Hyperkalaemia Algorithm

Safety

Red Flags — Life-Threatening Hyperkalaemia & Pseudohyperkalaemia

Done

Adult primary-care algorithm. IV treatment is hospital-only and appears in step 6 for reference — it is not a primary-care instruction.

One rule, everywhere: if K⁺ ≥6.5 mmol/L, there are ECG changes, significant symptoms, AKI or oliguria, or a rapidly rising potassium — initiate emergency transfer and do not wait for repeat confirmation. Obtain a repeat or point-of-care potassium in parallel where that does not delay treatment; a critical potassium is never converted into a routine repeat-blood task, and must not remain in an inbox or a routine repeat queue overnight. Categories used throughout: mild 5.5–5.9 · moderate 6.0–6.4 · severe ≥6.5 mmol/L; 5.1–5.4 is above the local reference range, not "mild hyperkalaemia". A normal ECG does not exclude severe hyperkalaemia.

K⁺ ≥6.5 mmol/L on any sample Severe hyperkalaemia — risk of ventricular fibrillation and cardiac arrest at any moment. Immediate emergency admission / ambulance transfer. Do not wait for repeat testing. Perform an ECG only if immediately available and it does not delay transfer. Do not attempt IV calcium in routine primary care unless an explicit local emergency protocol, equipment and trained, authorised staff are available — the decision to give calcium belongs to the receiving emergency or acute team.

ECG changes at any potassium level New broad QRS, bradyarrhythmia, sine-wave pattern, PR prolongation, loss of P waves, or peaked T waves (read in multiple leads and in clinical context) potentially attributable to hyperkalaemia — requires emergency clinical assessment and treatment. Compare with previous ECGs and consider alternative causes (an isolated broad QRS may be bundle branch block, ventricular pacing or sodium-channel blockade), but do not let this cause false reassurance or delay treatment when the clinical picture is consistent. Emergency transfer; hospital treatment is set out in step 6 for reference.

Significant symptoms at any potassium level Muscle weakness, paralysis, palpitations, syncope — neuromuscular toxicity, with ascending flaccid weakness that can reach the respiratory muscles. Emergency transfer. Any symptom attributable to hyperkalaemia is a life-threatening emergency, whatever the number.

AKI, oliguria or anuria — and the other escalation triggers Renal failure driving the potassium, which cannot be excreted; the risk compounds rapidly. Also escalate for a missed dialysis session, rhabdomyolysis or tumour lysis, and for a rapidly rising potassium. Emergency transfer. Withhold contributing drugs pending acute assessment — ACE inhibitor, ARB, MRA, potassium-sparing diuretic, NSAID, trimethoprim, potassium supplements and potassium-containing salt substitutes — and record what was withheld in the handover.

Suspected digoxin toxicity Not every incidental potassium rise on long-term digoxin. If toxicity is suspected — particularly with arrhythmia, bradycardia, gastrointestinal, visual or neurological symptoms, or significant hyperkalaemia — arrange emergency assessment with an ECG, a digoxin concentration and urgent toxicology or acute medical advice. Hyperkalaemia in acute digoxin toxicity is an emergency — discuss urgently with the acute medical/toxicology team regarding digoxin-specific antibody fragments, and do not delay emergency transfer for a digoxin level. Chronic stable digoxin use with a mild incidental rise is assessed on the usual criteria above. Calcium is neither categorically contraindicated nor inevitably harmful here — the receiving team follows the relevant toxicology and resuscitation protocol.

Pseudohyperkalaemia — only where no red flag applies Common enough to consider, particularly with haemolysis, thrombocytosis, leucocytosis, difficult venepuncture, a prolonged tourniquet or delayed processing. It must not be presumed when there are symptoms, ECG changes, AKI, oliguria, severe hyperkalaemia or a rapidly rising result. Consider plasma potassium where thrombocytosis or marked leucocytosis is present. Repeat with free-flow venepuncture (no tourniquet, or released after vein entry), minimal fist clenching, prompt processing under 30 minutes and no transit delay. Repeat first only when the patient is asymptomatic, the ECG is normal and none of the rows above applies — otherwise transfer, and confirm in parallel.

The cardiac membrane stabilisation principle of calcium gluconate is one of the most important emergency pharmacology facts in primary care — IV calcium gluconate does NOT lower the serum potassium. Its mechanism is to raise the threshold potential of the cardiac myocyte membrane, reducing the depolarisation risk from the elevated extracellular K⁺. It buys time while definitive K⁺-lowering measures are started, and the patient still has hyperkalaemia afterwards, so K⁺-lowering treatment remains mandatory. This is hospital pharmacology, given in a monitored environment by staff trained and authorised to administer IV calcium, at the dose and preparation set by the local UKKA-aligned protocol (step 6). In primary care the action is immediate transfer, not improvised IV treatment. Pseudohyperkalaemia is common enough to consider, but must not be presumed with symptoms, ECG changes, AKI, oliguria, severe hyperkalaemia or a rapid rise. The mechanism is potassium released from red blood cells during haemolysis in the sample tube, which can be caused by: prolonged tourniquet use (avoid or release after vein entry), repeated fist clenching (dramatically increases local K⁺), delayed sample processing (red cell K⁺ leaks into plasma over time), mechanical trauma during venepuncture, and extreme thrombocytosis or leucocytosis (release from platelets/WBCs — check FBC). The clinical implication is that a single asymptomatic K⁺ of 5.5–5.9 mmol/L in a patient without CKD, without precipitating drugs, and with a haemolysed or borderline sample can reasonably be repeated before acting. That logic applies only when no red flag is present — at 6.5 or above, or with ECG changes, significant symptoms, AKI or oliguria, or a rapidly rising potassium, transfer is arranged first and confirmation happens in parallel. A critical result must not remain in an inbox or a routine repeat queue overnight.

