Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/1636
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NITROPRESS (Injection, Solution, Concentrate)
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Dilution to proper strength for
infusion: Depending on the desired concentration, the solution containing
50 mg of NITROPRESS must be further diluted in 250-1000 mL of sterile 5% dextrose
injection. The diluted solution should be protected from light, using the
supplied opaque sleeve, aluminum foil, or other opaque material. It is not
necessary to cover the infusion drip chamber or the tubing. Verification of the chemical integrity of the product: Sodium
nitroprusside solution can be inactivated by reactions with trace contaminants.
The products of these reactions are often blue, green, or red, much brighter
than the faint brownish color of unreacted NITROPRESS. Discolored solutions,
or solutions in which particulate matter is visible, should not be used. If
properly protected from light, the freshly diluted solution is stable for
24 hours. No other drugs
should be administered in the same solution with sodium nitroprusside. Avoidance of excessive hypotension: While the
average effective rate in adults and children is about 3 mcg/kg/min, some
patients will become dangerously hypotensive when they receive NITROPRESS
at this rate. Infusion of sodium nitroprusside should therefore be started
at a very low rate (0.3 mcg/kg/min), with upward titration every few minutes
until the desired effect is achieved or the maximum recommended infusion rate
(10 mcg/kg/min) has been reached. Because sodium nitroprusside's
hypotensive effect is very rapid in onset and in dissipation, small variations
in infusion rate can lead to wide, undesirable variations in blood pressure. Sodium nitroprusside should not be infused through ordinary
I.V. apparatus, regulated only by gravity and mechanical clamps. Only an infusion
pump, preferably a volumetric pump, should be used. Because
sodium nitroprusside can induce essentially unlimited blood-pressure reduction, the blood pressure of a patient receiving this drug must
be continuously monitored, using either a continually reinflated
sphygmomanometer or (preferably) an intra-arterial pressure sensor. Special
caution should be used in elderly patients, since they may be more sensitive
to the hypotensive effects of the drug. When sodium
nitroprusside is used in the treatment of acute congestive heart failure,
titration of the infusion rate must be guided by the results of invasive hemodynamic
monitoring with simultaneous monitoring of urine output. Sodium nitroprusside
can be titrated by increasing the infusion rate until: The table below shows the infusion rates corresponding
to the recommended initial and maximal doses (0.3 mcg/kg/min and 10 mcg/kg/min,
respectively) for both adults and children of various weights. Some of the
listed infusion rates are so slow or so rapid as to be impractical, and these
practicalities must be considered when the concentration to be used is selected.
Note that when the concentration used in a given patient is changed, the tubing
is still filled with a solution at the previous concentration. Avoidance of cyanide toxicity: As described in
CLINICAL PHARMACOLOGY above, when more than 500 mcg/kg of sodium nitroprusside
is administered faster than 2 mcg/kg/min, cyanide is generated faster than
the unaided patient can eliminate it. Administration of sodium thiosulfate
has been shown to increase the rate of cyanide processing, reducing the hazard
of cyanide toxicity. Although toxic reactions to sodium thiosulfate have not
been reported, the co-infusion regimen has not been extensively studied, and
it cannot be recommended without reservation. In one study, sodium thiosulfate
appeared to potentiate the hypotensive effects of sodium nitroprusside. Co-infusions
of sodium thiosulfate have been administered at rates of 5-10 times that of
sodium nitroprusside. Care must be taken to avoid the indiscriminate use of
prolonged or high doses of sodium nitroprusside with sodium thiosulfate as
this may result in thiocyanate toxicity and hypovolemia. Incautious administration
of sodium nitroprusside must still be avoided, and all of the precautions
concerning sodium nitroprusside administration must still be observed. Consideration of methemoglobinemia
and thiocyanate toxicity: Rare patients receiving more than 10 mg/kg
of sodium nitroprusside will develop methemoglobinemia; other patients, especially
those with impaired renal function, will predictably develop thiocyanate toxicity
after prolonged, rapid infusions. In accordance with the descriptions in ADVERSE
REACTIONS above, patients with suggestive findings should be tested for these
toxicities. WARNING: Do
not use flexible container in series connections.
