Nifedipine

346.34

346.33

244-598-3

I9ZF7L6G2L

757242

DTXSID2025715

C29290

Yellow crystals

C08CA05|C - Cardiovascular system

29333990

110

2

yellow powder

1.2109 (rough estimate)

172-174 °C

475.3ºC at 760 mmHg

241.2ºC

1.584

H2O: <0.1 g/100 mL at 19.5 ºC;DMSO: soluble

2-8°C

2.6X10-8 mm Hg at 25 deg C

Oral-rat LD50: 1022 mg/kg; Oral-Mouse LD50: 310 mg/kg

Combustion produces toxic nitrogen oxide fumes; medicinal side effects: low blood pressure, cardiomyopathy, local blood flow disorders, hyperglycemia, psychosis

Henry's Law constant = 7.3X10-14 atm-cu m/mol at 25 °C (est)

169.4 Ų [M+H-H2O]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]

Very light sensitive in solution|Hydroxyl radical reaction rate constant = 1.1X10-10 cu cm/molec-sec at 25 °C (est)

Aqueous solutions are very sensitive to light. (NTP, 1992). Insoluble in water.

Amines, Phosphines, and Pyridines

NIFEDIPINE is sensitive to light.

IRRITANT

1

22-36/37/38

26-36

US7975000

Xn,Xi

Ventilated, low temperature and dry; stored separately from food materials in warehouse

Stable under normal temperatures and pressures.

P201, P202, P264, P270, P281, P301+P312, P308+P313, P330, P405, P501

H302

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.|SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl nifedipine, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

Flash point data for this chemical are not available; however, it is probably combustible. (NTP, 1992)

|Warning|H302 (98.87%): Harmful if swallowed [Warning Acute toxicity, oral]|P201, P202, P264, P270, P281, P301+P312, P308+P313, P330, P405, and P501|Aggregated GHS information provided by 177 companies from 16 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. A water spray may also be used. (NTP, 1992)

SMALL SPILLS AND LEAKAGE: If a spill of this chemical occurs, FIRST REMOVE ALL SOURCES OF IGNITION, then you should dampen the solid spill material with acetone and transfer the dampened material to a suitable container. Use absorbent paper dampened with acetone to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with acetone followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned. STORAGE PRECAUTIONS: You should protect this material from exposure to light, and store it under ambient temperatures. (NTP, 1992)

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

Nifedipine was not detected in influent or effluent samples from Jamaica Bay, NY, a sewage impacted estuary in New York City, NY; samples were collected in February 2005 from the 26th Ward Wastewater Treatment Plant, Brooklyn(1).

highly toxic

The oral LD50 in rats is 1022mg/kg and in mice is 202mg/kg. Patients experiencing an overdose may present with hypotension, sinus node dysfunction, atrioventricular node dysfunction, and reflex tachycardia. Overdose may be managed by monitoring cardiovascular and respiratory function; elevating extremities; and administering vasopressors, fluids, and calcium infusions.

Mild and transient elevations in serum aminotransferase levels may occur during nifedipine therapy, but often resolve even with continuation of therapy. Clinically apparent acute liver injury with jaundice due to nifedipine is rare and described only in isolated case reports. The time to onset of injury is typically 1 to 2 months and the pattern of serum enzyme elevations is usually hepatocellular or mixed. Rash, arthralgias, fever and eosinophilia can occur, but are not prominent. Chronic aminotransferase elevations during continued therapy with nifedipine have been described sometimes with histological features of alcoholic liver disease (steatosis and Mallory bodies), but chronic liver injury after withdrawal has not. Nifedipine has not been implicated in cases of vanishing bile duct syndrome or acute liver failure in the published literature.

Quinidine is a substrate of CYP3A and has been shown to inhibit CYP3A in vitro. Co-administration of multiple doses of quinidine sulfate, 200 mg t.i.d., and nifedipine, 20 mg t.i.d., increased Cmax and AUC of nifedipine in healthy volunteers by factors of 2.30 and 1.37, respectively. The heart rate in the initial interval after drug administration was increased by up to 17.9 beats/minute. The exposure to quinidine was not importantly changed in the presence of nifedipine. Monitoring of heart rate and adjustment of the nifedipine dose, if necessary, are recommended when quinidine is added to a treatment with nifedipine.|Pre-treatment of healthy volunteers with 30 mg or 90 mg t.i.d. diltiazem p.o. increased the AUC of nifedipine after a single dose of 20 mg nifedipine by factors of 2.2 and 3.1, respectively. The corresponding Cmax values of nifedipine increased by factors of 2.0 and 1.7, respectively. Caution should be exercised when co-administering diltiazem and nifedipine and a reduction of the dose of nifedipine should be considered.|Verapamil, a CYP3A inhibitor, can inhibit the metabolism of nifedipine and increase the exposure to nifedipine during concomitant therapy. Blood pressure should be monitored and reduction of the dose of nifedipine considered.|In healthy volunteers receiving single dose of 20 mg nifedipine ER and benazepril 10 mg, the plasma concentrations of benazeprilat and nifedipine in the presence and absence of each other were not statistically significantly different. A hypotensive effect was only seen after co-administration of the two drugs. The tachycardic effect of nifedipine was attenuated in the presence of benazepril.|For more Interactions (Complete) data for Nifedipine (22 total), please visit the HSDB record page.

LD50 Rat oral 1022 mg/kg|LD50 Rat ip 230 mg/kg|LD50 Mouse oral 310 mg/kg|LD50 Mouse ip 185 mg/kg|LD50 Rabbit oral 504 mg/kg

Nifedipine is 92-98% protein bound in serum. Nifedipine is 97±12% bound in a 40g/L solution of pure albumin. Nifedipine is 51.4±5.9% protein bound in a 50mg/100mL solution of alpha-1-acid glycoprotein, and 75.5±3.5% protein bound in a 150mg/mL solution.

