Vasopressin & SNP Flashcards
(27 cards)
Arginine vasopressin
endogenous hormone
ADH
produced in hypothalamus stores in posterior pituitary
ADH role
osmoregulation: release stimulated by increased osmolarity and hypovolemia
potent vasoconstrictor, but dilates renal afferent, pulmonary and cerebral arterioles
3 Types Vasopressin Receptors
V1, V2, V3
V1
mediates vasoconstriction (vasculature)
V2
mediates water reabsorption in the renal collecting ducts (kidney)
V3
found in CNS and stimulates modulation of corticotrophin secretion
Vasopressin Uses
post cardiopulm bypass shock refractory hypotension (ACE & ARB DOS) Reduce bleeding in VWB disease anti-diuresis in DI treatment of enuresis
Vasopressin Dosage
low dose infusion: 0.03-0.04 units/min, max 0.1 units/min bolus IV 1-2 units onset: 1-5 min DOA: 10-30 min peak effect: 5 min
Vasopressin Complications
only seen at dosages >0.04 units/min
GI ischemia
decreased CO
skin or digital necrosis
Peripheral Vasodilators: SNP
direct acting, nonselective peripheral vasodilator
relaxation of arterial and venous VSM
lacks significant effects on nonvascular SM and cardiac muscle
SNP MOA
SNP interacts with oxyhemoglobin to form methemoglobin, NO and cyanide
NO activates guanylate cyclase (increasing cGMP)
SNP Metabolism
transfer of an electron from iron of oxyhemoglobin to SNP yields metHgb and an UNSTABLE SNP radical, this breaks down to release 5 cyanide ions.
ONE cyanide ion interacts with metHGB to form cyano-methemoglobin (nontoxic)
remainder metabolized in liver and kidney and converted to thiocyanate
SNP Toxicity
occurs due to the effects of high plasma concentrations of THIOCYANATE
Cyanide Toxicity
occurs at rates >2mcg/kg/min for LONG PERIODS
suspect this when patients have resistance to hypotensive effects or previously responsive patient who is unresponsive (tachyphylaxis) rates >2-10 mcg/kg/min
May precipitate tissue anoxia, anaerobic metabolism and lactic acidosis
Thiocyanate Toxicity
rare, cleared by kidney in 3-7 days
less toxic than cyanide
S/S: N/V tinnutis, fatigue, CNS hyperrflexia, confusion, psychosis, miosis, seizure and coma
SNP Dosage
0.3 mcg/kg/min- 10 mcg/kg/min IV do not infuse >10 min immediate onset, short DOA extremely potent, monitor BP with aline requires continuous IV admin to maintain therapeutic effect
SNP Effects CV
venous and arterial vasodilation decreased venous capacitance d/t VR Increase HR (baroreflex) decrease SBP, SVR, PVR increased contractility decreased diastolic BP, reduced coronary perfusion
Clinical uses SNP
controlled hypotension: 0.3-0.5 mcg/kg/min (max 2mcg/kg/min)
hypertensive crisis: infusion 1-2mcg/kg IV (bolus also)
cardiac disease: decreases LV afterload, benefits management of MR or AR, CHF, and HF
consider coronary steal
cGMP role
inhibits calcium entry into VSMC but increases uptake of calcium into the smooth ER.
Results in vasodilation via NO
Cyanide Toxicity Tx
D/C SNP ASAP
100% FIO2 (even though sat is good)
Sodium bicarb
Sodium thiosulfate 150mg/kg over 15 min (sulfur donor to convert cyanide to thiocyanate
sodium nitrate 5mg/kg for SEVERE TOXICITY (coverts hemoglobin to metHgb which converts cyanide to cyanometHemoglobin
SNP Effects CNS
increased CBF and ICP
modest decrease in MAP or with greater decrease in MAP can reduce CBF (caution with carotid disease)
SNP Effects Pulmonary
attenuation of HPV
SNP Effects Blood
increased intracellular cGMP leads to inhibition of platelet aggregation and increase bleeding time.
