What it is:Five overlapping systems (sodium/water, calcium, phosphorus, potassium, magnesium) that the body keeps inside tight ranges using a handful of hormones and the kidney. This chapter is really five mini-topics stapled together, and every single one follows the same pattern: define it, figure out why it happened, decide if it's an emergency, then correct it at a safe speed.
The core problem:Two ideas explain almost everything here. First, "where sodium goes, water follows": water moves passively across membranes to chase osmotic gradients, so a sodium problem is nearly always a water problem in disguise. Second, fast correction is often more dangerous than the abnormality itself.Overcorrect sodium and you risk osmotic demyelination. Overcorrect calcium or potassium and you can cause the exact arrhythmia you were trying to prevent.
What you do about it:Match the urgency of your fix to the acuity of the problem. Symptomatic and acute means IV correction now, with frequent rechecks. Asymptomatic and chronic means oral repletion, find the cause, and don't rush it.
Almost every electrolyte on this page has a partner it travels with. Hypomagnesemia causes refractory hypokalemia and hypocalcemiathat won't correct until you replace the magnesium first. Loop and thiazide diuretics dump potassium andmagnesium together. When one electrolyte won't budge with straightforward replacement, check the other two before you assume treatment failure.
Memorize this table cold. Every treatment decision below hinges on where the patient's number sits relative to these lines.
| Electrolyte | Normal range | Abnormal cutoff | Critical / severe |
|---|---|---|---|
| Sodium | 135–145 mEq/L | Hypo <135 · Hyper >145 | Hypo <125 · Hyper >155 |
| Potassium | 3.5–5 mEq/L | Hypo <3.5 · Hyper >5 | Hypo <2.5–3 · Hyper >6 |
| Calcium (total) | 8.5–10.5 mg/dL | Hyper >10.2 · Hypo <8.6 | Crisis >15 mg/dL |
| Phosphorus | 2.5–4.5 mg/dL | Hyper >4.5 · Hypo <2.7 | Severe hypo <1.5 |
| Magnesium | 1.7–2.2 mg/dL | Hypo <1.4 mEq/L (<1.7 mg/dL) · Hyper >2 mEq/L (>2.4 mg/dL) | Symptoms rare below 4 mEq/L |
Corrected calcium = [(4 − albumin) × 0.8] + measured total calcium.Low albumin makes total calcium look falsely low because roughly 40–50% of calcium travels bound to albumin. Every 1 g/dL drop in albumin below 4 g/dL drags the reported total calcium down by about 0.8 mg/dL even though the physiologically active ionizedcalcium hasn't changed. If a hypoalbuminemic patient looks hypocalcemic, correct the number before you treat.
Skip memorizing each disorder as an island. Learn this once and the rest of the chapter is just plugging different variables into the same machine.
Total body water is 45–80% of body weight (varies by sex, age, and disease), split roughly two-thirds intracellular (ICF) and one-third extracellular (ECF). Sodium and potassium are "effective osmoles": they can't cross cell membranes freely, so they're what actually determines which way water moves. Add isotonic fluid and nothing shifts between compartments. Add hypertonic fluid (3% NaCl) and water gets pulled outof cells into the ECF. Add hypotonic fluid and water pushes intocells.
| IV fluid | Tonicity | % to ECF / ICF | Free water delivered |
|---|---|---|---|
| D5W | Hypotonic (dextrose metabolized off) | 33 / 67 | 1000 mL free water per liter |
| 0.45% NaCl (half normal) | Hypotonic | 67 / 33 | 500 mL/L |
| 0.9% NaCl (normal saline) | Isotonic | 100 / 0 | 0 mL/L |
| Lactated Ringer's | Isotonic | 97 / 3 | 0 mL/L |
| Plasma-Lyte / Normosol-R | Isotonic | 100 / 0 | 0 mL/L |
| 3% NaCl | Hypertonic | 100 / 0 | Pulls ~2331 mL water outof cells per liter given |
Dehydrationis loss of total body water producing hypertonicity (this is what causes hypernatremia). Hypovolemiais a symptomatic deficit of ECF volume, which can happen with a normal, high, orlow serum sodium. Students use these words interchangeably and they are not the same thing.
