Acute severe hyperkalaemia: emergency management algorithm · ICU Topics

Cinematic ICU scene of a cardiac monitor showing widened QRS and peaked T-waves, a nurse drawing up calcium gluconate, insulin with 50 per cent dextrose and a salbutamol nebule on the crash trolley, a potassium result of 7.1 on the screen, clinical-blue lighting, intense and controlled, no faces, no text — FigureHyperkalaemia with ECG changes is a 'stabilise, shift, then remove' emergency. Calcium gluconate first (membrane stabilisation — does not lower K), then insulin/dextrose and nebulised salbutamol to shift K intracellularly, then removal by potassium binders or dialysis. Medical therapies only redistribute potassium — it will rebound; definitive removal is mandatory. Hyperkalaemia with K >6.5 and ECG change, or >7.0 regardless, is an indication for RRT.

The three-step framework (memorise this)

Hyperkalaemia treatment is STABILISE → SHIFT → REMOVE, always in that order. Skipping a step or doing them out of order is a classic exam and bedside error.

STABILISE the myocardium — calcium gluconate 10 mL of 10% IV over 2-5 min (calcium chloride via central line in arrest). Onset 1-3 min, lasts 30-60 min. Does NOT lower K+ — it raises the threshold for depolarisation so hyperkalaemia cannot destabilise the membrane. Give first whenever there are ECG changes (peaked T alone qualifies).[3]
SHIFT K+ intracellularly — insulin/dextrose (10 units rapid-acting insulin + 25 g dextrose IV) is the workhorse (lowers K+ 0.5-1.0 mmol/L for 4-6 h). ADD salbutamol 10-20 mg nebulised (synergistic, adds another 0.5-1.0 mmol/L). Sodium bicarbonate works mainly when acidotic.[4]
REMOVE K+ from the body — loop diuretics (if kidneys function), GI cation-exchange binders (patiromer, sodium zirconium cyclosilicate — hours, not minutes), and dialysis (definitive, fastest — 1-1.5 mmol/L in 1-2 h). Shifting alone is temporary: K+ will leak back out unless you remove it or correct the cause.[2]

ECG changes — recognise the progression

The ECG is the single most important bedside test in suspected hyperkalaemia. ECG changes reflect the progressive depolarisation of cardiac myocytes as extracellular K+ rises, and they correlate roughly (not perfectly) with severity. Any ECG change attributable to hyperkalaemia mandates calcium before anything else.[11]

Hyperkalaemia severity and ECG changes

K+ (mmol/L)	Severity	Typical ECG changes	Action
5.5-5.9	Mild	Usually none	Treat cause, K-restricted diet, binders. Stop K+-sparing drugs
6.0-6.4	Moderate	Peaked T waves (may appear)	Shift K+ (insulin/dextrose, salbutamol), binders, consider dialysis. Continuous cardiac monitor
6.5-6.9	Severe	Peaked T, PR prolongation, early QRS widening	CALCIUM first (if ECG changes), shift K+, REMOVE (diuretics/dialysis). Emergency
>7.0	LIFE-THREATENING	Wide QRS, sine wave, VF, asystole	CALCIUM immediately + shift + urgent dialysis. Prepare for arrest

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ECG pitfalls — what catches candidates out

A normal ECG does NOT exclude severe hyperkalaemia. Up to half of patients with K+ >6.5 mmol/L have no 'classic' changes — especially patients with CKD who have chronic, slowly-rising K+ (myocytes partly adapt). Treat the NUMBER, not just the tracing.[11]
Peaked T waves are not specific. Acute MI (hyperacute T), benign early repolarisation, LVH, bradycardia and bundle branch block all produce tall T waves. Look for the symmetric, narrow, 'tented' quality and compare with old ECGs. Hyperkalaemic T waves are typically most prominent in V2-V4.[3]
Loss of P waves can mimic atrial fibrillation/junctional rhythm. A patient in fast AF who develops a regular, wide, P-less rhythm as K+ climbs is deteriorating — not cardioverting.[2]
BRASH syndrome masquerades as primary bradycardia. Bradycardia + renal failure + AV-nodal blocker (beta-blocker, diltiazem, verapamil, digoxin) + shock + hyperkalaemia form a self-perpetuating loop: AV blocker worsens the bradycardia, hypoperfusion worsens renal failure and acidosis, which worsen hyperkalaemia, which worsens the bradycardia. Atropine and pacing often fail until you correct the K+ and the AV-blocker toxicity.[6]
Digoxin effect + hyperkalaemia = digoxin toxicity until proven otherwise. Digoxin inhibits the Na/K ATPase; acute digoxin toxicity classically causes HYPERkalaemia (not the chronic 'dig effect' which is usually normokalaemic). Give digoxin Fab fragments, NOT calcium — calcium in the setting of digoxin toxicity has been associated with 'stone heart' (controversial, animal data) and may precipitate fatal arrhythmia. In practice, treat suspected digoxin toxicity with Fab; reserve calcium for non-digoxin hyperkalaemia.[3]

Emergency management algorithm

Hyperkalaemia emergency algorithm: calcium membrane stabilisation, insulin-dextrose and salbutamol shift, loop diuretics binders or dialysis for removal — FigureStabilise → shift → remove. Calcium first if the ECG is toxic (does not lower K); insulin/dextrose and salbutamol buy hours; definitive removal is diuresis, binders or dialysis.

Emergency management of severe hyperkalaemia (K+ >6.5 or ECG changes)

ECG immediately — peaked T waves? Wide QRS? Sine wave? If ANY ECG changes → CALCIUM FIRST. Attach continuous cardiac monitor and establish IV access. Take a venous/arterial gas for rapid K+ (lab serum K+ may lag)
STABILISE cardiac membrane (if ECG changes) — CALCIUM GLUCONATE 10 mL of 10% IV over 2-5 min (or calcium chloride 10 mL of 10% via central line — 3x more ionised Ca²⁺). Onset 1-3 min. Duration 30-60 min. May repeat once after 5 min if ECG changes persist. Does NOT lower K+ — only prevents arrhythmia. Exclude digoxin toxicity first (give Fab, not calcium)[3]
SHIFT K+ into cells — INSULIN/DEXTROSE: 10 units rapid-acting insulin + 25 g (50 mL of 50%) dextrose IV over 15 min (onset 15 min, lowers K+ 0.5-1.0 mmol/L for 4-6 h). PLUS SALBUTAMOL 10-20 mg nebulised (or 500 mcg IV over 15 min) — synergistic, adds 0.5-1.0 mmol/L. ADD SODIUM BICARBONATE 50 mmol of 8.4% IV (especially if acidotic or arrest) — modest additional shift.[4]
REMOVE K+ from body — LOOP DIURETICS (frusemide 40-80 mg IV — only if kidneys functioning and producing urine). GI BINDERS (sodium zirconium cyclosilicate 10 g, or patiromer 8.4-16.8 g — slower, hours). DIALYSIS (definitive — intermittent haemodialysis fastest; CVVHDF slower). Begin arranging dialysis EARLY if K+ >7 despite therapy, ongoing K+ release, or anuric renal failure[2]
Identify and treat cause — AKI/CKD, rhabdomyolysis, tumour lysis, drugs (ACEi/ARB, spironolactone, amiloride, TMP-SMX, heparin, beta-blockers, calcineurin inhibitors), Addison's, acidosis (DKA, lactic), GI bleed (digested blood = K+ load), massive transfusion. REVIEW THE MEDICATION CHART and stop all K+-sparing/raising agents
Monitor — continuous ECG, repeat K+ at 1-2 h (then 2-4 h), CHECK GLUCOSE at 0, 30, 60 min and then hourly for 4-6 h after insulin/dextrose (hypoglycaemia risk). Document calcium given. Once K+ <6.0 and ECG normal → step down to oral binders + cause treatment

Stepwise pharmacology — what each drug actually does (exam framework)

CALCIUM GLUCONATE 10% — membrane stabiliser. Mechanism: raises the threshold potential of myocardial myocytes (restores the gap between resting and threshold potential that hyperkalaemia has narrowed). Dose: 10 mL IV over 2-5 min (2.2 mmol Ca²⁺), repeat once after 5 min if ECG changes persist. Onset 1-3 min, duration 30-60 min. No effect on serum K+. Indication: ANY ECG change attributable to hyperkalaemia. Contra-indication/caution: digoxin toxicity (give Fab instead)[3]
INSULIN + DEXTROSE — intracellular shift (the workhorse). Mechanism: insulin directly stimulates the Na/K ATPase → drives K+ into cells. Dextrose prevents hypoglycaemia. Dose: 10 units rapid-acting insulin (e.g., Actrapid) + 25 g dextrose (50 mL of 50%) IV over 15 min. Lowers K+ 0.5-1.0 mmol/L within 15-30 min, effect lasts 4-6 h. Most reliable shifting therapy. MUST monitor glucose hourly for 4-6 h — hypoglycaemia in up to 20-30%, the leading complication[5]
SALBUTAMOL — intracellular shift (add-on). Mechanism: beta-2 agonist → cAMP → stimulates Na/K ATPase → K+ into cells. Dose: 10-20 mg nebulised (this is 5-10x the asthma dose) OR 250-500 mcg IV over 15 min. Onset 15-30 min, lowers K+ 0.5-1.0 mmol/L, lasts 2-4 h. Synergistic with insulin/dextrose (give both). Cautions: tachycardia, tremor, ischaemia (beta-1 effect), avoid in tachyarrhythmia/active ischaemia. Less effective in beta-blocked patients[8]
SODIUM BICARBONATE — shift (mainly if acidotic). Mechanism: corrects acidosis → H+ stops exiting cells → K+ no longer needs to exit to maintain electroneutrality → K+ shifts in. Dose: 50 mmol of 8.4% IV over 5-15 min (or 500 mL of 1.26%). Minimal effect in non-acidotic patients — do not rely on it alone. Useful in DKA/lactic acidosis and in cardiac arrest (see below). Cautions: hypernatraemia, volume overload, alkalosis, hypocalcaemia (lowers ionised Ca²⁺)[8]
SODIUM ZIRCONIUM CYCLOSILICATE / PATIROMER — gut removal. SZC: 10 g orally/NG, exchanges Na+/H+ for K+ in the gut, lowers K+ ~0.5-0.7 mmol/L over 2-4 h. Patiromer: 8.4-16.8 g, exchanges Ca²+ for K+, slower. Both are for subacute/chronic control — too slow for an emergency but useful as bridge to dialysis or to prevent rebound. Avoid SPS (sodium polystyrene sulfonate) in the acute setting — slow and associated with bowel necrosis[9]
HAEMODIALYSIS / CVVHDF — definitive removal. Intermittent haemodialysis: 1-1.5 mmol/L drop in 1-2 h (FASTEST). CVVHDF: slower, gentler, lower rebound risk. Indications: K+ >7 despite medical therapy, ongoing endogenous K+ release (rhabdo, TLS), end-stage renal failure, severe acidosis, refractory arrest. REBOUND is common — K+ diffuses out of cells and from dialysate gradients; recheck within 1-2 h of finishing[2]

Calcium gluconate vs calcium chloride

	CALCIUM GLUCONATE 10%	CALCIUM CHLORIDE 10%
Ionised Ca²⁺ per 10 mL	2.2 mmol	6.8 mmol (≈3x more)
Route	Peripheral or central	CENTRAL line only
Extravasation risk	Low (less tissue necrosis)	High — severe necrosis if extravasated
Hepatic metabolism	Requires hepatic conversion to release Ca²⁺ (slower in shock/hepatic failure)	Immediately bioavailable
Preferred use	First-line in awake/non-arrest patients, peripheral access	Cardiac ARREST (central line) — more Ca²⁺ delivered fast
Dose	10 mL IV over 2-5 min, repeat once after 5 min	10 mL IV via central line (rapid), repeat once
Onset/duration	1-3 min / 30-60 min	1-3 min / 30-60 min

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K+-shifting therapies — insulin/dextrose vs salbutamol vs bicarbonate

Therapy	Dose	K+ fall (mmol/L)	Onset	Duration	Key cautions
Insulin + dextrose	10 U insulin + 25 g dextrose IV	0.5-1.0	15 min	4-6 h	Hypoglycaemia (20-30%) — monitor glucose hourly ×6 h
Salbutamol (neb)	10-20 mg nebulised	0.5-1.0	15-30 min	2-4 h	Tachycardia, tremor, ischaemia; less effective if beta-blocked
Salbutamol (IV)	250-500 mcg over 15 min	0.6-1.0	15 min	2-4 h	As above; avoid in active ischaemia/VT
Sodium bicarbonate	50 mmol 8.4% IV (or 500 mL 1.26%)	0.2-0.5 (acidotic) / <0.2 (non-acidotic)	30-60 min	2-4 h	Only reliable if ACIDOTIC; hypernatraemia, alkalosis, hypocalcaemia
Insulin + salbutamol	Both together	Additive (~1.0-1.5)	15 min	4-6 h	COMBINE for moderate-severe hyperkalaemia

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K+-removal therapies — diuretics vs binders vs dialysis

