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Drug Reference

sodium nitroprusside

vasodilator (nitric oxide donor, balanced arterial and venous dilator)· Brands: Nitropress, NiprideIV

Mechanism of action
Sodium nitroprusside is a nitrovasodilator that releases nitric oxide non-enzymatically in the presence of oxyhaemoglobin in red cells and in vascular smooth muscle. Nitric oxide binds the haem iron of soluble guanylate cyclase and activates the enzyme, raising intracellular cyclic guanosine monophosphate. Cyclic guanosine monophosphate activates protein kinase G, which reduces cytosolic calcium availability and desensitises the contractile apparatus to calcium by promoting myosin light chain dephosphorylation. Smooth muscle relaxation follows in both arteriolar resistance vessels and venous capacitance vessels, so the drug lowers systemic vascular resistance and reduces both afterload and preload. Because the action is independent of the sympathetic nervous system, renin-angiotensin system or specific receptors, the effect is rapid, predictable and dose dependent across the whole vascular bed, including renal and splanchnic circulations. There is little or no direct effect on myocardial contractility (it is not an inotrope), but reduction in preload and afterload can improve cardiac output in acute decompensated heart failure with high filling pressures and reduce myocardial oxygen demand in hypertensive states.
Pharmacokinetics
Sodium nitroprusside is given only by intravenous infusion and acts within seconds to one or two minutes; blood pressure usually returns towards baseline within one to ten minutes of stopping the infusion, so it must be titrated continuously against measured blood pressure. It is highly water soluble, is not appreciably protein bound, and undergoes rapid metabolism in erythrocytes, where it reacts with oxyhaemoglobin to form cyanmethaemoglobin and liberate free cyanide. Cyanide is detoxified mainly in the liver by thiosulphate-sulphurtransferase (rhodanese), which transfers sulphur from endogenous thiosulphate to form thiocyanate; this step is rate limited by thiosulphate availability and is impaired in hepatic dysfunction and in malnutrition. Thiocyanate is eliminated almost entirely by the kidney, with a half-life of about three days when renal function is normal but markedly prolonged in renal impairment. Consequently, infusion for more than a short period, at high rates, or in patients with reduced hepatic or renal clearance predisposes to cyanide or thiocyanate accumulation. The infusion is light sensitive and must be protected from light; the diluted solution is usually used within 24 hours and discarded if it turns blue or dark.
Indications & dosing

Hypertensive emergency (severe hypertension with acute end-organ involvement)

Begin at 0.3 to 0.5 mcg/kg/min and titrate to effect using continuous or frequent blood pressure monitoring. Use the lowest effective rate and wean promptly; rates above 2 to 3 mcg/kg/min carry cyanide toxicity risk.

  • adult · IV: 0.3–10 mcg/kg/min continuous · Begin at 0.3 to 0.5 mcg/kg/min and titrate to effect using continuous or frequent blood pressure monitoring. Use the lowest effective rate and wean promptly; rates above 2 to 3 mcg/kg/min carry cyanide toxicity risk.

Controlled hypotension during surgery to reduce operative bleeding

Regional labelling varies; some formularies list this as an approved use and others as off-label. Requires invasive arterial monitoring and an anaesthetist familiar with rapid titration.

  • adult · IV: 0.5–5 mcg/kg/min continuous · Regional labelling varies; some formularies list this as an approved use and others as off-label. Requires invasive arterial monitoring and an anaesthetist familiar with rapid titration.

Acute decompensated heart failure with high afterload (afterload reduction)off-label

Off-label. Used as a short-term adjunct when systemic vascular resistance is high and blood pressure allows. Monitor for excessive hypotension and reflex tachycardia.

  • adult · IV: 0.1–5 mcg/kg/min continuous · Off-label. Used as a short-term adjunct when systemic vascular resistance is high and blood pressure allows. Monitor for excessive hypotension and reflex tachycardia.

Acute severe mitral or aortic regurgitation requiring afterload reductionoff-label

Off-label. Reduces regurgitant fraction by lowering systemic vascular resistance. Usually a bridge to surgery; echocardiographic and invasive monitoring needed.

  • adult · IV: 0.3–5 mcg/kg/min continuous · Off-label. Reduces regurgitant fraction by lowering systemic vascular resistance. Usually a bridge to surgery; echocardiographic and invasive monitoring needed.

Severe hypertension in children

Titrate slowly with continuous blood pressure monitoring. Children are at risk of cyanide and thiocyanate accumulation; limit duration and consider an alternative agent if infusion is prolonged.