Almost every abnormality in this chapter traces back to one of four regulatory systems misbehaving.
Controls free water excretion. Nonosmotic release (triggered by low effective circulating volume, not just true osmolality) is the engine behind most hyponatremia.
Retains Na+ and water, dumps K+ and Mg2+. Explains why RAAS blockers raise potassium and diuretics that block aldosterone spare it.
PTH pulls calcium from bone and kidney, dumps phosphate; vitamin D pulls both calcium and phosphate in from the gut. This is why calcium and phosphorus almost always move in opposite directions.
Both shove potassium into cells without changing total body stores. This is the entire basis of emergency hyperkalemia treatment.
Diuretics act at specific points along the nephron, and knowing the map explains their electrolyte side effects instead of forcing you to memorize them. Proximal tubule: carbonic anhydrase inhibitors, osmotic diuretics (mannitol). Thick ascending loop of Henle: loop diuretics block NKCC2, the transporter responsible for 20–25% of sodium reabsorption, which is why they're the most potent class and why they dump potassium, magnesium, and calcium. Distal convoluted tubule: thiazides, which lose less potassium than loops but actively retaincalcium (useful in idiopathic hypercalciuria, a classic exam trap). Collecting duct: potassium-sparing diuretics (amiloride, triamterene block ENaC directly) and aldosterone antagonists (spironolactone, eplerenone, finerenone competitively block the mineralocorticoid receptor). Sequential nephron blockade, stacking a loop with a thiazide like metolazone, works because you're hitting two different segments the nephron can't compensate around at once.
Hyponatremia means an excess of extracellular water relative to sodium, from impaired water excretion. The trigger is almost always nonosmotic AVP release: the body senses low effective circulating volume (true hypovolemia, or a "empty-feeling" circulation as in heart failure, cirrhosis, or nephrotic syndrome) and holds onto free water even though the sodium concentration is already low. SIADH does the same thing without a volume trigger, driven by cancers, CNS disease, lung disease, or drugs.
| Step | Category | Clue |
|---|---|---|
| 1. Osmolality | Isotonic | Pseudohyponatremia (severe hyperlipidemia/paraproteinemia) |
| Hypertonic | Hyperglycemia, mannitol pulling water out of cells | |
| Hypotonic (most common) | Go to step 2 | |
| 2. Volume status | Hypovolemic | Lost more sodium than water: diarrhea, sweating, diuretics. Signs of volume depletion present. |
| Euvolemic | Normal or slightly low ECF sodium, high TBW. Usually SIADH. | |
| Hypervolemic | Impaired renal Na/water excretion: HF, cirrhosis, kidney failure. Total body Na is up but relatively less than water. |
Clinical presentation:Most patients are completely asymptomatic. Symptoms track with how severe and how fastthe drop happened, not the absolute number alone: nausea and malaise progress to headache and lethargy, and severe or rapid drops can produce seizures, coma, and death. Hypovolemic patients add orthostatic hypotension, tachycardia, dry mucous membranes, and decreased skin turgor on top of the neuro symptoms.
Correcting serum sodium too fast causes an acute drop in brain cell volume and can trigger osmotic demyelination syndrome (ODS), permanent and severe. This is why acute symptomatic hyponatremia is treated to relief of symptoms, not to a normal number. A roughly 5% rise in serum sodium is often enough to resolve severe symptoms; some clinicians target an initial serum sodium around 120 mEq/L rather than racing to 140.
Treatment, acute/severely symptomatic (regardless of volume status):3% NaCl until symptoms resolve.
Treatment, nonemergent (chronic, mild-moderate):For SIADH, water-restrict to roughly 1000–1200 mL/day and fix the underlying cause; stop any contributing medication. If the patient can't tolerate that much restriction, add NaCl tablets plus a loop diuretic, or demeclocycline 300 mg PO two to four times daily (onset takes 3–6 days). Vaptans (tolvaptan 15 mg PO daily; conivaptan IV only) are options for euvolemic or hypervolemic hypotonic hyponatremia when water restriction alone isn't enough.