Diagnose

Classification — Causes of True Hyperkalaemia

Done

Reduced renal excretion (most common overall cause)

CKD/AKI: reduced glomerular filtration → reduced K⁺ excretion. CKD stage 3b+ significant risk; stage 4–5 = major risk. Drugs impairing renal K⁺ excretion: ACE inhibitors (reduce angiotensin II → reduce aldosterone → reduce K⁺ excretion), ARBs (same mechanism), K⁺-sparing diuretics (spironolactone, eplerenone — aldosterone antagonists; amiloride, triamterene — direct ENaC blockade), NSAIDs (reduce prostaglandin-mediated renin release → reduce aldosterone), trimethoprim (blocks ENaC — same mechanism as amiloride; greatest at the high doses used to treat Pneumocystis pneumonia, but can occur at standard doses in older people and in renal impairment), pentamidine.

Mineralocorticoid deficiency

Addison's disease (primary adrenal insufficiency): aldosterone deficiency → K⁺ retention + Na⁺ loss + hypotension. Classic electrolytes: hyponatraemia + hyperkalaemia. Pigmentation, postural hypotension, fatigue, weight loss. Short synacthen test. Hyporeninaemic hypoaldosteronism (type 4 RTA): diabetic nephropathy most common cause — low renin → low aldosterone without adrenal pathology. Heparin: suppresses aldosterone synthesis (rare, dose-dependent).

Transcellular shift (K⁺ moves from intracellular to extracellular)

Metabolic acidosis may contribute, particularly in advanced CKD and type 4 RTA, but the potassium response cannot be reliably calculated from the pH alone. DKA: total-body potassium is depleted despite an initially normal or high serum potassium — management follows the current DKA protocol, with frequent potassium and glucose monitoring in hospital. Insulin deficiency: insulin drives K⁺ into cells — absence = K⁺ exits. Beta-blockers: block beta2-mediated K⁺ uptake into cells. Digoxin toxicity: inhibits Na⁺/K⁺-ATPase. Succinylcholine: depolarising muscle relaxant.

Excessive K⁺ intake (rare cause alone) · specialist/acute causes

K⁺ supplements (oral or IV if excess), K⁺-containing salt substitutes (LoSalt, Miso, mineral-rich alternatives — significant K⁺ content). Specialist/acute causes (uncommon in primary care): blood transfusion (stored blood has high K⁺ from cell lysis), rhabdomyolysis (massive cell K⁺ release), tumour lysis syndrome (chemotherapy-induced cell death).

Drug review — high-yield causes

ACEi/ARB + spironolactone/eplerenone combination (heart failure triple therapy — very high risk) · NSAIDs (impair renal K⁺ excretion + worsen CKD) · Trimethoprim (high treatment doses, and standard doses in older people or CKD) · Heparin (LMWH > UFH) · Ciclosporin/tacrolimus (renal vasoconstriction) · K⁺ supplements in CKD · Digoxin toxicity

The ACEi/ARB + spironolactone triple therapy combination for heart failure is the highest-risk prescribing scenario for hyperkalaemia in primary care — RALES trial (spironolactone + ACEi in CHF) showed 30% reduction in mortality but a 2% rate of serious hyperkalaemia. When ARBs are added to ACEi + spironolactone (quadruple RAAS blockade, sometimes seen in complex heart failure management), the hyperkalaemia risk is very high. Guidelines recommend monitoring K⁺ and eGFR 1–2 weeks after each dose change and at risk-based intervals in stable patients. The trimethoprim hyperkalaemia mechanism is underappreciated — trimethoprim — most markedly at the high co-trimoxazole doses used to treat Pneumocystis jirovecii pneumonia, but also at standard doses in older people and CKD — structurally resembles amiloride and blocks the epithelial sodium channel (ENaC) in the distal nephron with the same mechanism as K⁺-sparing diuretics, causing meaningful K⁺ retention. This is clinically significant in patients on trimethoprim prophylaxis who also have CKD, are taking ACEi/ARB, or have other K⁺-elevating risk factors. K⁺-containing salt substitutes (LoSalt and similar products contain approximately 350 mg of K⁺ per gram — compared to approximately 0 mg in regular NaCl) are a recognised hazard and should be avoided in people with kidney disease, diabetes, older age, pregnancy and those taking ACE inhibitors or ARBs. These products can cause dangerous hyperkalaemia in at-risk patients. Asking about salt substitute use should be part of the dietary history in any patient with hyperkalaemia.

Diagnose

Investigations & ECG Interpretation

Done

Repeat K⁺ — but never before transfer

Confirm before acting only when no red flag applies; at K⁺ ≥6.5, with ECG changes, significant symptoms, AKI or oliguria, or a rapidly rising potassium, transfer first and confirm in parallel. Free-flow venepuncture: no prolonged tourniquet, no fist clenching, prompt processing under 30 minutes, non-haemolysed sample. Request "urgent". Plasma K⁺ (lithium heparin) is preferred to serum (SST) — less pseudohyperkalaemia artefact. Point-of-care or blood-gas potassium may be used for rapid decision-making; confirm with a laboratory sample when clinically safe. Blood-gas analysers may not reliably flag haemolysis, so a discrepancy needs clinical correlation, not automatic dismissal of either value.

ECG

Urgent 12-lead ECG at K⁺ ≥6.0, before any decision to manage in the community. At 5.5–5.9, arrange an ECG if there is cardiac disease, a rapid rise, significant renal impairment, concerning symptoms or inability to ensure prompt follow-up. Mild (5.5–5.9): tall, narrow, symmetrical peaked T waves — an early sign, best seen V2–V4, and interpreted in multiple leads and in clinical context rather than as a standalone diagnosis. Moderate (6.0–6.4): PR prolongation, P-wave flattening, broadening QRS. Severe (≥6.5): sine-wave pattern, loss of P waves, junctional rhythm, VF, asystole. New broad QRS, bradyarrhythmia, sine-wave pattern or another ECG abnormality potentially attributable to hyperkalaemia is an emergency — but a broad QRS may equally be bundle branch block, ventricular pacing or sodium-channel blockade, so compare with a previous ECG. At ≥6.5 the ECG must not delay transfer, and a normal ECG does not exclude severe hyperkalaemia.