  • pediatric · IV: 0.3–8 mcg/kg/min continuous · Titrate slowly with continuous blood pressure monitoring. Children are at risk of cyanide and thiocyanate accumulation; limit duration and consider an alternative agent if infusion is prolonged.

Severe hypertension in older adults

Start at the low end and titrate cautiously because of reduced baroreflex buffering and vascular disease. Lower rates reduce the risk of precipitous hypotension and cerebral or coronary hypoperfusion.

  • elderly · IV: 0.3–3 mcg/kg/min continuous · Start at the low end and titrate cautiously because of reduced baroreflex buffering and vascular disease. Lower rates reduce the risk of precipitous hypotension and cerebral or coronary hypoperfusion.
Contraindications & precautions
  • Compensatory hypertension, such as with an arteriovenous shunt or coarctation of the aorta · Blood pressure is raised to maintain flow across the narrowed or shunted circulation. Lowering it can cause collapse.
  • Inadequate cerebral perfusion or known cerebral insufficiency · Cerebral blood flow is pressure dependent in these patients. Hypotension risks cerebral ischaemia.
  • Congenital optic atrophy or tobacco amblyopia · Nitroprusside releases cyanide, which is toxic to the optic nerve. These patients may suffer further visual loss.
  • Severe renal impairment · Thiocyanate, a metabolite, is renally cleared and accumulates. Use only if no alternative, at reduced dose and with level monitoring.
  • Severe hepatic impairment · The liver converts cyanide to thiocyanate via rhodanese. Hepatic failure increases the risk of cyanide toxicity.
  • Raised intracranial pressure · Vasodilation may further raise intracranial pressure. Monitor neurological status closely and consider alternatives.
  • Severe hyponatraemia · The reconstituted solution delivers a sodium load. Account for this in the fluid balance.
  • Give by continuous intravenous infusion using a volumetric pump, titrated to effect, with continuous intra-arterial blood pressure monitoring wherever possible. Frequent cuff readings are a weak substitute in unstable patients.
  • Keep the infusion as short and as slow as the clinical situation allows. Doses and maximum rates vary between formularies and countries, so confirm the local limits before prescribing; prolonged high-rate infusion is the main driver of cyanide toxicity.
  • Reconstitute only in the diluent specified by the product literature, usually glucose 5%, protect the prepared solution and the giving set from light, and discard unused solution after the stated shelf life.
  • Monitor acid-base status, lactate and the anion gap during infusion. A falling bicarbonate or rising lactate with tachycardia suggests cyanide toxicity; stop the infusion and treat according to local protocols, which may include hydroxocobalamin or sodium thiosulfate.
  • Check thiocyanate concentrations and thyroid function if infusion continues beyond about 24 to 48 hours or if renal function is impaired. Check methaemoglobin if cyanosis persists despite adequate oxygenation.
  • Taper the infusion rather than stopping abruptly, and inspect the cannula site regularly because extravasation causes tissue damage.
Adverse effects
  • Excessive or rapid hypotension, sometimes with cardiovascular collapseserious
  • Headache
  • Reflex tachycardia and palpitations
  • Dizziness, flushing and sweating
  • Nausea, vomiting and abdominal pain
  • Cyanide toxicity: metabolic acidosis, arrhythmias, confusion, seizures and comaserious
  • Thiocyanate toxicity with prolonged infusion or renal impairment: weakness, tinnitus, hyperreflexia, psychosis and seizuresserious
  • Methaemoglobinaemia with cyanosis unresponsive to oxygenserious
  • Rebound hypertension after abrupt withdrawalserious
  • Venous irritation and pain at the infusion site, or tissue necrosis after extravasationserious
Renal & hepatic adjustment
  • eGFR 0–30: Avoid prolonged infusions and high doses. Thiocyanate, a metabolite, accumulates in renal impairment and can cause toxicity. If use is necessary, limit duration (usually less than 24 hours) and monitor cyanide and thiocyanate levels.
  • eGFR 30–60: Use with caution. Monitor for signs of cyanide or thiocyanate toxicity, especially with prolonged infusions. No specific dose reduction, but limit duration.
  • eGFR 60+: No dose adjustment required for normal renal function. Use standard doses with monitoring.
  • Hepatic impairment (mild): No specific dose adjustment. Use with caution; monitor for cyanide toxicity because hepatic metabolism via rhodanese may be impaired.
  • Hepatic impairment (moderate): Use with caution; consider reducing dose and duration. Monitor cyanide levels and acid-base status closely.