Vaptans cause dramatic, sometimes unpredictable free water excretion. Do not fluid-restrict during the first 24–48 hoursof starting one, or you can drive the sodium up too fast and trigger the exact ODS you're trying to avoid. Tolvaptan's label also warns against use beyond 30 days in chronic liver disease. Read the product labeling before you start one; this is a drug where the details actually change what you do.
Almost always a free water problem: insensible losses (skin, lungs), hypotonic GI losses, heat exposure, diabetes insipidus (a pure water diuresis), or iatrogenic sodium overload from hypertonic saline or concentrated IV/enteral formulas. Rising sodium pulls water out of brain cells, so symptoms are neurologic: weakness, lethargy, restlessness, irritability, twitching, confusion, and, if it develops fast, seizures, coma, and death.
Correct at approximately 1 mEq/L per hour if it developed in under 48 hours, and 0.5 mEq/L per hour if it developed more slowly(or is chronic/unknown duration). Same principle as hyponatremia in reverse: cells have adapted to the current tonicity, and moving too fast in either direction causes cerebral injury.
Treatment:Start hypovolemic hypernatremia with 0.9% NaCl to restore hemodynamic stability first. Once volume is repleted, switch to replacing the free-water deficit with D5W, 0.45% NaCl, or another hypotonic fluid. For sodium overload(iatrogenic), give loop diuretics (furosemide 20–40 mg IV q6h) plus D5W at an appropriate rate to get rid of the excess sodium while replacing free water.
Central DI(no ADH being made) is treated with intranasal desmopressin, starting at 5–10 mcg once or twice daily, titrated up to a max of 40 mcg every 8 hours. Oral tablets exist but have poor bioavailability, so switching dosage forms gives an unpredictable response, watch closely if you switch a patient's formulation.
Nephrogenic DI(kidney doesn't respond to ADH) is treated paradoxically with a thiazide diureticplus dietary sodium restriction (2000 mg/day), which can cut urine volume by up to 50%. The mechanism: mild volume contraction from the thiazide increases proximal sodium and water reabsorption, which passively reduces the amount of water delivered to the collecting duct for the kidney to fail to concentrate.
| Drug | Indication | Dose |
|---|---|---|
| Desmopressin | Central & nephrogenic | IN 5–20 mcg q12–24h · PO 0.05–0.8 mg divided (max 1.2 mg/day) |
| Hydrochlorothiazide | Central & nephrogenic | 25 mg PO q12–24h |
| Amiloride | Nephrogenic | 5–10 mg PO daily |
| Indomethacin | Central & nephrogenic | 50 mg PO q8–12h |
| Chlorpropamide / carbamazepine | Central | 125–250 mg daily / 100–300 mg BID |
Lithium-induced nephrogenic DI is the classic exam scenario for amiloride, since amiloride blocks the ENaC channel lithium uses to enter collecting duct cells in the first place.
Edema is a clinically detectable rise in interstitial fluid, from primary renal sodium retention or from the kidneys retaining sodium in response to a perceived drop in effective circulating volume, even when total ECF volume is already normal or high. Usual suspects are heart, kidney, or liver failure, alone or combined. It shows up first in the feet/pretibial area if ambulatory, or presacral if bed-bound, and "pitting" means a depression from pressure doesn't rapidly refill.
Treatmentis diuretics when the underlying disease and sodium/water restriction aren't enough. Potency order: loop > thiazide > potassium-sparing.
Cancer and hyperparathyroidism are the two big causes, working through increased bone resorption, increased GI absorption, and increased renal tubular reabsorption of calcium. Mild-moderate hypercalcemia (<13 mg/dL, or ionized <6 mg/dL) can be entirely asymptomatic.
| Severity | Presentation |
|---|---|
| Mild-moderate | Often asymptomatic |
| Hypercalcemia of malignancy | Develops fast: anorexia, nausea/vomiting, constipation, polyuria, polydipsia, nocturia |
| Hypercalcemic crisis (>15 mg/dL) | AKI, obtundation. Untreated: oliguric AKI, coma, life-threatening ventricular arrhythmias |
Chronic hypercalcemia (think chronic hyperparathyroidism) causes metastatic calcification, hypercalciuria, and CKD from interstitial nephrocalcinosis over time. ECG shows a shortened QT intervaland ST-T coving, the mirror image of hypocalcemia's prolonged QT.
