Hypertension is commonly seen in the perioperative setting as well as the intensive care unit (ICU). There are many agents to lower blood pressure with different mechanisms of action. One of the most potent vasodilators is sodium nitroprusside, which causes arteriolar and venous smooth muscle relaxation via nitric oxide-mediated mechanisms. It has a rapid onset and relatively short duration of action, making it a readily titratable agent. However, its dose must be limited because of its potential toxic side effects.

Toxicity from sodium nitroprusside is due to the cyanide groups released from metabolism of the nitroprusside molecule. After gaining an electron from the iron moiety of hemoglobin, the sodium nitroprusside produces an unstable radical and methemoglobin. The unstable nitroprusside radical produces five cyanide ions, which can have one of three fates. They can interact with methemoglobin to produce cyanomethemoglobin. They can produce thiosulfate and its end product thiocyanate. Additionally, cyanide ions can bind cytochrome oxidase and ultimately inhibit oxidative metabolism, leading to cyanide toxicity. Organs most susceptible to the effects of loss of oxidative metabolism are the heart and brain.

Clinically, patients with cyanide toxicity may exhibit altered mental status, cardiovascular instability, and an anion gap metabolic acidosis. Initially, patients may present with sinus tachycardia that may progress to sinus bradycardia or ventricular dysrhythmias and even asystole. Patients begin to have restlessness and agitation when the central nervous system is affected. With worsening toxicity, convulsions may occur and can ultimately lead to encephalopathy and coma. With loss of aerobic metabolism there is an increase in lactate, leading to an anion gap metabolic acidosis.