Drug information of Nitroprusside sodium
Mechanism of effect
Sodium nitroprusside breaks down in circulation to release nitric oxide (NO). It does this by binding to oxyhaemoglobin to release cyanide, methaemoglobin and nitric oxide.
NO activates guanylate cyclase in vascular smooth muscle and increases intracellular production of cGMP. cGMP activates protein kinase G which activates phosphatases which inactivate myosin light chains.Myosin light chains are involved in muscle contraction. The end result is vascular smooth muscle relaxation, which allow vessels to dilate.
Nitroprusside a powerful vasodilator relaxes the vascular smooth muscle and produce consequent dilatation of peripheral arteries and veins. Other smooth muscle (e.g., uterus, duodenum) is not affected. Sodium nitroprusside is more active on veins than on arteries.
Half-Life: parent drug: 2 min, metabolite (thiocyanate): 3 days, longer in patients with impaired renal function or hyponatremia
Onset of action: <2 min
Duration: 1-10 min
Metabolism: in blood (100%); ferrous ion in nitroprusside molecule reacts rapidly with sulfhydryl compounds in RBCs which results in cyanide release, which is then metabolized in liver and kidney by rhodanese to thiocyanate
Metabolites: Thiocyanate (inactive)
Excretion: Mainly in urine, excreted entirely as metabolites, principally thiocyanate
Dialyzable: Yes (HD)
Drug indicationsCongestive Heart Failure , Immediate reduction of blood pressure of patients in hypertensive crises , reduce bleeding during surgery
Hypertensive Emergency :
Initial dose: 0.3 mcg/kg/min IBW administered by continuous IV infusion. Maintenance dose: The dose may be titrated upward to a maximum of 10 mcg/kg/min IBW.
Congestive Heart Failure :
Initial dose: 10 to 15 mcg/min administered by continuous IV infusion.
Maintenance dose: The dose may be titrated to 10 to 200 mcg/min.
Maximum dose: 280 mcg/min (4 mcg/kg/min)
Toxicity with ergot alkaloid :
0.5 to 5 mcg/kg/min
Sodium Nitroprusside Injection is not suitable for direct injection. The solution must be further diluted in sterile 5% dextrose injection before infusion. Injection concentrate (25 mg/mL) must be further diluted prior to IV infusion.600 Dilute contents of one vial (50 mg) in 250–1000 mL of 5% dextrose injection.
Sodium Nitroprusside can cause precipitous decreases in blood pressure. In patients not properly monitored, these decreases can lead to irreversible ischemic injuries or death. Sodium nitroprusside should be used only when available equipment and personnel allow blood pressure to be continuously monitored.
Except when used briefly or at low (< 2 mcg/kg/min) infusion rates, sodium nitroprusside gives rise to important quantities of cyanide ion, which can reach toxic, potentially lethal levels. The usual dose rate is 0.5 to 10 mcg/kg/min, but infusion at the maximum dose rate should never last more than 10 minutes. If blood pressure has not been adequately controlled after 10 minutes of infusion at the maximum rate, administration of sodium nitroprusside should be terminated immediately.
Although acid-base balance and venous oxygen concentration should be monitored and may indicate cyanide toxicity, these laboratory tests provide imperfect guidance.
Use caution if high intracranial pressure or azotemia is present.
Other antihypertensive agents (e.g., hydralazine, labetalol, nifedipine) preferred for management of acute severe hypertension in preeclampsia; reserve sodium nitroprusside for treatment failures.
Points of recommendation
Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.
Importance of informing clinicians of existing or contemplated therapy, including prescription and OTC drugs and herbal supplements, as well as any concomitant illnesses.
Instruct patient to immediately report, ringing in the ears, headache, dizziness, blurred vision, or pain at the injection site.