Investigations — conditional, not a panel

All confirmed hyperkalaemia: U&E + eGFR bicarbonate glucose FBC (thrombocytosis or leucocytosis causing pseudohyperkalaemia), a medication review, and an ECG according to severity. Only if the trigger is present: muscle injury or tumour lysis → CK, urate, phosphate, calcium, LDH via acute services · hyponatraemia, hypotension or pigmentation → emergency adrenal assessment; cortisol only if it does not delay treatment · persistent unexplained hyperkalaemia with a low bicarbonate → renal assessment for type 4 RTA or hypoaldosteronism, where aldosterone and renin are specialist-directed. Do not order the whole list routinely — it generates inappropriate testing and distracts from transfer.

Risk stratification — one set of categories

Emergency transfer Severe: K⁺ ≥6.5, or ECG changes, significant symptoms, AKI or oliguria, missed dialysis, rhabdomyolysis, tumour lysis, or a rapidly rising potassium — at any level. Do not wait for a repeat · Same-day Moderate: K⁺ 6.0–6.4 — urgent 12-lead ECG; same-day hospital assessment if acutely unwell or with AKI; if well, repeat within 1 day after discussing with the renal/medical team; admission according to the ECG, symptoms, renal function, trend, cause and reliability of follow-up · Primary care with review Mild: K⁺ 5.5–5.9, asymptomatic, clinically stable, no AKI — review urgently (ideally the same working day), check for haemolysis, repeat K⁺ within 3 days (sooner if indicated), ECG if indicated as above — reversible contributors, AKI assessment, hydration and diet reviewed, with a named reviewer, a repeat date and a written escalation threshold · K⁺ 5.1–5.4 is above the local reference range rather than hyperkalaemia — recheck in context, review contributors in CKD or on RAAS therapy

The ECG changes of hyperkalaemia follow a predictable progression from mild to severe, and the QRS width is the single most important parameter for urgency — a widened QRS (>120 ms) from hyperkalaemia indicates that the ventricular conduction system is critically compromised, and VF or cardiac arrest can occur within minutes. This makes a new broad QRS more urgent than the absolute number: a K⁺ of 6.0 with a newly broad QRS is more immediately dangerous than a higher level with an unchanged narrow QRS — provided the broadening is genuinely new, since bundle branch block, pacing and sodium-channel blockade produce the same appearance. The peaked T waves are the earliest ECG sign and can appear in the mild range (5.5–5.9) — they are tall, narrow, and symmetrical, best seen in the precordial leads (V2–V4), and are often described as 'tented' (pointed rather than rounded apex). This contrasts with the tall broad asymmetric T waves of myocardial ischaemia. The sine wave pattern (QRS and T wave fusing into a continuous oscillating waveform) represents an immediately pre-arrest rhythm — any patient with a sine-wave ECG in primary care needs an immediate 999 transfer, with IV calcium given by the receiving team in a monitored setting. The risk stratification table is important for primary care decision-making — the dividing lines between 'phone 999,' 'send to hospital same day,' and 'urgent next-day review' are based on K⁺ level, ECG status, symptoms, and renal function. A K⁺ of 6.2 with a haemolysed sample, a normal ECG and no symptoms in a patient with CKD 3b warrants same-day assessment with a repeat rather than an ambulance — but the clinician must be certain the ECG is genuinely normal and the patient genuinely well, and a normal ECG does not exclude severe hyperkalaemia. At 6.5 or above, or with any red flag, the repeat happens in parallel with transfer, never instead of it.

Diagnose

Drug Review & Dietary Assessment

Done

Systematic drug review

List every current medication and check each against K⁺-elevating risk. High-risk combinations: ACEi + ARB (dual RAAS blockade — avoid in routine practice), ACEi/ARB + K⁺-sparing diuretic (spironolactone, eplerenone, amiloride), ACEi/ARB + NSAIDs (very common combination — NSAIDs impair renal K⁺ excretion via prostaglandin suppression + reduce GFR → less K⁺ filtered). Consider dose reduction or cessation of offending drug — weigh benefit vs risk (e.g., spironolactone in resistant hypertension may be more beneficial than its K⁺ risk warrants withdrawal).

Dietary potassium assessment

Start with the high-yield sources, not a long exclusion list. Potassium-containing salt substitutes (LoSalt, Nu-Salt and similar) — ask at every hyperkalaemia consultation; they should be avoided in CKD or on RAAS therapy. Then potassium supplements, and any concentrated sources the history actually points to — tomato concentrate, dried fruit, large amounts of fruit juice or chocolate. Advice is individualised and framed around substitution rather than broad exclusion: healthy foods such as milk, pulses, nuts and vegetables should not be restricted reflexively. Advanced CKD needs renal dietetic input rather than a generic list.