Three questions decide therapy: Is it symptomatic or life-threatening? What's the calcium level? Are the kidneys working?Asymptomatic and mild → just observe and fix reversible causes. Symptomatic with working kidneys → saline rehydration + loop diuretic, plus calcitonin and/or a glucocorticoid depending on cause. Severe renal insufficiency → hemodialysis with a low-calcium bath replaces the saline/loop step. Life-threatening → add an IV bisphosphonate on top of everything else.
Primary causes are postoperative hypoparathyroidism (accidental parathyroid removal/injury during neck surgery) and vitamin D deficiency. The pathway to remember: PTH and vitamin D control calcium handling at bone, gut, and kidney, so anything that knocks out either one drops calcium.
Severe symptomatic hypocalcemia that won't respond to calcium replacement is often actually a magnesium problem.Hypomagnesemia both impairs PTH secretion and induces PTH resistance at the receptor. You can pour in calcium all day and it won't normalize until the magnesium is replaced. If a hypocalcemic patient isn't responding as expected, check magnesium before increasing the calcium dose again.
Clinical presentation:Tetany is the hallmark of acute hypocalcemia: perioral and extremity paresthesias, muscle spasms and cramps, carpopedal spasm, and rarely laryngospasm or bronchospasm. Cardiac effects include a prolonged QT intervaland decreased contractility that can look like or worsen heart failure, plus arrhythmias, bradycardia, and hypotension that won't respond to fluids or pressors the way you'd expect.
Treatment, acute/symptomatic:IV calcium salts. Give 100–300 mg elemental calcium (1 g calcium chloride, or 2–3 g calcium gluconate) IV over 10–30 minutes, no faster than 60 mg elemental calcium/minute. The bolus only lasts 1–2 hours, so repeat hourly as needed until the patient is stable.
Calcium gluconate is preferred for peripheral IV administrationbecause calcium chloride is far more irritating/vesicant to peripheral veins. Chloride delivers roughly 3x more elemental calcium per gram, which is exactly why it's harsher, and it's generally reserved for central access or genuine emergencies (e.g., code situations).
Chronic, asymptomatic (hypoparathyroidism, vitamin D deficiency):Oral elemental calcium 1–3 g/day initially, titrating up to 2–8 g/day in divided doses. Add a vitamin D preparation if calcium doesn't normalize on calcium alone, since without vitamin D the gut can't absorb what you're giving.
Almost always from decreased excretion as GFR falls (AKI/CKD), the same mechanism covered in the CKD/mineral bone disease chapter. The other cause is a big cellular dump: rhabdomyolysis, hemolysis, or tumor lysis syndrome (a chemo complication, highest risk with acute leukemias and Burkitt lymphoma).
When serum calcium × serum phosphate exceeds 50–60 mg²/dL², calcium phosphate crystals precipitate into soft tissue, causing nephrolithiasis or obstructive uropathy. This is the mechanistic link between hyperphosphatemia and hypocalcemia, and why the two are managed together.
Treatment is mainly chronic-disease management: phosphate binders (see the CKD/CKD-MBD chapter for the full binder list) plus dietary phosphate restriction. Severe symptomatic hyperphosphatemia causing hypocalcemia and tetany gets treated with IV calcium.
From decreased GI absorption, decreased renal reabsorption, or a shift of phosphate into cells. Classic associations: alcohol use disorder, parenteral nutrition without adequate phosphate, chronic antacid use, DKA, and prolonged hyperventilation (respiratory alkalosis drives an intracellular shift).
Severe hypophosphatemia (<1.5 mg/dL)hits nearly every organ system: neurologic (irritability, confusion, seizures, coma), skeletal muscle (myalgia, bone pain, potentially fatal rhabdomyolysis), respiratory muscle weakness leading to acute respiratory failure, and cardiomyopathy, arrhythmias, hemolysis, and infection risk. Chronic hypophosphatemia causes osteopenia/osteomalacia from a lack of crystallization material for bone.