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Sodium nitroprusside is disodium pentacyanonitrosylferrate(2-)
dihydrate, an inorganic hypotensive agent whose structural formula is whose molecular formula is Na[Fe(CN)NO]���2HO, and whose molecular weight is 297.95. Dry sodium
nitroprusside is a reddish-brown powder, soluble in water. In an aqueous solution
infused intravenously, sodium nitroprusside is a rapid-acting vasodilator,
active on both arteries and veins. Sodium nitroprusside
solution is rapidly degraded by trace contaminants, often with resulting color
changes. (See DOSAGE AND ADMINISTRATION section.) The solution is also sensitive
to certain wavelengths of light, and it must be protected from light in clinical
use. NITROPRESS (Sodium Nitroprusside Injection) is
available as: 50 mg Fliptop Vial���Each 2 mL
vial contains the equivalent of 50 mg sodium nitroprusside dihydrate in sterile
water for injection.
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The principal pharmacological action of sodium nitroprusside
is relaxation of vascular smooth muscle and consequent dilatation of peripheral
arteries and veins. Other smooth muscle (e.g.
, uterus, duodenum) is not affected. Sodium nitroprusside is more
active on veins than on arteries, but this selectivity is much less marked
than that of nitroglycerin. Dilatation of the veins promotes peripheral pooling
of blood and decreases venous return to the heart, thereby reducing left ventricular
end-diastolic pressure and pulmonary capillary wedge pressure (preload). Arteriolar
relaxation reduces systemic vascular resistance, systolic arterial pressure,
and mean arterial pressure (afterload). Dilatation of the coronary arteries
also occurs. In association with the decrease in blood
pressure, sodium nitroprusside administered intravenously to hypertensive
and normotensive patients produces slight increases in heart rate and a variable
effect on cardiac output. In hypertensive patients, moderate doses induce
renal vasodilatation roughly proportional to the decrease in systemic blood
pressure, so there is no appreciable change in renal blood flow or glomerular
filtration rate. In normotensive subjects, acute reduction
of mean arterial pressure to 60-75 mm Hg by infusion of sodium nitroprusside
caused a significant increase in renin activity. In the same study, ten renovascular-hypertensive
patients given sodium nitroprusside had significant increases in renin release
from the involved kidney at mean arterial pressures of 90-137 mm Hg. The
hypotensive effect of sodium nitroprusside is seen within a minute or two
after the start of an adequate infusion, and it dissipates almost as rapidly
after an infusion is discontinued. The effect is augmented by ganglionic blocking
agents and inhaled anesthetics. Pharmacokinetics
and Metabolism: Infused sodium nitroprusside is rapidly distributed
to a volume that is approximately coextensive with the extracellular space.
The drug is cleared from this volume by intraerythrocytic reaction with hemoglobin
(Hgb), and sodium nitroprusside's resulting circulatory half-life is
about 2 minutes. The products of the nitroprusside/hemoglobin
reaction are cyanmethemoglobin (cyanmetHgb) and cyanide ion (CN��). Safe
use of sodium nitroprusside injection must be guided by knowledge of the further
metabolism of these products. As shown in the diagram
below, the essential features of nitroprusside metabolism are Cyanide
ion is normally found in serum; it is derived from dietary substrates and
from tobacco smoke. Cyanide binds avidly (but reversibly) to ferric ion (Fe),
most body stores of which are found in erythrocyte methemoglobin (metHgb)
and in mitochondrial cytochromes. When CN��is infused or generated
within the bloodstream, essentially all of it is bound to methemoglobin until
intraerythrocytic methemoglobin has been saturated. When
the Feof cytochromes is bound to cyanide, the cytochromes are
unable to participate in oxidative metabolism. In this situation, cells may
be able to provide for their energy needs by utilizing anaerobic pathways,
but they thereby generate an increasing body burden of lactic acid. Other
cells may be unable to utilize these alternate pathways, and they may die
hypoxic deaths. CN��levels in packed erythrocytes
are typically less than 1��mol/L (less than 25 mcg/L); levels are roughly
doubled in heavy smokers. At healthy steady state,
most people have less than 1% of their hemoglobin in the form of methemoglobin.