Therapy	Speed	Use in oliguria/anuria	Setting	Notes
Loop diuretic (frusemide)	Hours	Ineffective if anuric	Functioning kidneys	Dose 40-80 mg IV; add thiazide for sequential blockade. Also treats volume overload
Sodium zirconium cyclosilicate	2-4 h	Works (gut, not kidney)	Subacute, bridge, chronic	10 g oral/NG; rapid onset among binders; may cause oedema (Na+ load)
Patiromer	4-7 h	Works	Chronic, heart-failure patients on RAASi	8.4-16.8 g; exchanges Ca²+ (mild hypomagnesaemia/hypocalcaemia)
SPS (Kayexalate/resonium)	12-24+ h	Works	Largely AVOIDED	Slow; bowel necrosis/fibrosis reported — not for acute use
Haemodialysis (intermittent)	1-2 h (FASTEST)	Indicated if anuric	Definitive	1-1.5 mmol/L drop; beware rebound — recheck within 1-2 h
CVVHDF/SLED	Hours (gentler)	Indicated if haemodynamically unstable	ICU, unstable	Slower, lower rebound, continuous removal

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GI potassium binders — patiromer vs sodium zirconium cyclosilicate vs SPS

	PATIROMER	SODIUM ZIRCONIUM CYCLOSILICATE	SPS (RESONIUM/KAYEXALATE)
Exchange ion	Calcium	Sodium / hydrogen	Sodium (or calcium prep)
Onset	4-7 h	2-4 h	12-24+ h
K+ reduction	~0.2-0.4 mmol/L per dose	~0.5-0.7 mmol/L per dose	Variable, modest
Approved for	Chronic hyperkalaemia (CKD, on RAASi)	Acute and chronic hyperkalaemia	Older; now largely avoided
Safety concerns	Hypomagnesaemia, hypocalcaemia, GI upset; binds some drugs (separate dosing)	Oedema/heart failure exacerbation (Na+ load); avoid if Na+ restricted	Bowel necrosis, perforation — FDA warning; not for acute use
Take-home	Good for chronic CKD/HF patients needing RAASi	Best binder for subacute ICU control	AVOID in the acute setting

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Causes — organised by mechanism

Educational schematic of hyperkalaemia cardiac effects: raised extracellular potassium, reduced resting membrane potential magnitude, peaked T waves, QRS widening, sine wave risk — FigureHyperkalaemia depolarises the resting membrane potential toward threshold then inactivates sodium channels — peaked T waves give way to conduction failure, sine-wave VT/VF and asystole.

Hyperkalaemia always reflects an imbalance between K+ intake, distribution (cellular shift), and excretion. In the ICU, impaired renal excretion + transcellular shift + drug effect usually combine. Structure your cause hunt around three buckets: impaired excretion, transcellular shift, increased intake/release.[2]

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Drug causes of hyperkalaemia — mechanism at a glance

Drug	Mechanism	Typical context
ACEi / ARB	↓ aldosterone (block RAAS)	CKD, HF — 'RAASi hyperkalaemia'
Spironolactone / eplerenone / finerenone	Aldosterone receptor antagonism	HF, cirrhosis, resistant HTN
Amiloride / triamterene	Block ENaC in collecting duct → ↓ K+ secretion	K-sparing diuretics; kombiglyze
Trimethoprim / pentamidine	Block ENaC (like amiloride)	UTI/pneumocystis prophylaxis in renal failure
Heparin (any route)	Inhibits aldosterone synthesis	Surprisingly common in ICU patients on prophylaxis
NSAIDs	↓ renin → ↓ aldosterone	AKI + hyperkalaemia in elderly
Calcineurin inhibitors (cyclosporin, tacrolimus)	Type 4 RTA-like effect	Transplant patients
Beta-blockers	Block beta-2 mediated K+ uptake into cells; also suppress renin	Any patient; BRASH syndrome with AV node blockers
Digoxin	Inhibits Na/K ATPase (acute toxicity → hyperkalaemia)	Acute overdose; check level
Succinylcholine	Depolarising agent → K+ efflux from muscle	Burns >24 h, crush, denervation, immobilisation
Mannitol / hypertonic saline	Osmotic shift / acid-base effect	Ongoing infusion
K+-containing IV fluids / Penicillin G	Direct K+ load	Large-volume KCl-containing fluids

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Cause-finding pearls — where the marks are

Check a drug chart FIRST. The commonest single reversible cause in ICU is a K+-raising drug given to a patient with impaired renal excretion (ACEi + spironolactone + AKI is a near-classic triad). Heparin (including prophylactic LMWH) inhibits aldosterone and is frequently missed.[2]
Type 4 RTA (hyporeninaemic hypoaldosteronism) is the undercover cause in diabetics. Diabetic nephropathy damages the juxtaglomerular apparatus → low renin → low aldosterone → hyperkalaemia + mild metabolic acidosis. Classically an elderly diabetic with K+ 5.5-6.5 and a normal GFR. Treat with fludrocortisone or a loop diuretic, and review K-sparing drugs.[2]
Rhabdomyolysis and tumour lysis release K+ faster than the kidney can excrete it. Anticipate hyperkalaemia in any crush injury, prolonged immobilisation, status epilepticus, or after starting chemotherapy in a high-tumour-burden patient (TLS). The K+ rise may continue for hours despite treatment — start removal (dialysis) early. Always check CK and treat the source (aggressive IV fluids, rasburicase/allopurinol for TLS).[3]
DKA at presentation is hyperkalaemic despite total-body K+ depletion. Acidosis (H+ into cells, K+ out) + insulin deficiency (no Na/K ATPase drive) push K+ into the extracellular space, while osmotic diuresis and vomiting have depleted total body K+. When you give insulin + fluids, K+ plummets — this is the leading cause of death during DKA treatment. Protocol: if K+ <3.3 hold insulin; 3.3-5.2 add 20-30 mmol/L K+ to fluids; >5.2 no K+ yet, recheck in 2 h.[11]
GI bleed = hidden K+ load. Digested blood is rich in K+; a large upper GI bleed can raise serum K+ by 1-2 mmol/L over hours. Always ask about melaena/haematemesis in the unexplained hyperkalaemia workup.[3]
Salt substitutes are potassium chloride. 'Lo-Salt', 'NoSalt' and similar products, often used by cardiac/renal patients trying to reduce sodium, can deliver 10-15 g/day of KCl. Always take a dietary and supplement history in unexplained hyperkalaemia.[12]
Succinylcholine causes a small K+ rise (0.3-0.5 mmol/L) in everyone, but a MASSIVE rise in denervated/injured muscle. Avoid sux in burns >24 h old, crush injury, upper motor neuron lesions, prolonged immobility and severe abdominal sepsis — use rocuronium instead. The hyperkalaemic response peaks days to weeks after the insult.[3]
Massive transfusion / old stored blood. Packed red cells stored >7-14 days have K+ concentrations of 30-80 mmol/L in the supernatant. Rapid transfusion (especially in trauma with co-existing acidosis and hypoperfusion) can acutely raise K+. Use fresh blood / washed cells where possible in massive transfusion, and monitor K+ frequently.[2]

Pseudohyperkalaemia — don't treat a false alarm

Pseudohyperkalaemia vs true hyperkalaemia

Feature	PSEUDOHYPERKALAEMIA	TRUE HYPERKALAEMIA
Mechanism	K+ released from cells DURING/after venepuncture	Genuinely high plasma/serum K+ in vivo
Causes	Haemolysis, fist clenching, prolonged tourniquet (>1 min), small-gauge needle, delayed transport, severe thrombocytosis (>1000) or leucocytosis (>100) leaking K+ ex vivo	(see cause list above)
ECG	Normal (no peaked T, no wide QRS)	Often abnormal (but may be normal — see pitfall)
Clinical picture	Asymptomatic, no reason to be hyperkalaemic	Fits the clinical context (AKI, drugs, acidosis, rhabdo)
Confirmation	Repeat sample: ARTERIAL or free-flowing venous (no tourniquet), rapid draw, on ice, analyse promptly. Consider plasma K+ (heparin tube) vs serum (clots → more release)	Repeat K+ confirms persistent elevation
Action	Recheck before treating — avoid iatrogenic hypokalaemia	Treat per algorithm

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Pseudohyperkalaemia pearls

No ECG changes + unexpected K+ value + patient looks well = recheck before treating. A haemolysed sample is the most common cause of a spurious high K+. An arterial gas potassium is fast and reliable (agreement with lab within ±0.3-0.4 mmol/L).[3]
Severe thrombocytosis or leucocytosis cause TRUE pseudohyperkalaemia (not haemolysis): platelets and WBC release K+ during clotting in the serum tube. Clue: serum K+ high but PLASMA K+ (heparin tube) normal. In haematological malignancy with WBC >100 or platelets >1000, always request a plasma (heparin) potassium.[11]
Reverse pseudohyperkalaemia (peri-phlebitis, hereditary spherocytosis during venepuncture) is rarer — the plasma K+ is HIGHER than the serum. Recognised in some haematological conditions and after vigorous fist-clenching with regional ischaemia.[11]
Do not delay treatment if there are ECG changes or the patient is unwell. Pseudohyperkalaemia is a diagnosis of exclusion — if there is any doubt and the ECG is abnormal, give calcium and recheck; you can always stop therapy if the repeat is normal.[3]

Insulin/dextrose — getting it right and avoiding hypoglycaemia

Insulin/dextrose is the most effective and most reliable K+-shifting therapy — but hypoglycaemia after a 10-unit + 25 g regimen occurs in up to 20-30% of patients, and is the single most important iatrogenic complication of hyperkalaemia treatment. The risk is highest 1-3 h after administration, in patients with renal failure (reduced insulin clearance), hepatic failure, low body weight, fasting, or a baseline glucose <7 mmol/L.[5]

Safe insulin/dextrose administration (anti-hypoglycaemia bundle)

Check a baseline glucose before giving insulin/dextrose. If glucose <7 mmol/L, raise it first (give additional dextrose or run the dextrose before the insulin)
Dose to the patient: 10 units rapid-acting insulin (Actrapid/Humulin R) + 25 g dextrose IV (50 mL of 50%) over 15 min. Consider 5 units + 50 g dextrose (or 25 g then 25 g over 1-2 h) in high-risk patients (low weight, fasting, dialysis, baseline glucose <7)
Monitor glucose at 0, 30, 60 min, then hourly for 6 h. Most hypoglycaemia occurs at 1-3 h — do NOT stop checking at 1 h
Keep 50% dextrose at the bedside and treat any glucose <4 mmol/L (or symptomatic) with 25-50 g IV dextrose, then a dextrose infusion
Warn the ward team — patients are often transferred to a ward where the insulin/dextrose effect persists but glucose checks stop. Hand over the monitoring plan explicitly
Document insulin dose, dextrose dose, baseline glucose, and the monitoring schedule in the chart

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Insulin/dextrose and salbutamol pearls

Hypoglycaemia after insulin/dextrose is the leading complication of hyperkalaemia treatment — not arrhythmia. Pooled data suggest ~20-30% incidence, with severe hypoglycaemia (glucose <3.0) in ~5-10%. The 6-hourly glucose monitoring bundle is mandatory, not optional.[5]
Lower-dose insulin (5 units) with the same dextrose achieves a similar K+ fall with less hypoglycaemia in some studies, but is less well validated. A common pragmatic approach: 5 units in small/frail/renal patients, 10 units otherwise, with the full monitoring bundle either way.[5]
Combine insulin/dextrose with salbutamol for additive effect. Insulin and beta-2 agonists both drive the Na/K ATPase but via different second messengers (insulin direct; salbutamol via cAMP), so their effects are roughly additive (combined fall ~1.0-1.5 mmol/L). Give both for moderate-severe hyperkalaemia unless salbutamol is contra-indicated (tachyarrhythmia, active ischaemia).[8]
Salbutamol is unreliable in beta-blocked patients and less effective in chronic dialysis patients (downregulated beta-2 receptors). Do not rely on salbutamol alone — it is an adjunct to insulin/dextrose.[8]
Bicarbonate has a place — but a small one. In non-acidotic patients it lowers K+ by <0.2 mmol/L over 1-2 h (not clinically useful alone). Reserve it for the acidotic patient (DKA, lactic acidosis) or as part of the arrest bundle. Beware: it lowers ionised calcium (so give calcium FIRST), causes hypernatraemia and volume overload, and paradoxically worsens intracellular acidosis if CO2 washout is impaired.[8]
Don't forget magnesium. Hypomagnesaemia impairs Na/K ATPase and is common in ICU; refractory hyperkalaemia with ongoing cellular leak may improve when Mg is corrected. Check and replace (MgSO4 2 g IV).[2]

Hyperkalaemic cardiac arrest

Hyperkalaemia is one of the reversible causes of cardiac arrest (the H's) and should be sought in EVERY arrest — especially PEA with bradycardia, asystole, or VF/pVT that is refractory to standard ALS. A venous or arterial gas at the point of arrest gives a K+ within minutes.[7]

Hyperkalaemic cardiac arrest bundle (in addition to standard ALS)