Treatment:Severe or symptomatic (<1.5) gets IV phosphorus 0.32–0.64 mmol/kg (up to 1 mmol/kg described in critically ill trauma patients). Mild-moderate, asymptomatic (1.5–2.7) gets oral phosphorus 1–2 g (32–64 mmol) daily in divided doses, aiming to normalize over 7–10 days. Monitor calcium and phosphorus closely with IV repletion or renal dysfunction, since correcting one can drop the other.
| Product | Phosphate | Potassium | Sodium |
|---|---|---|---|
| Phos-NaK (packet) | 250 mg (8 mmol) | 280 mg (7.1 mEq) | 160 mg (6.9 mEq) |
| K-Phos Neutral (tablet) | 250 mg (8 mmol) | 45 mg (1.1 mEq) | 298 mg (13 mEq) |
| K-Phos No. 2 (tablet) | 250 mg (8 mmol) | 88 mg (2.3 mEq) | 134 mg (5.8 mEq) |
Every oral phosphate product delivers meaningful potassium and sodium along with it. That matters directly if the patient also has hyperkalemia or needs sodium restriction, don't reach for these on autopilot.
Develops when intake outpaces excretion, when tubules stop responding to aldosterone, or when potassium redistributes out of cells into serum. Often asymptomatic; patients might just mention palpitations or skipped beats, which is exactly why you can't rely on symptoms and have to trust the number and the ECG.
Peaked T wavesappear first, around K+ 5.5–6 mEq/L. As potassium keeps rising: widened PR interval → loss of the P wave → widened QRS complex → the QRS merges with the T wave into a sine wave pattern, which is pre-arrest. Know this order, it's tested constantly and it's also literally how you triage severity at the bedside.
There are three completely different jobs in hyperkalemia treatment, and mixing them up is the most common student error. Calcium stabilizes the cardiac membrane(raises the threshold potential) and reverses ECG changes, but it does notlower serum potassium at all, it's short-acting and must be repeated if symptoms recur. Insulin, sodium bicarbonate, and albuterol shift potassium into cells, temporarily lowering serum levels without changing total body potassium (the potassium comes right back out once the drug wears off). Only exchange resins and dialysis actually remove potassiumfrom the body. If you stop after the shifting agents wear off without a removal strategy in place, the potassium rebounds.
Algorithm logic:Abnormal ECG (peaked T, widened QRS) → give calcium gluconate and start continuous ECG monitoring. Then check glucose: hyperglycemic patients get insulin alone (following blood sugar closely); everyone else gets insulin with glucose to prevent hypoglycemia. Consider albuterol as an additional shifting agent, and consider sodium bicarbonate if the patient is also acidotic. Finally, give an exchange resin or consider dialysis for definitive removal, and recheck potassium every 2 hours until it's back under 5.
| Drug | Dose | Onset/Duration | Mechanism |
|---|---|---|---|
| Calcium gluconate/chloride | 1 g IV over 5–10 min | 1–2 min / 10–30 min | Membrane stabilization only, no K+ lowering |
| Regular insulin | 5–10 units IV/SC | 30 min / 2–6 h | Drives K+ intracellularly |
| Dextrose 10% or 50% | 1000 mL (10%) or 50 mL (50%) | 30 min / 2–6 h | Given with insulin to prevent hypoglycemia |
| Sodium bicarbonate | 50–100 mEq IV over 2–5 min | 30 min / 2–6 h | Raises pH, shifts K+ intracellularly |
| Albuterol | 10–20 mg nebulized (far above the standard bronchodilator dose) | 30 min / 1–2 h | β2-mediated intracellular K+ uptake |
| Furosemide | 20–40 mg IV | 5–15 min / 4–6 h | Increases urinary K+ loss |
| Sodium polystyrene sulfonate | 15–60 g PO/PR | 1 h / variable | Exchanges Na+ for K+ in the gut, 1:1 by weight |
| Patiromer | 8.4–25.2 g PO | Hours / variable | Exchanges Ca2+ for K+ |
| Sodium zirconium cyclosilicate | 5–15 g PO | 1 h / variable | Exchanges Na+ for K+ |
| Hemodialysis | ~4 hours | Immediate / variable | Direct removal, fastest definitive option |
SPS mechanics:each gram of resin exchanges 1 mEq of sodium for 1 mEq of potassium, and the sorbitol carrier promotes potassium excretion by causing diarrhea. Oral dosing is better tolerated and more effective than rectal.
