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SNP pharmaceutics

vial: reddish brown lypholized powder. Reconstitute with 5% dextrose


discard: when exposed to sunlight turns blue/dark brown as CN- have been liberated



colour and mixing substance


discard when:

dose

onset


duration of action




0.5-6mcg/kg/min


onset within 3 mins


duration: short lived



MOA

SCN enters RBC interacts with oxyHb produces Nitric oxide, CN, metHB


Nitric oxide-> increases enzyme guanylate cyclase -> increased intracellular cGMP-> reduced Ca influx into vasc SM -> vasodilation.

enters RBC....

PD- CVS

CVS: arterial vasodilation (fall in SVR, MAP


venodilation (fall in preload)


reflex tacchycardia


CO maintained

CVS

PD - Resp, CNS

Resp: inhibit pulm hypoxic vasoconstriction-> worsens V/Q mismatch


CNS: increased CBF-> increased ICP






PK- metabolism

M: SNP enters RBC, interacts with oxyHb-> NO, CN-, metHb


3 things happen to CN-


a. metHb + CN- -> cyanomethaemoglobin (non toxic)


b. CN- in liver/kidney -> SCN


- SCN converted by RBC -> CN-


or SCN excreted in urine


c. CN- + VitB12 -> cyanocobalamin



PK toxicity

CN>8mcg/ml



Cyanide toxicity: CN- bind to cytochrome oxidases -> interfer with normal oxygen utilisation = anaerobic metabolism. = metabolic acidosis




Rx: stop infusion.


- chelating agent (dicobalt edetate)


- sodium thiosulphate


- sodium nitrite or amyl nitrite




cyanide tox


SCN tox

PK tox (SCN)

SCN tox: 100x less toxic. causes anorexia, sedation,