Nitroprusside metabolism can lead to methemoglobin formation (a) through dissociation
of cyanmethemoglobin formed in the original reaction of sodium nitroprusside
with Hgb and (b) by direct oxidation of Hgb by the released nitroso group.
Relatively large quantities of sodium nitroprusside, however, are required
to produce significant methemoglobinemia. At physiologic
methemoglobin levels, the CN��binding capacity of packed red cells is
a little less than 200��mol/L (5 mg/L). Cytochrome toxicity is seen
at levels only slightly higher, and death has been reported at levels from
300 to 3000��mol/L (8���80 mg/L). Put another way, a patient with
a normal red-cell mass (35 mL/kg) and normal methemoglobin levels can buffer
about 175 mcg/kg of CN��, corresponding to a little less than 500 mcg/kg
of infused sodium nitroprusside. Some cyanide is eliminated
from the body as expired hydrogen cyanide, but most is enzymatically converted
to thiocyanate (SCN��) by thiosulfate-cyanide sulfur transferase (rhodanase,
EC 2.8.1.1), a mitochondrial enzyme. The enzyme is normally present in great
excess, so the reaction is rate-limited by the availability of sulfur donors,
especially thiosulfate, cystine, and cysteine. Thiosulfate
is a normal constituent of serum, produced from cysteine by way of��-mercaptopyruvate.
Physiological levels of thiosulfate are typically about 0.1 mmol/L (11 mg/L),
but they are approximately twice this level in children and in adults who
are not eating. Infused thiosulfate is cleared from the body (primarily by
the kidneys) with a half-life of about 20 minutes. When
thiosulfate is being supplied only by normal physiologic mechanisms, conversion
of CN��to SCN��generally proceeds at about 1 mcg/kg/min. This rate
of CN��clearance corresponds to steady-state processing of a sodium nitroprusside
infusion of slightly more than 2 mcg/kg/min. CN��begins to accumulate
when sodium nitroprusside infusions exceed this rate. Thiocyanate
(SCN��) is also a normal physiological constituent of serum, with normal
levels typically in the range of 50-250��mol/L (3-15 mg/L). Clearance
of SCN��is primarily renal, with a half-life of about 3 days. In renal
failure, the half-life can be doubled or tripled.<br/>Clinical Trials:: Baseline-controlled
clinical trials have uniformly shown that sodium nitroprusside has a prompt
hypotensive effect, at least initially, in all populations. With increasing
rates of infusion, sodium nitroprusside has been able to lower blood pressure
without an observed limit of effect. Clinical trials have also shown that the hypotensive
effect of sodium nitroprusside is associated with reduced blood loss in a
variety of major surgical procedures. In patients with acute congestive heart failure and
increased peripheral vascular resistance, administration of sodium nitroprusside
causes reductions in peripheral resistance, increases in cardiac output, and
reductions in left ventricular filling pressure. Many trials have verified the clinical significance
of the metabolic pathways described above. In patients receiving unopposed
infusions of sodium nitroprusside, cyanide and thiocyanate levels have increased
with increasing rates of sodium nitroprusside infusion. Mild to moderate metabolic
acidosis has usually accompanied higher cyanide levels, but peak base deficits
have lagged behind the peak cyanide levels by an hour or more. Progressive tachyphylaxis
to the hypotensive effects of sodium nitroprusside has been reported in several
trials and numerous case reports. This tachyphylaxis has frequently been attributed
to concomitant cyanide toxicity, but the only evidence adduced for this assertion
has been the observation that in patients treated with sodium nitroprusside
and found to be resistant to its hypotensive effects, cyanide levels are often
found to be elevated. In the only reportedcomparisons
of cyanide levels in resistant and nonresistant patients, cyanide
levels did not correlate with tachyphylaxis.