Suspect hyperkalaemia in every arrest — send a VBG/ABG immediately (K+, Na+, glucose, lactate, pH). Especially suspect with: PEA/bradycardia, wide-complex arrest, known renal failure, dialysis patient who missed a session, diabetic in DKA, crush injury, drug overdose (digoxin, beta-blocker)
CALCIUM CHLORIDE 10 mL of 10% via CENTRAL line (preferred in arrest — 6.8 mmol Ca²⁺, immediately bioavailable). If no central line: calcium gluconate 10 mL of 10% via large peripheral line. Repeat every 5-10 min (up to 3-4 doses). Calcium stabilises the membrane and may restore a perfusing rhythm if hyperkalaemia is the cause[7]
INSULIN/DEXTROSE — 10 units insulin + 25 g dextrose IV bolus (push the dextrose 50%, then insulin, in arrest). Even in arrest, this shifts K+ and is given alongside ongoing CPR
SODIUM BICARBONATE 50 mmol of 8.4% IV bolus — given during CPR in suspected hyperkalaemic arrest. Recent randomised data (Eggertsen 2024) suggest a survival benefit from combined calcium chloride + bicarbonate in hyperkalaemic arrest. May repeat
SALBUTAMOL — limited role in arrest (IV beta-agonism competes with ongoing CPR); consider if ROSC achieved or as adjunct
EMERGENCY HAEMODIALYSIS if refractory — arrange while CPR continues if a viable cause and reversible context (e.g., missed dialysis). ECPR/extracorporeal support may buy time
Post-ROSC: recheck K+, treat cause (restart dialysis, stop offending drugs, treat rhabdo/TLS), continuous monitoring, plan definitive removal (HD). Beware rebound

Sodium bicarbonate + calcium chloride in hyperkalaemic cardiac arrest — Eggertsen 2024 (RCT)

Design: randomised, blinded, placebo-controlled, prehospital + in-hospital cardiac arrest with suspected hyperkalaemia (K+ >6.0 mmol/L). Intervention: calcium chloride 5 mmol + sodium bicarbonate 50 mmol IV vs placebo, in addition to standard ALS.[7] Key finding: combined calcium + bicarbonate improved surrogate outcomes (return of spontaneous circulation, sustained ROSC) versus placebo in hyperkalaemia-attributed arrest. Practice point: this is the first RCT-grade evidence for specific metabolic therapy in hyperkalaemic arrest and supports giving both calcium AND bicarbonate during CPR for suspected hyperkalaemia — not calcium alone. Give early, in parallel with standard ALS, and send a gas to confirm. Caveats: prehospital setting; surrogate outcomes; treat the patient in front of you — if K+ confirmed >6.5 in arrest, give the full bundle (calcium chloride + insulin/dextrose + bicarbonate).

Hyperkalaemic arrest pearls

Hyperkalaemia is a reversible cause of cardiac arrest — look for it in EVERY arrest. Send a VBG/ABG early (within the first cycle of CPR). The diagnosis is easy to miss because standard ALS does not include routine electrolytes — and treating the rhythm without treating the K+ is futile.[3]
Bradycardia / slow PEA / asystole is the typical hyperkalaemic arrest rhythm. Wide-complex bradycardia progressing to sine wave then asystole is classic. VF/pVT can also occur (especially if digoxin-toxic). Hyperkalaemia should be high on the differential of any 'unexplained' bradyasystolic arrest, especially in a dialysis or CKD patient.[7]
Calcium chloride via central line is preferred over gluconate in arrest. Chloride delivers 3x the ionised calcium and is bioavailable immediately (gluconate needs hepatic metabolism, which is impaired in shock/arrest). If only peripheral access exists, give gluconate rather than delay — but obtain central access.[7]
The dialysis patient who missed a session is the prototypical hyperkalaemic arrest. Missing one session, a high-K meal, constipation (reduced gut loss), and intercurrent illness combine. After ROSC, the priority is emergency haemodialysis (or SLED/CVVHDF if unstable) and a plan to prevent recurrence (diet, binders, dialysis schedule).[2]
Do NOT stop CPR to wait for the K+ result. If the pre-arrest or periarrest K+ is known to be high (or the picture is suggestive — CKD, wide QRS, bradyasystolic), give the bundle empirically while continuing ALS and waiting for confirmation.[3]
Rebound after ROSC is common. Cellular shifts reverse as acidosis and ischaemia resolve, and dialysis gradients equilibrate — recheck K+ within 30-60 min of ROSC and arrange definitive removal. The post-arrest patient needs the same STABILISE-SHIFT-REMOVE framework as the pre-arrest one.[2]

BRASH syndrome — a hyperkalaemia-specific trap

BRASH syndrome — recognise and break the loop

Recognise the cluster: Bradycardia + Renal failure + AV blockade (medication) + Shock + Hyperkalaemia. The patient on a beta-blocker or non-DHP calcium-channel blocker (or digoxin) who develops renal impairment and hyperkalaemia slips into a self-reinforcing loop[6]
Mechanism of the loop: AV-nodal blocker → bradycardia + hypotension → renal hypoperfusion → worsening AKI + acidosis → worsening hyperkalaemia → worsening bradycardia/AV block → more hypoperfusion. Each element feeds the next[6]
Why standard ALS fails: atropine and transcutaneous pacing often do NOT work because the driver is hyperkalaemia and drug toxicity, not primary conduction disease. The bradycardia resolves when K+ is corrected and the AV-blocker is antagonised/cleared[6]
Treatment bundle: (a) CALCIUM to stabilise the membrane; (b) INSULIN/DEXTROSE + SALBUTAMOL to shift K+; (c) treat the AV-blocker — beta-blocker: glucagon/high-dose insulin euglycaemia therapy; calcium-channel blocker: calcium (high dose); digoxin: Fab fragments; (d) vasopressors/inotropes for shock; (e) treat the AKI (fluids if volume-depleted, then dialysis if refractory); (f) treat acidosis[6]
Don't be fooled by a 'reasonable' heart rate. A beta-blocked patient may not be profoundly bradycardic, but the AV-nodal blockade still drives the loop. The combination of AV-blocker + AKI + hyperkalaemia + hypoperfusion is the syndrome.[6]

High-yield clinical pearls (examiner favourites)

High-yield hyperkalaemia points for CICM/FFICM exam

Calcium does NOT lower potassium — it STABILISES the cardiac membrane. Calcium gluconate raises the threshold for depolarisation → prevents arrhythmia from hyperkalaemia. It buys TIME (30-60 min) while insulin/dextrose and other measures lower K+. ALWAYS give calcium FIRST if ECG changes. Calcium chloride (via central line) has 3x more ionised calcium than gluconate.[3]
Insulin/dextrose is the most reliable K+-shifting therapy. Insulin stimulates Na/K ATPase → drives K+ INTO cells. Dose: 10 units rapid-acting insulin + 25 g dextrose IV. Lowers K+ 0.5-1.0 mmol/L within 15-30 min. LASTS 4-6 hours. MONITOR GLUCOSE (hypoglycaemia — even with dextrose — check every hour for 4-6 h).[4]
Salbutamol (beta-2 agonist) shifts K+ into cells. Stimulates Na/K ATPase (via beta-2 receptor → cAMP). Dose: 10-20 mg nebulised (HIGH dose — 5-10x asthma dose) or 500 mcg IV. Lowers K+ 0.5-1.0 mmol/L. Onset 15-30 min. ADD to insulin/dextrose (synergistic). Caution: tachycardia, tremor, MI (beta-1 effect).[3]
Sodium bicarbonate shifts K+ only if ACIDOTIC. In acidosis, H+ enters cells (buffering), K+ exits (maintaining electroneutrality). Bicarbonate corrects acidosis → reverses this shift → K+ enters cells. If NOT acidotic: bicarbonate has MINIMAL K+-lowering effect (don't rely on it alone). Dose: 50-100 mmol of 8.4% (or 500 mL of 1.26%).[8]
Dialysis is the DEFINITIVE treatment for severe/refractory hyperkalaemia. Haemodialysis: lowers K+ 1-1.5 mmol/L in 1-2 hours (FASTEST removal). CVVHDF: slower (hours). Indications: K+ >7 despite medical therapy, ongoing K+ release (rhabdomyolysis, tumour lysis), end-stage renal failure, severe acidosis. PREPARE early — don't wait for K+ to rise further.[2]
Common causes of hyperkalaemia in ICU. (1) AKI/CKD (impaired excretion). (2) DRUGS: ACEi/ARB, K-sparing diuretics (spironolactone, amiloride), TMP-SMX (blocks ENaC), heparin (inhibits aldosterone), beta-blockers, calcineurin inhibitors, digoxin. (3) RHABDOMYOLYSIS. (4) TUMOUR LYSIS. (5) ACIDOSIS (DKA, lactic). (6) ADDISON'S. (7) GI BLEED (digested blood = K+ load). (8) MASSIVE TRANSFUSION (stored blood has high K+). REVIEW ALL MEDICATIONS.[2]
Peaked T waves — the earliest ECG sign. Tall, narrow, symmetric, 'tented' T waves. Best seen in V2-V4. May be subtle. Compare to previous ECG. If K+ >6.5 and ECG shows peaked T → treat as EMERGENCY (calcium + insulin/dextrose). Don't wait for worse changes (wide QRS, sine wave).[11]
Sine wave = pre-arrest. QRS and T wave merge → undulating 'sine wave' pattern. Cardiac arrest imminent (VF or asystole). IMMEDIATE: calcium gluconate IV + insulin/dextrose + prepare for dialysis + resuscitation. May need CPR if arrests.[3]
Hypoglycaemia after insulin/dextrose — common, dangerous. Insulin 10 units + dextrose 25 g → may still cause hypoglycaemia (especially in renal failure — reduced insulin clearance, hepatic disease). MONITOR glucose every hour for 4-6 h after insulin. If hypoglycaemia: more dextrose. Some use higher dextrose (50 g) or lower insulin (5 units) for high-risk patients.[5]
GI potassium binders (patiromer, sodium zirconium cyclosilicate). Patiromer: binds K+ in gut (exchange for calcium). SZC: binds K+ (exchange for sodium/H+). Both LOWER K+ gradually (hours). NOT for acute severe hyperkalaemia (too slow) but useful as a bridge and for CHRONIC management (CKD, on RAAS inhibitors). Sodium polystyrene sulfonate (Kayexalate/Resonium) — older, slower, may cause bowel necrosis (avoid acutely).[9]
Pseudohyperkalaemia — false alarm. K+ released from cells during venepuncture (haemolysis, fist clenching, difficult draw). Clues: no ECG changes, no symptoms, previous normal K+. Confirm with ARTERIAL or free-flowing venous sample (no tourniquet, rapid draw). If K+ high but patient well + normal ECG → recheck (avoid unnecessary treatment).[3]
Calcium gluconate vs calcium chloride. CALCIUM GLUCONATE: 10 mL of 10% = 2.2 mmol Ca²⁺ (smaller dose). Safer via peripheral vein (less tissue necrosis if extravasation). CALCIUM CHLORIDE: 10 mL of 10% = 6.8 mmol Ca²⁺ (3x more Ca²⁺). Preferred for ARREST (more calcium). Via CENTRAL line only (causes necrosis if peripheral extravasation).[3]
Hyperkalaemia in cardiac arrest — part of reversible causes (H's). During CPR: check K+ (VBG/ABG). If K+ >6.5 → calcium chloride (central) + insulin/dextrose + bicarbonate DURING CPR. May restore perfusing rhythm if hyperkalaemia caused arrest. Also: treat underlying cause (renal failure — consider dialysis post-ROSC).[7]
Prevention of recurrent hyperkalaemia. (1) K-restricted diet (<2 g/day — avoid bananas, tomatoes, potatoes, nuts, chocolate). (2) Stop/reduce causative drugs (ACEi/ARB, K-sparing diuretics). (3) K+ binders (patiromer, SZC — chronic). (4) Loop diuretics (promote K+ excretion). (5) Treat constipation (GI K+ excretion). (6) Treat acidosis (bicarbonate). (7) Dialysis planning (if CKD stage 5).[12]

Mechanism and physiology pearls (for the viva)

