CLASS
- an inorganic complex
MECHANISM OF ACTION
- vasodiator & hypotension
- dilates both resistance & capacitance vessels by direction on vascular smooth muscle.
- acts by interacting with sulphdryl groups in smooth muscle membrane & preventing Ca2+ influx necessary for initiation of contraction
PHARMACEUTICS
- solution: 10mg/mL
- must be diluted before administration
- must be protected from light
- IV
DOSE
- 0.5 – 4mcg/kg/min
- titrated according to response
- need art line
- onset: immediate
Indications
(1) hypertensive crises
(2) aortic dissection
(3) LVF
(4) produce hypotension during surgery
Adverse Effects
- reversible decrease in PaO2 from decrease in hypoxic pulmonary vasoconstriction
- cerebral vasodilation -> increase in ICP
- increase in catecholamine
- increase in renin
- lactic acidosis may occur
- toxicity from cyanide production
PHARMACOKINETICS
- Absorption – n/a
- Distribution – confined to the plasma
- Metabolism
(1) reaction with sulphdryl groups on amino acids in plasma
(2) rapid, non-enzymatic hydrolysis within RBC’s
- 5 cyanide ions are produced by the degradation of each molecule of Na nitroprusside
- 1 reacts with metHb -> cyanometHb
- 3 react with thiosulphate -> thiocyanate (catalysed by hepatic rhodanese)
- 1 reacts with hydoxy-cobalamin -> forms cyanocobalamin (vitamin B12)
- Elimination – thiocyanate & cyanocobalamin -> urine, t1/2 of thiocyanate = 3 days
EVIDENCE
Major issue – liability to cyanide toxicity
- risk increased by hypothermia, malnutrition, vitamin B12 deficiency, hepatic or renal impairment
- related to rate of infusion rather than total dose.
- cyanide ion combines with cytochrome C -> impairment of aerobic metabolism -> metabolic lactic acidosis
- signs:
- tachycardia
- dysrhythmias
- hyperventilation
- sweating
- treatment:
- stop SNP infusion
- supportive measures
- sodium thiosulphate
- dicobalt edentate
- sodium nitrite
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