The mechanism of tachyphylaxis to sodium nitroprusside remains unknown.
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Sodium nitroprusside should not be used in the treatment
of compensatory hypertension, where the primary hemodynamic lesion is aortic
coarctation or arteriovenous shunting. Sodium nitroprusside
should not be used to produce hypotension during surgery in patients with
known inadequate cerebral circulation, or in moribund patients (A.S.A. Class
5E) coming to emergency surgery. Patients with congenital
(Leber's) optic atrophy or with tobacco amblyopia have unusually high
cyanide/thiocyanate ratios. These rare conditions are probably associated
with defective or absent rhodanase, and sodium nitroprusside should be avoided
in these patients. Sodium nitroprusside should not
be used for the treatment of acute congestive heart failure associated with
reduced peripheral vascular resistance such as high-output heart failure that
may be seen in endotoxic sepsis.
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NITROPRESS (sodium nitroprusside injection) is supplied in
amber-colored, single-dose 50 mg/2 mL Fliptop Vials (List No. 3024). Store
at 20 to 25��C (68 to 77��F). [See USP Controlled Room Temperature.] To
protect NITROPRESS from light, it should be stored in its carton until it
is used. Revised: March, 2006 ��Hospira
2006 EN-1157 Printed in USA HOSPIRA,
INC., LAKE FOREST, IL 60045 USA
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NITROPRESS (Sodium Nitroprusside
Injection) is not suitable for direct injection. The solution must be further
diluted in sterile 5% dextrose injection before infusion. NITROPRESS can cause precipitous decreases in blood pressure
(see DOSAGE AND ADMINISTRATION). In patients not properly monitored, these
decreases can lead to irreversible ischemic injuries or death. Sodium nitroprusside
should be used only when available equipment and personnel allow blood pressure
to be continuously monitored. Except
when used briefly or at low (<2 mcg/kg/min) infusion rates, sodium nitroprusside
gives rise to important quantities of cyanide ion, which can reach toxic,
potentially lethal levels (see WARNINGS). The usual dose rate is 0.5-10 mcg/kg/min,
but infusion at the maximum dose rate should never last more than 10 minutes.
If blood pressure has not been adequately controlled after 10 minutes of infusion
at the maximum rate, administration of sodium nitroprusside should be terminated
immediately. Although
acid-base balance and venous oxygen concentration should be monitored and
may indicate cyanide toxicity, these laboratory tests provide imperfect guidance. This package insert
should be thoroughly reviewed before administration of NITROPRESS.
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General:: Like other vasodilators, sodium nitroprusside can cause increases
in intracranial pressure. In patients whose intracranial pressure is already
elevated, sodium nitroprusside should be used only with extreme caution. Hepatic: Use caution when administering nitroprusside
to patients with hepatic insufficiency. Use
in Anesthesia: When sodium nitroprusside (or any other vasodilator)
is used for controlled hypotension during anesthesia, the patient's
capacity to compensate for anemia and hypovolemia may be diminished. If possible,
pre-existing anemia and hypovolemia should be corrected prior to administration
of NITROPRESS. Hypotensive anesthetic techniques may
also cause abnormalities of the pulmonary ventilation/perfusion ratio. Patients
intolerant of these abnormalities may require a higher fraction of inspired
oxygen. Extreme caution should be exercised in patients
who are especially poor surgical risks (A.S.A. Class 4 and 4E).<br/>Laboratory Tests:: The cyanide-level assay is technically difficult, and cyanide
levels in body fluids other than packed red blood cells are difficult to interpret.