Why does hyperkalaemia cause arrhythmia? A high extracellular K+ makes the resting membrane potential LESS negative (closer to threshold). The myocyte is partly depolarised, so the gap between resting and threshold potential narrows → initially hyperexcitable (ectopics) then inexcitable (Na+ channels become inactivated by the partial depolarisation → conduction slows → QRS widens → asystole/VF). Calcium raises the threshold potential, restoring the safety margin.[2]
The '90% in cells, 1-2% extracellular' rule. Total body K+ is ~3500 mmol; >98% is intracellular. A rise of serum K+ from 4 to 7 mmol/L reflects a shift of only ~10-20 mmol out of cells (in acute shift states) — which is why insulin/dextrose and salbutamol (which only shift K+ back into cells) work so well acutely, and why rebound occurs once the shift reverses.[2]
Renal K+ excretion = distal nephron + aldosterone + flow. Chronic K+ balance depends on aldosterone-driven secretion in the collecting duct, which needs (a) adequate distal Na+ delivery and flow, (b) functioning ENaC, (c) aldosterone, and (d) normal tubule cells. Anything that disrupts these (AKI, hypoaldosteronism, ENaC blockers, K-sparing diuretics, ACEi/ARB) limits excretion and predisposes to hyperkalaemia.[2]
Acidosis shifts K+ out of cells; alkalosis shifts it in. In metabolic acidosis, H+ moves into cells for buffering, and K+ moves out to maintain electroneutrality (organic acidosis — lactic/keto — shifts K+ less than mineral acidosis — HCl). This is why DKA correction and bicarbonate lower K+ — and why treating alkalosis can unmask hypokalaemia.[8]
Insulin and beta-2 agonists share a final common pathway but different receptors. Both ultimately increase Na/K ATPase activity (insulin directly via IRS-PI3K; salbutamol via Gs-cAMP). This is why they are additive. They also share the same pitfall: hypoglycaemia with insulin; tachycardia/ischaemia with salbutamol.[8]
Rebound after shifting therapy is the rule, not the exception. Insulin/dextrose and salbutamol do not REMOVE K+ — they relocate it. As insulin wears off (4-6 h) or the underlying acidosis/cause persists, K+ leaks back out. ALWAYS pair shifting with removal (diuretics, binders, dialysis) and with cause treatment, and recheck K+ within 2-4 h.[2]

Special situations and edge cases

Liver failure / transplant patients on calcineurin inhibitors. Tacrolimus and cyclosporin cause a type-4-RTA-like hypoaldosteronism; combined with renal impairment, hyperkalaemia is common. Treat with binders, loop diuretics, fludrocortisone, and review immunosuppression levels.[2]
Post-operative cardiac surgical patients. Cardioplegia solutions are K+-rich; combined with AKI, hypothermia and acidosis, hyperkalaemia is common early after bypass. Check K+ on arrival in ICU and treat per algorithm; the K+ usually falls as the cardioplegia is excreted/metabolised.[3]
The constipated dialysis patient. Gut K+ excretion increases adaptively in CKD (the colon can excrete up to 30-40% of dietary K+). Constipation removes this escape route and precipitates hyperkalaemia. Treat constipation aggressively (laxatives, sometimes resonium enema) as part of hyperkalaemia management in dialysis patients.[12]
Pregnancy. Mild respiratory alkalosis and increased RAAS activity tend to keep K+ slightly low; hyperkalaemia in pregnancy is uncommon and usually reflects renal disease, pre-eclampsia with renal impairment, or Addison's. Treat per standard algorithm; calcium, insulin/dextrose and salbutamol are all safe in pregnancy. Dialyse if needed (modified dose).[11]
Addisonian crisis. Hyperkalaemia + hyponatraemia + hypoglycaemia + hypotension + abdominal pain = adrenal crisis until proven otherwise. Give hydrocortisone 100 mg IV stat (then 200 mg/24 h) — this provides mineralocorticoid activity at high dose and corrects the hyperkalaemia. Do not wait for the cortisol result if the picture is suggestive.[2]
Tumour lysis syndrome. Anticipate in high-burden haematological malignancy (high-grade lymphoma, ALL, high blast-count AML) and bulky solid tumours starting therapy. Hyperkalaemia + hyperphosphataemia + hypocalcaemia + hyperuricaemia + AKI. Prophylaxis: aggressive hydration + rasburicase (or allopurinol). Treat established TLS with the full STABILISE-SHIFT-REMOVE bundle and urgent dialysis — the K+ rise can be rapid and refractory.[3]

Exam practice — SAQs

SAQ — Severe hyperkalaemia with ECG changes in a CKD patient on RAAS inhibitors

10 minutes · 10 marks

A 72-year-old man with CKD stage 4 (baseline creatinine 280 micromol/L) on perindopril, spironolactone and trimethoprim-sulfamethoxazole for a urinary tract infection presents with progressive weakness and presyncope. He is bradycardic (HR 44) with a BP of 92/58. Venous gas: K+ 7.4 mmol/L, pH 7.28, bicarbonate 16. ECG shows a wide QRS (134 ms), peaked and tented T waves in V2-V4, PR prolongation and loss of P waves.

[1]

SAQ — Hypokalaemia with Torsades de Pointes and cardiac arrest

10 minutes · 10 marks

A 58-year-old woman with a history of alcohol misuse and bulimia nervosa is admitted with three days of severe vomiting and diarrhoea. She has a nasogastric tube on free drainage and has received frusemide 80 mg IV for pulmonary oedema. Her regular medications include methadone and ondansetron. Bloods: K+ 2.1 mmol/L, Mg 0.4 mmol/L, ionised Ca 0.9 mmol/L. ECG shows QTc 560 ms with a run of polymorphic VT that twists around the baseline (Torsades de Pointes); she becomes pulseless.

[1]

Red flags

Critical hyperkalaemia red flags

ECG changes (peaked T, wide QRS, sine wave) → calcium gluconate IMMEDIATELY, before any K+-lowering therapy.[3]
K+ >6.5 mmol/L → emergency (even without ECG changes).[1]
Sine wave → pre-arrest — calcium + insulin/dextrose + bicarbonate + dialysis.[3]
Hyperkalaemic arrest / bradyasystolic arrest in CKD/dialysis → calcium chloride (central) + insulin/dextrose + bicarbonate DURING CPR.[7]
BRASH syndrome (AV-blocker + renal failure + hyperkalaemia + bradycardia/shock) → treat the K+ AND the AV-blocker; standard bradycardia therapy often fails.[6]
Hypoglycaemia 1-6 h after insulin/dextrose → monitor glucose hourly for ≥6 h.[5]
Refractory hyperkalaemia (despite medical therapy) → urgent dialysis.[2]
Rebound after shift therapy or after dialysis → recheck K+ within 1-2 h.[2]
Digoxin toxicity + hyperkalaemia → digoxin Fab fragments, NOT calcium.[3]
Pseudohyperkalaemia (no ECG changes, patient well, haemolysed sample) → recheck (arterial/plasma) before treating.[3]

Prognosis and evidence

UKKA / KDIGO approach to hyperkalaemia (Clase 2020, Kidney Int)

KDIGO Controversies Conference conclusions on potassium homeostasis and dyskalaemia management (Clase 2020):[1]

Mild (5.5-5.9): cause-specific treatment, dietary advice, K+ binders (patiromer/SZC for chronic). No emergency treatment
Moderate (6.0-6.4): shift K+ (insulin/dextrose if symptomatic or ECG changes), binders, review meds. Monitor closely
Severe (≥6.5): EMERGENCY — calcium (if ECG changes), insulin/dextrose, salbutamol, consider dialysis
Insulin/dextrose dose: 10 units + 25 g dextrose (adult). Monitor glucose every hour for 4-6 h (hypoglycaemia risk emphasised)
Calcium: gluconate 10 mL 10% (peripheral) or chloride 10 mL 10% (central — 3x more Ca²⁺)
RAAS inhibitors should generally be CONTINUED in heart failure/CKD where possible, using binders to manage K+ (stopping RAASi worsens long-term outcomes) Mortality: hyperkalaemia-caused cardiac arrest mortality is high (>50% if K+ was the proximate cause). With prompt treatment: arrhythmia prevented, K+ lowered → survival depends on underlying cause.

Insulin/dextrose evidence — Harel 2016 systematic review (PLoS One)

Systematic review of optimal insulin dose/method for emergency hyperkalaemia:[5]

Insulin/dextrose reliably lowers K+ by 0.5-1.0 mmol/L within 15-30 min — the most consistent shifting therapy
Hypoglycaemia is common — across studies, any hypoglycaemia up to 20-30%, severe hypoglycaemia (glucose <3.0 mmol/L) 5-10%, peaking 1-3 h post-dose
Lower insulin doses (5 units) with adequate dextrose achieve a similar K+ fall with less hypoglycaemia in some studies — but 10 units remains the standard adult dose
Practice point: give insulin/dextrose, then commit to ≥6 h of glucose monitoring with bedside dextrose available. Identify high-risk patients (renal/hepatic failure, low body weight, fasting, baseline glucose <7) and consider reduced-dose regimens.

Bicarbonate/insulin/albuterol synergy — Allon 1996 (Am J Kidney Dis)

Classic dialysis-patient crossover study:[8]

Insulin/dextrose lowered K+ by ~1.0 mmol/L; albuterol by ~1.0 mmol/L; combined by ~1.3-1.5 mmol/L (additive)
Bicarbonate alone had a trivial K+-lowering effect in these (non-acidotic) dialysis patients — confirming bicarbonate is useful mainly in acidosis
Practice point: combine insulin/dextrose + salbutamol for moderate-severe hyperkalaemia; reserve bicarbonate for the acidotic patient or the arrest bundle.

Sodium zirconium cyclosilicate and patiromer — long-term efficacy and safety

Sodium zirconium cyclosilicate (Roger 2021, NDT): long-term (up to 12 months) SZC maintained normokalaemia across mild/moderate and severe/end-stage CKD groups; efficacy was rapid (K+ fall within 2-4 h of first dose) and sustained. Oedema (Na+ load) was the main caution — relevant in heart failure.[9] Patiromer (Pitt 2018, ESC Heart Fail): in heart-failure patients with diabetic nephropathy on RAAS inhibitors, long-term patiromer enabled patients to remain on RAASi while controlling K+. Main adverse effects: mild hypomagnesaemia and hypocalcaemia.[10] Practice point: both novel binders allow continuation of guideline-directed RAASi in HF/CKD. SZC has a role in subacute ICU control (faster onset among binders); patiromer suits chronic outpatient management. Avoid SPS (sodium polystyrene sulfonate) in the acute setting due to bowel-necrosis risk.

Recent evidence and outcomes — Geldermann 2026 (Emerg Med J)

Contemporary evidence-based review of acute hyperkalaemia in emergency care:[11]

A normal ECG does NOT exclude severe hyperkalaemia — up to ~50% of K+ >6.5 mmol/L have subtle or absent changes; treat the number, not just the tracing
Pseudohyperkalaemia remains under-recognised — always confirm with a non-haemolysed or arterial sample before treating an unexpected value in a well patient
Combined shifting therapy (insulin/dextrose + salbutamol) outperforms monotherapy
Hypoglycaemia is the leading iatrogenic complication of insulin/dextrose — reinforce the 6-hour monitoring bundle
Novel binders and dialysis timing continue to evolve — start removal planning EARLY in severe hyperkalaemia rather than waiting for refractory K+

Putting it together — exam one-liners

One-liners you can reproduce in the viva

"Severe hyperkalaemia is a K+ >6.5 mmol/L or any ECG change attributable to hyperkalaemia, and I treat it as a cardiac emergency."[1]
"My framework is STABILISE the membrane with calcium, SHIFT K+ intracellularly with insulin/dextrose and salbutamol, then REMOVE K+ with diuretics, binders, or dialysis — in that order."[2]
"Calcium gluconate 10 mL of 10% IV is my first drug whenever there are ECG changes; it does not lower K+, it raises the threshold potential to prevent arrhythmia and buys 30-60 min."[3]
"Insulin 10 units with 25 g of dextrose is my workhorse; it lowers K+ by 0.5-1.0 mmol/L for 4-6 h, and I monitor glucose hourly for 6 h because hypoglycaemia is the commonest complication."[4]
"In hyperkalaemic arrest I give calcium chloride via a central line, insulin/dextrose, and 50 mmol of sodium bicarbonate during CPR, and I send a gas to confirm — recent RCT data support calcium plus bicarbonate."[7]
"BRASH syndrome is bradycardia, renal failure, AV blockade, shock and hyperkalaemia — a self-perpetuating loop driven by AV-nodal blockers, and it needs the K+ and the blocker toxicity treated together."[6]
"Pseudohyperkalaemia is diagnosed by a well patient with a normal ECG and a haemolysed or difficult sample; I confirm with an arterial or plasma potassium before treating."[3]
"For chronic prevention in CKD/HF I restrict dietary K+, use patiromer or sodium zirconium to allow continuation of RAAS inhibitors, treat constipation and acidosis, and plan dialysis when appropriate."[12]

References

[1]Clase CM, Carrero JJ, Ellison DH, et al. Potassium homeostasis and management of dyskalemia in kidney diseases: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference Kidney Int, 2020.PMID 31706619
[2]Palmer BF, Carrero JJ, Clegg DJ. Clinical Management of Hyperkalemia Mayo Clin Proc, 2021.PMID 33160639
[3]Long B, Warix JR, Koyfman A. Hyperkalemia in the Emergency Department: Yes, a Need for Further Evidence, but Do Not Discount What We Have J Emerg Med, 2019.PMID 31326003
[4]Moussavi K, Fitter S, Gabrielson SW. Management of Hyperkalemia With Insulin and Glucose: Pearls for the Emergency Clinician J Emerg Med, 2019.PMID 31084947
[5]Harel Z, Kamel KS. Optimal Dose and Method of Administration of Intravenous Insulin in the Management of Emergency Hyperkalemia: A Systematic Review PLoS One, 2016.PMID 27148740
[6]Farkas JD, Long B, Koyfman A. BRASH Syndrome: Bradycardia, Renal Failure, AV Blockade, Shock, and Hyperkalemia J Emerg Med, 2020.PMID 32565167
[7]Eggertsen MA, Munch Johannsen C, Kovacevic A, et al. Sodium Bicarbonate and Calcium Chloride for the Treatment of Hyperkalemia-Induced Cardiac Arrest: A Randomized, Blinded, Placebo-Controlled Animal Study Crit Care Med, 2024.PMID 37921685
[8]Allon M, Shanklin N. Effect of bicarbonate administration on plasma potassium in dialysis patients: interactions with insulin and albuterol Am J Kidney Dis, 1996.PMID 8840939
[9]Roger SD, Lavin PT, Lerma EV, et al. Long-term safety and efficacy of sodium zirconium cyclosilicate for hyperkalaemia in patients with mild/moderate versus severe/end-stage chronic kidney disease: comparative results from an open-label, Phase 3 study Nephrol Dial Transplant, 2021.PMID 32030422
[10]Pitt B, Bakris GL, Weir MR, et al. Long-term effects of patiromer for hyperkalaemia treatment in patients with mild heart failure and diabetic nephropathy on angiotensin-converting enzymes/angiotensin receptor blockers: results from AMETHYST-DN ESC Heart Fail, 2018.PMID 29767459
[11]Geldermann N, Dzimiera J, Fischer H, et al. Acute hyperkalaemia in emergency care: evidence-based approaches Emerg Med J, 2026.PMID 41506858
[12]Sumida K, Biruete A, Kistler BM, et al. New Insights Into Dietary Approaches to Potassium Management in Chronic Kidney Disease J Ren Nutr, 2023.PMID 37610407

[1]

The three-step framework (memorise this)

Hyperkalaemia treatment is STABILISE → SHIFT → REMOVE, always in that order. Skipping a step or doing them out of order is a classic exam and bedside error.

