# Electrolyte Imbalance Nursing

> Electrolyte imbalance in Nursing: sodium, potassium, calcium and magnesium derangements, ECG changes, safe correction rates and monitoring.

- Canonical URL: https://prepelephant.com/topics/allied/nursing/electrolyte-imbalance-nursing
- Exam / course: Allied Health · Subject: Nursing
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-02
- Last updated: 2026-10-02
- How to cite: "Electrolyte Imbalance Nursing", PrepElephant, https://prepelephant.com/topics/allied/nursing/electrolyte-imbalance-nursing

## Direct answer

Peaked T waves on the monitor are potassium until proven otherwise — hyperkalaemia above 5.0-5.5 mmol/L, the electrolyte emergency that widens the QRS and stops the heart. Electrolyte Nursing revolves around sodium (135-145 mmol/L), potassium (3.5-5.0), calcium and magnesium: each one's reference range, its signature signs and its safe correction speed, because fast corrections kill — sodium corrected too quickly causes osmotic demyelination, and potassium drifting either way causes arrhythmia. The nurse's sequence is constant: recognise the pattern (confusion and seizures point to sodium, cramps and arrhythmias to potassium, tetany to calcium), send or verify the sample, treat per orders, and recheck after every intervention.

## What you must remember

- **Sodium 135-145 mmol/L:** low — headache, confusion, seizures, correction capped (commonly 8 mmol/L in 24 hours) to avoid osmotic demyelination; high — intense thirst, lethargy, corrected slowly to avoid cerebral oedema.
- **Potassium 3.5-5.0 mmol/L:** low — weakness, cramps, ileus, ECG with flattened T waves, ST depression and U waves; high — peaked T waves, widening QRS, then a sine wave.
- **Hyperkalaemia ladder:** intravenous calcium gluconate first (membrane stabilisation, buys time), then insulin with dextrose and nebulised salbutamol (shift potassium into cells), then definitive removal — dialysis, binders, or treating the cause.
- **Potassium safety:** never intravenous push; diluted, pump-controlled infusion; hold when urine output is poor; oral replacement preferred for mild deficits.
- **Insulin's sting:** insulin drives potassium into cells, so DKA correction can precipitate hypokalaemia — monitor potassium and replace per protocol; hypokalaemia is a classic danger of DKA treatment.
- **Calcium (corrected total about 8.5-10.5 mg/dL):** low — perioral tingling, carpopedal spasm, Chvostek and Trousseau signs, prolonged QT; high — stones, bones, abdominal groans and psychiatric overtones.
- **Magnesium:** hypomagnesaemia mimics and perpetuates hypocalcaemia and hypokalaemia — refractory hypokalaemia usually means replace the magnesium too.
- **Monitoring bundle:** telemetry for potassium derangements, intake-output, daily weight, and a repeat level after every treatment step.

## Working a potassium emergency

A post-operative patient with a rising creatinine and urine output of 15 mL/hour reports weakness; the potassium returns at 6.8 mmol/L. Sequence the nursing: stay with the patient and attach continuous cardiac monitoring — peaked T waves and a widening QRS confirm the threat; inform the physician with the value in hand; then execute the ladder as ordered — intravenous calcium gluconate over minutes with the ECG watched (it does not lower potassium; it stabilises the myocardium), short-acting insulin in a dextrose infusion with hourly glucose checks, nebulised salbutamol, and the nephrology conversation for dialysis. Meanwhile, audit the ward's contribution: is he still on a potassium supplement or an ACE inhibitor? And question the sample — a fist-clenched or haemolysed draw falsely elevates potassium, so a clean repeat with gentle technique is part of the thinking, not a delay. Recheck the potassium and the ECG after every step; the trend, not one number, ends the emergency.

## Where students slip

The flips that cost marks: U waves belong to hypokalaemia and peaked T waves to hyperkalaemia; calcium gluconate is mistaken for a potassium-lowering drug (it only protects the heart); and the correction limits swap — rapid correction of hyponatraemia causes osmotic demyelination (central pontine myelinolysis), rapid correction of hypernatraemia causes cerebral oedema. The bedside slip is treating the number over the patient: a sodium drifting slowly to 125 in a chronic, asymptomatic person is managed gently, while 128 with a seizure is an emergency. And the hidden answer to "hypokalaemia that will not correct" is magnesium.

## Frequently asked questions

### What are the ECG changes of hyperkalaemia?

Tall peaked T waves first, then a widening QRS, loss of P waves and, untreated, a sine-wave pattern ending in asystole.

### Why does calcium gluconate come first in hyperkalaemia?

It immediately stabilises the myocardial membrane, protecting the heart while insulin-dextrose, salbutamol and dialysis actually lower the potassium.

### How fast should hyponatraemia be corrected?

Commonly no more than 8 mmol/L in 24 hours — faster correction risks osmotic demyelination (central pontine myelinolysis), which may be irreversible.

### Which two bedside signs suggest hypocalcaemia?

Chvostek's sign — facial twitch when the facial nerve is tapped — and Trousseau's sign — carpal spasm after the cuff is held above systolic for a few minutes.

### Why check magnesium in refractory hypokalaemia?

Hypomagnesaemia drives renal potassium loss, so potassium will not correct until magnesium is replaced.