Introduction
Sodium nitroprusside is a potent, fast-acting vasodilator used in hypertensive emergencies and acute heart failure. It dilates both arteries and veins, reducing both preload and afterload, which improves cardiac output and lowers blood pressure.
Pharmacokinetics
Nitroprusside is administered intravenously and has an immediate onset of action. It is rapidly metabolized in the red blood cells, with a half-life of less than 2 minutes. Its metabolites, including cyanide, are excreted in the urine.
Mechanism of Action
Sodium nitroprusside releases nitric oxide, which stimulates guanylate cyclase and increases cyclic GMP levels. This leads to smooth muscle relaxation in both veins and arteries, reducing preload, afterload, and systemic vascular resistance.
Pharmacodynamics
Sodium nitroprusside reduces blood pressure rapidly and significantly, making it ideal for hypertensive crises. Its effects on both arterial and venous dilation help to improve cardiac function in acute heart failure.
Adverse Effects
Cyanide Toxicity: Prolonged use or high doses of nitroprusside can lead to cyanide poisoning.
Hypotension: Excessive vasodilation can cause severe hypotension, leading to organ hypoperfusion.
Reflex Tachycardia: Rapid blood pressure reduction may lead to compensatory tachycardia.
Drug Interactions
Antihypertensives: Use with other blood pressure-lowering agents may cause excessive hypotension.
Phosphodiesterase inhibitors: Concurrent use can potentiate vasodilation, increasing the risk of hypotension.
Dosages
Adults (Hypertensive Crisis): Start at 0.3 mcg/kg/min IV, titrate every few minutes to a maximum of 10 mcg/kg/min.