11.3 Electrolyte Disorders
Key Takeaways
- Sodium disorders are disorders of water balance relative to sodium: correct chronic hyponatremia carefully—overly rapid sodium rise risks osmotic demyelination syndrome (ODS); overly rapid falls can worsen cerebral edema.
- Hypokalemia causes weakness and arrhythmias and increases digoxin toxicity risk; hyperkalemia can show peaked T waves and is a true emergency when severe or ECG-unstable—treat per protocol while stopping potassium sources.
- IV potassium chloride is never given IV push; it is always pump-controlled, diluted per policy, with typical peripheral rate teaching often ≤10 mEq/hr (higher rates usually require central access and cardiac monitoring per protocol).
- Magnesium, calcium, and phosphorus are tightly linked: low Mg makes K repletion difficult; calcium–phosphorus product and solubility matter; ionized calcium is the physiologically active fraction; low phosphorus is a refeeding red flag.
- Infusion nurses prevent harm by verifying concentration/route/rate, monitoring ECG and labs during repletion, watching IV sites for chemical irritation, and recognizing tetany/neuromuscular irritability with low calcium or magnesium.
Electrolytes as high-alert infusion content
Electrolyte repletion and free-water management sit at the center of Domain 3G.3. Mistakes here cause arrhythmias, seizures, osmotic demyelination, tissue necrosis from extravasation, and cardiac arrest from IV push potassium. Master relationships, ECG clues, correction-rate caution, and route/rate safety—not trivia lists of every rare syndrome name.
Quick Answer: Na disorders = water vs sodium balance; correct chronic hyponatremia slowly enough to avoid ODS. K: hypo → weakness/arrhythmia/dig toxicity risk; hyper → peaked T/emergency; never IV push KCl; peripheral rates often ≤10 mEq/hr teaching limit, always on a pump. Mg repletion supports K repletion. Ca (use ionized when relevant) and Phos interact; watch tetany and refeeding low Phos.
Sodium (Na⁺)
Why sodium rules extracellular water
Serum sodium concentration reflects water balance relative to sodium, not a simple “total body sodium meter.” Hyponatremia usually means relatively too much free water (or impaired water excretion); hypernatremia usually means relatively too little free water.
Approximate adult reference teaching range often cited near 135–145 mEq/L (facility labs vary).
Hyponatremia — causes and clinical picture
| Mechanism cluster | Examples | Notes |
|---|---|---|
| Excess free water / impaired excretion | SIADH, hypotonic IV fluids, polydipsia, postoperative ADH | Classic iatrogenic contribution from hypotonic fluids |
| Hypovolemic hyponatremia | GI losses replaced with free water | Needs volume + thoughtful Na/water strategy |
| Hypervolemic hyponatremia | HF, cirrhosis, renal failure | Total body sodium may be high with low [Na] |
| Factitious / other | Hyperglycemia (translocational), lab issues | Interpret with glucose |
Symptoms: headache, nausea, confusion, seizures, coma as severity/acuity rise. Acute drops are more symptomatic than chronic at the same number.
Correction rate caution — ODS risk
In chronic hyponatremia, brain cells adapt by extruding osmoles. If serum sodium is raised too rapidly, water leaves brain cells excessively → osmotic demyelination syndrome (ODS) (central pontine myelinolysis is the classic related term in older literature).
Exam-ready principles:
- Symptomatic acute severe hyponatremia may need careful hypertonic saline under protocol—this is specialist, high-alert care.
- Chronic asymptomatic or mildly symptomatic hyponatremia is corrected gradually with free-water restriction, cause treatment, and measured repletion—not aggressive rapid Na climbs.
- Know the direction of risk: overly rapid rise in chronic hyponatremia → ODS; overly rapid fall or free-water load → cerebral edema risk.
- Exact mEq/L-per-day limits are protocol-specific—CRNI tests the caution concept, not an invented universal number you must fabricate.
Hypernatremia
Usually a free-water deficit (inadequate intake, DI, osmotic diuresis, insensible losses) or sodium gain (less common, e.g., hypertonic saline excess).
Signs: thirst, dry mucosa, confusion, seizures in severe cases; often volume deficit signs if water losses dominate.
