About 60% of adult body weight is water: two-thirds is intracellular fluid (ICF) and one-third is extracellular fluid (ECF) (plasma plus interstitial fluid). Water moves toward the compartment with the higher solute concentration (osmolality). Balance is kept by thirst, antidiuretic hormone (ADH), which makes the kidney retain water, aldosterone, which retains sodium and excretes potassium, and natriuretic peptides.

Key mechanisms tested

• Sodium controls water movement. Low serum sodium (hypotonic plasma) pulls water into brain cells → cerebral edema; high sodium pulls water out of cells → cell shrinkage.
• Potassium, calcium, and magnesium control nerve and muscle excitability, so their imbalances show up as muscle and heart rhythm changes.
• Third spacing: fluid shifts from the vessels into the interstitial space. In major burns, the first 24–48 hours bring a plasma-to-interstitial shift (edema, hypovolemia, hyperkalemia from cell destruction). As capillaries recover (roughly after 48–72 hours), fluid returns to the vessels → diuresis, hypokalemia, and risk of fluid overload.

Common clinical patterns

IV solutions

Fluid volume

Older adults have a blunted thirst response and are at high risk of dehydration; skin turgor is unreliable in them — check mucosa, mental status, and weight.

Electrolyte imbalances at a glance

Ranges vary slightly by laboratory.

• Low albumin lowers total calcium without changing ionized calcium. Corrected calcium ≈ measured calcium + 0.8 × (4.0 − albumin in g/dL); in SI units, corrected calcium (mmol/L) ≈ measured + 0.02 × (40 − albumin in g/L). Ionized calcium is more reliable.
• A hemolyzed sample falsely raises potassium. For an unexpected high value, get a 12-lead ECG at once while the repeat sample is sent; if the ECG shows hyperkalemic changes, treat without waiting.
• Continuous ECG for significant potassium, calcium, or magnesium abnormalities.
• Urine sodium and osmolality help separate SIADH from volume loss.

Sodium

• Hypovolemic hyponatremia (vomiting, diarrhea): 0.9% NaCl. Euvolemic (SIADH) or hypervolemic (heart failure, cirrhosis): fluid restriction and treat the cause.
• Severe symptoms (seizures, coma): small boluses of 3% saline (commonly 100–150 mL) per protocol to stop symptoms.
• Correct slowly. Limit the rise to no more than 8–10 mEq/L in 24 hours, and 8 mEq/L or less in high-risk clients (alcohol use disorder, malnutrition, hypokalemia, liver disease, sodium ≤ 105 mEq/L). Overcorrection causes osmotic demyelination syndrome (dysarthria, dysphagia, paralysis, days later). If sodium rises too fast, notify at once — the provider may give D5W or desmopressin to lower it again. Potassium replacement also raises sodium.
• Tolvaptan (a vasopressin antagonist) for selected hyponatremia: start in hospital, avoid fluid restriction in the first 24 hours, monitor sodium closely for overcorrection; risk of liver injury, so use is time-limited.
• Hypernatremia: replace free water (oral water, D5W, or 0.45% NaCl) gradually — in chronic hypernatremia, lower sodium by no more than about 10 mEq/L (mmol/L) in 24 hours (about 0.5 mEq/L per hour); faster lowering causes cerebral edema.

Potassium

• Hypokalemia: oral replacement when possible (take with food and fluid to reduce GI irritation). IV potassium is always diluted, given by infusion pump, never IV push or IM. A common maximum is 10 mEq/h via a peripheral line (peripheral concentration commonly ≤ 40 mEq/L); higher rates (usually ≤ 20 mEq/h) only via a central line with continuous ECG, per protocol. Use premixed bags and never add potassium to a hanging IV bag. Confirm adequate urine output first. Correct low magnesium, or hypokalemia will not resolve.
• Hyperkalemia (emergency sequence):
  1. Stabilize the heart: IV calcium gluconate when ECG changes are present
  2. Shift potassium into cells: IV regular insulin with dextrose (check glucose hourly — hypoglycemia risk); inhaled albuterol; sodium bicarbonate only if metabolic acidosis is present
  3. Remove potassium: potassium binders (sodium zirconium cyclosilicate, patiromer; sodium polystyrene sulfonate is less favored because of rare intestinal necrosis), loop diuretics if kidneys respond, hemodialysis if severe or kidneys fail
• Review drugs that raise potassium: ACE inhibitors, ARBs, spironolactone, potassium supplements, salt substitutes, trimethoprim.

