Potassium: the most tested electrolyte
Potassium governs cardiac conduction, which is why both hypokalaemia and hyperkalaemia are emergencies rather than merely abnormal numbers. Hypokalaemia arises from vomiting, diarrhoea, nasogastric suction, loop and thiazide diuretics, and insulin therapy. Findings include muscle weakness, leg cramps, decreased bowel motility progressing to ileus, shallow respirations from respiratory muscle weakness, and electrocardiogram changes with flattened T waves and prominent U waves. Hypokalaemia also potentiates digoxin toxicity, a pairing the exam loves.
Hyperkalaemia arises from renal failure, potassium-sparing diuretics, ACE inhibitors, crush injuries, burns, acidosis and massive transfusion. Findings include muscle weakness that begins in the legs, paraesthesia, hyperactive bowel sounds with diarrhoea, and peaked T waves progressing to a widened QRS and cardiac arrest. Treatment layers three strategies: stabilize the myocardium with calcium gluconate, shift potassium into cells with insulin and dextrose, beta agonists or bicarbonate, then remove it with binders or dialysis.
Administration safety is examined constantly. Potassium chloride is never given by intravenous push or as a bolus, is always diluted, is infused via a pump at a controlled rate, and requires confirmed urine output before administration. Infusion site pain or phlebitis is common and should be assessed; the infusion is not simply increased to finish faster.
| Electrolyte | Normal range | Low | High |
|---|---|---|---|
| Potassium | 3.5–5.0 mEq/L | Weakness, ileus, flat T waves, U waves | Peaked T waves, wide QRS, diarrhoea |
| Sodium | 135–145 mEq/L | Confusion, seizures, headache | Thirst, dry mucosa, agitation |
| Calcium | 9.0–10.5 mg/dL | Tetany, Chvostek, Trousseau, tingling | Weakness, constipation, kidney stones |
| Magnesium | 1.3–2.1 mEq/L | Hyperreflexia, tremor, torsades risk | Depressed reflexes, hypotension, respiratory depression |
| Phosphate | 3.0–4.5 mg/dL | Weakness, refeeding risk | Often with renal failure, causes low calcium |
Sodium and the neurological pattern
Sodium disorders present neurologically because water follows sodium across the blood-brain barrier. Hyponatraemia causes cerebral swelling with headache, confusion, lethargy, muscle cramps and, at severe levels, seizures and coma. Common causes include the syndrome of inappropriate antidiuretic hormone, excessive hypotonic fluids, heart failure, and diuretic use. Management depends on the cause and may involve fluid restriction or, in severe symptomatic cases, hypertonic saline given cautiously with close monitoring.
Hypernatraemia usually reflects water loss rather than salt gain: fever, diabetes insipidus, inadequate intake in older adults, and excessive tube feeding without free water. Findings include intense thirst, dry sticky mucous membranes, restlessness, agitation and, when severe, seizures. Correction uses hypotonic fluids given slowly.
The universal safety rule is that sodium is corrected gradually. Correcting hyponatraemia too fast risks osmotic demyelination, and correcting hypernatraemia too fast risks cerebral oedema. Exam answers that involve rapid correction are almost always wrong, and answers that involve frequent neurological checks are usually right.
- •Low sodium: think swollen brain cells — confusion, seizures
- •High sodium: think dehydrated cells — thirst, dry mucosa, agitation
- •Correct either direction slowly with neuro checks
- •SIADH retains water and dilutes sodium; diabetes insipidus loses water and concentrates it
Calcium and magnesium move together
Calcium and magnesium behave similarly enough that learning one gives you the other. Low levels of either produce neuromuscular excitability: tingling around the mouth and fingers, muscle twitching, hyperactive reflexes, a positive Chvostek sign when the facial nerve is tapped, a positive Trousseau sign when a blood pressure cuff is inflated, and in severe cases tetany, laryngospasm and seizures. Hypocalcaemia follows thyroid or parathyroid surgery, so postoperative airway monitoring for laryngospasm is a classic exam point.
High levels of either depress the neuromuscular system: lethargy, weakness, diminished or absent deep tendon reflexes, hypotension and, with magnesium, respiratory depression. Hypercalcaemia additionally causes constipation, kidney stones and bone pain, and is often related to malignancy or hyperparathyroidism; hydration with isotonic fluids and mobilization are core interventions.
Magnesium deficiency deserves separate attention because it predisposes to torsades de pointes and makes hypokalaemia resistant to correction — you cannot fix the potassium until the magnesium is replaced. Alcohol use disorder, malnutrition and prolonged diarrhoea are the common causes, which links this topic back to both mental health and gastrointestinal content.
How to answer electrolyte items reliably
Start by identifying whether the value is high or low and whether the client's findings match. If they do not, question the data — a stem that reports hyperkalaemia with flattened T waves is testing whether you notice the mismatch. Next, ask whether the finding is cardiac, respiratory or neurological, because those three categories dictate urgency. Cardiac and respiratory findings are always reported before gastrointestinal ones.
Then look at the cause in the stem. Diuretics, nasogastric suction, vomiting and diarrhoea point toward loss; renal failure, tissue destruction and potassium-sparing drugs point toward retention. Matching mechanism to value converts a memory question into a reasoning question, which is what next-generation items increasingly ask.
Finally, practise these values inside clinical scenarios rather than as flashcards. Fundamentals and adult health sets both include fluid and electrolyte items, and pairing them with the fluid balance and IV therapy guide gives you the full picture of how volume and electrolytes interact.