Electrolyte Abnormalities for Nursing Students
Electrolyte Abnormalities every nursing student should memorize
Educational use This material supplements, but does not replace, laboratory-specific ranges, organizational protocols, medication labeling, prescribing guidance, or individualized clinical judgment.
This page does not cover ABG analysis, for help with ABG interpretation go here!
Core principles
- Interpret the patient, trend, rate of change, symptoms, ECG findings, renal function, medications, fluid balance, specimen quality, and units—not the laboratory value alone.
- Reference intervals vary by laboratory, age, albumin, pH, kidney function, and assay method.
- Confirm an unexpected potassium result when safe because hemolysis can cause pseudohyperkalemia; do not delay treatment for instability or dangerous ECG changes.
- Correction and replacement must be protocolized and reassessed frequently to prevent overcorrection or treatment-related complications.
Quick reference
| Electrolyte | Common adult serum range* | Primary functions | Immediate high-risk concerns |
|---|---|---|---|
| Sodium | 135–145 mmol/L | Extracellular tonicity, water balance, neurologic function. | Seizure, coma, severe encephalopathy; harm from overly rapid correction. |
| Potassium | 3.5–5.0 mmol/L | Cardiac and skeletal-muscle membrane conduction. | Weakness, paralysis, ventricular dysrhythmia, cardiac arrest. |
| Total calcium | ~8.5–10.5 mg/dL | Neuromuscular function, coagulation, bone. | Tetany/seizure/QT prolongation when low; encephalopathy/dehydration when high. |
| Ionized calcium | ~1.12–1.32 mmol/L | Biologically active calcium. | Preferred in critical illness or major albumin/pH disturbance. |
| Magnesium | ~1.7–2.4 mg/dL | Enzymes, conduction, potassium/calcium regulation. | Torsades/seizure when low; hyporeflexia/respiratory depression when high. |
| Phosphate | ~2.5–4.5 mg/dL | ATP, oxygen delivery, muscle, neurologic function, bone. | Respiratory failure/rhabdomyolysis when severely low; hypocalcemia when high. |
| Chloride | ~98–106 mmol/L | Electroneutrality, volume and acid-base balance. | Usually interpreted with sodium, bicarbonate, volume status, and acid-base data. |
*Use the reporting laboratory’s reference interval and units.
Sodium disorders
Hyponatremia: Na⁺ <135 mmol/L
Hyponatremia is excess water relative to sodium. Severity depends on concentration, symptoms, duration, and speed of decline; classify by serum osmolality and volume status.
| Etiology / mechanisms | Signs and symptoms | Diagnostics / assessment | Treatment / nursing priorities |
|---|---|---|---|
| • Hypovolemic: GI losses, renal losses, diuretics, sweating, burns. • Euvolemic: SIADH, medications, glucocorticoid deficiency, hypothyroidism, excess water. • Hypervolemic: heart failure, cirrhosis, advanced kidney disease. • Hyperglycemia can cause translocational hyponatremia; marked lipid/protein elevation may cause pseudohyponatremia with selected assays. | • Mild: headache, nausea, fatigue, weakness, cramps. • Moderate: confusion, decreased attention, gait/cognitive change. • Severe/rapid: vomiting, marked encephalopathy, seizure, coma, respiratory compromise. | • Repeat/confirm and trend Na⁺; assess serum osmolality, glucose, volume status, medications, renal/endocrine context. • Urine osmolality and urine sodium help distinguish etiologies. • Frequent neurologic assessment and sodium checks during active correction. | • Treat the cause and volume category; fluid restriction is not universal. • Hypovolemic: restore volume, commonly with isotonic crystalloid. • SIADH: fluid restriction is common; medication/cause-directed therapies vary. • Hypervolemic: fluid/sodium and diuretic strategy based on the underlying disease. • Severe neurologic symptoms: protocolized 3% saline boluses with frequent reassessment. |
| Special consideration Avoid excessive correction in chronic or unknown-duration hyponatremia. Many guidelines limit correction to ≤8 mmol/L in 24 hours in patients at high risk for osmotic demyelination. ODS is demyelination after overly rapid correction—not intracellular brain swelling. |
Hypernatremia: Na⁺ >145 mmol/L
Hypernatremia usually represents water deficit relative to sodium. Neurologic risk depends on concentration and speed of development.
