Sodium nitroprusside is an immediate-acting vasodilator used only in hospital, by drip, to lower very high blood pressures in emergencies (hypertensive emergency, aortic dissection).
Also known as: Nipride, Nitroprussiato
Nitroprusside vasodilation adds to that of enalapril, with a risk of profound hypotension, particularly with the first dose and in hypovolaemic patients or those with renal artery stenosis.
Additive hypotensive effect through complementary mechanisms: nitroprusside is a nitric oxide donor causing direct arterial and venous vasodilation, while the ACE inhibitor reduces angiotensin II and aldosterone; the Prontuário (Annex 7, ARA II table) lists sodium nitroprusside among drugs that increase the hypotensive effect.
Invasive or continuous blood pressure, renal function and potassium, urine output; during prolonged infusion monitor cyanide/thiocyanate toxicity (particularly in renal impairment — Prontuário: "avoid prolonged use in renal impairment").
Hypotension, bradycardia, oliguria, metabolic acidosis, altered mental state.
Start nitroprusside at the lowest dose and titrate by invasive blood pressure; correct volume status before starting in a hypertensive emergency with an ongoing ACE inhibitor; stop the ACE inhibitor if hypotension is refractory.
INFARMED Prontuário Terapêutico (11th ed., 2012), Annex 7 — "Increase the hypotensive effect ... Sodium nitroprusside" and note on prolonged use in renal impairment; EMC-Portugal — PT INN names.
Metoprolol blunts the reflex tachycardia that compensates nitroprusside-induced vasodilation, potentially worsening hypotension and bradycardia.
Additive hypotensive effect: nitroprusside dilates arterioles and veins while the beta-blocker prevents the compensatory chronotropic response; the Prontuário (Annex 7) lists beta-adrenergic blockers among drugs that increase the hypotensive effect.
Continuous blood pressure, heart rate, ECG, urine output, lactate; during prolonged infusion, cyanide/thiocyanate toxicity.
Hypotension, bradycardia, syncope, oliguria, confusion.
Reduce the initial infusion rate and titrate slowly by invasive blood pressure; if symptomatic bradycardia occurs, reduce or stop the beta-blocker and consider an alternative vasodilator.
INFARMED Prontuário Terapêutico (11th ed., 2012), Annex 7 — ARA II table: "Beta-adrenergic blockers ... Sodium nitroprusside" among drugs that increase the hypotensive effect.
No documented food or drink interactions.
Nitroprusside is a potent hypotensive — invasive titration mandatory; never in hypotension.
ICU use only with invasive arterial monitoring (site monograph).
Site monograph (nitroprusside — ICU use only).
Metabolism releases cyanide — in renal impairment thiocyanate accumulates (neurotoxicity) and cyanide is not efficiently eliminated.
Limit dose and duration; monitor lactate and acidosis; alternative: clevidipine/nicardipine.
Site monograph (nitroprusside — do not exceed 2 mcg/kg/min for > 3 h — toxicity).
Cyanide is hepatically metabolised — liver disease worsens cyanide toxicity.
Limit dose/duration; monitor lactic acidosis.
EMC-UK — nitroprusside SmPC 4.4 (liver function, cyanide).
No specific Annex 1 entry; nitroprusside is reserved for severe refractory hypertensive crises: the cyanide metabolite crosses the placenta and, with prolonged infusions or high doses (>2 µg/kg/min, >24 h), can cause fetal cyanide toxicity. Prefer IV labetalol, hydralazine or nicardipine; if used, limit time/dose and avoid in the 3rd trimester whenever possible.
Last-line use in severe hypertensive crises (ICU); limit time and dose (≤2 µg/kg/min, avoid >24 h); prefer alternatives in pregnancy.
Compatible as an emergency drug (minutes half-life).
EMC-UK (MHRA) — Sodium Nitroprusside SmPC (section 4.6 — "not recommended in pregnancy").
Clinical and educational support tool. The information does not replace a medical prescription or the opinion of a qualified healthcare professional.
Immediate preload and afterload reduction; onset in seconds, 1–2 min duration (continuous titration).
Non-enzymatic NO donor: released NO activates guanylate cyclase → ↑ cyclic GMP → arterial and venous smooth muscle relaxation.
IV exclusive; immediate action.
Reaction with haemoglobin → methaemoglobin + cyanide; cyanide is converted to thiocyanate by hepatic rhodanese (with thiosulfate cofactor); renal thiocyanate excretion.
~ 2–4 min (nitroprusside); thiocyanate ~ 3–4 days (renal failure: accumulation).
Medicines from the same therapeutic group (ATC classification) or the same pharmacological class.