Treatment concepts: restore free water enterally when safe, or IV free-water sources (e.g., D5W) per orders; correct underlying cause; avoid reckless rapid swings. Hypovolemic hypernatremia may need isotonic volume first if shock is present, then free-water strategy—sequence follows perfusion priority.
Exam trap: Treating hypernatremia by dumping free water without monitoring, or giving hypotonic fluids in elevated ICP contexts without specialist direction.
Potassium (K⁺)
Hypokalemia
Causes: GI losses, diuretics, shift into cells (insulin, alkalosis, beta-agonists), poor intake, magnesium depletion.
Clinical: muscle weakness, cramps, constipation/ileus, arrhythmias, ECG changes (flattening T waves, U waves teaching pattern), and increased digoxin toxicity risk even when digoxin level seems borderline.
Repletion principles:
- Oral preferred when mild and GI tract works.
- IV when severe, symptomatic, or NPO—high-alert.
- Replete magnesium if low—refractory hypokalemia often means concurrent hypomagnesemia.
- Continuous cardiac monitoring when policy requires for higher rates/concentrations.
Hyperkalemia
Causes: renal failure, cell lysis (rhabdo, tumor lysis), acidosis shift, excess K administration, drugs (ACEI/ARB, potassium-sparing diuretics, succinylcholine in risk contexts).
Clinical/ECG: peaked T waves, widened QRS, sine-wave progression, ventricular arrhythmias, asystole risk. Weakness can occur.
Emergency pathway concepts (know roles, not every mg dose by memory unless your materials specify):
- Stabilize cardiac membrane (e.g., IV calcium when ECG changes—protocol)
- Shift K intracellularly (insulin+glucose, beta-agonists, bicarbonate in selected acidosis—per protocol)
- Remove K (diuretics if renal function allows, potassium binders, dialysis)
- Stop all potassium in fluids/feeds and salt substitutes
IV potassium safety — non-negotiable
| Rule | Rationale |
|---|---|
| NEVER IV push KCl | Can cause fatal arrhythmia/asystole |
| Always on an infusion pump | Prevents accidental bolus |
| Dilute per pharmacy/policy | Reduces vein irritation and dosing errors |
| Peripheral rate teaching | Often ≤10 mEq/hr typical teaching maximum for peripheral lines |
| Central higher rates | May be allowed with monitoring per policy—still not push |
| Site surveillance | Concentrated K is a vesicant-like chemical irritant—extravasation harms tissue |
| Verify access patency | Do not run concentrated electrolytes into infiltrated tissue |
Exam trap: Selecting IV push potassium “because the level is 2.4 and the patient is weak.” The correct action is controlled IV infusion (or oral if appropriate), never push.
Magnesium (Mg²⁺)
Magnesium supports enzyme function, neuromuscular stability, and potassium homeostasis.
Hypomagnesemia causes: GI losses, alcohol use disorder, diuretics, refeeding, poor intake.
Signs: neuromuscular irritability, tremors, hyperreflexia, seizures, arrhythmias (including association with torsades teaching pattern), concurrent refractory hypokalemia.
Hypermagnesemia: often iatrogenic (over-repletion) or renal failure—flushing, hypotension, bradycardia, hyporeflexia, respiratory depression when severe.
Infusion notes: IV magnesium sulfate is common; rates and dilution follow protocol; monitor reflexes/vitals during larger repletions (especially obstetrics protocols—concept of monitoring applies broadly).
Key relationship: Low Mg → hard to fix low K. Always check and replete Mg when potassium will not rise.
Calcium (Ca²⁺)
Total vs ionized
- Total calcium includes albumin-bound fraction—falls when albumin is low even if ionized calcium is acceptable.
- Ionized calcium is the physiologically active fraction preferred when acid–base, transfusion, or critical illness confounds total Ca.
Hypocalcemia signs: tetany, perioral numbness, Chvostek/Trousseau signs, laryngospasm risk, prolonged QT, seizures. Causes include hypoparathyroidism, vitamin D deficiency, citrate-binding with massive transfusion, alkalosis, pancreatitis, and high phosphate states.