| Etiology / mechanisms | Signs and symptoms | Diagnostics / assessment | Treatment / nursing priorities |
|---|---|---|---|
| • Inadequate access to water, impaired thirst, fever/sweating, diarrhea, burns. • Central or nephrogenic diabetes insipidus, osmotic diuresis, loop diuresis. • Less commonly sodium gain from hypertonic sodium administration or mineralocorticoid states. | • Thirst, restlessness, irritability, weakness, hyperreflexia. • Confusion, seizure, coma when severe or rapidly developing. • Polyuria with DI/osmotic diuresis; tachycardia/orthostasis with hypovolemia. | • Trend Na⁺, glucose, renal function, urine output, fluid balance and neurologic status. • Urine osmolality and history help identify DI or osmotic diuresis. • Estimate free-water deficit only as a guide; ongoing losses and response must be included. | • Treat shock first with isotonic fluid when present. • Then replace free water orally/enterally or with an appropriate IV hypotonic solution. • Treat the cause; desmopressin may be used for central DI. • Correct chronic/unknown-duration disease gradually with frequent monitoring; acute sodium loading requires specialist-directed care. |
Potassium disorders
Hypokalemia: K⁺ <3.5 mmol/L
Hypokalemia reflects potassium loss, inadequate intake, or intracellular shift. Clinical risk rises with severity, rapid decline, heart disease, digoxin, QT-prolonging drugs, and concurrent hypomagnesemia.
| Etiology / mechanisms | Signs and symptoms | Diagnostics / assessment | Treatment / nursing priorities |
|---|---|---|---|
| • GI losses, loop/thiazide diuretics, renal wasting, poor intake. • Insulin, beta-agonists, alkalosis, refeeding. • Mineralocorticoid excess. • Hypomagnesemia promotes renal potassium wasting and refractory hypokalemia. | • Weakness, cramps, fatigue, constipation or ileus. • Severe deficiency may cause paralysis or rhabdomyolysis. • ECG: flattened T waves, ST depression, U waves, apparent QU prolongation, ectopy, atrial/ventricular dysrhythmias. | • Repeat/trend K⁺; check magnesium, renal function, acid-base status, medications, GI losses, urine output. • Telemetry for severe/symptomatic abnormalities or significant cardiac risk. | • Oral replacement preferred when feasible. • IV replacement for severe/symptomatic disease or inability to use enteral route. • Never IV push potassium; use pump and follow line, concentration, and rate policies. • Correct magnesium; reassess K⁺ at the ordered interval. |
Hyperkalemia: commonly K⁺ >5.0 mmol/L
Hyperkalemia can rapidly impair cardiac conduction. The ECG may be normal despite clinically important elevation.
| Etiology / mechanisms | Signs and symptoms | Diagnostics / assessment | Treatment / nursing priorities |
|---|---|---|---|
| • Reduced excretion: AKI/CKD, hypoaldosteronism. • Medications: ACEI, ARB, MRA, potassium supplements and selected others. • Cell release/shift: acidosis, insulin deficiency, rhabdomyolysis, tumor lysis, burns, hemolysis. • Pseudohyperkalemia from specimen hemolysis or collection factors. | • Often asymptomatic. • Weakness, paresthesias, flaccid paralysis, palpitations. • ECG progression may include peaked T waves, PR prolongation, loss of P waves, QRS widening, sine wave, ventricular dysrhythmia or asystole. | • Immediate ECG/telemetry when severe, symptomatic, rapidly rising, or clinically high-risk. • Verify unexpected values when safe; assess renal function, glucose, acid-base status, medication/exposure history, and tissue injury. • Serial K⁺ and glucose after treatment. | • Stabilize: IV calcium for significant ECG change/severe toxicity; calcium protects myocardium but does not lower K⁺. • Shift: IV regular insulin with dextrose; inhaled beta-agonist; bicarbonate for selected significant metabolic acidosis. • Remove: renal excretion/diuresis when appropriate, binders, or dialysis. • Treat the cause and monitor for rebound. |
| Special consideration In DKA, serum potassium may be normal or high despite total-body depletion. Insulin and correction of acidosis can rapidly lower serum potassium; protocolized monitoring and replacement are essential. |
Calcium disorders
Total calcium is affected by albumin and pH. Ionized calcium is the biologically active fraction and is preferred when albumin/pH is substantially abnormal or in critical illness.