Renal function review

Potassium rises progressively from CKD stage 3b. Do not make eGFR-based stop decisions in isolation — ACE inhibitors and ARBs are often appropriately continued at low eGFR, and the decision depends on the indication, albuminuria, the potassium, the change in creatinine, blood pressure and specialist context. Follow CKD and heart-failure guidance, and seek renal or cardiology advice where RAAS therapy is clinically important. CKD (NICE NG203): do not routinely start RAAS inhibition if pretreatment K⁺ >5.0 mmol/L; stop it at K⁺ ≥6.0 mmol/L after reviewing other potassium-raising drugs; repeat eGFR and K⁺ 1–2 weeks after initiation and each dose increase; do not routinely modify the dose for an eGFR fall <25% or creatinine rise <30%. Heart failure: review the potassium trend, renal function, congestion, blood pressure and the importance of prognostic therapy; discuss with the heart-failure or renal team when hyperkalaemia is persistent or limits treatment, and do not discontinue prognostic therapy indefinitely without a reintroduction plan. Acute illness: UKKA advises withholding RAAS drugs during sepsis, hypovolaemia or AKI at all severities of hyperkalaemia — distinct from stable chronic hyperkalaemia. AKI: any acute potassium rise with a rising creatinine is AKI until proved otherwise — look for dehydration, obstruction, nephrotoxins and infection.

Context assessment

Diabetes: insulin deficiency + renal insufficiency = highest-risk combination. DKA: total-body potassium is depleted despite an initially normal or high serum potassium — management follows the current DKA protocol, with frequent potassium and glucose monitoring in hospital. Type 4 RTA (diabetic nephropathy): hyporeninaemic hypoaldosteronism — K⁺ chronically elevated despite only moderate CKD. Adrenal: Addison's = bilateral adrenal failure. Hyponatraemia + hyperkalaemia = Addison's pattern — check morning cortisol.

The ACEi + ARB + spironolactone combination (sometimes called 'triple RAAS blockade') is explicitly discouraged in most UK guidelines because of the high risk of hyperkalaemia and AKI without additional cardiovascular benefit compared to optimal single-agent RAAS blockade. NICE NG203 (CKD, 2021) specifically states that dual RAAS blockade (ACEi + ARB together) should not be used. The prescribing scenario that commonly creates triple RAAS blockade is: a GP prescribes ACEi for hypertension/heart failure, a cardiologist adds spironolactone for resistant hypertension or heart failure, and the patient also self-medicates with ibuprofen — neither prescriber sees the complete picture. Medication reconciliation at each consultation (reviewing the full drug list including OTC medications) is the single most important preventive action for iatrogenic hyperkalaemia. The salt substitute issue deserves special attention because it creates a false sense of safety: patients with CKD or heart failure who have been advised to reduce salt intake appropriately switch to salt substitutes — which contain potassium chloride instead of sodium chloride and can deliver several grams of potassium per day. A patient with CKD-4 on spironolactone who uses LoSalt liberally and eats a high-potassium diet can have K⁺ levels that are genuinely dangerous. Ask specifically about salt substitute use in the dietary history of any patient with hyperkalaemia.

Refer

Referral Pathways

Done

Emergency transfer

K⁺ ≥6.5 on any sample — do not wait for repeat testing · any ECG change potentially attributable to hyperkalaemia at any level (new broad QRS, bradyarrhythmia, sine wave, PR prolongation, loss of P waves, peaked T waves in context) · significant symptoms — weakness, paralysis, palpitations, syncope · AKI, oliguria or anuria · missed dialysis, rhabdomyolysis, tumour lysis · a rapidly rising potassium · suspected digoxin toxicity (arrhythmia, bradycardia, GI, visual or neurological symptoms). ECG only if immediately available and it does not delay transfer. Withhold contributing drugs and record what was withheld

Same-day assessment

Moderate: K⁺ 6.0–6.4 — urgent ECG; same-day hospital assessment if acutely unwell or with AKI; if well, repeat within 1 day after discussing with the renal/medical team · K⁺ 5.5–5.9 with a rising creatinine, acute illness, concerning symptoms, a rapid rise or unreliable follow-up · significant hyperkalaemia on an MRA plus an ACE inhibitor or ARB · suspected type 4 RTA with significant renal impairment or acidosis · hyperkalaemia with hypotension and hyponatraemia — treat a suspected adrenal crisis as an emergency in its own right, ahead of any cortisol test · unable to obtain an ECG or reliable follow-up with a confirmed K⁺ ≥5.5

Nephrology / cardiology

CKD with persistent hyperkalaemia despite removal of reversible contributors · where RAAS therapy is clinically important and hyperkalaemia is limiting it — heart failure, albuminuric CKD · potassium-binder consideration where the NICE TA1148/TA623 criteria are met (CKD 3b–5 or heart failure, not on dialysis, RAAS inhibition not optimised because of hyperkalaemia, with confirmed K⁺ ≥5.5 for sodium zirconium cyclosilicate under NICE TA1148 or ≥6.0 for patiromer under NICE TA623; sodium zirconium cyclosilicate may also be started in primary care, UKKA July 2026) · persistent unexplained hyperkalaemia with a low bicarbonate — type 4 RTA or hypoaldosteronism · pre-dialysis assessment. Do not make eGFR-based stop decisions in isolation.

Endocrinology

Suspected adrenal crisis is an emergency, not a test request — hypotension with hyponatraemia and hyperkalaemia goes for emergency assessment, and cortisol is taken only if it does not delay treatment. Routine endocrine referral is for stable suspected Addison's (pigmentation, postural symptoms) for a short synacthen test, and for specialist assessment of hypoaldosteronism — aldosterone and renin are specialist-directed, not routine primary-care tests.

Renal dietitian

CKD with dietary potassium genuinely contributing — advanced CKD needs renal dietetic input rather than a generic restriction, and any target is set by that service, not applied universally. Clarify salt substitute use. Advice is framed around substitution rather than broad exclusion, so healthy foods are not restricted unnecessarily.

Patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma) are two novel K⁺-binding agents recommended by NICE (TA623 for patiromer, TA1148 for SZC — TA1148 updated and replaced TA599 in April 2026) that represent a significant advance in chronic hyperkalaemia management in primary care. Unlike the older polystyrene sulphonate resins — which UKKA removed from the acute protocol in 2023 (and, in July 2026, from chronic hyperkalaemia management) because their efficacy is slow and unpredictable and they carry important gastrointestinal risks including intestinal injury and necrosis — patiromer and SZC are tolerated oral preparations designed for long-term outpatient use. They work by binding K⁺ in the gastrointestinal tract and preventing its absorption, providing a sustained K⁺-lowering effect over days to weeks. Clinical significance: they allow patients who could not otherwise tolerate optimal RAAS blockade for heart failure or CKD to remain on prognostically important medication. But the NICE TA1148/TA623 criteria are specific — selected adults with CKD 3b–5 or heart failure, not on dialysis, where hyperkalaemia is limiting optimised RAAS-inhibitor therapy (TA1148, TA623). The eligibility criteria matter as much as the drugs. NICE TA1148 (April 2026, which updated and replaced TA599) recommends sodium zirconium cyclosilicate from a confirmed K⁺ ≥5.5 mmol/L; NICE TA623 (2020) still requires a confirmed K⁺ ≥6.0 mmol/L for patiromer — so the threshold now depends on which binder is being considered. Sodium zirconium cyclosilicate may now be started in primary care (NICE TA1148; UKKA July 2026); otherwise initiation and prescribing responsibility follow local renal or cardiology arrangements and the local formulary or shared-care protocol, rather than generic prescribing from the algorithm. Neither is emergency treatment or a substitute for emergency transfer: SZC's hospital correction phase is typically 10 g three times daily for up to 72 hours, and patiromer does not act quickly enough to be an emergency option at all.

Treat

Hospital acute treatment — reference only, not for primary-care administration

Done

⚠ Hospital treatment only — not for routine primary-care administration. This module is here so you know what the receiving team is likely to do, what to hand over, and when to contact renal or critical care. Every dose and rate below follows the local UKKA-aligned protocol, given in a monitored environment by staff trained and authorised to administer it. In primary care the action is immediate transfer.

What to hand overThe potassium and its trend and timing, whether the sample was haemolysed, renal function and urine output, the ECG if one was done, the full drug list and which drugs were withheld, dialysis status and last session, comorbidity (heart failure, CKD, diabetes), and any suspected precipitant — AKI, rhabdomyolysis, tumour lysis, adrenal insufficiency, digoxin toxicity.

1. Calcium — cardioprotectionGiven only in an appropriately monitored clinical environment by staff trained and authorised to give IV calcium. The UKKA adult hospital algorithm uses 10% calcium gluconate 30 mL IV over 10 minutes, or 10% calcium chloride 10 mL IV, according to the local protocol and the access available — calcium chloride is more irritant and is generally reserved for large-bore or central access and for cardiac arrest. 30 mL of 10% calcium gluconate provides about 6.8 mmol calcium and 10 mL of 10% calcium chloride an equivalent dose — the preparations are not dose-equivalent by volume (MHRA). Calcium is given for myocardial stabilisation when indicated. In cardiac arrest, follow the current Resuscitation Council UK/European Resuscitation Council hyperkalaemia cardiac-arrest algorithm — do not rely solely on the non-arrest UKKA hospital algorithm. Calcium does not lower the potassium — it raises the myocyte threshold potential and buys time, so K⁺-lowering treatment must follow. Do not attempt IV calcium in routine primary care unless an explicit local emergency protocol, equipment and trained staff are available.

2. Insulin–glucose — and the hypoglycaemia regimen10 units soluble insulin IV with 25 g glucose — equivalently 50 mL of 50%, 125 mL of 20% or 250 mL of 10% glucose. Check the glucose immediately before treatment. If the pre-treatment glucose is below 7.0 mmol/L, follow with 10% glucose at 50 mL/hour for 5 hours (UKKA). Monitor glucose at baseline and at 30, 60, 90, 120, 180, 240, 300 and 360 minutes — six hours, because hypoglycaemia occurs after the bolus has been metabolised while the insulin is still acting. This is the most reliably effective acute K⁺-lowering treatment.

3. Salbutamol nebuliserSalbutamol 10–20 mg nebulised — a beta-2 agonist that drives K⁺ into cells, additive to insulin–glucose and given alongside it. Causes tachycardia; less reliable in patients already on a beta-blocker. It is an adjunct, not a substitute for insulin–glucose.

4. Sodium bicarbonate — not routineDo not use sodium bicarbonate routinely for hyperkalaemia. Consider it only for selected patients with significant metabolic acidosis, or in hyperkalaemic cardiac arrest, according to the local renal, critical-care or resuscitation protocol. No fixed volume applies — a standard 500 mL may be hazardous in heart failure, renal failure or fluid overload, and concentrated bicarbonate has a role in selected resuscitation protocols under specialist guidance.

5. Potassium binders — hospital adjunctCalcium resonium is not a substitute for emergency treatment and should not be used as the primary acute potassium-lowering intervention in life-threatening hyperkalaemia — follow the current acute-hospital protocol (UKKA 2023 removed it from the acute protocol); its efficacy is slow and unpredictable and it carries important gastrointestinal risks including intestinal injury and necrosis. Consider current potassium binders only in accordance with the hospital protocol and specialist decision-making. Sodium zirconium cyclosilicate may be considered alongside standard emergency treatment per the local acute protocol — it does not replace calcium where indicated, or insulin–glucose. Patiromer is not an immediate emergency potassium-lowering treatment. Outpatient use is a separate question — see step 7.

6. Dialysis — escalate earlyContact renal or critical care early if severe hyperkalaemia is refractory or recurrent, or associated with anuria or oliguria, severe AKI or advanced renal failure, severe metabolic acidosis, fluid overload, ongoing potassium release (rhabdomyolysis, tumour lysis), failure of initial medical treatment, or hyperkalaemic cardiac arrest, or in a dialysis patient with significant hyperkalaemia — and whenever definitive potassium removal is likely to be needed. Do not wait for K⁺ above 7.0 mmol/L.