The nephroprotective agents that cause hyperkalemia (ACEi, ARB, and especially MRAs like spironolactone, eplerenone, and finerenone, which carries more hyperkalemia risk than an ACEi/ARB alone) are usually the same drugs slowing CKD or heart failure progression. Current teaching for CKD management is to manage the hyperkalemia around the drug (dietary counseling, a potassium binder like patiromer or SZC) rather than reflexively discontinuing a mortality- or kidney-protective medication. This mirrors the heart failure teaching point about RAAS blockers and MRAs.
Either a true total-body potassium deficit or a shift of potassium into cells. Loop and thiazide diuretics are the most common cause in practice; diarrhea, vomiting, and hypomagnesemia round out the usual suspects.
Transcellular shift(no total body deficit, just moved into cells): β2-agonists (albuterol, decongestants), caffeine, theophylline, insulin overdose. Enhanced renal excretion(true deficit): every diuretic class, high-dose penicillins, mineralocorticoids, aminoglycosides, amphotericin B, cisplatin. Enhanced fecal elimination: laxatives, and, worth remembering because it's counterintuitive, the same potassium binders used to treat hyperkalemia(SPS, patiromer, SZC) can overshoot into hypokalemia.
Clinical presentation:Mild hypokalemia is often silent. Moderate produces muscle weakness, cramping, malaise, and myalgias. Cardiac effects include arrhythmias (heart block, atrial flutter, paroxysmal atrial tachycardia, ventricular fibrillation, and potentiation of digoxin toxicity). Severe hypokalemia (<2.5 mEq/L) produces ECG changes: ST-segment depression or flattening, T-wave inversion, and U waves.
Treatment:Roughly every 1 mEq/L drop below 3.5 corresponds to a total-body deficit of 100–400 mEq. Patients on chronic loop or thiazide therapy typically need 40–100 mEq to correct a mild deficit.
Usually from GI or renal losses. Medication causes include aminoglycosides, amphotericin B, cyclosporine, diuretics, digitalis, and cisplatin; alcoholism is a classic clinical association. Typically asymptomatic, but the neuromuscular and cardiovascular systems bear the brunt when it's severe: palpitations, tetany, twitching, generalized convulsions, and ventricular arrhythmias are the most dangerous complication. ECG shows widened QRS and peaked T waves in mild deficiency, progressing to prolonged PR, worsening QRS widening, and flattened T waves as it gets worse.
Hypomagnesemia rarely travels alone: it commonly coexists with hypokalemia and hypocalcemia, and neither of those two will fully correct until the magnesium does. If you're chasing a low potassium or calcium that keeps bouncing back, check magnesium before repeating the same fix.
Treatment:Severity and symptoms dictate the route. IM magnesium is painful and reserved for severe deficiency with no venous access; IV bolus causes flushing, sweating, and warmth.
Rises as GFR drops below 30 mL/min/1.73m², essentially always tied to advanced CKD. Other causes: magnesium-containing antacids in renal insufficiency, TPN in multiorgan failure, magnesium given for eclampsia, lithium, hypothyroidism, and Addison disease.
Symptoms are rare below 4 mEq/L. Two escalating sequences to know: neuromuscular(5–12 mEq/L): sedation → hypotonia → hyporeflexia → somnolence → coma → paralysis → respiratory depression. Cardiovascular(3–15 mEq/L): hypotension → cutaneous vasodilation → QT prolongation → bradycardia → heart block → nodal rhythm → bundle branch block → complete heart block → asystole.