STABILISE the myocardium — calcium gluconate 10 mL of 10% IV over 2-5 min (calcium chloride via central line in arrest). Onset 1-3 min, lasts 30-60 min. Does NOT lower K+ — it raises the threshold for depolarisation so hyperkalaemia cannot destabilise the membrane. Give first whenever there are ECG changes (peaked T alone qualifies).[3]
SHIFT K+ intracellularly — insulin/dextrose (10 units rapid-acting insulin + 25 g dextrose IV) is the workhorse (lowers K+ 0.5-1.0 mmol/L for 4-6 h). ADD salbutamol 10-20 mg nebulised (synergistic, adds another 0.5-1.0 mmol/L). Sodium bicarbonate works mainly when acidotic.[4]
REMOVE K+ from the body — loop diuretics (if kidneys function), GI cation-exchange binders (patiromer, sodium zirconium cyclosilicate — hours, not minutes), and dialysis (definitive, fastest — 1-1.5 mmol/L in 1-2 h). Shifting alone is temporary: K+ will leak back out unless you remove it or correct the cause.[2]

ECG changes — recognise the progression

Hyperkalaemia severity and ECG changes

K+ (mmol/L)	Severity	Typical ECG changes	Action
5.5-5.9	Mild	Usually none	Treat cause, K-restricted diet, binders. Stop K+-sparing drugs
6.0-6.4	Moderate	Peaked T waves (may appear)	Shift K+ (insulin/dextrose, salbutamol), binders, consider dialysis. Continuous cardiac monitor
6.5-6.9	Severe	Peaked T, PR prolongation, early QRS widening	CALCIUM first (if ECG changes), shift K+, REMOVE (diuretics/dialysis). Emergency
>7.0	LIFE-THREATENING	Wide QRS, sine wave, VF, asystole	CALCIUM immediately + shift + urgent dialysis. Prepare for arrest

[1]

ECG pitfalls — what catches candidates out

A normal ECG does NOT exclude severe hyperkalaemia. Up to half of patients with K+ >6.5 mmol/L have no 'classic' changes — especially patients with CKD who have chronic, slowly-rising K+ (myocytes partly adapt). Treat the NUMBER, not just the tracing.[11]
Peaked T waves are not specific. Acute MI (hyperacute T), benign early repolarisation, LVH, bradycardia and bundle branch block all produce tall T waves. Look for the symmetric, narrow, 'tented' quality and compare with old ECGs. Hyperkalaemic T waves are typically most prominent in V2-V4.[3]
Loss of P waves can mimic atrial fibrillation/junctional rhythm. A patient in fast AF who develops a regular, wide, P-less rhythm as K+ climbs is deteriorating — not cardioverting.[2]
BRASH syndrome masquerades as primary bradycardia. Bradycardia + renal failure + AV-nodal blocker (beta-blocker, diltiazem, verapamil, digoxin) + shock + hyperkalaemia form a self-perpetuating loop: AV blocker worsens the bradycardia, hypoperfusion worsens renal failure and acidosis, which worsen hyperkalaemia, which worsens the bradycardia. Atropine and pacing often fail until you correct the K+ and the AV-blocker toxicity.[6]
Digoxin effect + hyperkalaemia = digoxin toxicity until proven otherwise. Digoxin inhibits the Na/K ATPase; acute digoxin toxicity classically causes HYPERkalaemia (not the chronic 'dig effect' which is usually normokalaemic). Give digoxin Fab fragments, NOT calcium — calcium in the setting of digoxin toxicity has been associated with 'stone heart' (controversial, animal data) and may precipitate fatal arrhythmia. In practice, treat suspected digoxin toxicity with Fab; reserve calcium for non-digoxin hyperkalaemia.[3]

Emergency management algorithm

Emergency management of severe hyperkalaemia (K+ >6.5 or ECG changes)

ECG immediately — peaked T waves? Wide QRS? Sine wave? If ANY ECG changes → CALCIUM FIRST. Attach continuous cardiac monitor and establish IV access. Take a venous/arterial gas for rapid K+ (lab serum K+ may lag)
STABILISE cardiac membrane (if ECG changes) — CALCIUM GLUCONATE 10 mL of 10% IV over 2-5 min (or calcium chloride 10 mL of 10% via central line — 3x more ionised Ca²⁺). Onset 1-3 min. Duration 30-60 min. May repeat once after 5 min if ECG changes persist. Does NOT lower K+ — only prevents arrhythmia. Exclude digoxin toxicity first (give Fab, not calcium)[3]
SHIFT K+ into cells — INSULIN/DEXTROSE: 10 units rapid-acting insulin + 25 g (50 mL of 50%) dextrose IV over 15 min (onset 15 min, lowers K+ 0.5-1.0 mmol/L for 4-6 h). PLUS SALBUTAMOL 10-20 mg nebulised (or 500 mcg IV over 15 min) — synergistic, adds 0.5-1.0 mmol/L. ADD SODIUM BICARBONATE 50 mmol of 8.4% IV (especially if acidotic or arrest) — modest additional shift.[4]
REMOVE K+ from body — LOOP DIURETICS (frusemide 40-80 mg IV — only if kidneys functioning and producing urine). GI BINDERS (sodium zirconium cyclosilicate 10 g, or patiromer 8.4-16.8 g — slower, hours). DIALYSIS (definitive — intermittent haemodialysis fastest; CVVHDF slower). Begin arranging dialysis EARLY if K+ >7 despite therapy, ongoing K+ release, or anuric renal failure[2]
Identify and treat cause — AKI/CKD, rhabdomyolysis, tumour lysis, drugs (ACEi/ARB, spironolactone, amiloride, TMP-SMX, heparin, beta-blockers, calcineurin inhibitors), Addison's, acidosis (DKA, lactic), GI bleed (digested blood = K+ load), massive transfusion. REVIEW THE MEDICATION CHART and stop all K+-sparing/raising agents
Monitor — continuous ECG, repeat K+ at 1-2 h (then 2-4 h), CHECK GLUCOSE at 0, 30, 60 min and then hourly for 4-6 h after insulin/dextrose (hypoglycaemia risk). Document calcium given. Once K+ <6.0 and ECG normal → step down to oral binders + cause treatment

Stepwise pharmacology — what each drug actually does (exam framework)

CALCIUM GLUCONATE 10% — membrane stabiliser. Mechanism: raises the threshold potential of myocardial myocytes (restores the gap between resting and threshold potential that hyperkalaemia has narrowed). Dose: 10 mL IV over 2-5 min (2.2 mmol Ca²⁺), repeat once after 5 min if ECG changes persist. Onset 1-3 min, duration 30-60 min. No effect on serum K+. Indication: ANY ECG change attributable to hyperkalaemia. Contra-indication/caution: digoxin toxicity (give Fab instead)[3]
INSULIN + DEXTROSE — intracellular shift (the workhorse). Mechanism: insulin directly stimulates the Na/K ATPase → drives K+ into cells. Dextrose prevents hypoglycaemia. Dose: 10 units rapid-acting insulin (e.g., Actrapid) + 25 g dextrose (50 mL of 50%) IV over 15 min. Lowers K+ 0.5-1.0 mmol/L within 15-30 min, effect lasts 4-6 h. Most reliable shifting therapy. MUST monitor glucose hourly for 4-6 h — hypoglycaemia in up to 20-30%, the leading complication[5]
SALBUTAMOL — intracellular shift (add-on). Mechanism: beta-2 agonist → cAMP → stimulates Na/K ATPase → K+ into cells. Dose: 10-20 mg nebulised (this is 5-10x the asthma dose) OR 250-500 mcg IV over 15 min. Onset 15-30 min, lowers K+ 0.5-1.0 mmol/L, lasts 2-4 h. Synergistic with insulin/dextrose (give both). Cautions: tachycardia, tremor, ischaemia (beta-1 effect), avoid in tachyarrhythmia/active ischaemia. Less effective in beta-blocked patients[8]
SODIUM BICARBONATE — shift (mainly if acidotic). Mechanism: corrects acidosis → H+ stops exiting cells → K+ no longer needs to exit to maintain electroneutrality → K+ shifts in. Dose: 50 mmol of 8.4% IV over 5-15 min (or 500 mL of 1.26%). Minimal effect in non-acidotic patients — do not rely on it alone. Useful in DKA/lactic acidosis and in cardiac arrest (see below). Cautions: hypernatraemia, volume overload, alkalosis, hypocalcaemia (lowers ionised Ca²⁺)[8]
SODIUM ZIRCONIUM CYCLOSILICATE / PATIROMER — gut removal. SZC: 10 g orally/NG, exchanges Na+/H+ for K+ in the gut, lowers K+ ~0.5-0.7 mmol/L over 2-4 h. Patiromer: 8.4-16.8 g, exchanges Ca²+ for K+, slower. Both are for subacute/chronic control — too slow for an emergency but useful as bridge to dialysis or to prevent rebound. Avoid SPS (sodium polystyrene sulfonate) in the acute setting — slow and associated with bowel necrosis[9]
HAEMODIALYSIS / CVVHDF — definitive removal. Intermittent haemodialysis: 1-1.5 mmol/L drop in 1-2 h (FASTEST). CVVHDF: slower, gentler, lower rebound risk. Indications: K+ >7 despite medical therapy, ongoing endogenous K+ release (rhabdo, TLS), end-stage renal failure, severe acidosis, refractory arrest. REBOUND is common — K+ diffuses out of cells and from dialysate gradients; recheck within 1-2 h of finishing[2]

Calcium gluconate vs calcium chloride

	CALCIUM GLUCONATE 10%	CALCIUM CHLORIDE 10%
Ionised Ca²⁺ per 10 mL	2.2 mmol	6.8 mmol (≈3x more)
Route	Peripheral or central	CENTRAL line only
Extravasation risk	Low (less tissue necrosis)	High — severe necrosis if extravasated
Hepatic metabolism	Requires hepatic conversion to release Ca²⁺ (slower in shock/hepatic failure)	Immediately bioavailable
Preferred use	First-line in awake/non-arrest patients, peripheral access	Cardiac ARREST (central line) — more Ca²⁺ delivered fast
Dose	10 mL IV over 2-5 min, repeat once after 5 min	10 mL IV via central line (rapid), repeat once
Onset/duration	1-3 min / 30-60 min	1-3 min / 30-60 min

[1]

K+-shifting therapies — insulin/dextrose vs salbutamol vs bicarbonate

Therapy	Dose	K+ fall (mmol/L)	Onset	Duration	Key cautions
Insulin + dextrose	10 U insulin + 25 g dextrose IV	0.5-1.0	15 min	4-6 h	Hypoglycaemia (20-30%) — monitor glucose hourly ×6 h
Salbutamol (neb)	10-20 mg nebulised	0.5-1.0	15-30 min	2-4 h	Tachycardia, tremor, ischaemia; less effective if beta-blocked
Salbutamol (IV)	250-500 mcg over 15 min	0.6-1.0	15 min	2-4 h	As above; avoid in active ischaemia/VT
Sodium bicarbonate	50 mmol 8.4% IV (or 500 mL 1.26%)	0.2-0.5 (acidotic) / <0.2 (non-acidotic)	30-60 min	2-4 h	Only reliable if ACIDOTIC; hypernatraemia, alkalosis, hypocalcaemia
Insulin + salbutamol	Both together	Additive (~1.0-1.5)	15 min	4-6 h	COMBINE for moderate-severe hyperkalaemia

[1]

