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Pronunciation |
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(nye
troe PRUS
ide) |
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U.S. Brand
Names |
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Nitropress® |
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Generic
Available |
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Yes |
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Synonyms |
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Nitroprusside Sodium; Sodium Nitroferricyanide; Sodium
Nitroprusside |
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Pharmacological Index |
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Vasodilator |
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Use |
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Management of hypertensive crises; congestive heart failure; used for
controlled hypotension to reduce bleeding during surgery |
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Pregnancy Risk
Factor |
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C |
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Contraindications |
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Hypersensitivity to nitroprusside or any component; treatment of compensatory
hypertension (aortic coarctation, arteriovenous shunting); high output failure;
congenital optic atrophy or tobacco amblyopia |
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Warnings/Precautions |
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Except when used briefly or at low (<2 mcg/kg/minute) infusion rates,
nitroprusside gives rise to large cyanide quantities. Do not use the maximum
dose for more than 10 minutes. Use with extreme caution in patients with
elevated intracranial pressure. Use extreme caution in patients with hepatic or
renal dysfunction. Watch for cyanide toxicity in patients with impaired hepatic
function. Use the lowest end of the dosage range with renal impairment.
Thiocyanate toxicity occurs in patients with renal impairment or those on
prolonged infusions. Continuous blood pressure monitoring is
needed. |
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Adverse
Reactions |
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1% to 10%:
Central nervous system: Disorientation, psychosis, headache, restlessness
Endocrine & metabolic: Thyroid suppression
Gastrointestinal: Nausea, vomiting
Neuromuscular & skeletal: Weakness, muscle spasm
Otic: Tinnitus
Respiratory: Hypoxia
Miscellaneous: Sweating, thiocyanate toxicity |
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Overdosage/Toxicology |
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Symptoms of overdose include hypotension, vomiting, hyperventilation,
tachycardia, muscular twitching, hypothyroidism, cyanide or thiocyanate
toxicity. Thiocyanate toxicity includes psychosis, hyper-reflexia, confusion,
weakness, tinnitus, seizures, and coma; cyanide toxicity includes acidosis
(decreased HCO3, decreased pH, increased lactate), increase in mixed
venous blood oxygen tension, tachycardia, altered consciousness, coma,
convulsions, and almond smell on breath.
Nitroprusside has been shown to release cyanide in vivo with
hemoglobin. Cyanide toxicity does not usually occur because of the rapid uptake
of cyanide by erythrocytes and its eventual incorporation into cyanocobalamin.
However, prolonged administration of nitroprusside or its reduced elimination
can lead to cyanide intoxication. In these situations, airway support with
oxygen therapy is germane, followed closely with antidotal therapy of amyl
nitrate perles, sodium nitrate 300 mg I.V. (6 mg/kg for children) and sodium
thiosulfate 12.5 g I.V. (1.5 mL/kg for children); nitrates should not be
administered to neonates and small children. Thiocyanate is dialyzable. May be
mixed with sodium thiosulfate in I.V. to prevent cyanide toxicity.
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Drug
Interactions |
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None noted |
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Stability |
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Nitroprusside sodium should be reconstituted freshly by diluting 50 mg in
250-1000 mL of D5W
Use only clear solutions; solutions of nitroprusside exhibit a color
described as brownish, brown, brownish-pink, light orange, and straw. Solutions
are highly sensitive to light. Exposure to light causes decomposition, resulting
in a highly colored solution of orange, dark brown or blue. A blue color
indicates almost complete degradation and breakdown to cyanide.
Solutions should be wrapped with aluminum foil or other opaque material
to protect from light (do as soon as possible)
Stability of parenteral admixture at room temperature
(25°C) and at refrigeration temperature
(4°C): 24 hours |
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Mechanism of
Action |
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Causes peripheral vasodilation by direct action on venous and arteriolar
smooth muscle, thus reducing peripheral resistance; will increase cardiac output
by decreasing afterload; reduces aortal and left ventricular
impedance |
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Pharmacodynamics/Kinetics |
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Onset of hypotensive effect: <2 minutes
Duration: Within 1-10 minutes following discontinuation of therapy, effects
cease
Metabolism: Nitroprusside is converted to cyanide ions in the bloodstream;
decomposes to prussic acid which in the presence of sulfur donor is converted to
thiocyanate (liver and kidney rhodanase systems)
Half-life: Parent drug: <10 minutes; Thiocyanate: 2.7-7 days
Elimination: Thiocyanate renally eliminated |
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Usual Dosage |
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Administration requires the use of an infusion pump. Average dose: 5
mcg/kg/minute.