7. After treatment — reboundPotassium at approximately 1, 2, 4, 6 and 24 hours after moderate or severe treatment; glucose monitored to 6 hours after insulin–glucose. Insulin, salbutamol and bicarbonate shift potassium into cells rather than removing it, so rebound is expected unless the cause is corrected or the potassium is removed — clear re-treatment and escalation thresholds must be documented before step-down.

The insulin-dextrose infusion is the cornerstone of acute hospital hyperkalaemia management and works via a beautifully simple physiological mechanism — insulin activates the Na⁺/K⁺-ATPase pump on skeletal muscle cells, driving K⁺ from the extracellular space into the intracellular compartment. This is why hyperkalaemia is a key feature of diabetic ketoacidosis (absent insulin) despite total body K⁺ depletion (K⁺ cannot enter cells without insulin). The dextrose is given simultaneously to prevent the hypoglycaemia that the exogenous insulin would otherwise cause. The glucose monitoring protocol after insulin–glucose is mandatory because hypoglycaemia occurs after the glucose bolus has been metabolised while the insulin is still acting — which is why UKKA specifies monitoring to six hours and a follow-on 10% glucose infusion at 50 mL/hour for 5 hours when the pre-treatment glucose is below 7.0 mmol/L. The salbutamol additive effect is clinically important — the combination of insulin-dextrose + salbutamol is superior to either alone for acute K⁺ reduction, and both treatments can be administered simultaneously in the emergency department. The total K⁺ reduction from combined insulin + salbutamol is approximately 1.0–2.0 mmol/L — which is often sufficient to convert an immediately dangerous ECG pattern to a manageable one while dialysis is arranged if needed. GPs need these treatments in order to hand over well and to explain them — not to administer them. The insulin and glucose are being given to move potassium into cells, not to manage diabetes. Note too that insulin, salbutamol and bicarbonate all shift potassium rather than removing it, so the level rebounds unless the cause is corrected or dialysis removes it — the reason early renal or critical-care contact matters more than any particular number.

Treat

Primary Care Management — Chronic Hyperkalaemia

Done

Above the reference range (K⁺ 5.1–5.4) on RAAS therapy

This is above the local reference range, not "mild hyperkalaemia". 1. Repeat to exclude pseudohyperkalaemia. 2. Remove reversible contributors first — NSAIDs, potassium supplements, potassium-containing salt substitutes, trimethoprim. 3. Assess for AKI, and assess volume status. 4. Individualised dietary advice (step 4). 5. Recheck in 1–4 weeks with a named reviewer. Only then consider dose adjustment or specialist advice — and in heart failure or albuminuric CKD, document a plan for reintroduction or optimisation rather than indefinite discontinuation.

Mild hyperkalaemia (K⁺ 5.5–5.9) confirmed

1. Review urgently (ideally the same working day) and check for haemolysis; ECG if cardiac disease, a rapid rise, significant renal impairment, concerning symptoms or unreliable follow-up — any change potentially attributable to hyperkalaemia means emergency transfer. 2. Stop NSAIDs and potassium supplements and salt substitutes. 3. Assess for AKI and check renal function and volume status. 4. Review the potassium-sparing diuretic and the ACE inhibitor or ARB — reduce or withhold on the clinical picture, not on a formula, and in heart failure or albuminuric CKD plan the reintroduction rather than stopping indefinitely; seek renal or cardiology advice where the drug matters. 5. Individualised dietary review. 6. Repeat potassium within 3 days (sooner if clinically indicated), with a named reviewer, a repeat date and a written escalation threshold. 7. Same-day assessment if an ECG or reliable follow-up cannot be arranged. Moderate (6.0–6.4): urgent ECG; same-day hospital assessment if acutely unwell or with AKI; if well, repeat within 1 day after discussing with the renal/medical team.

Potassium binders — persistent outpatient hyperkalaemia

Not for every raised potassium. NICE TA1148 and TA623 recommend sodium zirconium cyclosilicate or patiromer in defined settings: CKD stage 3b–5 or heart failure · not on dialysis · RAAS inhibition not optimised because of hyperkalaemia · confirmed K⁺ ≥5.5 mmol/L for sodium zirconium cyclosilicate (NICE TA1148, April 2026, which updated and replaced TA599) or ≥6.0 mmol/L for patiromer (NICE TA623). Sodium zirconium cyclosilicate may be started in primary care when these criteria are met (NICE TA1148; UKKA July 2026); patiromer is initiated by the specialist service unless a current local protocol explicitly states otherwise — check the local formulary and shared-care protocol rather than prescribing generically, and distinguish NICE eligibility from what is clinically appropriate for the individual patient. Practical points: patiromer also binds magnesium, so monitor it; separate binders from other oral medicines by the interval the product specifies. Neither agent is emergency treatment or a substitute for emergency transfer — SZC's correction phase in hospital is typically 10 g three times daily for up to 72 hours, and patiromer is not an immediate potassium-lowering treatment at all.

Type 4 RTA / hypoaldosteronism

Persistent unexplained hyperkalaemia with a low bicarbonate warrants renal assessment for type 4 RTA or hypoaldosteronism. Fludrocortisone is not a primary-care treatment for hyperkalaemia — it can worsen hypertension, fluid retention, heart failure and oedema, and can cause hypokalaemia. Specialist endocrine or renal initiation only, with the contraindications considered and monitoring specified by the initiating team; primary care may continue a specialist-initiated prescription within that plan.