K+-removal therapies — diuretics vs binders vs dialysis

Therapy	Speed	Use in oliguria/anuria	Setting	Notes
Loop diuretic (frusemide)	Hours	Ineffective if anuric	Functioning kidneys	Dose 40-80 mg IV; add thiazide for sequential blockade. Also treats volume overload
Sodium zirconium cyclosilicate	2-4 h	Works (gut, not kidney)	Subacute, bridge, chronic	10 g oral/NG; rapid onset among binders; may cause oedema (Na+ load)
Patiromer	4-7 h	Works	Chronic, heart-failure patients on RAASi	8.4-16.8 g; exchanges Ca²+ (mild hypomagnesaemia/hypocalcaemia)
SPS (Kayexalate/resonium)	12-24+ h	Works	Largely AVOIDED	Slow; bowel necrosis/fibrosis reported — not for acute use
Haemodialysis (intermittent)	1-2 h (FASTEST)	Indicated if anuric	Definitive	1-1.5 mmol/L drop; beware rebound — recheck within 1-2 h
CVVHDF/SLED	Hours (gentler)	Indicated if haemodynamically unstable	ICU, unstable	Slower, lower rebound, continuous removal

[1]

GI potassium binders — patiromer vs sodium zirconium cyclosilicate vs SPS

	PATIROMER	SODIUM ZIRCONIUM CYCLOSILICATE	SPS (RESONIUM/KAYEXALATE)
Exchange ion	Calcium	Sodium / hydrogen	Sodium (or calcium prep)
Onset	4-7 h	2-4 h	12-24+ h
K+ reduction	~0.2-0.4 mmol/L per dose	~0.5-0.7 mmol/L per dose	Variable, modest
Approved for	Chronic hyperkalaemia (CKD, on RAASi)	Acute and chronic hyperkalaemia	Older; now largely avoided
Safety concerns	Hypomagnesaemia, hypocalcaemia, GI upset; binds some drugs (separate dosing)	Oedema/heart failure exacerbation (Na+ load); avoid if Na+ restricted	Bowel necrosis, perforation — FDA warning; not for acute use
Take-home	Good for chronic CKD/HF patients needing RAASi	Best binder for subacute ICU control	AVOID in the acute setting

[1]

Causes — organised by mechanism

[1]

Drug causes of hyperkalaemia — mechanism at a glance

Drug	Mechanism	Typical context
ACEi / ARB	↓ aldosterone (block RAAS)	CKD, HF — 'RAASi hyperkalaemia'
Spironolactone / eplerenone / finerenone	Aldosterone receptor antagonism	HF, cirrhosis, resistant HTN
Amiloride / triamterene	Block ENaC in collecting duct → ↓ K+ secretion	K-sparing diuretics; kombiglyze
Trimethoprim / pentamidine	Block ENaC (like amiloride)	UTI/pneumocystis prophylaxis in renal failure
Heparin (any route)	Inhibits aldosterone synthesis	Surprisingly common in ICU patients on prophylaxis
NSAIDs	↓ renin → ↓ aldosterone	AKI + hyperkalaemia in elderly
Calcineurin inhibitors (cyclosporin, tacrolimus)	Type 4 RTA-like effect	Transplant patients
Beta-blockers	Block beta-2 mediated K+ uptake into cells; also suppress renin	Any patient; BRASH syndrome with AV node blockers
Digoxin	Inhibits Na/K ATPase (acute toxicity → hyperkalaemia)	Acute overdose; check level
Succinylcholine	Depolarising agent → K+ efflux from muscle	Burns >24 h, crush, denervation, immobilisation
Mannitol / hypertonic saline	Osmotic shift / acid-base effect	Ongoing infusion
K+-containing IV fluids / Penicillin G	Direct K+ load	Large-volume KCl-containing fluids

[1]

Cause-finding pearls — where the marks are

Check a drug chart FIRST. The commonest single reversible cause in ICU is a K+-raising drug given to a patient with impaired renal excretion (ACEi + spironolactone + AKI is a near-classic triad). Heparin (including prophylactic LMWH) inhibits aldosterone and is frequently missed.[2]
Type 4 RTA (hyporeninaemic hypoaldosteronism) is the undercover cause in diabetics. Diabetic nephropathy damages the juxtaglomerular apparatus → low renin → low aldosterone → hyperkalaemia + mild metabolic acidosis. Classically an elderly diabetic with K+ 5.5-6.5 and a normal GFR. Treat with fludrocortisone or a loop diuretic, and review K-sparing drugs.[2]
Rhabdomyolysis and tumour lysis release K+ faster than the kidney can excrete it. Anticipate hyperkalaemia in any crush injury, prolonged immobilisation, status epilepticus, or after starting chemotherapy in a high-tumour-burden patient (TLS). The K+ rise may continue for hours despite treatment — start removal (dialysis) early. Always check CK and treat the source (aggressive IV fluids, rasburicase/allopurinol for TLS).[3]
DKA at presentation is hyperkalaemic despite total-body K+ depletion. Acidosis (H+ into cells, K+ out) + insulin deficiency (no Na/K ATPase drive) push K+ into the extracellular space, while osmotic diuresis and vomiting have depleted total body K+. When you give insulin + fluids, K+ plummets — this is the leading cause of death during DKA treatment. Protocol: if K+ <3.3 hold insulin; 3.3-5.2 add 20-30 mmol/L K+ to fluids; >5.2 no K+ yet, recheck in 2 h.[11]
GI bleed = hidden K+ load. Digested blood is rich in K+; a large upper GI bleed can raise serum K+ by 1-2 mmol/L over hours. Always ask about melaena/haematemesis in the unexplained hyperkalaemia workup.[3]
Salt substitutes are potassium chloride. 'Lo-Salt', 'NoSalt' and similar products, often used by cardiac/renal patients trying to reduce sodium, can deliver 10-15 g/day of KCl. Always take a dietary and supplement history in unexplained hyperkalaemia.[12]
Succinylcholine causes a small K+ rise (0.3-0.5 mmol/L) in everyone, but a MASSIVE rise in denervated/injured muscle. Avoid sux in burns >24 h old, crush injury, upper motor neuron lesions, prolonged immobility and severe abdominal sepsis — use rocuronium instead. The hyperkalaemic response peaks days to weeks after the insult.[3]
Massive transfusion / old stored blood. Packed red cells stored >7-14 days have K+ concentrations of 30-80 mmol/L in the supernatant. Rapid transfusion (especially in trauma with co-existing acidosis and hypoperfusion) can acutely raise K+. Use fresh blood / washed cells where possible in massive transfusion, and monitor K+ frequently.[2]

Pseudohyperkalaemia — don't treat a false alarm

Pseudohyperkalaemia vs true hyperkalaemia

Feature	PSEUDOHYPERKALAEMIA	TRUE HYPERKALAEMIA
Mechanism	K+ released from cells DURING/after venepuncture	Genuinely high plasma/serum K+ in vivo
Causes	Haemolysis, fist clenching, prolonged tourniquet (>1 min), small-gauge needle, delayed transport, severe thrombocytosis (>1000) or leucocytosis (>100) leaking K+ ex vivo	(see cause list above)
ECG	Normal (no peaked T, no wide QRS)	Often abnormal (but may be normal — see pitfall)
Clinical picture	Asymptomatic, no reason to be hyperkalaemic	Fits the clinical context (AKI, drugs, acidosis, rhabdo)
Confirmation	Repeat sample: ARTERIAL or free-flowing venous (no tourniquet), rapid draw, on ice, analyse promptly. Consider plasma K+ (heparin tube) vs serum (clots → more release)	Repeat K+ confirms persistent elevation
Action	Recheck before treating — avoid iatrogenic hypokalaemia	Treat per algorithm

[1]

Pseudohyperkalaemia pearls

No ECG changes + unexpected K+ value + patient looks well = recheck before treating. A haemolysed sample is the most common cause of a spurious high K+. An arterial gas potassium is fast and reliable (agreement with lab within ±0.3-0.4 mmol/L).[3]
Severe thrombocytosis or leucocytosis cause TRUE pseudohyperkalaemia (not haemolysis): platelets and WBC release K+ during clotting in the serum tube. Clue: serum K+ high but PLASMA K+ (heparin tube) normal. In haematological malignancy with WBC >100 or platelets >1000, always request a plasma (heparin) potassium.[11]
Reverse pseudohyperkalaemia (peri-phlebitis, hereditary spherocytosis during venepuncture) is rarer — the plasma K+ is HIGHER than the serum. Recognised in some haematological conditions and after vigorous fist-clenching with regional ischaemia.[11]
Do not delay treatment if there are ECG changes or the patient is unwell. Pseudohyperkalaemia is a diagnosis of exclusion — if there is any doubt and the ECG is abnormal, give calcium and recheck; you can always stop therapy if the repeat is normal.[3]

Insulin/dextrose — getting it right and avoiding hypoglycaemia

Safe insulin/dextrose administration (anti-hypoglycaemia bundle)

Check a baseline glucose before giving insulin/dextrose. If glucose <7 mmol/L, raise it first (give additional dextrose or run the dextrose before the insulin)
Dose to the patient: 10 units rapid-acting insulin (Actrapid/Humulin R) + 25 g dextrose IV (50 mL of 50%) over 15 min. Consider 5 units + 50 g dextrose (or 25 g then 25 g over 1-2 h) in high-risk patients (low weight, fasting, dialysis, baseline glucose <7)
Monitor glucose at 0, 30, 60 min, then hourly for 6 h. Most hypoglycaemia occurs at 1-3 h — do NOT stop checking at 1 h
Keep 50% dextrose at the bedside and treat any glucose <4 mmol/L (or symptomatic) with 25-50 g IV dextrose, then a dextrose infusion
Warn the ward team — patients are often transferred to a ward where the insulin/dextrose effect persists but glucose checks stop. Hand over the monitoring plan explicitly
Document insulin dose, dextrose dose, baseline glucose, and the monitoring schedule in the chart

[1]

Insulin/dextrose and salbutamol pearls

Hypoglycaemia after insulin/dextrose is the leading complication of hyperkalaemia treatment — not arrhythmia. Pooled data suggest ~20-30% incidence, with severe hypoglycaemia (glucose <3.0) in ~5-10%. The 6-hourly glucose monitoring bundle is mandatory, not optional.[5]
Lower-dose insulin (5 units) with the same dextrose achieves a similar K+ fall with less hypoglycaemia in some studies, but is less well validated. A common pragmatic approach: 5 units in small/frail/renal patients, 10 units otherwise, with the full monitoring bundle either way.[5]
Combine insulin/dextrose with salbutamol for additive effect. Insulin and beta-2 agonists both drive the Na/K ATPase but via different second messengers (insulin direct; salbutamol via cAMP), so their effects are roughly additive (combined fall ~1.0-1.5 mmol/L). Give both for moderate-severe hyperkalaemia unless salbutamol is contra-indicated (tachyarrhythmia, active ischaemia).[8]
Salbutamol is unreliable in beta-blocked patients and less effective in chronic dialysis patients (downregulated beta-2 receptors). Do not rely on salbutamol alone — it is an adjunct to insulin/dextrose.[8]
Bicarbonate has a place — but a small one. In non-acidotic patients it lowers K+ by <0.2 mmol/L over 1-2 h (not clinically useful alone). Reserve it for the acidotic patient (DKA, lactic acidosis) or as part of the arrest bundle. Beware: it lowers ionised calcium (so give calcium FIRST), causes hypernatraemia and volume overload, and paradoxically worsens intracellular acidosis if CO2 washout is impaired.[8]
Don't forget magnesium. Hypomagnesaemia impairs Na/K ATPase and is common in ICU; refractory hyperkalaemia with ongoing cellular leak may improve when Mg is corrected. Check and replace (MgSO4 2 g IV).[2]

Hyperkalaemic cardiac arrest

Hyperkalaemic cardiac arrest bundle (in addition to standard ALS)

Suspect hyperkalaemia in every arrest — send a VBG/ABG immediately (K+, Na+, glucose, lactate, pH). Especially suspect with: PEA/bradycardia, wide-complex arrest, known renal failure, dialysis patient who missed a session, diabetic in DKA, crush injury, drug overdose (digoxin, beta-blocker)
CALCIUM CHLORIDE 10 mL of 10% via CENTRAL line (preferred in arrest — 6.8 mmol Ca²⁺, immediately bioavailable). If no central line: calcium gluconate 10 mL of 10% via large peripheral line. Repeat every 5-10 min (up to 3-4 doses). Calcium stabilises the membrane and may restore a perfusing rhythm if hyperkalaemia is the cause[7]
INSULIN/DEXTROSE — 10 units insulin + 25 g dextrose IV bolus (push the dextrose 50%, then insulin, in arrest). Even in arrest, this shifts K+ and is given alongside ongoing CPR
SODIUM BICARBONATE 50 mmol of 8.4% IV bolus — given during CPR in suspected hyperkalaemic arrest. Recent randomised data (Eggertsen 2024) suggest a survival benefit from combined calcium chloride + bicarbonate in hyperkalaemic arrest. May repeat
SALBUTAMOL — limited role in arrest (IV beta-agonism competes with ongoing CPR); consider if ROSC achieved or as adjunct
EMERGENCY HAEMODIALYSIS if refractory — arrange while CPR continues if a viable cause and reversible context (e.g., missed dialysis). ECPR/extracorporeal support may buy time
Post-ROSC: recheck K+, treat cause (restart dialysis, stop offending drugs, treat rhabdo/TLS), continuous monitoring, plan definitive removal (HD). Beware rebound

