Electrolyte Imbalance Nursing
On this page
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.