Next steps: see Chronic kidney disease · Heart failure · Addison's disease · Acute kidney injury

Patiromer (Veltassa) is a particularly useful drug for the very common clinical scenario of heart failure + CKD + spironolactone-induced hyperkalaemia — the RAAS inhibitor combination is the cornerstone of HFrEF management with proven mortality benefit (RALES showed 30% reduction in all-cause mortality with spironolactone + ACEi), but is frequently stopped or under-dosed in primary care because of hyperkalaemia. Patiromer allows the clinician to maintain optimal RAAS blockade while controlling the K⁺ rise. The AMBER trial (Agarwal et al., Lancet 2019, n=295) showed that in patients with CKD and resistant hypertension, patiromer allowed more patients to stay on spironolactone at 12 weeks (86% vs 66% with placebo). This is a meaningful clinical benefit — GPs managing complex heart failure patients with CKD should be aware of patiromer as an enabling strategy. Fludrocortisone is a specialist decision, not a primary-care option. Mechanistically it replaces the deficient aldosterone in type 4 RTA and restores distal nephron potassium secretion — the only K⁺-lowering drug that corrects the underlying defect rather than binding potassium in the gut or shifting it into cells. But its sodium-retaining effect raises blood pressure and causes fluid retention, and it can precipitate hypokalaemia and decompensate heart failure — precisely the comorbidities that accompany type 4 RTA in diabetic nephropathy. It therefore belongs to endocrinology or renal, with primary care continuing a specialist-initiated prescription within the specialist's monitoring plan.

Lifestyle

Dietary Modification, Patient Education & Monitoring Plan

Done

Dietary potassium — individualised, substitution not exclusion Target the high-yield sources first: potassium-containing salt substitutes, potassium supplements, and the major dietary contributors the history actually identifies. Do not reflexively restrict milk, pulses, nuts and vegetables — unnecessary restriction of healthy foods has its own harms. Lower-potassium swaps (rice, pasta, bread, eggs, apples, pears, berries) are offered as substitutions. Boiling and discarding the water is a practical dietetic technique whose effect varies with the food, how finely it is cut, the water volume and the method — not a guaranteed percentage. Any numeric target belongs to the renal dietetic service, not to a universal rule for CKD 4–5.

Salt substitute elimination LoSalt, Nu-Salt, and similar products contain potassium chloride and are potentially dangerous in CKD or on RAAS therapy. Ask every patient with hyperkalaemia specifically: "Do you use any low-sodium salt or salt substitute?" Advise stopping immediately. Document in clinical records. Remind at each review — patients may restart without telling their GP. Advise against potassium-containing salt substitutes in people with kidney disease, diabetes, older age, pregnancy, or taking ACE inhibitors or ARBs.

Hydration — assess individually Dehydration reduces GFR and raises potassium, so avoiding it matters. Do not prescribe a standard fluid target in CKD, heart failure, oliguria or suspected obstruction — a generic 30 mL/kg/day instruction risks pulmonary oedema and hyponatraemia. Follow the renal or heart-failure fluid plan where one exists, and individualise otherwise. Avoid excess alcohol.

Sick-day plan — personalised, with restart advice Not a blanket instruction. A personalised plan naming which medicines to pause and when, with explicit restart advice and a clinician review if the illness persists — a blanket rule causes interruption of essential medicines, failure to restart, confusion about which drug is meant, and avoidable decompensation in heart failure. The usual trigger is significant vomiting or diarrhoea, or being unable to drink normally. NSAIDs are different: they should generally be avoided altogether in relevant CKD and heart-failure contexts rather than treated as a medicine to pause during illness. RAAS inhibitors, diuretics, metformin and SGLT2 inhibitors may require temporary interruption depending on the circumstances. Where AKI or significant hyperkalaemia occurred, arrange renal function and potassium review after the acute illness before restarting or re-titrating. Give it in writing.

Medication compliance and education Explain clearly why drugs are being changed or stopped (language: "This medication has been building up potassium to a level that could affect your heart rhythm — we need to adjust it"). Give written list of current medications including changes made today. Advise not to restart stopped medications without GP review. Structured medication review (for example by the practice or PCN clinical pharmacist) for complex polypharmacy patients.

Home BP and symptom monitoring Teach patients with CKD to recognise symptoms of hyperkalaemia: unexplained muscle weakness (especially legs), palpitations, feeling of fluttering in chest. Any of these symptoms → call GP same day. Home BP monitoring helps detect the hypotension of Addison's. Pulse check (irregular pulse = possible arrhythmia from electrolyte disturbance → urgent ECG and K⁺; emergency transfer if attributable to hyperkalaemia).

Monitoring schedule Use NICE NG203 Table 2 as the minimum framework; monitor more often after medication changes, during intercurrent illness, after AKI, and in advanced CKD, heart failure, diabetes, a rising potassium or unstable renal function. Stable on RAAS therapy (SPS): heart failure U&E every 3–6 months once stable; hypertension at least annually, more often if high risk; and whenever acutely unwell. After any RAAS dose change: K⁺ and eGFR at 1–2 weeks. Post-AKI: 2–4 weeks. On a potassium binder: as specified by the initiating service. After hospital treatment of moderate or severe hyperkalaemia the inpatient schedule is K⁺ at about 1, 2, 4, 6 and 24 hours, with glucose to 6 hours after insulin–glucose — know it so the discharge plan can be checked. All results on a monitoring register so missed checks are flagged.

NSAID awareness NSAIDs (ibuprofen, naproxen, diclofenac, aspirin at anti-inflammatory doses) significantly worsen K⁺ in CKD or on RAAS therapy. OTC ibuprofen is the most dangerous — patients do not consider it a "real medication." Explicitly advise: "Do not take any ibuprofen or anti-inflammatory painkillers without checking with your GP first." Paracetamol is generally preferred to NSAIDs for analgesia in CKD, but check the dose and maximum daily dose in frailty, low body weight, liver disease, alcohol excess and polypharmacy.