Adults: I.V. Initial: 0.3-0.5 mcg/kg/minute; increase in increments of 0.5
mcg/kg/minute, titrating to the desired hemodynamic effect or the appearance of
headache or nausea; usual dose: 3 mcg/kg/minute; rarely need >4
mcg/kg/minute; maximum: 10 mcg/kg/minute. When administered by prolonged
infusion faster than 2 mcg/kg/minute, cyanide is generated faster than an
unaided patient can handle. |
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Monitoring
Parameters |
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Blood pressure, heart rate; monitor for cyanide and thiocyanate toxicity;
monitor acid-base status as acidosis can be the earliest sign of cyanide
toxicity; monitor thiocyanate levels if requiring prolonged infusion (>3
days) or dose greater than or equal to 4 mcg/kg/minute or patient has renal
dysfunction; monitor cyanide blood levels in patients with decreased hepatic
function; cardiac monitor and blood pressure monitor
required |
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Reference Range |
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Monitor thiocyanate levels if requiring prolonged infusion (>4 days) or
greater than or equal to 4 mg/kg/minute; not to
exceed 100
mg/mL (or 10 mg/dL) plasma thiocyanate
Therapeutic: 6-29 mg/mL
Toxic: 35-100 mg/mL
Fatal: >200 mg/mL
Cyanide: Normal <0.2 mg/mL; normal (smoker):
<0.4
mg/mL
Toxic: >2 mg/mL
Potentially lethal: >3 mg/mL
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Cardiovascular
Considerations |
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Nitroprusside preparations must be wrapped with aluminum foil to protect from
light in order to prevent breakdown of the parent drug to cyanide. A bluish tint
to the solution indicates breakdown to cyanide. Thiocyanate levels should be
monitored if high doses are used for more than 24 hours, particularly in
patients with renal dysfunction and hepatic dysfunction. Nitroprusside is a very
effective agent for controlled blood pressure lowering because of the very short
half-life. Reasonably accurate titrations, based on target blood pressure can be
achieved. Nitroprusside may also be useful for afterload reduction in patients
with severe heart failure. Because of restricted cardiac output conditions,
nitroprusside should be avoided in patients with aortic stenosis or coarctation.
Nitroprusside should also be used cautiously in patients with acute myocardial
infarction, because of hemodynamic effects and possible coronary
steal. |
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Mental Health: Effects
on Mental Status |
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May cause restlessness, disorientation, or psychosis |
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Mental Health:
Effects on Psychiatric
Treatment |
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None reported, but monitor for hypotension if receiving a
psychotropic |
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Dental Health: Local
Anesthetic/Vasoconstrictor
Precautions |
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No information available to require special precautions |
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Dental Health:
Effects on Dental Treatment |
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No effects or complications reported |
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Patient
Information |
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Patient condition should indicate extent of education and instruction needed.
This drug can only be given I.V. You will be monitored at all times during
infusion. Promptly report any chest pain or pain/burning at site of infusion.
Breast-feeding precautions: Consult prescriber if
breast-feeding. |
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Nursing
Implications |
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Brownish solution is usable, discard if bluish in color |
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Dosage Forms |
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Injection, as sodium: 10 mg/mL (5 mL); 25 mg/mL (2 mL) |
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References |
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Cohn JN and Burke LP, "Nitroprusside," Ann Intern Med, 1979,
91(5):752-7.
Harmon C and Wohlreich MM, "Sodium Nitroprusside-Induced Delirium,"
Psychosomatics, 1995, 36(1):83-5.
Palmer RF and Lasseter KC, "Drug Therapy: Sodium Nitroprusside," N Engl J
Med, 1975, 292(6):294-7.
Schulz V,
"Clinical Pharmacokinetics of Nitroprusside, Cyanide, Thiosulfate, and Thiocyanate,"
Clin Pharmacokinet, 1984, 9(3):239-51.
Vesey CJ and Cole PV,
"Blood Cyanide and Thiocyanate Concentrations Produced by Long-Term Therapy With Sodium Nitroprusside,"
Br J Anaesth, 1985, 57(2):148-55.
Walters BN, "Urgent Treatment of Acute Hypertension," Br J Hosp Med,
1984, 31(1):49-52.
Wesson DE, Foley R, Sabatini S, et al,
"Treatment of Acute Cyanide Intoxication With Hemodialysis," Am J
Nephrol, 1985, 5(2):121-6. |
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