Sodium bicarbonate + calcium chloride in hyperkalaemic cardiac arrest — Eggertsen 2024 (RCT)

Hyperkalaemic arrest pearls

Hyperkalaemia is a reversible cause of cardiac arrest — look for it in EVERY arrest. Send a VBG/ABG early (within the first cycle of CPR). The diagnosis is easy to miss because standard ALS does not include routine electrolytes — and treating the rhythm without treating the K+ is futile.[3]
Bradycardia / slow PEA / asystole is the typical hyperkalaemic arrest rhythm. Wide-complex bradycardia progressing to sine wave then asystole is classic. VF/pVT can also occur (especially if digoxin-toxic). Hyperkalaemia should be high on the differential of any 'unexplained' bradyasystolic arrest, especially in a dialysis or CKD patient.[7]
Calcium chloride via central line is preferred over gluconate in arrest. Chloride delivers 3x the ionised calcium and is bioavailable immediately (gluconate needs hepatic metabolism, which is impaired in shock/arrest). If only peripheral access exists, give gluconate rather than delay — but obtain central access.[7]
The dialysis patient who missed a session is the prototypical hyperkalaemic arrest. Missing one session, a high-K meal, constipation (reduced gut loss), and intercurrent illness combine. After ROSC, the priority is emergency haemodialysis (or SLED/CVVHDF if unstable) and a plan to prevent recurrence (diet, binders, dialysis schedule).[2]
Do NOT stop CPR to wait for the K+ result. If the pre-arrest or periarrest K+ is known to be high (or the picture is suggestive — CKD, wide QRS, bradyasystolic), give the bundle empirically while continuing ALS and waiting for confirmation.[3]
Rebound after ROSC is common. Cellular shifts reverse as acidosis and ischaemia resolve, and dialysis gradients equilibrate — recheck K+ within 30-60 min of ROSC and arrange definitive removal. The post-arrest patient needs the same STABILISE-SHIFT-REMOVE framework as the pre-arrest one.[2]

BRASH syndrome — a hyperkalaemia-specific trap

BRASH syndrome — recognise and break the loop

Recognise the cluster: Bradycardia + Renal failure + AV blockade (medication) + Shock + Hyperkalaemia. The patient on a beta-blocker or non-DHP calcium-channel blocker (or digoxin) who develops renal impairment and hyperkalaemia slips into a self-reinforcing loop[6]
Mechanism of the loop: AV-nodal blocker → bradycardia + hypotension → renal hypoperfusion → worsening AKI + acidosis → worsening hyperkalaemia → worsening bradycardia/AV block → more hypoperfusion. Each element feeds the next[6]
Why standard ALS fails: atropine and transcutaneous pacing often do NOT work because the driver is hyperkalaemia and drug toxicity, not primary conduction disease. The bradycardia resolves when K+ is corrected and the AV-blocker is antagonised/cleared[6]
Treatment bundle: (a) CALCIUM to stabilise the membrane; (b) INSULIN/DEXTROSE + SALBUTAMOL to shift K+; (c) treat the AV-blocker — beta-blocker: glucagon/high-dose insulin euglycaemia therapy; calcium-channel blocker: calcium (high dose); digoxin: Fab fragments; (d) vasopressors/inotropes for shock; (e) treat the AKI (fluids if volume-depleted, then dialysis if refractory); (f) treat acidosis[6]
Don't be fooled by a 'reasonable' heart rate. A beta-blocked patient may not be profoundly bradycardic, but the AV-nodal blockade still drives the loop. The combination of AV-blocker + AKI + hyperkalaemia + hypoperfusion is the syndrome.[6]

High-yield clinical pearls (examiner favourites)

High-yield hyperkalaemia points for CICM/FFICM exam

Calcium does NOT lower potassium — it STABILISES the cardiac membrane. Calcium gluconate raises the threshold for depolarisation → prevents arrhythmia from hyperkalaemia. It buys TIME (30-60 min) while insulin/dextrose and other measures lower K+. ALWAYS give calcium FIRST if ECG changes. Calcium chloride (via central line) has 3x more ionised calcium than gluconate.[3]
Insulin/dextrose is the most reliable K+-shifting therapy. Insulin stimulates Na/K ATPase → drives K+ INTO cells. Dose: 10 units rapid-acting insulin + 25 g dextrose IV. Lowers K+ 0.5-1.0 mmol/L within 15-30 min. LASTS 4-6 hours. MONITOR GLUCOSE (hypoglycaemia — even with dextrose — check every hour for 4-6 h).[4]
Salbutamol (beta-2 agonist) shifts K+ into cells. Stimulates Na/K ATPase (via beta-2 receptor → cAMP). Dose: 10-20 mg nebulised (HIGH dose — 5-10x asthma dose) or 500 mcg IV. Lowers K+ 0.5-1.0 mmol/L. Onset 15-30 min. ADD to insulin/dextrose (synergistic). Caution: tachycardia, tremor, MI (beta-1 effect).[3]
Sodium bicarbonate shifts K+ only if ACIDOTIC. In acidosis, H+ enters cells (buffering), K+ exits (maintaining electroneutrality). Bicarbonate corrects acidosis → reverses this shift → K+ enters cells. If NOT acidotic: bicarbonate has MINIMAL K+-lowering effect (don't rely on it alone). Dose: 50-100 mmol of 8.4% (or 500 mL of 1.26%).[8]
Dialysis is the DEFINITIVE treatment for severe/refractory hyperkalaemia. Haemodialysis: lowers K+ 1-1.5 mmol/L in 1-2 hours (FASTEST removal). CVVHDF: slower (hours). Indications: K+ >7 despite medical therapy, ongoing K+ release (rhabdomyolysis, tumour lysis), end-stage renal failure, severe acidosis. PREPARE early — don't wait for K+ to rise further.[2]
Common causes of hyperkalaemia in ICU. (1) AKI/CKD (impaired excretion). (2) DRUGS: ACEi/ARB, K-sparing diuretics (spironolactone, amiloride), TMP-SMX (blocks ENaC), heparin (inhibits aldosterone), beta-blockers, calcineurin inhibitors, digoxin. (3) RHABDOMYOLYSIS. (4) TUMOUR LYSIS. (5) ACIDOSIS (DKA, lactic). (6) ADDISON'S. (7) GI BLEED (digested blood = K+ load). (8) MASSIVE TRANSFUSION (stored blood has high K+). REVIEW ALL MEDICATIONS.[2]
Peaked T waves — the earliest ECG sign. Tall, narrow, symmetric, 'tented' T waves. Best seen in V2-V4. May be subtle. Compare to previous ECG. If K+ >6.5 and ECG shows peaked T → treat as EMERGENCY (calcium + insulin/dextrose). Don't wait for worse changes (wide QRS, sine wave).[11]
Sine wave = pre-arrest. QRS and T wave merge → undulating 'sine wave' pattern. Cardiac arrest imminent (VF or asystole). IMMEDIATE: calcium gluconate IV + insulin/dextrose + prepare for dialysis + resuscitation. May need CPR if arrests.[3]
Hypoglycaemia after insulin/dextrose — common, dangerous. Insulin 10 units + dextrose 25 g → may still cause hypoglycaemia (especially in renal failure — reduced insulin clearance, hepatic disease). MONITOR glucose every hour for 4-6 h after insulin. If hypoglycaemia: more dextrose. Some use higher dextrose (50 g) or lower insulin (5 units) for high-risk patients.[5]
GI potassium binders (patiromer, sodium zirconium cyclosilicate). Patiromer: binds K+ in gut (exchange for calcium). SZC: binds K+ (exchange for sodium/H+). Both LOWER K+ gradually (hours). NOT for acute severe hyperkalaemia (too slow) but useful as a bridge and for CHRONIC management (CKD, on RAAS inhibitors). Sodium polystyrene sulfonate (Kayexalate/Resonium) — older, slower, may cause bowel necrosis (avoid acutely).[9]
Pseudohyperkalaemia — false alarm. K+ released from cells during venepuncture (haemolysis, fist clenching, difficult draw). Clues: no ECG changes, no symptoms, previous normal K+. Confirm with ARTERIAL or free-flowing venous sample (no tourniquet, rapid draw). If K+ high but patient well + normal ECG → recheck (avoid unnecessary treatment).[3]
Calcium gluconate vs calcium chloride. CALCIUM GLUCONATE: 10 mL of 10% = 2.2 mmol Ca²⁺ (smaller dose). Safer via peripheral vein (less tissue necrosis if extravasation). CALCIUM CHLORIDE: 10 mL of 10% = 6.8 mmol Ca²⁺ (3x more Ca²⁺). Preferred for ARREST (more calcium). Via CENTRAL line only (causes necrosis if peripheral extravasation).[3]
Hyperkalaemia in cardiac arrest — part of reversible causes (H's). During CPR: check K+ (VBG/ABG). If K+ >6.5 → calcium chloride (central) + insulin/dextrose + bicarbonate DURING CPR. May restore perfusing rhythm if hyperkalaemia caused arrest. Also: treat underlying cause (renal failure — consider dialysis post-ROSC).[7]
Prevention of recurrent hyperkalaemia. (1) K-restricted diet (<2 g/day — avoid bananas, tomatoes, potatoes, nuts, chocolate). (2) Stop/reduce causative drugs (ACEi/ARB, K-sparing diuretics). (3) K+ binders (patiromer, SZC — chronic). (4) Loop diuretics (promote K+ excretion). (5) Treat constipation (GI K+ excretion). (6) Treat acidosis (bicarbonate). (7) Dialysis planning (if CKD stage 5).[12]

Mechanism and physiology pearls (for the viva)

Why does hyperkalaemia cause arrhythmia? A high extracellular K+ makes the resting membrane potential LESS negative (closer to threshold). The myocyte is partly depolarised, so the gap between resting and threshold potential narrows → initially hyperexcitable (ectopics) then inexcitable (Na+ channels become inactivated by the partial depolarisation → conduction slows → QRS widens → asystole/VF). Calcium raises the threshold potential, restoring the safety margin.[2]
The '90% in cells, 1-2% extracellular' rule. Total body K+ is ~3500 mmol; >98% is intracellular. A rise of serum K+ from 4 to 7 mmol/L reflects a shift of only ~10-20 mmol out of cells (in acute shift states) — which is why insulin/dextrose and salbutamol (which only shift K+ back into cells) work so well acutely, and why rebound occurs once the shift reverses.[2]
Renal K+ excretion = distal nephron + aldosterone + flow. Chronic K+ balance depends on aldosterone-driven secretion in the collecting duct, which needs (a) adequate distal Na+ delivery and flow, (b) functioning ENaC, (c) aldosterone, and (d) normal tubule cells. Anything that disrupts these (AKI, hypoaldosteronism, ENaC blockers, K-sparing diuretics, ACEi/ARB) limits excretion and predisposes to hyperkalaemia.[2]
Acidosis shifts K+ out of cells; alkalosis shifts it in. In metabolic acidosis, H+ moves into cells for buffering, and K+ moves out to maintain electroneutrality (organic acidosis — lactic/keto — shifts K+ less than mineral acidosis — HCl). This is why DKA correction and bicarbonate lower K+ — and why treating alkalosis can unmask hypokalaemia.[8]
Insulin and beta-2 agonists share a final common pathway but different receptors. Both ultimately increase Na/K ATPase activity (insulin directly via IRS-PI3K; salbutamol via Gs-cAMP). This is why they are additive. They also share the same pitfall: hypoglycaemia with insulin; tachycardia/ischaemia with salbutamol.[8]
Rebound after shifting therapy is the rule, not the exception. Insulin/dextrose and salbutamol do not REMOVE K+ — they relocate it. As insulin wears off (4-6 h) or the underlying acidosis/cause persists, K+ leaks back out. ALWAYS pair shifting with removal (diuretics, binders, dialysis) and with cause treatment, and recheck K+ within 2-4 h.[2]

