Electrolytes: sodium, potassium, calcium, magnesium, phosphate

Learn each ion the same way: what it does, then low vs high, then causes and treatment. When that map is solid, NCLEX items become pattern recognition.

The ions that carry most of the exam

Volume asks how much water is in the tank. Electrolytes ask which charged particle is putting the brain, heart, airway, or reflexes at risk right now. Phosphate rides with calcium and with feeding: miss it and the stem looks like a calcium or respiratory item.

Sodium (Na+) - brain water

Sodium is the main extracellular cation. It holds water outside cells and sets serum osmolarity. Low relative sodium → water into brain cells. High relative sodium → cells shrink. Sodium items are almost always neurologic first. Adult serum range is near 135–145 mEq/L - treat the picture and the rate of change, not a lone digit.

Hyponatremia

Causes: SIADH, excess free water / hypotonic IV fluids, thiazides, HF/cirrhosis/CKD dilution, GI losses with hypotonic replacement.

• Mild euvolemic SIADH pattern: fluid restriction first-line.
• Hypovolemic: restore volume with isotonic saline as ordered.
• Seizures / deep neuro change: controlled 3% saline in a monitored setting.
• Correct slowly - fast jumps risk osmotic demyelination.

Hypernatremia

Causes: inadequate free water, fever/tachypnea/burns, diabetes insipidus, osmotic losses, hypertonic saline or bicarb loads.

• Restore free water gradually (oral or hypotonic IV as ordered).
• Treat the driver (e.g. DI pathway when that is the diagnosis).
• Question more hypertonic saline when water deficit is already the problem.
• Correct gradually to avoid cerebral edema from an overly fast drop.

Potassium (K+) - heart

Potassium is the main intracellular cation; serum levels set cardiac and muscle resting potential. Items are cardiac and muscle first. Range near 3.5–5.0 mEq/L. Never IV push potassium.

Hypokalemia

Causes: loop/thiazide diuretics, vomiting/NG/diarrhea, shift into cells (insulin, alkalosis, beta-agonists), poor intake, low Mg (K will not hold).

• Monitor cardiac rhythm when low or symptomatic.
• Replace orally when possible; controlled IV infusion when needed.
• Never IV push K+. Check and replace magnesium if low.
• IV potassium runs on a pump at facility rate limits (often no faster than about 10 mEq/hr on general units unless a monitored higher-rate protocol exists) - never “catch up” a missed bag by bolusing.

Hyperkalemia

Causes: kidney failure, ACE/ARB / K-sparing diuretics, acidosis or cell lysis, excess replacement.

1. ECG changes: IV calcium first to stabilize membranes.
2. Shift into cells: insulin + glucose (and selected other shifts).
3. Remove: binders, diuretics if kidneys work, or dialysis.
4. Stop K intake and review drugs that raise potassium.

Calcium (Ca2+) - excite vs sedate

Calcium stabilizes nerve membranes, couples muscle contraction, supports clotting, and builds bone. Low → nerves fire too easily. High → nerves and muscles quiet. Total serum near 8.5–10.5 mg/dL; interpret with albumin and the clinical picture.

Hypocalcemia

Causes: hypoparathyroidism / neck surgery, CKD, vitamin D deficiency, pancreatitis, massive transfusion, severe low Mg.

• Airway readiness and tetany/seizure precautions (laryngospasm risk).
• Replace calcium; fix Mg / vitamin D / CKD driver so it holds.
• After neck surgery, new tingling or stridor is a now problem.
• Chvostek (facial twitch after tap) and Trousseau (carpal spasm with BP cuff) support hypocalcemia when stems name them - still treat the airway picture first.

Calcium and phosphorus often move as a pair in opposite directions in CKD and parathyroid disease. A high phosphate with low calcium fits that map - treat the clinical priority (tetany/airway or the ordered binders/replacement) rather than chasing one number in isolation.

Hypercalcemia

Causes: hyperparathyroidism, malignancy, vitamin D excess, thiazides/lithium, prolonged immobilization.