Hypocalcemia: below the laboratory reference range
True hypocalcemia should be assessed with ionized calcium when indicated.
| Etiology / mechanisms | Signs and symptoms | Diagnostics / assessment | Treatment / nursing priorities |
|---|---|---|---|
| • Hypoparathyroidism, vitamin D deficiency, CKD. • Pancreatitis, massive transfusion/citrate, sepsis. • Hypomagnesemia can impair PTH release/action. | • Perioral/finger paresthesia, cramps, tetany, hyperreflexia. • Seizure, laryngospasm, hypotension. • ECG: QT prolongation and dysrhythmia risk. | • Confirm total and/or ionized calcium; review albumin, pH, magnesium, phosphate, renal function, vitamin D/PTH context. • ECG/telemetry for severe or symptomatic disease. | • IV calcium for severe symptoms, seizure, marked QT prolongation, or instability. • Oral calcium/vitamin D for selected stable cases. • Correct magnesium and treat the underlying cause. |
Hypercalcemia: above the laboratory reference range
Symptoms correlate with severity and rate of rise. Primary hyperparathyroidism and malignancy are common causes.
| Etiology / mechanisms | Signs and symptoms | Diagnostics / assessment | Treatment / nursing priorities |
|---|---|---|---|
| • Primary hyperparathyroidism, malignancy. • Calcium/vitamin D or selected medication exposure. • Granulomatous disease, immobilization, endocrine causes. | • Polyuria, dehydration, thirst, constipation, nausea. • Weakness, confusion, lethargy, kidney stones. • ECG: shortened QT; severe disease may cause dysrhythmia. | • Confirm calcium/ionized calcium and assess albumin, renal function, volume status, medications, PTH and malignancy context. • ECG and neurologic monitoring when severe. | • Isotonic fluid when appropriate after volume assessment. • Calcitonin for faster temporary effect; antiresorptive therapy for selected causes. • Dialysis for selected severe/refractory cases or when fluids are unsafe. • Avoid indiscriminate aggressive fluids in HF or renal failure. |
Magnesium disorders
Hypomagnesemia: below the laboratory reference range
Serum magnesium may underestimate total-body deficiency. Hypomagnesemia commonly coexists with refractory hypokalemia or hypocalcemia.
| Etiology / mechanisms | Signs and symptoms | Diagnostics / assessment | Treatment / nursing priorities |
|---|---|---|---|
| • GI/renal losses, alcohol use disorder, malnutrition. • Loop/thiazide diuretics, PPIs and selected nephrotoxic drugs. • Refeeding and other intracellular shifts. | • Weakness, tremor, hyperreflexia, cramps. • Seizure, prolonged QT, ventricular dysrhythmia and torsades. • Refractory hypokalemia or hypocalcemia. | • Trend Mg²⁺, K⁺, Ca²⁺, renal function and ECG. • Review losses, nutrition and medication exposure. | • Oral or IV magnesium based on severity and symptoms. • IV magnesium for torsades. • Adjust dosing for renal dysfunction; monitor reflexes, respiratory status and hemodynamics during substantial IV replacement. |
Hypermagnesemia: above the laboratory reference range
Clinically important hypermagnesemia most often occurs when impaired kidney excretion is combined with magnesium exposure.