Special situations and edge cases

Liver failure / transplant patients on calcineurin inhibitors. Tacrolimus and cyclosporin cause a type-4-RTA-like hypoaldosteronism; combined with renal impairment, hyperkalaemia is common. Treat with binders, loop diuretics, fludrocortisone, and review immunosuppression levels.[2]
Post-operative cardiac surgical patients. Cardioplegia solutions are K+-rich; combined with AKI, hypothermia and acidosis, hyperkalaemia is common early after bypass. Check K+ on arrival in ICU and treat per algorithm; the K+ usually falls as the cardioplegia is excreted/metabolised.[3]
The constipated dialysis patient. Gut K+ excretion increases adaptively in CKD (the colon can excrete up to 30-40% of dietary K+). Constipation removes this escape route and precipitates hyperkalaemia. Treat constipation aggressively (laxatives, sometimes resonium enema) as part of hyperkalaemia management in dialysis patients.[12]
Pregnancy. Mild respiratory alkalosis and increased RAAS activity tend to keep K+ slightly low; hyperkalaemia in pregnancy is uncommon and usually reflects renal disease, pre-eclampsia with renal impairment, or Addison's. Treat per standard algorithm; calcium, insulin/dextrose and salbutamol are all safe in pregnancy. Dialyse if needed (modified dose).[11]
Addisonian crisis. Hyperkalaemia + hyponatraemia + hypoglycaemia + hypotension + abdominal pain = adrenal crisis until proven otherwise. Give hydrocortisone 100 mg IV stat (then 200 mg/24 h) — this provides mineralocorticoid activity at high dose and corrects the hyperkalaemia. Do not wait for the cortisol result if the picture is suggestive.[2]
Tumour lysis syndrome. Anticipate in high-burden haematological malignancy (high-grade lymphoma, ALL, high blast-count AML) and bulky solid tumours starting therapy. Hyperkalaemia + hyperphosphataemia + hypocalcaemia + hyperuricaemia + AKI. Prophylaxis: aggressive hydration + rasburicase (or allopurinol). Treat established TLS with the full STABILISE-SHIFT-REMOVE bundle and urgent dialysis — the K+ rise can be rapid and refractory.[3]

Exam practice — SAQs

SAQ — Severe hyperkalaemia with ECG changes in a CKD patient on RAAS inhibitors

10 minutes · 10 marks

[1]

SAQ — Hypokalaemia with Torsades de Pointes and cardiac arrest

10 minutes · 10 marks

[1]

Red flags

Critical hyperkalaemia red flags

ECG changes (peaked T, wide QRS, sine wave) → calcium gluconate IMMEDIATELY, before any K+-lowering therapy.[3]
K+ >6.5 mmol/L → emergency (even without ECG changes).[1]
Sine wave → pre-arrest — calcium + insulin/dextrose + bicarbonate + dialysis.[3]
Hyperkalaemic arrest / bradyasystolic arrest in CKD/dialysis → calcium chloride (central) + insulin/dextrose + bicarbonate DURING CPR.[7]
BRASH syndrome (AV-blocker + renal failure + hyperkalaemia + bradycardia/shock) → treat the K+ AND the AV-blocker; standard bradycardia therapy often fails.[6]
Hypoglycaemia 1-6 h after insulin/dextrose → monitor glucose hourly for ≥6 h.[5]
Refractory hyperkalaemia (despite medical therapy) → urgent dialysis.[2]
Rebound after shift therapy or after dialysis → recheck K+ within 1-2 h.[2]
Digoxin toxicity + hyperkalaemia → digoxin Fab fragments, NOT calcium.[3]
Pseudohyperkalaemia (no ECG changes, patient well, haemolysed sample) → recheck (arterial/plasma) before treating.[3]

Prognosis and evidence

UKKA / KDIGO approach to hyperkalaemia (Clase 2020, Kidney Int)

KDIGO Controversies Conference conclusions on potassium homeostasis and dyskalaemia management (Clase 2020):[1]

Mild (5.5-5.9): cause-specific treatment, dietary advice, K+ binders (patiromer/SZC for chronic). No emergency treatment
Moderate (6.0-6.4): shift K+ (insulin/dextrose if symptomatic or ECG changes), binders, review meds. Monitor closely
Severe (≥6.5): EMERGENCY — calcium (if ECG changes), insulin/dextrose, salbutamol, consider dialysis
Insulin/dextrose dose: 10 units + 25 g dextrose (adult). Monitor glucose every hour for 4-6 h (hypoglycaemia risk emphasised)
Calcium: gluconate 10 mL 10% (peripheral) or chloride 10 mL 10% (central — 3x more Ca²⁺)
RAAS inhibitors should generally be CONTINUED in heart failure/CKD where possible, using binders to manage K+ (stopping RAASi worsens long-term outcomes) Mortality: hyperkalaemia-caused cardiac arrest mortality is high (>50% if K+ was the proximate cause). With prompt treatment: arrhythmia prevented, K+ lowered → survival depends on underlying cause.

Insulin/dextrose evidence — Harel 2016 systematic review (PLoS One)

Systematic review of optimal insulin dose/method for emergency hyperkalaemia:[5]

Insulin/dextrose reliably lowers K+ by 0.5-1.0 mmol/L within 15-30 min — the most consistent shifting therapy
Hypoglycaemia is common — across studies, any hypoglycaemia up to 20-30%, severe hypoglycaemia (glucose <3.0 mmol/L) 5-10%, peaking 1-3 h post-dose
Lower insulin doses (5 units) with adequate dextrose achieve a similar K+ fall with less hypoglycaemia in some studies — but 10 units remains the standard adult dose
Practice point: give insulin/dextrose, then commit to ≥6 h of glucose monitoring with bedside dextrose available. Identify high-risk patients (renal/hepatic failure, low body weight, fasting, baseline glucose <7) and consider reduced-dose regimens.

Bicarbonate/insulin/albuterol synergy — Allon 1996 (Am J Kidney Dis)

Classic dialysis-patient crossover study:[8]

Insulin/dextrose lowered K+ by ~1.0 mmol/L; albuterol by ~1.0 mmol/L; combined by ~1.3-1.5 mmol/L (additive)
Bicarbonate alone had a trivial K+-lowering effect in these (non-acidotic) dialysis patients — confirming bicarbonate is useful mainly in acidosis
Practice point: combine insulin/dextrose + salbutamol for moderate-severe hyperkalaemia; reserve bicarbonate for the acidotic patient or the arrest bundle.

Sodium zirconium cyclosilicate and patiromer — long-term efficacy and safety

Recent evidence and outcomes — Geldermann 2026 (Emerg Med J)

Contemporary evidence-based review of acute hyperkalaemia in emergency care:[11]

A normal ECG does NOT exclude severe hyperkalaemia — up to ~50% of K+ >6.5 mmol/L have subtle or absent changes; treat the number, not just the tracing
Pseudohyperkalaemia remains under-recognised — always confirm with a non-haemolysed or arterial sample before treating an unexpected value in a well patient
Combined shifting therapy (insulin/dextrose + salbutamol) outperforms monotherapy
Hypoglycaemia is the leading iatrogenic complication of insulin/dextrose — reinforce the 6-hour monitoring bundle
Novel binders and dialysis timing continue to evolve — start removal planning EARLY in severe hyperkalaemia rather than waiting for refractory K+

Putting it together — exam one-liners

One-liners you can reproduce in the viva

"Severe hyperkalaemia is a K+ >6.5 mmol/L or any ECG change attributable to hyperkalaemia, and I treat it as a cardiac emergency."[1]
"My framework is STABILISE the membrane with calcium, SHIFT K+ intracellularly with insulin/dextrose and salbutamol, then REMOVE K+ with diuretics, binders, or dialysis — in that order."[2]
"Calcium gluconate 10 mL of 10% IV is my first drug whenever there are ECG changes; it does not lower K+, it raises the threshold potential to prevent arrhythmia and buys 30-60 min."[3]
"Insulin 10 units with 25 g of dextrose is my workhorse; it lowers K+ by 0.5-1.0 mmol/L for 4-6 h, and I monitor glucose hourly for 6 h because hypoglycaemia is the commonest complication."[4]
"In hyperkalaemic arrest I give calcium chloride via a central line, insulin/dextrose, and 50 mmol of sodium bicarbonate during CPR, and I send a gas to confirm — recent RCT data support calcium plus bicarbonate."[7]
"BRASH syndrome is bradycardia, renal failure, AV blockade, shock and hyperkalaemia — a self-perpetuating loop driven by AV-nodal blockers, and it needs the K+ and the blocker toxicity treated together."[6]
"Pseudohyperkalaemia is diagnosed by a well patient with a normal ECG and a haemolysed or difficult sample; I confirm with an arterial or plasma potassium before treating."[3]
"For chronic prevention in CKD/HF I restrict dietary K+, use patiromer or sodium zirconium to allow continuation of RAAS inhibitors, treat constipation and acidosis, and plan dialysis when appropriate."[12]

References

[1]Clase CM, Carrero JJ, Ellison DH, et al. Potassium homeostasis and management of dyskalemia in kidney diseases: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference Kidney Int, 2020.PMID 31706619
[2]Palmer BF, Carrero JJ, Clegg DJ. Clinical Management of Hyperkalemia Mayo Clin Proc, 2021.PMID 33160639
[3]Long B, Warix JR, Koyfman A. Hyperkalemia in the Emergency Department: Yes, a Need for Further Evidence, but Do Not Discount What We Have J Emerg Med, 2019.PMID 31326003
[4]Moussavi K, Fitter S, Gabrielson SW. Management of Hyperkalemia With Insulin and Glucose: Pearls for the Emergency Clinician J Emerg Med, 2019.PMID 31084947
[5]Harel Z, Kamel KS. Optimal Dose and Method of Administration of Intravenous Insulin in the Management of Emergency Hyperkalemia: A Systematic Review PLoS One, 2016.PMID 27148740
[6]Farkas JD, Long B, Koyfman A. BRASH Syndrome: Bradycardia, Renal Failure, AV Blockade, Shock, and Hyperkalemia J Emerg Med, 2020.PMID 32565167
[7]Eggertsen MA, Munch Johannsen C, Kovacevic A, et al. Sodium Bicarbonate and Calcium Chloride for the Treatment of Hyperkalemia-Induced Cardiac Arrest: A Randomized, Blinded, Placebo-Controlled Animal Study Crit Care Med, 2024.PMID 37921685
[8]Allon M, Shanklin N. Effect of bicarbonate administration on plasma potassium in dialysis patients: interactions with insulin and albuterol Am J Kidney Dis, 1996.PMID 8840939
[9]Roger SD, Lavin PT, Lerma EV, et al. Long-term safety and efficacy of sodium zirconium cyclosilicate for hyperkalaemia in patients with mild/moderate versus severe/end-stage chronic kidney disease: comparative results from an open-label, Phase 3 study Nephrol Dial Transplant, 2021.PMID 32030422
[10]Pitt B, Bakris GL, Weir MR, et al. Long-term effects of patiromer for hyperkalaemia treatment in patients with mild heart failure and diabetic nephropathy on angiotensin-converting enzymes/angiotensin receptor blockers: results from AMETHYST-DN ESC Heart Fail, 2018.PMID 29767459
[11]Geldermann N, Dzimiera J, Fischer H, et al. Acute hyperkalaemia in emergency care: evidence-based approaches Emerg Med J, 2026.PMID 41506858
[12]Sumida K, Biruete A, Kistler BM, et al. New Insights Into Dietary Approaches to Potassium Management in Chronic Kidney Disease J Ren Nutr, 2023.PMID 37610407

Your progress

ECG changes — recognise the progression

Emergency management algorithm

Causes — organised by mechanism

Pseudohyperkalaemia — don't treat a false alarm

Insulin/dextrose — getting it right and avoiding hypoglycaemia

Hyperkalaemic cardiac arrest

Sodium bicarbonate + calcium chloride in hyperkalaemic cardiac arrest — Eggertsen 2024 (RCT)

BRASH syndrome — a hyperkalaemia-specific trap

High-yield clinical pearls (examiner favourites)

Exam practice — SAQs

SAQ — Severe hyperkalaemia with ECG changes in a CKD patient on RAAS inhibitors

SAQ — Hypokalaemia with Torsades de Pointes and cardiac arrest

Red flags

Prognosis and evidence

UKKA / KDIGO approach to hyperkalaemia (Clase 2020, Kidney Int)

Insulin/dextrose evidence — Harel 2016 systematic review (PLoS One)

Bicarbonate/insulin/albuterol synergy — Allon 1996 (Am J Kidney Dis)

Sodium zirconium cyclosilicate and patiromer — long-term efficacy and safety

Recent evidence and outcomes — Geldermann 2026 (Emerg Med J)

Putting it together — exam one-liners

References

Your progress

ECG changes — recognise the progression

Emergency management algorithm

Causes — organised by mechanism

Pseudohyperkalaemia — don't treat a false alarm

Insulin/dextrose — getting it right and avoiding hypoglycaemia

Hyperkalaemic cardiac arrest

Sodium bicarbonate + calcium chloride in hyperkalaemic cardiac arrest — Eggertsen 2024 (RCT)

BRASH syndrome — a hyperkalaemia-specific trap

High-yield clinical pearls (examiner favourites)

Exam practice — SAQs

SAQ — Severe hyperkalaemia with ECG changes in a CKD patient on RAAS inhibitors

SAQ — Hypokalaemia with Torsades de Pointes and cardiac arrest

Red flags

Prognosis and evidence

UKKA / KDIGO approach to hyperkalaemia (Clase 2020, Kidney Int)

Insulin/dextrose evidence — Harel 2016 systematic review (PLoS One)

Bicarbonate/insulin/albuterol synergy — Allon 1996 (Am J Kidney Dis)

Sodium zirconium cyclosilicate and patiromer — long-term efficacy and safety

Recent evidence and outcomes — Geldermann 2026 (Emerg Med J)

Putting it together — exam one-liners

References