PharmacologyTier 2Medical Sciences concept

Management options for hyperkalaemia - mechanisms (insulin/dextrose, salbutamol, resonium, dialysis)

Core concept

Three jobs, in order: protect the myocardium, shift K+ into cells, remove K+ from the body.

Step	Agent	Mechanism	Onset	Duration	Lowers serum K?
1. Stabilise	Calcium gluconate/chloride	Raises the threshold potential, restoring the gap between resting and threshold potential	1-3 min	30-60 min	NO
2. Shift	Insulin + dextrose	inc Na/K-ATPase activity	15-30 min	4-6 h	Yes (~0.6-1.2)
	Salbutamol (neb)	beta-2 -> cAMP -> Na/K-ATPase + Na/K/2Cl	30 min	2-4 h	Yes (~0.5-1.0)
	Sodium bicarbonate	H+/K+ exchange; only useful if acidotic	30-60 min	variable	Modest
3. Remove	Loop diuretic	Distal Na delivery -> K secretion	30-60 min	hours	Yes, if urine output
	Binders (SZC, patiromer, resonium)	GI cation exchange	hours	ongoing	Yes, slowly
	Dialysis	Direct removal	minutes	-	Definitive

Calcium does not lower potassium. Giving it alone and walking away is the classic error - the ECG improves while the potassium stays lethal.
Insulin-dextrose and salbutamol move potassium; they do not remove it. It comes back in 4-6 hours.

Doses

Calcium gluconate 10% 10-30 mL IV over 5-10 min, repeat if ECG changes persist
- Gluconate peripherally; calcium chloride 10% 10 mL gives ~3x the elemental calcium but needs a central line
- Caution with digoxin toxicity - give slowly, diluted
Actrapid 10 units IV + 50 mL 50% dextrose (or 250 mL 10%)
- Hypoglycaemia occurs in up to 1 in 5-6 - it is the commonest iatrogenic complication; monitor BGL hourly for 6 hours
- Consider 5 units if BGL <7, small, elderly or CKD
Salbutamol 10-20 mg nebulised (4-8x the bronchodilator dose)
- Additive with insulin; ~20-40% of patients are non-responders
- Tachycardia, tremor, lactate rise
Sodium zirconium cyclosilicate (SZC) - onset ~1 hr, Na load; patiromer - onset ~7 hr, binds Mg
- Sodium polystyrene sulfonate (Resonium) - slow, poor evidence, *rare but catastrophic colonic necrosis, especially with sorbitol or post-operatively*
Dialysis for: refractory hyperkalaemia, oliguric AKI, ESKD, tumour lysis, severe rhabdomyolysis
- Beware rebound as potassium redistributes out of cells after the session

ECG progression - not reliably sequential

Peaked T waves -> flattened P, PR prolongation -> widened QRS -> sine wave -> VF/asystole
*A normal ECG does not exclude life-threatening hyperkalaemia* - treat the number and the rate of rise

Confirm it is real before anything drastic: haemolysis, fist clenching, prolonged tourniquet, delayed processing, extreme leucocytosis or thrombocytosis (pseudohyperkalaemia)
- A whole-blood gas potassium gives an answer in 2 minutes and avoids the haemolysed sample
Find and stop the cause
- Drugs: ACEi/ARB, spironolactone/eplerenone, trimethoprim, heparin, NSAIDs, tacrolimus/ciclosporin, digoxin, non-selective beta-blockers, potassium supplements, salt substitutes
- AKI/CKD, adrenal insufficiency, type 4 RTA, rhabdomyolysis, tumour lysis, massive transfusion, acidosis
Do not reflexively and permanently stop RAAS inhibition in heart failure or CKD - it is prognostic therapy. Potassium binders exist precisely to allow it to continue.
Dietary potassium restriction and dietitian referral for chronic management
Recheck potassium at 2 and 4-6 hours after treatment - rebound is expected

Diuretic classes - site and mechanism of action
Evidence-based pharmacotherapy in heart failure (MRA and RAAS inhibitor tolerability)
Renal tubular acidosis (type 4); adrenal insufficiency
Tumour lysis syndrome; rhabdomyolysis
Digoxin mechanism and toxicity
Catecholamine metabolic effects (beta-2-mediated potassium shift)
Dialysability of drugs in overdose

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