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Quick facts
- How it is given
- intravenous
- Type
- human prescription drug
- RxNorm ID
- 240793
We do not publish dosing. How much of this medicine to take, how often, and for how long depends on your age, weight, kidney and liver function, other conditions and other medicines. That is a decision for the person who prescribes or dispenses it. Follow the directions on your own pack and ask your pharmacist if anything is unclear.
What it is used to treat
INDICATIONS & USAGE Sodium nitroprusside is indicated for the immediate reduction of blood pressure of adult and pediatric patients in hypertensive crises. Concomitant longer-acting antihypertensive medication should be administered so that the duration of treatment with sodium nitroprusside can be minimized. Sodium nitroprusside is also indicated for producing controlled hypotension in order to reduce bleeding during surgery. Sodium nitroprusside is also indicated for the treatment of acute congestive heart failure.
About this medicine
DESCRIPTION Sodium nitroprusside is disodium pentacyanonitrosylferrate(2-) dihydrate, a hypotensive agent whose structural formula is whose molecular formula is Na 2 [Fe(CN) 5 NO] 2H 2 O, and whose molecular weight is 297.95. Dry sodium nitroprusside, USP available as reddish-brown powder or crystals, freely soluble in water and slightly soluble in alcohol. In an aqueous solution infused intravenously, sodium nitroprusside is a rapid-acting vasodilator, active on both arteries and veins. Sodium nitroprusside solution is rapidly degraded by trace contaminants, often with resulting color changes. (See DOSAGE AND ADMINISTRATION section.) The solution is also sensitive to certain wavelengths of light, and it must be protected from light in clinical use. Sodium nitroprusside injection is available as: 50 mg Fliptop Vial – Each 2 mL vial contains the equivalent of 50 mg sodium nitroprusside dihydrate in sterile water for injection. structure
Who should not take it
CONTRAINDICATIONS Sodium nitroprusside should not be used in the treatment of compensatory hypertension, where the primary hemodynamic lesion is aortic coarctation or arteriovenous shunting. Sodium nitroprusside should not be used to produce hypotension during surgery in patients with known inadequate cerebral circulation, or in moribund patients (A.S.A. Class 5E) coming to emergency surgery. Patients with congenital (Leber’s) optic atrophy or with tobacco amblyopia have unusually high cyanide/thiocyanate ratios. These rare conditions are probably associated with defective or absent rhodanase, and sodium nitroprusside should be avoided in these patients. Sodium nitroprusside should not be used for the treatment of acute congestive heart failure associated with reduced peripheral vascular resistance such as high-output heart failure that may be seen in endotoxic sepsis.
Warnings
WARNINGS (See also the boxed warning at the beginning of this insert.) The principal hazards of sodium nitroprusside injection administration are excessive hypotension and excessive accumulation of cyanide (see also OVERDOSAGE and DOSAGE AND ADMINISTRATION ). Excessive Hypotension: Small transient excesses in the infusion rate of sodium nitroprusside can result in excessive hypotension, sometimes to levels so low as to compromise the perfusion of vital organs. These hemodynamic changes may lead to a variety of associated symptoms; see ADVERSE REACTIONS . Nitroprusside-induced hypotension will be self-limited within 1 to 10 minutes after discontinuation of the nitroprusside infusion; during these few minutes, it may be helpful to put the patient into a head-down (Trendelenburg) position to maximize venous return. If hypotension persists more than a few minutes after discontinuation of the infusion of sodium nitroprusside injection, sodium nitroprusside injection is not the cause, and the true cause must be sought. Cyanide Toxicity: As described in CLINICAL PHARMACOLOGY above, sodium nitroprusside infusions at rates above 2 mcg/kg/min generate cyanide ion (CN – ) faster than the body can normally dispose of it. (When sodium thiosulfate is given, as described under DOSAGE AND ADMINISTRATION , the body’s capacity for CN – elimination is greatly increased.) Methemoglobin normally present in the body can buffer a certain amount of CN–, but the capacity of this system is exhausted by the CN – produced from about 500 mcg/kg of sodium nitroprusside. This amount of sodium nitroprusside is administered in less than an hour when the drug is administered at 10 mcg/kg/min (the maximum recommended rate). Thereafter, the toxic effects of CN – may be rapid, serious, and even lethal. The true rates of clinically important cyanide toxicity cannot be assessed from spontaneous reports or published data. […]
Reported side effects
