Structure/Class |
- It functions as an intravenous vasodilator.
- It is a complex consisting of cyanide group, iron and a nitroso group.
|
Pharmacodynamics |
- It releases NO, which stimulates guanylyl cyclase to increase cGMP levels. This leads to both venodilation and arteriolar dilation.
- In the absence of heart failure, there is a fall in BP due to decreased vascular resistance. Cardiac output generally does not change (or it may fall slightly).
- In patients with heart failure and low cardiac output, SNP may increase cardiac output by decreasing afterload.
|
Absorption/administration |
- IV only.
- It has a T ½ of two minutes, and overall duration of action of 1-10 minutes.
- Its metabolite thiocyanate has a T ½ of 3 days.
|
Distribution |
|
Metabolism |
- SNP is taken up by RBCs and readily metabolized to release NO and cyanide.
- Cyanide is metabolized in the liver by the mitochondrial enzyme rhodanase to thiocyanate.
- Thiocyanate is then distributed to the extracellular fluid and excreted renally.
|
Excretion |
- Renal
|
Indications |
- Hypertensive emergency
|
Contraindications |
|
Interactions |
|
Special precautions |
- Renal impairment (due to reduced excretion of thiocyanate)
- High doses and long infusion times may cause toxicity
|
Adverse effects |
- Excessive fall in BP (requires arterial line to use)
- Cyanide toxicity – metabolic acidosis, arrhythmia, tachypnea, pink skin and dilated pupils.
- Thiocyanate toxicity – CNS effects, e.g. ataxia, weakness, disorientation, psychosis, N/V and seizures.
|
Dosing/administration |
|
Toxicology |
- Sodium thiosulphate provides a sulphur group to assist with cyanide metabolism.
- Hydroxycobalamin (Vit B12) can also be used – it is metabolized to a non-toxic byproduct known as cyanocobalamin.
|
Withdrawal states |
|
Special notes |
|