| Etiology / mechanisms | Signs and symptoms | Diagnostics / assessment | Treatment / nursing priorities |
|---|---|---|---|
| • Kidney failure plus magnesium-containing laxatives, antacids or infusions. • Excessive replacement; less commonly major cell injury/endocrine causes. | • Nausea, flushing, lethargy. • Hyporeflexia, hypotension, bradycardia. • Respiratory depression, heart block or cardiac arrest when severe. | • Trend Mg²⁺, renal function, ECG, blood pressure, reflexes and respiratory status. • Review all medication and supplement sources. | • Stop magnesium exposure. • IV calcium for clinically significant toxicity. • Fluids and loop diuresis when renal/cardiac status permits. • Dialysis for severe toxicity or kidney failure. |
Phosphate disorders
Hypophosphatemia: below the laboratory reference range
Phosphate is essential for ATP production, diaphragmatic function, neurologic function and oxygen delivery.
| Etiology / mechanisms | Signs and symptoms | Diagnostics / assessment | Treatment / nursing priorities |
|---|---|---|---|
| • Refeeding syndrome, insulin therapy, alcohol use disorder, malnutrition. • Respiratory alkalosis/hyperventilation. • GI loss, renal wasting and phosphate binders. | • Weakness, paresthesia, encephalopathy, seizure. • Respiratory muscle failure, reduced cardiac function. • Rhabdomyolysis, hemolysis and impaired leukocyte function when severe. | • Trend phosphate, calcium, potassium, magnesium, renal function and nutrition/feeding history. • Assess respiratory strength and neurologic status in severe deficiency. | • Oral replacement for many stable cases. • IV replacement for severe or symptomatic deficiency. • Monitor for hypocalcemia, hyperphosphatemia, hypotension and renal limitations. • Prevent/treat refeeding syndrome with protocolized nutrition and electrolyte monitoring. |
Hyperphosphatemia: above the laboratory reference range
Hyperphosphatemia commonly reflects impaired renal excretion or massive cell breakdown and can lower ionized calcium.
| Etiology / mechanisms | Signs and symptoms | Diagnostics / assessment | Treatment / nursing priorities |
|---|---|---|---|
| • AKI/CKD. • Tumor lysis, rhabdomyolysis, hemolysis. • Hypoparathyroidism or excessive phosphate exposure. | • Often asymptomatic. • Symptoms of hypocalcemia: paresthesia, cramps, tetany or seizure. • Chronic elevation promotes vascular/soft-tissue calcification and bone-mineral disease. | • Trend phosphate, calcium, renal function and ECG when calcium is significantly affected. • Evaluate cell breakdown, kidney failure and phosphate-containing medications/enemas. | • Treat the cause. • Dietary phosphate restriction and phosphate binders for selected patients. • Dialysis for severe disease with kidney failure or other indications. • Avoid phosphate-containing products. |
Chloride and acid-base context
| Topic | Talking points |
|---|---|
| Hypochloremia | Often accompanies vomiting, gastric suction, chloride-responsive metabolic alkalosis, diuretics or dilutional states. Assess volume status, sodium, potassium and bicarbonate. Treatment is cause-directed and may include chloride/volume and potassium replacement. |
| Hyperchloremia | May occur with diarrhea, renal tubular acidosis, kidney dysfunction or large-volume 0.9% sodium chloride. Interpret with bicarbonate, anion gap, sodium and volume status. |
| Saline-associated acidosis | Large-volume 0.9% sodium chloride can contribute to hyperchloremic normal-anion-gap metabolic acidosis by lowering the plasma strong-ion difference—not simply by causing renal bicarbonate excretion. |
| Nursing focus | Trend fluid source/volume, electrolytes, bicarbonate, renal function, intake/output and acid-base status; communicate worsening acidosis, oliguria or hemodynamic change. |
Nursing safety checklist
- Verify the specimen, units, reference interval, trend, renal function, glucose, albumin/pH context, medications, intake/output, and ECG indication.
- Use infusion pumps and approved concentrations; confirm line access, compatibility, maximum rates, and monitoring requirements for IV electrolyte replacement.
- Reassess laboratory values at ordered intervals; monitor glucose after insulin for hyperkalemia and telemetry for clinically significant potassium, calcium, or magnesium disorders.
- Escalate seizure, severe weakness, respiratory compromise, dysrhythmia, rapidly changing values, oliguria, or neurologic deterioration immediately.