Calcium

• Hypocalcemia: IV calcium gluconate for tetany (calcium chloride is a vesicant — central line preferred). Give slowly with ECG monitoring; calcium increases digoxin toxicity risk. Never mix calcium with bicarbonate or phosphate in the same line.
• Hypercalcemia: IV 0.9% NaCl to restore volume and increase calcium excretion; calcitonin for rapid short-term effect; bisphosphonates (zoledronic acid — check kidney function, dental risk of jaw osteonecrosis) or denosumab (can cause hypocalcemia); treat the cause (hyperparathyroidism, malignancy). Loop diuretics only after volume is restored.

Magnesium

• Hypomagnesemia: IV magnesium sulfate by pump; check deep tendon reflexes, respiratory rate, and urine output during infusion; watch for flushing and hypotension — rapid infusion can cause cardiac arrest.
• Hypermagnesemia: stop magnesium sources (antacids, laxatives, infusions); IV calcium gluconate is the antagonist; dialysis if kidneys fail.

Phosphate

• Hypophosphatemia: replace orally or IV (IV potassium phosphate also counts toward potassium limits); start nutrition slowly in malnourished clients to prevent refeeding syndrome (phosphate, potassium, and magnesium fall as glucose drives them into cells).
• Hyperphosphatemia (CKD): dietary phosphate restriction and phosphate binders with meals — calcium acetate (monitor for hypercalcemia), sevelamer, lanthanum. Avoid long-term aluminum- or magnesium-containing binders in kidney failure.

Listed in priority order.

1. Airway, breathing, and cardiac rhythm
   • Continuous ECG for serious potassium, calcium, or magnesium changes; keep emergency equipment ready
   • Hypocalcemia: watch for laryngeal stridor. Hypermagnesemia and severe hypokalemia: watch for respiratory depression or weakness
   • Volume excess: upright position, oxygen as ordered, prepare diuretics
2. Neurologic safety
   • Sodium and calcium imbalances: seizure precautions, frequent neuro checks, orient the confused client
   • Monitor sodium every few hours during active correction; report a rise faster than ordered
3. Circulation and fluid balance
   • Volume deficit: IV access, isotonic fluids as ordered, orthostatic vital signs, fall precautions
   • Daily weight (same time, scale, clothing), strict intake and output, urine output at least 0.5 mL/kg/h
4. IV and medication safety
   • Potassium: pump, dilution, site checks (it burns and irritates veins; stop the infusion if infiltration occurs)
   • Double-check high-alert infusions (hypertonic saline, concentrated potassium, insulin)
5. Diet and comfort — encourage or restrict fluids, sodium, and potassium as ordered; oral care for dry mucosa

• Weigh daily when on diuretics or with heart or kidney disease; report rapid gain or loss
• Potassium-rich foods: bananas, oranges, potatoes, tomatoes, dried fruit, beans, leafy greens — increase with diuretic-related hypokalemia, limit in CKD
• Salt substitutes contain potassium — avoid with CKD or potassium-sparing drugs unless prescribed
• Calcium sources: dairy, small fish with bones, fortified foods; take vitamin D as advised
• Replace fluids early during vomiting, diarrhea, or heat exposure; oral rehydration solution is better than plain water or soft drinks
• Do not overuse magnesium-containing antacids or laxatives, especially with kidney disease
• Report muscle weakness, palpitations, cramps, numbness around the mouth, or confusion

• Daily weight is the best indicator of fluid status: 1 kg ≈ 1 L
• Hyponatremia → cerebral edema; correct no faster than 8–10 mEq/L per 24 h (≤ 8 in high-risk clients)
• IV potassium: never IV push, pump only, confirm urine output; common peripheral maximum 10 mEq/h
• Hypokalemia → weakness, U wave; hyperkalemia → peaked T, cardiac arrest
• Hyperkalemia order: calcium gluconate → insulin + dextrose → remove potassium
• Hypocalcemia → Chvostek, Trousseau, tetany, laryngospasm; hypercalcemia → constipation, stones, polyuria
• Hypomagnesemia → hyperreflexia; hypermagnesemia → loss of DTRs, respiratory depression
• Vomiting/NG suction → hypokalemic metabolic alkalosis; diarrhea → metabolic acidosis
• Addison disease → low sodium, high potassium; hyperparathyroidism → high calcium, low phosphate
• Burns: early plasma shift + hyperkalemia; later fluid remobilization, diuresis, hypokalemia
• Hypotonic fluids are avoided in increased intracranial pressure