Potassium chloride plus enalapril (ACE inhibitor) increases the risk of severe hyperkalaemia, with potentially fatal arrhythmias.
ACE inhibitors reduce aldosterone and renal potassium excretion; Annex 7 (Potassium-sparing drugs): "Potassium supplements: additive hyperkalaemic effect in the presence of renal impairment".
Serum potassium, ECG (peaked T waves, QRS widening), renal function.
Muscle weakness, paraesthesia, bradycardia, ECG changes, cardiac arrest.
Avoid routine potassium supplementation with ACE inhibitors; if needed, monitor serum potassium and ECG; review diet and other hyperkalaemic drugs.
INFARMED Prontuário Terapêutico (11th ed., 2012), Annex 7 — Potassium-sparing diuretics/ACE inhibitors: additive hyperkalaemic effect; DailyMed — Enalapril Maleate Tablet label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=a88902bd-742f-4ea6-b625-cc9df1709efc
Spironolactone + potassium: risk of severe hyperkalaemia.
Spironolactone is a potassium-sparing diuretic that antagonises aldosterone in the distal convoluted tubule, reducing renal potassium excretion. Concomitant potassium supplements (potassium chloride) additively increase the risk of hyperkalaemia, which can be severe and potentially fatal (ventricular arrhythmias, cardiac arrest). The risk is even higher in patients with renal impairment, diabetes or advanced age, and with other potassium-raising drugs (ACE inhibitors, ARBs, other potassium-sparing agents). The combination should generally be avoided; if clinically unavoidable (e.g., severe hypokalaemia in an already treated patient), use the lowest potassium dose, monitor serum potassium frequently and watch the ECG, warning the patient about symptoms such as muscle weakness, palpitations or paraesthesias.
Spironolactone + potassium: risk of severe, potentially fatal hyperkalaemia. Avoid the combination; if unavoidable, monitor serum potassium and ECG.
Spironolactone (potassium-sparing diuretic) reduces renal K+ excretion; additive supplementation may cause potentially fatal hyperkalaemia.
Serum potassium, ECG, renal function.
Weakness, arrhythmias, peaked T waves, cardiac arrest.
Avoid the combination; if unavoidable, monitor potassium frequently and stop the supplement.
DailyMed (FDA) — approved Spironolactone label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ac487ae2-e15f-4781-bae3-a03058cfcfe4 ; approved Potassium chloride label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=eb56a807-ea94-4edb-9811-a04b19568468 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Adding pharmacological supplementation to potassium-rich foods (bananas, oranges, tomatoes, potatoes, KCl salt substitutes) can raise serum potassium to toxic levels.
Do not use salt substitutes; moderate potassium-rich fruits and juices; keep potassium blood tests up to date (site monograph).
Site monograph (potassium chloride — avoid potassium supplements and salt substitutes); EMC-UK KCl SmPC 4.4.
Salt substitutes contain potassium chloride and increase K+ intake.
Advise patients on potassium supplements not to use salt substitutes.
EMC-UK (MHRA) — approved Potassium chloride SmPC: https://www.medicines.org.uk/emc/product/959/smpc
In severe renal impairment, oral/IV potassium supplementation causes potentially fatal hyperkalaemia (arrhythmias, cardiac arrest).
Contraindicated in severe renal impairment (markedly reduced clearance); in milder grades, monitor serum potassium rigorously.
Prontuário Terapêutico INFARMED (electrolytes): renal precaution; EMC-UK KCl SmPC 4.3 (severe renal impairment, hyperkalaemia).
Potassium supplementation in established hyperkalaemia can precipitate cardiac arrest.
Measure potassium before and during therapy; discontinue if serum K+ > 5.5 mmol/l.
EMC-UK — Potassium chloride SmPC § 4.3 (hyperkalaemia).
No documented pregnancy or breastfeeding information.
Clinical and educational support tool. The information does not replace a medical prescription or the opinion of a qualified healthcare professional.
Restoration of serum and intracellular potassium; normalisation of neuromuscular and cardiac membrane potential.
Primary intracellular electrolyte: maintains the K+ gradient via Na/K-ATPase (3 Na+ out / 2 K+ in), stabilising the membrane resting potential (~ −90 mV).
Oral: passive intestinal absorption 20–40%; prolonged-release formulations improve tolerance; IV: 100%.
No metabolism; strict renal regulation via aldosterone and pH; renal (90%) and faecal excretion.
~ 1–1.5 h (oral); intracellular equilibrium in 24–48 h.
Medicines from the same therapeutic group (ATC classification) or the same pharmacological class.