ADVERSE REACTIONS The most important adverse reactions to sodium nitroprusside are the avoidable ones of excessive hypotension and cyanide toxicity, described above under WARNINGS . The adverse reactions described in this section develop less rapidly and, as it happens, less commonly. Methemoglobinemia: As described in CLINICAL PHARMACOLOGY above, sodium nitroprusside infusions can cause sequestration of hemoglobin as methemoglobin. The back-conversion process is normally rapid, and clinically significant methemoglobinemia (>10%) is seen only rarely in patients receiving sodium nitroprusside injection. Even patients congenitally incapable of back-converting methemoglobin should demonstrate 10% methemoglobinemia only after they have received about 10 mg/kg of sodium nitroprusside, and a patient receiving sodium nitroprusside at the maximum recommended rate (10 mcg/kg/min) would take over 16 hours to reach this total accumulated dose. Methemoglobin levels can be measured by most clinical laboratories. The diagnosis should be suspected in patients who have received >10 mg/kg of sodium nitroprusside and who exhibit signs of impaired oxygen delivery despite adequate cardiac output and adequate arterial pO2. Classically, methemoglobinemic blood is described as chocolate brown, without color change on exposure to air. When methemoglobinemia is diagnosed, the treatment of choice is 1 to 2 mg/kg of methylene blue, administered intravenously over several minutes. In patients likely to have substantial amounts of cyanide bound to methemoglobin as cyanmethemoglobin, treatment of methemoglobinemia with methylene blue must be undertaken with extreme caution. Thiocyanate Toxicity: As described in CLINICAL PHARMACOLOGY above, most of the cyanide produced during metabolism of sodium nitroprusside is eliminated in the form of thiocyanate. When cyanide elimination is accelerated by the co-infusion of thiosulfate, thiocyanate production is increased. Thiocyanate is mildly neurotoxic (tinnitus, miosis, hyperreflexia) at serum levels of 1 mmol/L (60 mg/L). Thiocyanate toxicity is life-threatening when levels are 3 or 4 times higher (200 mg/L). […]
Interactions with other medicines
DRUG INTERACTIONS The hypotensive effect of sodium nitroprusside is augmented by that of most other hypotensive drugs, including ganglionic blocking agents, negative inotropic agents, and inhaled anesthetics.
If too much is taken
OVERDOSAGE Overdosage of nitroprusside can be manifested as excessive hypotension or cyanide toxicity (see WARNINGS ) or as thiocyanate toxicity (see ADVERSE REACTIONS ). The acute intravenous mean lethal doses (LD50) of nitroprusside in rabbits, dogs, mice, and rats are 2.8, 5.0, 8.4, and 11.2 mg/kg, respectively. Treatment of cyanide toxicity: Cyanide levels can be measured by many laboratories, and blood-gas studies that can detect venous hyperoxemia or acidosis are widely available. Acidosis may not appear until more than an hour after the appearance of dangerous cyanide levels, and laboratory tests should not be awaited. Reasonable suspicion of cyanide toxicity is adequate grounds for initiation of treatment. Treatment of cyanide toxicity consists of • discontinuing the administration of sodium nitroprusside; • providing a buffer for cyanide by using sodium nitrite to convert as much hemoglobin into methemoglobin as the patient can safely tolerate; and then • infusing sodium thiosulfate in sufficient quantity to convert the cyanide into thiocyanate. The necessary medications for this treatment are contained in commercially available Cyanide Antidote Kits. Alternatively, discrete stocks of medications can be used. Hemodialysis is ineffective in removal of cyanide, but it will eliminate most thiocyanate. Cyanide Antidote Kits contain both amyl nitrite and sodium nitrite for induction of methemoglobinemia. The amyl nitrite is supplied in the form of inhalant ampoules, for administration in environments where intravenous administration of sodium nitrite may be delayed. In a patient who already has a patent intravenous line, use of amyl nitrite confers no benefit that is not provided by infusion of sodium nitrite. Sodium nitrite is available in a 3% solution, and 4 to 6 mg/kg (about 0.2 mL/kg) should be injected over 2 to 4 minutes. This dose can be expected to convert about 10% of the patient’s hemoglobin into methemoglobin; this level of methemoglobinemia is not associated with any important hazard of its own. The nitrite infusion may cause transient vasodilatation and hypotension, and this hypotension must, if it occurs, be routinely managed. […]
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This page is built from the openFDA record of the U.S. Food and Drug Administration's approved labelling for this product, effective 22 July 2021. Label text has been shortened and reformatted for readability; safety wording has not been altered in meaning. FDA labelling describes products approved in the United States — brand names, strengths, formulations and approved uses may differ in your country. Always read the leaflet that comes with your own pack. PocketsInfo is not affiliated with, and is not endorsed by, the FDA. Retrieved 2026-07-30.