Physiology
Electrolyte Balance
Sodium, potassium, calcium, magnesium — the ions that run the body
Electrolytes are charged ions essential for nerve conduction, muscle contraction, fluid balance, and acid-base homeostasis. Sodium (135-145 mEq/L) drives extracellular volume; the kidney regulates via aldosterone and ADH. Potassium (3.5-5.0 mEq/L) sets resting membrane potential; 98% intracellular; aldosterone and insulin shift K. Calcium (8.5-10.5 mg/dL) is regulated by PTH, vitamin D, calcitonin; 99% in bone. Magnesium (1.7-2.2 mg/dL) is a cofactor for 300+ enzymes; deficiency causes refractory hypokalemia. Disturbances are common in hospitalized patients — diuretics, vomiting, diarrhea, kidney disease, endocrine disease, drugs. Severe disturbances cause arrhythmias, seizures, coma.
- Normal sodium135-145 mEq/L
- Normal potassium3.5-5.0 mEq/L
- Normal calcium8.5-10.5 mg/dL (ionized 4.5-5.3)
- Normal magnesium1.7-2.2 mg/dL
- Hyponatremia threshold<135 mEq/L; severe <120
- ECG hyperkalemiaPeaked T waves >5.5; widened QRS >6.5
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Why electrolytes matter
- Cardiac arrhythmias. K, Mg, Ca disturbances trigger torsades, VF, asystole.
- Altered mental status. Hyponatremia causes seizures and herniation if severe.
- Diuretic monitoring. Loops cause hypoK, hypoMg, hypoCa, hyponatremia.
- Endocrine disease. Aldosterone, PTH, ADH disorders manifest as electrolyte abnormalities.
- Critical care. Sepsis, DKA, AKI, refeeding require constant correction.
- Renal disease. CKD causes hyperK, hyperphosphatemia, hypoCa, acidosis.
- Drug toxicity. Digoxin toxicity worsened by hypoK, hypoMg, hyperCa.
Common errors
- Correcting sodium too fast. Central pontine myelinolysis if Na rises >8 mEq/L per 24 hours.
- Treating hypokalemia without checking magnesium. Refractory until Mg replaced.
- Calcium gluconate via peripheral line for hyperK code. Calcium chloride extravasation causes tissue necrosis — use central or gluconate peripherally.
- Ignoring pseudohyponatremia. Hyperglycemia, hyperlipidemia, hyperproteinemia mimic low Na.
- Stopping potassium when level normalizes. Total body deficit much larger than serum suggests.
- Aggressive bicarb for acidosis. Worsens intracellular acidosis and hypocalcemia; treat the cause.
Frequently asked questions
How is hyponatremia worked up?
First check serum osmolality. High (pseudohyponatremia) — hyperglycemia, mannitol; correct sodium up by 1.6 for every 100 glucose >100. Normal — pseudohyponatremia from hyperlipidemia or hyperproteinemia. Low (true) — assess volume. Hypovolemic (vomiting, diuretics) — saline. Euvolemic (SIADH, hypothyroid, adrenal insufficiency) — fluid restriction. Hypervolemic (heart failure, cirrhosis) — diuresis. Correct slowly — max 8 mEq/L per 24 hours to avoid central pontine myelinolysis.
How do you treat hyperkalemia?
First stabilize the heart — calcium gluconate 1 g IV over 2 minutes (or calcium chloride via central line). Then shift K into cells — insulin 10 units IV with 25 g dextrose, beta-2 agonist albuterol 10-20 mg nebulized, sodium bicarbonate 50 mEq if acidotic. Then remove K — loop diuretic, sodium polystyrene or patiromer or sodium zirconium, dialysis if severe or refractory. Monitor ECG continuously.
What causes hypokalemia?
GI losses (diarrhea, vomiting — actually causes alkalosis driving K into cells), renal losses (diuretics, hyperaldosteronism, Bartter, Gitelman, type 1 RTA, Liddle), transcellular shift (insulin, beta-2 agonists, alkalosis, hypothermia, refeeding), inadequate intake. Treat — oral KCl 40-80 mEq/day for mild; IV 10 mEq/hr peripheral, 20 mEq/hr central with monitoring. Replace magnesium concurrently — hypokalemia is refractory without it.
How does calcium homeostasis work?
PTH rises when ionized Ca falls. PTH increases renal Ca reabsorption, activates 1-alpha-hydroxylase to make calcitriol (active vitamin D), which boosts gut Ca absorption. PTH also pulls Ca from bone via osteoclasts. Calcitonin from thyroid C-cells lowers Ca but minor in adults. Hypercalcemia causes — primary hyperparathyroidism, malignancy (PTHrP, bone mets, multiple myeloma), vitamin D toxicity, granulomatous disease, immobilization. Treat with IV saline, calcitonin, bisphosphonates.
Why is magnesium so important?
Cofactor for ATP, sodium-potassium ATPase, many enzymes. Hypomagnesemia (<1.7) causes hypokalemia and hypocalcemia (suppresses PTH release and end-organ response), refractory arrhythmias, torsades de pointes. Causes — diuretics, alcoholism, diarrhea, PPIs, refeeding, aminoglycosides, cisplatin. Treat — magnesium sulfate 2 g IV over 1 hour for severe. Always replace Mg before treating refractory K and Ca.
What is SIADH?
Syndrome of inappropriate ADH — unsuppressed ADH despite low osmolality. Euvolemic hyponatremia, urine osm >100 (inappropriately concentrated), urine Na >40. Causes — small cell lung cancer, CNS pathology, drugs (SSRIs, carbamazepine, ecstasy, oxytocin), pulmonary disease (pneumonia, TB), HIV. Treat — fluid restriction <1 L/day, salt tablets, loop diuretic, vaptans (tolvaptan blocks V2 receptor) for refractory. Treat underlying cause.
What about acid-base?
pH 7.35-7.45, HCO3 22-26, PaCO2 35-45. Anion gap = Na − (Cl + HCO3); normal 8-12. High anion gap acidosis (MUDPILES) — methanol, uremia, DKA, paraldehyde/propylene glycol, INH/iron, lactic acidosis, ethylene glycol, salicylates. Normal gap acidosis — diarrhea, RTA, carbonic anhydrase inhibitors. Metabolic alkalosis from vomiting (loss of HCl), diuretics. Respiratory acidosis from hypoventilation; alkalosis from hyperventilation.