Cyanide toxicity will lead to lactic acidosis and venous hyperoxemia, but
these findings may not be present until an hour or more after the cyanide
capacity of the body's red-cell mass has been exhausted.<br/>Drug Interactions:: The hypotensive effect of sodium nitroprusside is augmented
by that of most other hypotensive drugs, including ganglionic blocking agents,
negative inotropic agents, and inhaled anesthetics.<br/>Carcinogenesis, Mutagenesis, and Impairment of Fertility:: Animal studies assessing sodium nitroprusside's carcinogenicity
and mutagenicity have not been conducted. Similarly, sodium nitroprusside
has not been tested for effects on fertility.<br/>Pregnancy:: Teratogenic effects: Pregnancy Category C. There
are no adequate, well-controlled studies of NITROPRESS in either laboratory
animals or pregnant women. It is not known whether NITROPRESS can cause fetal
harm when administered to a pregnant woman or can affect reproductive capacity.
NITROPRESS should be given to a pregnant woman only if clearly needed. Nonteratogenic
effects: In three studies in pregnant ewes, nitroprusside was shown to cross
the placental barrier. Fetal cyanide levels were shown to be dose-related
to maternal levels of nitroprusside. The metabolic transformation of sodium
nitroprusside given to pregnant ewes led to fatal levels of cyanide in the
fetuses. The infusion of 25 mcg/kg/min of sodium nitroprusside for one hour
in pregnant ewes resulted in the death of all fetuses. Pregnant ewes infused
with 1 mcg/kg/min of sodium nitroprusside for one hour delivered normal lambs. According
to one investigator, a pregnant woman at 24 weeks gestation was given sodium
nitroprusside to control gestational hypertension secondary to mitral valve
disease. Sodium nitroprusside was infused at 3.9 mcg/kg/min for a total of
3.5 mg/kg over 15 hours prior to delivery of a 478 gram stillborn infant without
any obvious anomalies. Cyanide levels in the fetal liver were less than 10
mcg/mL. Toxic levels have been reported to be more than 30-40 mcg/mL. The
mother demonstrated no cyanide toxicity. The effects
of administering sodium thiosulfate in pregnancy, either by itself or as a
co-infusion with sodium nitroprusside, are completely unknown.<br/>Nursing Mothers:: It is not known whether sodium nitroprusside and its metabolites
are excreted in human milk. Because many drugs are excreted in human milk
and because of the potential for serious adverse reactions in nursing infants
from sodium nitroprusside, a decision should be made whether to discontinue
nursing or to discontinue the drug, taking into account the importance of
the drug to the mother.<br/>Pediatric Use:: See DOSAGE AND ADMINISTRATION.
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Overdosage of nitroprusside can be manifested as excessive
hypotension or cyanide toxicity (see WARNINGS) or as thiocyanate toxicity
(see ADVERSE REACTIONS). The acute intravenous mean
lethal doses (LD) of nitroprusside in rabbits, dogs, mice, and
rats are 2.8, 5.0, 8.4, and 11.2 mg/kg, respectively. Treatment of cyanide toxicity: Cyanide levels can
be measured by many laboratories, and blood-gas studies that can detect venous
hyperoxemia or acidosis are widely available. Acidosis
may not appear until more than an hour after the appearance of dangerous cyanide
levels, and laboratory tests should not be awaited. Reasonable suspicion of
cyanide toxicity is adequate grounds for initiation of treatment. Treatment
of cyanide toxicity consists of The necessary medications for this treatment are contained
in commercially available Cyanide Antidote Kits. Alternatively, discrete stocks
of medications can be used. Hemodialysis is ineffective
in removal of cyanide, but it will eliminate most thiocyanate. Cyanide
Antidote Kits contain both amyl nitrite and sodium nitrite for induction of
methemoglobinemia. The amyl nitrite is supplied in the form of inhalant ampoules,
for administration in environments where intravenous administration of sodium
nitrite may be delayed. In a patient who already has a patent intravenous
line, use of amyl nitrite confers no benefit that is not provided by infusion
of sodium nitrite. Sodium nitrite is available in a
3% solution, and 4-6 mg/kg (about 0.2 mL/kg) should be injected over 2-4 minutes.