• IV hydration as ordered to restore volume and promote excretion.
• Stop contributors (thiazides, excess Ca/D) when appropriate.
• Fall precautions while weak or lethargic; treat the driver.

Magnesium (Mg2+) - reflexes / breathing

Magnesium calms neuromuscular transmission and supports enzymes that move potassium into cells. Too little → irritable. Too much → reflexes and breathing flatten. Serum near 1.5–2.5 mg/dL. Obstetric infusions make toxicity a favorite exam scenario.

Hypomagnesemia

Causes: alcohol use / malnutrition, diarrhea and other GI losses, loop/thiazide diuretics, refeeding.

• Replace Mg; monitor rhythm when low or replacing IV.
• If potassium will not correct, check magnesium.
• Seizure precautions when neuromuscular irritability is high.

Hypermagnesemia / toxicity

Causes: Mg infusions (preeclampsia protocols), Mg antacids/laxatives in kidney failure, impaired renal excretion.

1. Stop the magnesium infusion / source immediately.
2. Support airway and breathing.
3. Give calcium gluconate as the antidote.
4. Promote excretion or dialysis when needed.

Phosphate (PO4) - energy and the calcium pair

Phosphate is the ATP and bone ion that exams hide inside CKD, tumor lysis, and refeeding stems. Serum orientation is often about 2.5–4.5 mg/dL. It usually moves opposite calcium: when phosphate climbs, ionized calcium falls and nerves get twitchy. When phosphate crashes, muscles (including the diaphragm) lose fuel.

Hypophosphatemia

Causes: refeeding (insulin drives phosphate into cells as calories restart), alcohol use and malnutrition, phosphate-binding antacids, respiratory alkalosis, and insulin therapy. The mechanism trap is treating the calorie plan as finished work while the diaphragm is starving for phosphate. New dyspnea, extra effort, or failing tidal volumes during refeeding is a chemistry problem until proven otherwise, not “anxiety about eating.”

• Replace phosphate as ordered; cardiac and respiratory monitoring when severely low.
• Watch potassium and magnesium at the same time; refeeding drops the cluster.
• Do not “catch up” with an unmonitored large IV load; follow the ordered rate.

Hyperphosphatemia

Causes: failed renal excretion (CKD), cell burst (tumor lysis, rhabdomyolysis), and phosphate enemas or laxatives when kidneys cannot clear the load. High phosphate binds calcium. The bedside picture can look like hypocalcemia: tingling, Chvostek or Trousseau signs, laryngospasm risk. Binders only work if they meet food in the gut, so calcium acetate and similar binders go with meals, not on an empty-stomach “vitamin schedule.” Full CKD binder and dialysis teaching lives in Renal and urinary care. Tumor-lysis potassium still outranks phosphate when the ECG is changing; see Oncology care.

• Give phosphate binders with meals so they capture dietary phosphate.
• Protect the airway and treat tetany if calcium has fallen.
• Stop phosphate enemas and cola-heavy intake in advanced CKD teaching.

Cross-cutting rules that win items

Pairs that travel together

• Low magnesium often keeps potassium (and sometimes calcium) low until Mg is replaced.
• Acidosis tends to raise serum potassium; alkalosis tends to lower it (shifts).
• After thyroid/parathyroid surgery, new tingling is hypocalcemia until proven otherwise.
• Phosphate and calcium often move opposite in CKD and parathyroid disease; treat tetany or binders-with-meals, not one number in isolation.
• SIADH: too much ADH → water retained → dilute low Na (often euvolemic) → fluid restriction first-line when mild.
• Diabetes insipidus: too little ADH effect → water loss → high Na and big dilute urine → replace free water and treat the DI pathway.

How to reason under time pressure

1. Name the ion.
2. Name the organ at risk (brain, heart, airway, reflexes).
3. Decide low vs high from the stem cues.
4. Pick the first protective action, then the definitive fix.