The sick day rules concept is one of the most important and underused patient safety interventions in CKD management — studies have shown that acute kidney injury (AKI) is responsible for approximately 10–15% of hospital admissions, and a significant proportion are caused by dehydration + continued nephrotoxic/RAAS drug use during illness in patients who were not told to temporarily stop these drugs. The 'STOP' mnemonic for sick day rules (Stop: Spironolactone, Trimethoprim, ACEi/ARBs, and NSAIDs during illness causing dehydration) is used in many NHS kidney patient education programmes. Written sick day rules cards (available from NHS Kidney Care/Kidney Research UK) should be given to every patient with CKD-3b or above on any combination of these drugs. The key message: 'These drugs are generally safe and important, but they can harm your kidneys and raise your potassium to a dangerous level if you become dehydrated from vomiting, diarrhoea, or not drinking enough during illness. Stop them temporarily if you can't keep fluids down for more than 24 hours, and restart them when you're better and eating and drinking normally.' The NSAID over-the-counter problem is a genuine patient safety crisis — ibuprofen is available at supermarkets and petrol stations without any prescription, and patients with CKD, heart failure, or on RAAS therapy frequently self-medicate with it for pain without realising it can cause AKI and hyperkalaemia. Verbal and written advice at each consultation, and recording the allergy/intolerance to NSAIDs in the patient's record (even if it is a relative contraindication rather than an absolute allergy) helps flag this when the patient or other prescribers attempt to prescribe it.

Safety

Follow-Up & Safety-Netting

Done

After acute treatment / hospital discharge

The interval is individualised to the inpatient course, renal function and the ongoing cause — typically a potassium and eGFR within days of discharge, sooner where renal function is still moving or the cause is unresolved, and it should be named explicitly in the discharge plan rather than left as "routine". Insulin, salbutamol and bicarbonate shift potassium into cells rather than removing it, so rebound is expected unless the cause was corrected or potassium was removed. Check what was stopped in hospital and document a plan for reintroduction or optimisation — particularly ACE inhibitor, ARB or MRA in heart failure or albuminuric CKD — rather than leaving them indefinitely discontinued. Personalised sick-day plan in writing, dietetic referral if relevant, and the cause of any AKI identified.

Chronic CKD monitoring

Tailored to eGFR and ACR category, rate of decline, heart failure, diabetes, hypertension, RAAS inhibitor/MRA/diuretic/NSAID use, intercurrent illness and treatment changes — NICE NG203 Table 2 as the minimum framework. Any K⁺ result >5.0 mmol/L in CKD should prompt drug and dietary review before the next routine check. Log on monitoring register. Recalls for overdue bloods.

RAAS therapy dose changes

Any change to ACEi/ARB/spironolactone dose → recheck K⁺ + eGFR at 1–2 weeks (NICE NG203). Do not routinely increase ACEi/ARB to maximum dose without intermediate K⁺ check in CKD-3b+. Document monitoring in records for medicolegal protection.

MRA (spironolactone / eplerenone) monitoring

Before starting: check K⁺, creatinine/eGFR and blood pressure; avoid initiation if K⁺ >5.0 mmol/L or eGFR <30 mL/min/1.73 m² unless specialist-directed. After initiation or dose increase: U&E at about 1 week, then monthly for the first 3 months, then at least every 3 months during the first year, then every 3–4 months adjusted for risk — following the indication, product information, heart-failure pathway and local protocol (UKKA). MHRA: potentially fatal hyperkalaemia with spironolactone combined with an ACE inhibitor or ARB.

Potassium-binder monitoring

Per the initiating service and the local shared-care protocol: potassium after starting and on titration, then at the agreed interval. Patiromer also binds magnesium — monitor it. SZC contains sodium — monitor blood pressure and for fluid retention. Separate the binder from other oral medicines by the interval the product specifies. Confirm the shared-care arrangement is in place before taking over prescribing.

Return immediately

Any muscle weakness in legs or arms not explained by other cause → emergency assessment (999 or acute team) with ECG + K⁺ · Palpitations or irregular pulse → emergency assessment with ECG + K⁺ · Collapse or syncope → 999 · Any symptom of adrenal crisis (collapse + vomiting + hypotension) → call 999 and treat according to the emergency steroid protocol; if trained and authorised, give IM hydrocortisone without delaying transfer, and take cortisol and other bloods only if this does not delay treatment

Result handling

K⁺ 5.5–5.9 on routine bloods → urgent review (ideally the same working day) and repeat within 3 days, ECG if indicated — never left in a routine inbox · K⁺ 6.0–6.4 → urgent ECG; same-day hospital assessment if acutely unwell or with AKI; if well, repeat within 1 day after discussing with the renal/medical team · K⁺ ≥6.5, or any red flag, is an emergency transfer, not a repeat request · a new medicine that could raise potassium (NSAID, trimethoprim, another RAAS agent) → K⁺ at 1 week. A critical result must not remain in an inbox or a routine repeat queue overnight — name who is responsible for acting on it out of hours.

The 1–2 week K⁺ recheck after any ACEi/ARB dose change is a NICE NG203 (CKD, 2021) monitoring requirement that is frequently missed in general practice — the most common pattern of iatrogenic severe hyperkalaemia is: GP increases ACEi/ARB dose (appropriately, for blood pressure or CKD proteinuria), K⁺ rises to dangerous levels over 1–2 weeks, no repeat bloods are taken, patient develops ECG changes or cardiac arrest before the next routine blood test. The monitoring requirement is not bureaucratic box-ticking — it reflects the genuine physiological reality that RAAS agent dose increases can raise K⁺ by 0.5–1.0 mmol/L within 1–2 weeks of dose change, and this rise is unpredictable (patients with CKD-3b can have dramatic K⁺ rises to dangerous levels from a relatively small dose change). Implementing a simple practice recall system for 'K⁺ + eGFR at 1–2 weeks post-RAAS dose change' is a high-yield, low-effort patient safety intervention.