This dose can be expected to convert about 10% of the patient's hemoglobin
into methemoglobin; this level of methemoglobinemia is not associated with
any important hazard of its own. The nitrite infusion may cause transient
vasodilatation and hypotension, and this hypotension must, if it occurs, be
routinely managed. Immediately after infusion of the
sodium nitrite, sodium thiosulfate should be infused. This agent is available
in 10% and 25% solutions, and the recommended dose is 150-200 mg/kg; a typical
adult dose is 50 mL of the 25% solution. Thiosulfate treatment of an acutely
cyanide-toxic patient will raise thiocyanate levels,but not to a dangerous
degree. The nitrite/thiosulfate regimen may be repeated,
at half the original doses, after two hours.
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Sodium Nitroprusside
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NITROPRESS (Injection, Solution, Concentrate)
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The most important adverse reactions to sodium nitroprusside
are the avoidable ones of excessive hypotension and cyanide toxicity, described
above under WARNINGS. The adverse reactions described in this section develop
less rapidly and, as it happens, less commonly. Methemoglobinemia: As described in CLINICAL PHARMACOLOGY
above, sodium nitroprusside infusions can cause sequestration of hemoglobin
as methemoglobin. The back-conversion process is normally rapid, and clinically
significant methemoglobinemia (>10%) is seen only rarely in patients receiving
NITROPRESS. Even patients congenitally incapable of back-converting methemoglobin
should demonstrate 10% methemoglobinemia only after they have received about
10 mg/kg of sodium nitroprusside, and a patient receiving sodium nitroprusside
at the maximum recommended rate (10 mcg/kg/min) would take over 16 hours to
reach this total accumulated dose. Methemoglobin levels
can be measured by most clinical laboratories. The diagnosis should be suspected
in patients who have received>10 mg/kg of sodium nitroprusside and who exhibit
signs of impaired oxygen delivery despite adequate cardiac output and adequate
arterial pO. Classically, methemoglobinemic blood is described
as chocolate brown, without color change on exposure to air. When
methemoglobinemia is diagnosed, the treatment of choice is 1-2 mg/kg of methylene
blue, administered intravenously over several minutes. In patients likely
to have substantial amounts of cyanide bound to methemoglobin as cyanmethemoglobin,
treatment of methemoglobinemia with methylene blue must be undertaken with
extreme caution. Thiocyanate
Toxicity: As described in CLINICAL PHARMACOLOGY above, most of the
cyanide produced during metabolism of sodium nitroprusside is eliminated in
the form of thiocyanate. When cyanide elimination is accelerated by the co-infusion
of thiosulfate, thiocyanate production is increased. Thiocyanate
is mildly neurotoxic (tinnitus, miosis, hyperreflexia) at serum levels of
1 mmol/L (60 mg/L). Thiocyanate toxicity is life-threatening when levels are
3 or 4 times higher (200 mg/L). The steady-state thiocyanate
level after prolonged infusions of sodium nitroprusside is increased with
increased infusion rate, and the half-time of accumulation is 3-4 days. To
keep the steady-state thiocyanate level below 1 mmol/L, a prolonged infusion
of sodium nitroprusside should not be more rapid than 3 mcg/kg/min; in anuric
patients, the corresponding limit is just 1 mcg/kg/min. When prolonged infusions
are more rapid than these, thiocyanate levels should be measured daily. Physiologic
maneuvers (e.g., those that alter the
pH of the urine) are not known to increase the elimination of thiocyanate.