Hypercalcemia signs: “stones, bones, groans, psychiatric overtones” teaching mnemonic—polyuria, dehydration, confusion; causes include hyperparathyroidism and malignancy.
Infusion notes:
- IV calcium (gluconate vs chloride) choice and route follow protocol—calcium chloride is more irritating and often central-preferred.
- Do not mix calcium-containing fluids casually with products that precipitate (classic compatibility concern with certain phosphate-containing mixtures and with some blood product contexts—follow pharmacy).
- Massive transfusion: watch ionized hypocalcemia from citrate.
Phosphorus (phosphate)
Phosphate is essential for ATP and 2,3-DPG. Hypophosphatemia causes weakness, respiratory muscle failure risk, hemolysis, and altered mentation when severe.
Refeeding syndrome risk: after prolonged starvation, carbohydrate reintroduction drives phosphate (and K/Mg) intracellularly → dangerous drops. Parenteral nutrition and aggressive feeding are classic settings—monitor Phos/K/Mg closely (links to Domain 3H).
Hyperphosphatemia: common in renal failure; may complex with calcium → soft-tissue calcification risk; treat underlying cause, binders as ordered, dialysis when indicated.
Calcium–phosphorus relationship
High phosphate can lower calcium; solubility product concerns matter when both are high (metastatic calcification teaching). In refeeding and PN, unbalanced repletion invites precipitation and metabolic chaos—pharmacy-driven compounding exists for a reason.
Integrated electrolyte relationships (memory grid)
| Pairing | Clinical pearl |
|---|---|
| Na ↔ water | [Na] is mostly water story; correction rate protects brain |
| K ↔ Mg | Replete Mg to enable K repletion |
| K ↔ digoxin | HypoK increases dig toxicity risk |
| K ↔ ECG | HyperK peaked T; severe → QRS widening |
| Ca ↔ albumin | Low albumin lowers total Ca; check ionized |
| Ca ↔ Phos | Product/solubility; reciprocal trends common |
| Phos ↔ refeeding | Low Phos after feeding restart is a red flag |
| Ca/Mg ↔ tetany | Neuromuscular irritability when low |
Nursing process for electrolyte infusions
- Verify order, concentration, diluent, route (peripheral vs central), rate, and indication.
- Review latest labs and ECG when indicated; hold and call if values conflict with the plan.
- Prime and pump—no free-flow electrolyte concentrates.
- Monitor during infusion: HR/rhythm, symptoms, urine output, IV site, repeat labs per protocol.
- Document response and adverse effects; educate patients to report palpitations, weakness, tingling, or site pain.
Integrated scenarios
Scenario A — Chronic hyponatremia: Na 118, mildly confused, known SIADH, not seizing. Aggressive rapid correction with large hypertonic boluses outside protocol risks ODS. Follow controlled correction and free-water management orders.
Scenario B — Hypokalemia on digoxin: K 2.7, patient on digoxin with new ectopy. Replete K (and check Mg) carefully IV on pump; never push; monitor rhythm.
Scenario C — Hyperkalemia emergency: K 7.1 with peaked T waves in ESKD. Activate emergency treatment pathway, stop K-containing fluids, prepare for possible dialysis—do not start a potassium-rich maintenance bag.
Scenario D — Refeeding: Severely malnourished patient starts PN; Phos and K plummet. Anticipate refeeding electrolyte shifts; replete and adjust nutrition rate with the team.
High-yield exam traps
- IV push KCl for any reason
- Rapid chronic hyponatremia correction without ODS awareness
- Free water for hypernatremia without rate/ICP caution
- Repleting K endlessly while ignoring low Mg
- Treating low total Ca without considering albumin/ionized Ca
- Missing peaked T waves as hyperkalemia urgency
- Running concentrated electrolytes peripherally at central-only rates
- Ignoring refeeding hypophosphatemia when nutrition restarts
What is the primary neurologic risk of raising serum sodium too rapidly in a patient with chronic severe hyponatremia?
Which statement about IV potassium chloride administration is correct for CRNI-level safety practice?
A patient has persistent hypokalemia despite repeated potassium repletion. Which related electrolyte problem should the infusion nurse anticipate checking?
Which ECG teaching finding is most classically associated with severe hyperkalemia?