Treatment:IV calcium (100–200 mg elemental, e.g., calcium gluconate 2 g IV) directly antagonizes the neuromuscular and cardiovascular effects, repeated hourly if life-threatening. Forced diuresis with 0.45% NaCl plus a loop diuretic (furosemide 40 mg IV) promotes magnesium elimination in patients with normal function or CKD stage 1–3. Dialysis patients need a magnesium-free dialysate instead.
| Hyponatremia / Hypernatremia | ||
| Agent | Dose | Use |
|---|---|---|
| 3% NaCl | Per protocol until symptoms resolve | Acute symptomatic hyponatremia, any volume status |
| 0.9% NaCl | Per volume deficit | Hypovolemic hyponatremia; initial hypovolemic hypernatremia |
| Tolvaptan | 15 mg PO daily | Euvolemic/hypervolemic hyponatremia; avoid >30 days in chronic liver disease |
| Demeclocycline | 300 mg PO 2–4x/day | SIADH, can't restrict water; onset 3–6 days |
| Desmopressin | IN 5–20 mcg q12–24h | Central DI |
| Hypercalcemia | ||
| Agent | Dose | Onset |
| 0.9% saline | 200–300 mL/h | 24–48 h to normalize |
| Furosemide (equivalent) | 40–80 mg IV q1–4h | With saline, functioning kidneys only |
| Calcitonin | 4 units/kg SC/IM q12h | 1–2 h, unpredictable magnitude |
| Pamidronate | 30–90 mg IV over 2–24 h | 2 days, nadir ~day 7 |
| Zoledronic acid | 4 mg IV over 15 min | 1–2 days |
| Corticosteroid | 40–60 mg prednisone equiv daily | 3–5 days |
| Cinacalcet | 30 mg PO BID | Parathyroid carcinoma specifically |
| Hypocalcemia | ||
| Calcium gluconate/chloride | 100–300 mg elemental Ca IV over 10–30 min | Acute symptomatic; repeat hourly PRN |
| Oral elemental calcium | 1–3 g/day, up to 2–8 g/day divided | Chronic; add vitamin D if not normalizing |
| Phosphorus | ||
| IV phosphorus | 0.32–0.64 mmol/kg (up to 1 mmol/kg critically ill) | Severe/symptomatic (<1.5 mg/dL) |
| Oral phosphorus | 1–2 g (32–64 mmol)/day divided | Mild-moderate, normalize over 7–10 days |
| Potassium | ||
| Oral KCl | 40–100 mEq to correct mild deficit | Preferred route whenever possible |
| IV KCl | 10–20 mEq in 100 mL NS over 1 h | Severe/symptomatic only; dilute in saline, never dextrose |
| Insulin + dextrose | 5–10 units regular insulin IV/SC + dextrose | Emergency hyperkalemia, shifts K+ intracellularly |
| Patiromer / SZC | 8.4–25.2 g PO / 5–15 g PO | Nonacute hyperkalemia, allows continued RAASi/MRA use |
| Magnesium | ||
| Oral MgSO4 | 8–12 g divided over 24h, then 4–6 g/day × 3–5 days | Serum Mg >1 mEq/L, asymptomatic |
| IV magnesium | 4–6 g over 12–24 h, repeat as needed | Serum Mg <1 mEq/L or symptomatic; reduce 25–50% in renal insufficiency |
| IV calcium (for hyperMg) | 100–200 mg elemental (e.g. Ca gluconate 2 g IV) | Antagonizes neuromuscular/CV effects; repeat hourly if severe |
| Parameter | When | Watching for |
|---|---|---|
| Serum sodium | q2–4h during 3% NaCl or vaptan initiation | Rate of correction; ODS if too fast |
| Serum potassium | During any IV K+ repletion or binder therapy; q2h during acute hyperK treatment | Overcorrection, rebound after shifting agents wear off |
| Serum calcium (+ albumin, or ionized Ca) | q24–48h during IV therapy; 1–2x/week during chronic oral therapy | Normalization; recheck corrected value if albumin is abnormal |
| Serum phosphorus | Frequently with IV repletion or renal dysfunction | Concurrent calcium changes, since they move opposite each other |
| Serum magnesium | Before each repeat dose; with any renal impairment | Accumulation, and whether hypoK/hypoCa are actually responding |
| Continuous ECG / telemetry | Any acute IV correction of K+, Ca2+, or Mg2+ | Arrhythmia, the whole reason these are emergencies |
| Renal function | Baseline and periodically on RAASi, MRA, or diuretic therapy | Drug-induced electrolyte shifts before they become severe |
| Full electrolyte panel (not just the one abnormal value) | Whenever any single electrolyte is off | Coexisting derangements: hypoMg driving refractory hypoK/hypoCa, hyperphos driving hypoCa |