Thiocyanate clearance rates during dialysis, on the other hand, can approach
the blood flow rate of the dialyzer. Thiocyanate interferes
with iodine uptake by the thyroid. Abdominal pain,
apprehension, diaphoresis,���dizziness,���headache, muscle twitching,
nausea, palpitations, restlessness, retching, and retrosternal discomfort
have been noted when the blood pressure was too rapidly reduced. These symptoms
quickly disappeared when the infusion was slowed or discontinued, and they
did not reappear with a continued (or resumed) slower infusion. Other
adverse reactions reported are: Cardiovascular:
Bradycardia, electrocardiographic changes, tachycardia. Dermatologic: Rash. Endocrine: Hypothyroidism. Gastrointestinal: Ileus. Hematologic: Decreased platelet aggregation. Neurologic: Increased intracranial pressure. Miscellaneous: Flushing, venous streaking, irritation
at the infusion site.
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(See also the boxed warning at the beginning of this insert.) The
principal hazards of NITROPRESS administration are excessive hypotension and
excessive accumulation of cyanide (see also OVERDOSAGE AND DOSAGE AND ADMINISTRATION). Excessive Hypotension: Small transient excesses
in the infusion rate of sodium nitroprusside can result in excessive hypotension,
sometimes to levels so low as to compromise the perfusion of vital organs.
These hemodynamic changes may lead to a variety of associated symptoms; see
ADVERSE REACTIONS. Nitroprusside-induced hypotension will be self-limited
within 1-10 minutes after discontinuation of the nitroprusside infusion; during
these few minutes, it may be helpful to put the patient into a head-down (Trendelenburg)
position to maximize venous return. If hypotension persists more than a few
minutes after discontinuation of the infusion of NITROPRESS, NITROPRESS is
not the cause, and the true cause must be sought. Cyanide Toxicity: As described in CLINICAL PHARMACOLOGY
above, sodium nitroprusside infusions at rates above 2 mcg/kg/min generate
cyanide ion (CN��) faster than the body can normally dispose of it. (When
sodium thiosulfate is given, as described under DOSAGE AND ADMINISTRATION,
the body's capacity for CN��elimination is greatly increased.)
Methemoglobin normally present in the body can buffer a certain amount of
CN��, but the capacity of this system is exhausted by the CN��produced
from about 500 mcg/kg of sodium nitroprusside. This amount of sodium nitroprusside
is administered in less than an hour when the drug is administered at 10 mcg/kg/min
(the maximum recommended rate). Thereafter, the toxic effects of CN��may be rapid, serious, and even lethal. The true rates
of clinically important cyanide toxicity cannot be assessed from spontaneous
reports or published data. Most patients reported to have experienced such
toxicity have received relatively prolonged infusions, and the only patients
whose deaths have been unequivocally attributed to nitroprusside-induced cyanide
toxicity have been patients who had received nitroprusside infusions at rates
(30-120 mcg/kg/min) much greater than those now recommended. Elevated cyanide
levels, metabolic acidosis, and marked clinical deterioration, however, have
occasionally been reported in patients who received infusions at recommended
rates for only a few hours and even, in one case, for only 35 minutes. In
some of these cases, infusion of sodium thiosulfate caused dramatic clinical
improvement, supporting the diagnosis of cyanide toxicity. Cyanide
toxicity may manifest itself as venous hyperoxemia with bright red venous
blood, as cells become unable to extract the oxygen delivered to them; metabolic
(lactic) acidosis; air hunger; confusion; and death. Cyanide toxicity due
to causes other than nitroprusside has been associated with angina pectoris
and myocardial infarction; ataxia, seizures, and stroke; and other diffuse
ischemic damage. Hypertensive patients, and patients
concomitantly receiving other antihypertensive medications, may be more sensitive
to the effects of sodium nitroprusside than normal subjects.
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Sodium nitroprusside is indicated for the immediate reduction
of blood pressure of patients in hypertensive crises. Concomitant longer-acting
antihypertensive medication should be administered so that the duration of
treatment with sodium nitroprusside can be minimized. Sodium
nitroprusside is also indicated for producing controlled hypotension in order
to reduce bleeding during surgery. Sodium nitroprusside
is also indicated for the treatment of acute congestive heart failure.
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NITROPRESS
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