Hypokalaemia and Hyperkalaemia: Emergency Assessment, ECG Recognition and Treatment

Learning objectives

• Explain potassium physiology and the difference between a concentration problem and a total-body deficit or excess.
• Recognise symptoms and ECG changes of hypokalaemia and hyperkalaemia.
• Identify renal, gastrointestinal, endocrine, medication, acid–base and cellular-shift causes.
• Manage life-threatening hyperkalaemia and severe hypokalaemia using a structured ABCDE approach.
• Replace potassium safely, correct magnesium, monitor glucose/ECG/urine output and prevent recurrence.

Potassium physiology

Most potassium is intracellular. The sodium–potassium pump, insulin, catecholamines and acid–base balance move potassium between the intracellular and extracellular spaces, while the kidneys determine long-term excretion. A normal serum value can occasionally hide a depleted total-body store, and a high value can be caused by a shift out of cells rather than excess total potassium. Treat the patient and the cause, not the number alone.

Definitions and severity

Causes of hypokalaemia

• Reduced intake: malnutrition, prolonged fasting, alcoholism or inability to swallow.
• Gastrointestinal loss: vomiting, diarrhoea, fistula, laxative misuse or high-output stoma.
• Renal loss: loop/thiazide diuretics, osmotic diuresis, renal tubular disease, mineralocorticoid excess or certain antibiotics.
• Cellular shift: insulin, beta-agonists, alkalosis, refeeding and periodic paralysis.
• Low magnesium: promotes renal potassium wasting and makes replacement difficult.
• Endocrine: hyperaldosteronism, Cushing syndrome and some inherited tubulopathies.

Causes of hyperkalaemia

• Reduced excretion: acute kidney injury, chronic kidney disease, adrenal insufficiency, hypoaldosteronism or urinary obstruction.
• Medicines: potassium supplements, ACE inhibitors, ARBs, mineralocorticoid antagonists, potassium-sparing diuretics, NSAIDs, trimethoprim, heparin and some chemotherapy.
• Cellular release: metabolic acidosis, insulin deficiency, rhabdomyolysis, tumour lysis, haemolysis, burns and massive tissue injury.
• Excess intake: usually important when kidney excretion is impaired or a medication blocks excretion.
• Pseudohyperkalaemia: haemolysis, prolonged tourniquet/fist clenching, delayed processing, thrombocytosis or leukocytosis.

Clinical features

Hypokalaemia

• Fatigue, cramps, myalgia, paraesthesia, constipation or ileus.
• Generalised weakness, hyporeflexia, ascending paralysis and respiratory muscle weakness in severe cases.
• Palpitations, syncope and dysrhythmia; symptoms may be absent despite a dangerous ECG.
• Polyuria and polydipsia when renal concentrating ability is impaired.

Hyperkalaemia

• Often asymptomatic until the rhythm becomes unstable.
• Perioral or limb paraesthesia, muscle weakness, flaccid paralysis, nausea or abdominal discomfort.
• Palpitations, chest discomfort, syncope, bradycardia or sudden collapse.

Immediate contact and safety

1. Use ABCDE and call for help if the patient is weak, confused, hypotensive, breathless or has an abnormal rhythm.
2. Place the patient on continuous cardiac monitoring and obtain a 12-lead ECG urgently.
3. Confirm the potassium result with a non-haemolysed sample when pseudohyperkalaemia is plausible, but do not delay treatment for ECG-positive or unstable hyperkalaemia.
4. Establish IV access, check bedside glucose and review medicines, kidney function, urine output and recent fluid losses.
5. Stop potassium-containing fluids and medications that worsen the abnormality while a senior clinician reviews the full prescription.

ABCDE assessment

A and B — Airway and breathing

• Assess speech, respiratory effort and ability to protect the airway.
• Weakness or paralysis may impair ventilation; provide oxygen for hypoxaemia and prepare assisted ventilation if required.

C — Circulation

• Check pulse, blood pressure, capillary refill, peripheral temperature and rhythm.
• Treat dysrhythmia as a resuscitation emergency and prepare defibrillation/pacing equipment.
• Assess volume status, urine output and evidence of kidney failure, sepsis, burns or rhabdomyolysis.

D and E — Disability and exposure

• Check GCS, glucose, muscle power, reflexes, sensation, cramps, bowel sounds and pain.
• Look for burns, crush injury, renal disease, dehydration, diarrhoea, vomiting or medication patches and infusions.

ECG patterns

Investigations

• Repeat electrolytes using a properly collected sample; check sodium, chloride, bicarbonate, magnesium, calcium, phosphate, urea and creatinine.
• Venous or arterial blood gas for pH, bicarbonate, lactate and urgent potassium when laboratory delay is significant.
• Glucose to identify insulin deficiency, diabetic ketoacidosis or treatment-related hypoglycaemia.
• Urine potassium and acid–base testing when renal wasting or endocrine causes are suspected.
• Creatine kinase, urinalysis and renal assessment for rhabdomyolysis or tumour lysis.
• Digoxin level when toxicity is possible; review all medicines, supplements and salt substitutes.
• Serial ECGs and repeat potassium after every urgent intervention.

Emergency management of hyperkalaemia

Management has three simultaneous goals: protect the cardiac membrane, shift potassium into cells and remove potassium from the body. A normal ECG does not guarantee safety.

1. Stabilise the myocardium

• For ECG changes, malignant arrhythmia or severe hyperkalaemia with clinical instability, give IV calcium under the local protocol. Calcium antagonises membrane excitability but does not lower serum potassium.
• Reassess the ECG after administration and repeat calcium if changes persist according to senior/local guidance.
• Use a secure IV line and monitor for extravasation; calcium chloride is more concentrated and more tissue-irritant than calcium gluconate.

2. Shift potassium intracellularly

• Give IV insulin with glucose according to protocol; check glucose before treatment and monitor repeatedly for delayed hypoglycaemia, especially in kidney failure.
• Nebulised salbutamol can provide additional intracellular shift, but response may be variable and it does not replace insulin/glucose or calcium when indicated.
• Consider bicarbonate only for selected patients with significant metabolic acidosis and senior advice; it is not routine monotherapy.

3. Remove potassium from the body

• Stop exogenous potassium and offending medicines; treat the underlying cause.
• Use a loop diuretic only if the patient can produce urine and volume status allows.
• Use an appropriate potassium binder when available and suitable, understanding that onset is slower than membrane stabilisation and cellular shifting.
• Arrange urgent dialysis for refractory or severe hyperkalaemia, anuria, advanced kidney failure, severe acidosis, ongoing tissue breakdown or recurrent arrhythmia.

Emergency management of hypokalaemia

1. Place the patient on ECG monitoring when severe, symptomatic, rapidly falling, digoxin-treated or associated with ECG changes.
2. Identify and stop ongoing losses where possible: review diuretics, laxatives, vomiting, diarrhoea and renal wasting.
3. Measure and correct magnesium because low magnesium promotes continued potassium loss and refractory replacement.
4. Use oral potassium for stable, mild-to-moderate hypokalaemia when the gut works and there is no urgent ECG or neuromuscular threat.
5. Use IV potassium for severe/symptomatic hypokalaemia, ECG changes, paralysis or inability to absorb orally. Use a pump, a secure line, the prescribed concentration and the local maximum rate—never give IV potassium as a rapid push.
6. Recheck potassium, magnesium, renal function and ECG after replacement; avoid overshoot, especially in kidney disease.

Medication and cause-specific management

• Diuretics: review indication and dose; replace losses and consider a potassium-sparing strategy only under clinician supervision.
• DKA or insulin therapy: follow the DKA protocol; insulin can lower potassium rapidly, so assess potassium before and during treatment.
• Renal failure: adjust replacement and medication, involve nephrology early and consider dialysis for severe hyperkalaemia.
• Gastrointestinal loss: restore volume, potassium and magnesium and treat vomiting/diarrhoea.
• Rhabdomyolysis or tumour lysis: manage the cause, renal injury and rapidly rising potassium in a critical-care setting.
• Adrenal insufficiency: assess shock, glucose and sodium; give urgent steroid therapy under the relevant emergency protocol.

Monitoring after treatment

Nursing interventions

• Confirm the sample, label the urgency and report critical values immediately.
• Maintain continuous ECG monitoring and document rhythm changes with times and interventions.
• Use an infusion pump and independent double-check for IV potassium, calcium, insulin and concentrated electrolytes.
• Check IV patency, inspect for extravasation and never administer IV potassium by bolus.
• Monitor capillary glucose frequently after insulin–glucose therapy and provide rescue glucose according to protocol.
• Measure urine output, fluid balance, neurological status, muscle power and respiratory effort.
• Educate about medication, salt substitutes, supplements, renal follow-up and dietary advice from the clinical team.

Complications

• Ventricular tachycardia, ventricular fibrillation, conduction block and sudden cardiac arrest.
• Respiratory failure from muscle weakness or fluid overload.
• Rhabdomyolysis, acute kidney injury and metabolic acidosis.
• Hypoglycaemia after insulin therapy, tissue injury from extravasated calcium and potassium, and rebound hyperkalaemia.
• Neurological injury from hypoperfusion, falls and prolonged paralysis.

Scenario-based application

Prevention and patient education

• Review renal function and electrolytes after medication changes, illness, vomiting, diarrhoea or diuretic adjustment.
• Do not self-start potassium tablets, herbal remedies or potassium-containing salt substitutes.
• Teach people with kidney disease or heart failure which medicines and foods require professional advice.
• Provide sick-day guidance where appropriate and ensure access to follow-up blood testing.
• Prevent recurrent diarrhoea, vomiting, malnutrition and uncontrolled diabetes.

Common errors to avoid

• Treating the laboratory number without an ECG, repeat sample or cause assessment.
• Assuming a normal ECG rules out dangerous hyperkalaemia.
• Giving calcium as if it removes potassium—it stabilises the myocardium only.
• Giving insulin without glucose planning and prolonged glucose monitoring.
• Giving IV potassium by bolus, using an unmonitored infusion or ignoring renal failure.
• Failing to correct magnesium in refractory hypokalaemia.
• Discharging a symptomatic, severe or ECG-positive patient without monitored follow-up.

Documentation checklist

• Symptoms, onset, comorbidities, medicines, supplements, fluid losses and kidney function.
• Initial and repeat potassium, magnesium, glucose, acid–base results and ECG findings.
• Time, dose, route and response to calcium, insulin/glucose, beta-agonist, potassium and fluids.
• Monitoring frequency, urine output, adverse events, senior/nephrology discussion and disposition.
• Cause-specific prevention advice, medication changes and follow-up plan.

Quick revision questions

1. Why can a serum potassium value misrepresent total-body stores?
2. List five causes of hypokalaemia and five causes of hyperkalaemia.
3. What ECG changes suggest dangerous hyperkalaemia?
4. What are the three simultaneous treatment goals in severe hyperkalaemia?
5. Why must magnesium be checked in hypokalaemia?
6. When is IV rather than oral potassium replacement appropriate?
7. Why is glucose monitoring essential after insulin–glucose therapy?
8. When should urgent dialysis be considered?

Key takeaways

Further reading

• KDIGO: Acute hyperkalaemia in the emergency department
• Clinical guideline: Hyperkalaemia
• Clinical guideline: Hypokalaemia
• NHS England: Safe and timely management of hyperkalaemia