  • Hepatic impairment (severe): Avoid if possible. Impaired cyanide detoxification increases risk of cyanide toxicity. If essential, use the lowest effective dose for the shortest time with intensive monitoring. (avoid)
Monitoring, pregnancy & toxicity
  • Blood pressure · Continuous intra-arterial monitoring if possible, or at least every 5-15 minutes during infusion and until stable after stopping.
  • Heart rate · Continuous or every 5-15 minutes during infusion.
  • Cyanide and thiocyanate levels · If prolonged infusion (more than 24-48 hours), high dose, or renal impairment; at least every 24 hours.
  • Acid-base status (arterial or venous blood gas, lactate) · Every 4-6 hours during prolonged infusion or if toxicity suspected.
  • Methaemoglobin · If hypoxia or cyanosis is unexplained despite adequate oxygenation.
  • Renal function (creatinine, eGFR) · Baseline and at least daily in patients with renal impairment or prolonged infusion.
  • Pregnancy: Use in pregnancy only for life-threatening hypertension when other agents are ineffective or contraindicated. Sodium nitroprusside crosses the placenta and can cause fetal cyanide toxicity. Monitor fetal heart rate and maternal acid-base status. Avoid prolonged infusions and high doses. Regional practice varies; some guidelines recommend alternatives such as labetalol, hydralazine or nifedipine first.
  • Toxicity: Cyanide toxicity: early signs include confusion, headache, dizziness, tachycardia, then metabolic acidosis, venous hyperoxaemia (bright red venous blood), seizures, coma, cardiovascular collapse. · Stop infusion immediately. Administer hydroxocobalamin (preferred) or sodium thiosulphate. Consider sodium nitrite only if no hydroxocobalamin and not smoke inhalation. Give 100% oxygen and supportive care.
  • Toxicity: Thiocyanate toxicity: nausea, vomiting, tinnitus, blurred vision, weakness, confusion, seizures, and in severe cases coma. More likely with prolonged infusion, renal impairment, or high doses. · Stop infusion. Supportive care. Haemodialysis can remove thiocyanate in severe cases or renal failure.
  • Toxicity: Severe hypotension: excessive vasodilation causing symptomatic low blood pressure, dizziness, syncope, shock. · Stop or reduce infusion rate. Place patient supine, give IV fluids if appropriate, and use vasopressors (e.g. noradrenaline) if hypotension persists. Monitor blood pressure closely.
  • Toxicity: Methaemoglobinaemia: rare, presents with cyanosis, hypoxia, chocolate-brown blood, low oxygen saturation unresponsive to oxygen. · Stop infusion. Give methylene blue 1-2 mg/kg IV if symptomatic or methaemoglobin greater than 30%. Consider exchange transfusion in severe cases.
Antidotes & reversal
  • Sodium thiosulfate with hydroxocobalamin · Cyanide toxicity: sodium thiosulfate IV and hydroxocobalamin; monitor lactate and thiocyanate levels.
Clinical notes
Sodium nitroprusside is used in critical care and perioperative settings for severe hypertensive emergencies, controlled hypotension during some surgical procedures, and acute decompensated heart failure with raised systemic vascular resistance. Title dosing is by continuous infusion, often starting at 0.3 to 0.5 microgram/kg/min and titrated against an intra-arterial line, with teaching ranges commonly quoted up to about 10 micrograms/kg/min for short periods; when infusion exceeds roughly 2 micrograms/kg/min, or continues for many hours, the risk of cyanide toxicity rises and alternatives such as nitroglycerin, nicardipine, clevidipine or labetalol may be preferred according to local protocol. Cyanide toxicity presents with unexplained deepening metabolic acidosis, raised lactate, tachyphylaxis, altered consciousness, seizures or arrhythmias and is treated by stopping the infusion plus hydroxocobalamin or sodium thiosulphate; thiocyanate toxicity, seen mainly in renal impairment, causes tinnitus, blurred vision, confusion and seizures and is managed by stopping the drug and considering renal replacement. The drug is contraindicated in compensatory hypertension such as coarctation of the aorta or arteriovenous shunting, and in inadequate cerebral perfusion; it should be used with caution in raised intracranial pressure, coronary steal, hepatic impairment, hypothyroidism and severe renal failure, and it can worsen hypoxaemia by increasing perfusion of poorly ventilated lung. It may be given with sodium thiosulphate or hydroxocobalamin in prolonged infusions as a cyanide-sparing strategy, and it should not be mixed with other drugs in the same bag. Because practice and monitoring requirements vary by region and unit, always confirm dose limits, monitoring and antidote availability against the local formulary and prescribing information.

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BNF; local critical care formulary and infusion guidelines; manufacturer prescribing information (SPC or equivalent); national hypertensive emergency guideline