly — no faster than 10–12 mEq/L per 24 hours |
| Nursing Priorities | |
| Monitor neuro status hourly if severe; seizure precautions; restrict free water per orders; accurate I&O | Offer oral water frequently for conscious patients; seizure precautions; monitor mental status; accurate I&O |
Potassium (K⁺)
Normal: 3.5–5.0 mEq/L| Hypokalemia (< 3.5 mEq/L) | Hyperkalemia (> 5.0 mEq/L) |
|---|---|
| Causes | |
| Diuretics (loop, thiazide), vomiting, diarrhea, NG suction, poor oral intake, excess insulin, alkalosis, steroid use | Renal failure (most common), ACE inhibitors, potassium-sparing diuretics, metabolic acidosis, hemolysis, excessive supplementation, adrenal insufficiency |
| Signs & Symptoms | |
| Muscle weakness, cramps, fatigue, constipation, paralytic ileus; ECG: flat T waves, U waves, prolonged QT | Muscle weakness, paresthesias, bradycardia; ECG: peaked T waves → widened QRS → sine wave → VF |
| Treatment | |
| PO potassium chloride for mild–moderate; IV KCl for severe (never IV push — max 10 mEq/hr via peripheral, 40 mEq/hr via central with monitoring) | Calcium gluconate (stabilizes cardiac membrane — FIRST if ECG changes); insulin + dextrose (shifts K into cells); sodium bicarbonate; sodium polystyrene sulfonate or patiromer (eliminates K); dialysis for severe |
| Nursing Priorities | |
| Never give IV K⁺ undiluted; monitor ECG; assess for digitalis toxicity (hypokalemia potentiates digoxin); assess muscle strength | Continuous ECG monitoring; hold K-sparing agents; restrict dietary potassium; calcium gluconate ready at bedside |
Calcium (Ca²⁺)
Normal: 8.5–10.5 mg/dL (ionized: 4.6–5.1 mg/dL)| Hypocalcemia (< 8.5 mg/dL) | Hypercalcemia (> 10.5 mg/dL) |
|---|---|
| Causes | |
| Hypoparathyroidism (post-thyroidectomy or parathyroidectomy), vitamin D deficiency, pancreatitis, hypomagnesemia, alkalosis (ionized Ca decreases), massive blood transfusion (citrate) | Hyperparathyroidism (most common overall), malignancy (most common in hospitalized patients), immobility, thiazide diuretics, excess vitamin D, sarcoidosis |
| Signs & Symptoms | |
| Tetany, muscle cramps, Chvostek sign (facial twitch with facial nerve tap), Trousseau sign (carpal spasm with BP cuff inflation), perioral numbness, seizures, prolonged QT | Bones, stones, groans, and psychic moans — bone pain, kidney stones, constipation/nausea, depression/confusion; shortened QT |
| Treatment | |
| IV calcium gluconate (emergency); oral calcium carbonate + vitamin D for chronic; correct hypomagnesemia first | IV normal saline hydration; furosemide after hydration; bisphosphonates (pamidronate); calcitonin; dialysis for severe |
| Nursing Priorities | |
| Assess Chvostek and Trousseau signs; seizure precautions; monitor QT interval; have IV calcium gluconate available post-thyroid surgery | Encourage oral fluids; mobilize patient; monitor cardiac rhythm; strain urine for stones; assess mental status |
Magnesium (Mg²⁺)
Normal: 1.5–2.5 mEq/L| Hypomagnesemia (< 1.5 mEq/L) | Hypermagnesemia (> 2.5 mEq/L) |
|---|---|
| Causes | |
| Malnutrition, alcoholism, loop diuretics, prolonged NG suction, diarrhea, amphotericin B, cisplatin, PPIs (chronic use), diabetes | Renal failure (most common); excessive Mg supplementation; antacid/laxative overuse; eclampsia treatment (IV MgSO4) |
| Signs & Symptoms | |
| Tremors, muscle weakness, tetany, positive Trousseau/Chvostek, dysrhythmias, torsades de pointes; often coexists with hypokalemia and hypocalcemia (prevents correction) | Flushing, nausea, depressed reflexes (DTRs first to go), respiratory depression, cardiac arrest at very high levels |
| Treatment | |
| IV magnesium sulfate for severe; PO magnesium oxide for mild; must correct Mg before K and Ca will normalize | Calcium gluconate (antagonizes Mg — give if respiratory depression or cardiac instability); stop all Mg sources; dialysis for severe |
| Nursing Priorities | |
| Monitor DTRs (loss of knee-jerk = early Mg toxicity with IV infusion); have calcium gluconate at bedside; assess for coexisting hypo-K and hypo-Ca | Monitor DTRs every 1–2 hours during IV MgSO4 (absent patellar reflex = stop infusion); monitor RR (hold if < 12); calcium gluconate at bedside |
Phosphate (PO₄³⁻)
Normal: 2.5–4.5 mg/dL| Hypophosphatemia (< 2.5 mg/dL) | Hyperphosphatemia (> 4.5 mg/dL) |
|---|---|
| Causes | |
| Malnutrition and refeeding syndrome (insulin drives P into cells), antacid use (phosphate binders), alcoholism, DKA treatment, hyperparathyroidism | Renal failure (most common — kidney cannot excrete P), excess vitamin D, hypoparathyroidism, excessive phosphate intake |
| Signs & Symptoms | |
| Muscle weakness, fatigue, confusion, respiratory muscle weakness (risk of vent failure), hemolytic anemia, impaired WBC and platelet function | Often asymptomatic; hypocalcemia symptoms (calcium-phosphate reciprocal relationship); calcifications in soft tissue with chronic disease |
| Treatment | |
| PO or IV phosphate; treat the underlying cause; slow enteral feeding initiation in malnourished patients (refeeding protocol) | Phosphate binders with meals (calcium carbonate, sevelamer, lanthanum); dietary phosphate restriction; dialysis |
| Nursing Priorities | |
| Monitor respiratory status closely in ventilated patients; avoid antacid overuse; watch for refeeding syndrome in patients starting TPN | Administer phosphate binders WITH meals (not before or after); assess for signs of hypocalcemia; reinforce dietary restrictions |
NCLEX Pearls
K⁺ IV safety: Never give IV potassium as an IV push or bolus — always diluted, always with a pump, always with monitoring.
Mg²⁺ priority: Correct hypomagnesemia before expecting hypokalemia or hypocalcemia to respond to treatment.
Na⁺ correction rate: Correct sodium no faster than 10–12 mEq/L per 24 hours — too-rapid correction of hyponatremia causes osmotic demyelination syndrome (central pontine myelinolysis).
Ca²⁺ and albumin: Corrected calcium = measured Ca + (0.8 × [4 − albumin]). Low albumin falsely lowers serum calcium.
Hyperkalemia emergency: First drug = calcium gluconate (stabilizes cardiac membrane). Second = insulin + dextrose (shifts K intracellularly).
MgSO4 toxicity: Loss of patellar reflex (DTR) is the first sign — stop infusion immediately and notify provider.
Phosphate binders: Must be given WITH meals to bind dietary phosphate in the gut — not effective if given without food.
Related Resources
Standards & sources
Fact-checked Jun 20, 2026This page is written to align with Infusion Nurses Society (INS) Standards of Practice · Institute for Safe Medication Practices (ISMP) · Standard laboratory reference ranges. It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →