Potassium disorders — high and low potassium in Australian general practice

Potassium is the principal intracellular cation, essential for nerve conduction, muscle contraction, and stable cardiac rhythm. The normal serum range is 3.5–5.0 mmol/L. Disorders in either direction are common in Australian general practice and carry significant arrhythmia risk.

Both hyperkalaemia and hypokalaemia are frequently driven by medicines — the same drugs that protect the heart and kidneys can push potassium up (ACE inhibitors, ARBs, spironolactone, NSAIDs), while diuretics tend to push it down. The clinical task is always to classify severity, identify the cause, and match the urgency of response to the clinical picture.

A. Core clinical — the AU general-practice framework

History

The most important historical question is what medications is this person taking? Per eTG and KHA-CARI, the following drug review is non-negotiable at every potassium-derangement visit:

• Raising potassium: ACE inhibitors, angiotensin receptor blockers, aldosterone antagonists (spironolactone, eplerenone, finerenone), NSAIDs (including over-the-counter ibuprofen and naproxen), trimethoprim (including in co-trimoxazole), heparin, calcineurin inhibitors, non-selective beta-blockers, digoxin, potassium-containing salt substitutes
• Lowering potassium: loop diuretics (frusemide, ethacrynic acid), thiazide diuretics, beta-2-agonists (salbutamol at high doses), insulin, laxative or diuretic misuse

Symptom screen for hyperkalaemia: weakness (legs first, ascending), paraesthesia, palpitations, nausea. For hypokalaemia: muscle cramps, fatigue, weakness, constipation, palpitations, excessive urination. Absence of symptoms is common at mild-to-moderate levels — it does not exclude meaningful derangement.

Risk-factor inventory: chronic kidney disease (CKD), diabetes mellitus, heart failure, eating disorder (laxative or diuretic misuse in a young woman), recent gastrointestinal illness with vomiting or diarrhoea, recent chemotherapy (tumour-lysis syndrome), recent heat exposure or strenuous exercise.

Examination

• Volume status — jugular venous pressure, lung-base crackles, peripheral oedema (CKD, heart failure context); postural hypotension (hypovolaemia driving hypokalaemia or pre-renal hyperkalaemia)
• Blood pressure — hypertension with hypokalaemia raises suspicion of primary aldosteronism or Cushing syndrome; hypotension with hyperkalaemia suggests Addison’s disease
• Cardiovascular — rhythm (AF, ectopy), pulse rate and character
• Neurological — flaccid weakness, areflexia, ascending paralysis in severe hypokalaemia
• Abdomen — bowel sounds (ileus in hypokalaemia); palpable bladder (obstruction causing AKI and hyperkalaemia)
• Skin — hyperpigmentation (Addison’s), striae and central obesity (Cushing’s)

Investigations

Per eTG and the Australian Medicines Handbook:

First line (every episode):

• UEC (urea, electrolytes, creatinine, eGFR, bicarbonate) — note anion gap and chloride
• Magnesium — co-deficiency is universal in refractory hypokalaemia
• Glucose and HbA1c
• Repeat potassium in lithium-heparin tube if haemolysis or pseudohyperkalaemia suspected
• ECG — mandatory for K above 6.0 mmol/L, K below 2.5 mmol/L, or any cardiac symptom

Pseudohyperkalaemia check: when an isolated high potassium has no clinical correlate, repeat with free-flowing venesection before any treatment. Tourniquet use, fist clenching, haemolysis, extreme thrombocytosis or leukaemia all artificially raise the measured level.

Second line (aetiology workup):

• Aldosterone-renin ratio — for hypertension plus hypokalaemia, or resistant hypertension; withhold aldosterone antagonists for 4–6 weeks before sampling per Endocrine Society 2025 and RACGP guidance
• Morning cortisol and short Synacthen test — if Addison’s disease is suspected (hypotension, hyperpigmentation, hyponatraemia with hyperkalaemia)
• Thyroid function tests — thyrotoxic periodic paralysis (sudden severe hypokalaemia in Asian males)
• CK — rhabdomyolysis
• Uric acid, phosphate, LDH — tumour-lysis syndrome
• Urine potassium — to distinguish renal loss (>20 mmol/24 h) from extra-renal loss (vomiting, diarrhoea) when the cause is unclear

Severity grading

Condition	Mild	Moderate	Severe
Hyperkalaemia	5.1–5.5 mmol/L	5.6–6.0 mmol/L	>6.0 mmol/L OR any ECG change OR symptomatic
Hypokalaemia	3.0–3.4 mmol/L	2.5–2.9 mmol/L	Under 2.5 mmol/L OR ECG change OR symptomatic

B. ECG changes and cardiac arrhythmia risk

The AHA ACLS 2020 algorithm and KDIGO 2024 both mandate ECG in all symptomatic or severe potassium disorders because the absolute level does not reliably predict the ECG pattern, and ECG changes guide the aggressiveness of treatment.

Hyperkalaemia ECG progression:

• K 5.5–6.5: peaked, narrow-based, symmetric T-waves — most prominent in V2–V4
• K 6.5–7.5: PR prolongation, flattened or absent P-waves, AV block
• K 7.5–8.5: widened QRS, bundle-branch morphology, fascicular block
• K >8.5: sine-wave pattern (QRS merging with T), VF, or asystole

The ECG can appear normal even with dangerous levels. A normal ECG in the context of K >6.5 does not eliminate the urgency of treatment.

Hypokalaemia ECG findings:

• T-wave flattening or inversion
• Prominent U-waves (most visible in V2–V3) — pathognomonic when marked
• ST-segment depression
• QTc prolongation — risk of torsades de pointes, especially when co-existing hypomagnesaemia or QT-prolonging drugs are present

C. Management — severity-guided

Severe hyperkalaemia (K >6.0 OR any ECG change OR symptomatic)

This is a medical emergency. In a community setting, call 000 for transfer to hospital. Initiate on-site:

1. IV calcium gluconate 10% — 10 mL slow push over 2–3 minutes — membrane stabilisation; onset 1–3 minutes, duration 30–60 minutes. Repeat every 5–10 minutes if ECG changes persist. Does not lower potassium — it protects the heart while other measures take effect. Per AHA ACLS 2020.
2. Insulin 10 units actrapid + 50 mL of 50% dextrose IV — shifts potassium intracellularly; onset 15–30 minutes. Monitor blood glucose hourly for at least six hours (delayed hypoglycaemia is common in CKD).
3. Salbutamol 10–20 mg nebulised — additive intracellular potassium shift; onset 15–30 minutes; tachycardia expected.
4. Sodium bicarbonate 8.4% 50–100 mL IV — only if pH below 7.20; ineffective if pH is normal.
5. Definitive potassium removal — per eTG: patiromer (Veltassa) or sodium zirconium cyclosilicate (Lokelma) for chronic management in CKD on RAS blockade (PBS Authority Required); sodium polystyrene sulfonate (Resonium A, PBS general schedule) as second-line due to slower onset and intestinal necrosis risk in post-operative or ileus settings.
6. Dialysis — for anuria, AKI with refractory hyperkalaemia, or levels unresponsive to treatment.

Moderate hyperkalaemia (5.6–6.0, no ECG change)

• Dietary potassium review — written list of high-potassium foods to reduce (bananas, citrus, tomatoes, avocado, potatoes, spinach, salt substitutes)
• Medication review — assess each drug’s necessity and consider whether a potassium-binder enables continuation of the cardiorenal protective drug
• Recheck within 2–3 days

Mild hyperkalaemia (5.1–5.5)

Address the cause — medication review, salt-substitute elimination, sick-day rules — and recheck in one to two weeks.

Chronic hyperkalaemia in CKD

The KDIGO 2024 four-pillar strategy supports continuing ACE inhibitors, ARBs, and mineralocorticoid receptor antagonists alongside a potassium-binding agent rather than abandoning proven cardiorenal therapy. Patiromer or sodium zirconium cyclosilicate, both PBS Authority listed for CKD on RAS blockade, enable this approach. Advise patients to avoid potassium-containing salt substitutes (Lo-Salt, No-Salt) — a single tablespoon can deliver a substantial potassium load.

Hypokalaemia — severity-guided correction

• Mild (3.0–3.4): oral potassium chloride 40–80 mmol/day in divided doses (Slow-K, Span-K, effervescent sachets), plus dietary repletion
• Moderate (2.5–2.9): oral 80–120 mmol/day or IV if unable to eat or vomiting
• Severe (K below 2.5 OR ECG change OR symptomatic): IV KCl — peripheral line maximum 10 mmol/hour in concentrations ≤40 mmol/L; central line maximum 20–40 mmol/hour with cardiac monitoring. Never administer undiluted IV KCl — this has caused cardiac arrest (nationally classified sentinel event)

Replace magnesium first in refractory hypokalaemia. Per eTG, hypomagnesaemia causes renal potassium wasting through the ROMK channel. Give magnesium sulfate 2–4 g IV (10–20 mmol) for severe depletion, or oral magnesium aspartate or glycinate 5–10 mmol/day for chronic repletion.

D. Australian operations

MBS item numbers relevant to potassium disorders:

• Standard consultations: Level B (item 23), Level C (item 36, ≥20 minutes, appropriate for complex electrolyte review), Level D (item 44)
• Telehealth: video item 91790, phone Level B item 92029 for stable monitoring follow-up
• GP Chronic Condition Management Plan (items 965 and 967) — CKD with recurrent electrolyte disorders qualifies
• ECG: item 11700 — bill this for every patient with K above 6.0 or below 2.5 in your rooms
• ATSI Health Assessment: item 715 — annual; appropriate vehicle for CKD electrolyte surveillance

PBS medicines: Potassium chloride oral preparations are PBS general schedule. Patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma) are PBS Authority Required for chronic hyperkalaemia in CKD on RAS blockade — verify current criteria at pbs.gov.au. Sodium polystyrene sulfonate (Resonium A) is PBS general schedule. Spironolactone, amiloride, and frusemide are PBS general schedule.

Primary aldosteronism testing — aldosterone-renin ratio is Medicare rebatable. Confirmatory testing and adrenal vein sampling occur at specialist level. The MJA 2022 Australian study found ~14% of hypertensive Australian adults in general practice had primary aldosteronism — a readily treatable and commonly missed diagnosis.

Referral pathways:

• Routine nephrology: CKD with persistent K >5.5, suspected Bartter or Gitelman syndrome, renal tubular acidosis
• Routine endocrinology: positive aldosterone-renin ratio, suspected Cushing’s, confirmed Addison’s
• Urgent ED transfer: K above 6.0, K below 2.5, any ECG change, paralysis, suspected adrenal crisis, dialysis patient off schedule

E. Special populations

CKD stages 4–5. The most high-risk group for hyperkalaemia. Target lithium level 0.4–0.6 mmol/L in dialysis-dependent patients. The KDIGO 2024 approach: individualise dietary potassium counselling rather than blanket restriction — fruit and vegetable intake has cardiovascular benefit that matters more in CKD 1–3 than the modest potassium load.

Older adults. Age-related decline in renal function, combined with polypharmacy including multiple antihypertensive and diuretic agents, makes both hyperkalaemia and hypokalaemia more frequent and more dangerous. Falls risk is amplified by hypokalaemia-driven weakness. Reassess the medication burden at each visit using a STOPP/START framework.

Eating disorders. Recurrent, unexplained hypokalaemia in a young woman — especially without an obvious diuretic — should prompt careful enquiry about laxative or diuretic misuse and vomiting. The clinical approach is sensitive and non-confrontational; use the SCOFF questionnaire. Refer to a multidisciplinary eating-disorder service.

Pregnancy. Vomiting in hyperemesis gravidarum drives significant hypokalaemia and requires intravenous replacement and correction of hypomagnesaemia. ACE inhibitors and ARBs are contraindicated in pregnancy — medication review is essential when hyperkalaemia is detected in a pregnant person with CKD or hypertension.

Dialysis-dependent CKD. A missed haemodialysis session can produce K >7.0 mmol/L within 24–48 hours. Patients presenting unwell after a missed session need urgent ECG and blood potassium — do not wait for a scheduled dialysis slot.

When to escalate

Call 000 or arrange immediate transfer to hospital:

• Serum K >6.0 mmol/L with any ECG change
• Serum K >6.5 mmol/L (regardless of ECG)
• Serum K below 2.5 mmol/L with ECG change, paralysis, or rhabdomyolysis
• Any potassium disorder with new weakness, arrhythmia, loss of consciousness, or ileus
• Dialysis-dependent patient with missed session and high potassium
• Suspected Addisonian crisis (hyperkalaemia + hyponatraemia + hypotension)
• Suspected tumour-lysis syndrome in a patient on chemotherapy

Refer to nephrology or endocrinology for: persistent hyperkalaemia >5.5 not correctable in general practice, confirmed primary aldosteronism, suspected Cushing’s or Addison’s, Bartter or Gitelman syndrome.

What this article is and is not

This is general health information drawn from current Australian guidelines — Therapeutic Guidelines, Australian Medicines Handbook, NPS MedicineWise, Kidney Health Australia, and the KDIGO 2024 CKD guideline. It is not personal medical advice and does not create a doctor–patient relationship. Decisions about potassium replacement or reduction, medication adjustment, and escalation are made in the context of the individual clinical situation with the treating GP and specialist team.

For Australian consumer-friendly information: HealthDirect, Better Health Channel, Kidney Health Australia.

For a life-threatening cardiac emergency: call 000 immediately.

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Sources cited

1. Therapeutic Guidelines — Electrolyte disorders
2. Kidney Health Australia / KHA-CARI Guidelines
3. RACGP AJGP — Hyperkalaemia in general practice
4. Australian Medicines Handbook
5. NPS MedicineWise — Diuretics and electrolytes
6. KDIGO 2024 CKD Clinical Practice Guideline
7. American Heart Association — ACLS hyperkalaemia algorithm 2020
8. Endocrine Society 2025 Primary Aldosteronism Guideline
9. Libianto et al. — Prevalence of primary aldosteronism in Australian general practice (MJA 2022)
10. TGA — Resonium safety alert
11. HealthDirect — Potassium
12. Better Health Channel — Body fluids and electrolytes