Nifedipine's production and use as antianginal and antihypertensive medicines(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 370(SRC), determined from a log Kow of 2.20(2) and a regression-derived equation(3), indicates that Nifedipine is expected to have moderate mobility in soil(SRC). Volatilization of Nifedipine from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 7.3X10-14 atm-cu m/mole(SRC), using a fragment constant estimation method(4). Nifedipine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.6X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(5). Biodegradation data for Nifedipine were not available(SRC,2009).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 370(SRC), determined from a log Kow of 2.20(2) and a regression-derived equation(3), indicates that Nifedipine is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(4) based upon an estimated Henry's Law constant of 7.3X10-14 atm-cu m/mole(SRC), developed using a fragment constant estimation method(5). According to a classification scheme(6), an estimated BCF of 13(SRC), from its log Kow(2) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data for Nifedipine were not available(SRC,2009).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), Nifedipine, which has an estimated vapor pressure of 2.6X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase Nifedipine may be removed from the air by wet or dry deposition(SRC). Nifedipine contains chromophores that absorb at wavelengths >290 nm(3) and therefore may be susceptible to direct photolysis by sunlight(SRC). Nifedipine is photosensitive and decomposes rapidly(4).

The rate constant for the vapor-phase reaction of Nifedipine with photochemically-produced hydroxyl radicals has been estimated as 1.1X10-10 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 3.4 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The rate constant for the vapor-phase reaction of Nifedipine with ozone has been estimated as 1.5X10-16 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(1). This corresponds to an atmospheric half-life of about 1.9 hours at an atmospheric concentration of 7X10+11 ozone molecules per cu cm(2). A base-catalyzed second-order hydrolysis rate constant of 4.1X10-3 L/mole-sec(SRC) was estimated using a structure estimation method(3); this corresponds to half-lives of 53 and 5.3 years at pH values of 7 and 8, respectively(3). Nifedipine contains chromophores that absorb at wavelengths >290 nm(4) and therefore may be susceptible to direct photolysis by sunlight(SRC). Nifedipine is photosensitive and decomposes rapidly(5).

An estimated BCF of 13 was calculated for Nifedipine(SRC), using a log Kow of 2.20(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Koc of Nifedipine is estimated as 370(SRC), using a log Kow of 2.20(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that Nifedipine is expected to have moderate mobility in soil.

The Henry's Law constant for Nifedipine is estimated as 7.3X10-14 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that Nifedipine is expected to be essentially nonvolatile from water surfaces(2). Nifedipine's Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to occur(SRC). Nifedipine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.6X10-8 mm Hg(SRC), determined from a fragment constant method(3).

SURFACE WATER: Nifedipine was detected in 3 of 32 surface water samples collected in October 2004 and 2005 from Jamaica Bay, NY, a wastewater-impacted estuary in the area of the large urbanized watershed of Brooklyn and Queens, New York City, at concentrations of up to or exceeding 1,000 ng/L(1).

Occupational exposure to Nifedipine may occur through inhalation of dust and dermal contact with this compound at workplaces where Nifedipine is produced or used. Exposure to Nifedipine among the general population may be limited to those administered the drug Nifedipine, a cardiovascular agent. (SRC)

Nifedipine capsules are indicated to treat vasospastic angina and chronic stable angina. Extended release tablets are indicated to treat vasospastic angina, chronic stable angina, and hypertension.|FDA Label|Treatment of essential hypertension

Nifedipine is a first generation calcium channel blocker used to treat hypertension and angina pectoris. Nifedipine therapy is associated with a low rate of serum enzyme elevations and has been linked to several instances of clinically apparent acute liver injury.

Cardiovascular Agents

Calcium Channel Blockers; Tocolytic Agents; Vasodilator Agents|Nifedipine extended-release tablets are indicated for the management of vasospastic angina confirmed by any of the following criteria: 1) classical pattern of angina at rest accompanied by ST segment elevation, 2) angina or coronary artery spasm provoked by ergonovine, or 3) angiographically demonstrated coronary artery spasm. In those patients who have had angiography, the presence of significant fixed obstructive disease is not incompatible with the diagnosis of vasospastic angina, provided that the above criteria are satisfied. Nifedipine extended-release may also be used where the clinical presentation suggests a possible vasospastic component but where vasospasm has not been confirmed, eg, where pain has a variable threshold on exertion or in unstable angina where electrocardiographic findings are compatible with intermittent vasospasm, or when angina is refractory to nitrates and/or adequate doses of beta blockers. /Included in US product label/|Nifedipine extended-release tablets are indicated for the management of chronic stable angina (effort-associated angina) without evidence of vasospasm in patients who remain symptomatic despite adequate doses of beta blockers and/or organic nitrates or who cannot tolerate those agents. /Included in US product label/|Nifedipine extended-release tablets (ADALAT CC) is indicated for the treatment of hypertension. It may be used alone or in combination with other antihypertensive agents. /Included in US product label/

The National Heart, Lung, and Blood Institute (NHLBI) concluded from the apparent concordance of findings from observational studies in hypertensive patients and from randomized studies principally in acute myocardial infarction and unstable angina patients that it seems prudent and consistent with current evidence to recommend that short-acting nifedipine, especially at high doses, be used in the management of hypertension, angina, or myocardial infarction with great caution, if at all.|The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), which compared long-term therapy with an ACE inhibitor (lisinopril) or dihydropyridine-derivative calcium-channel blocker (amlodipine) revealed no difference in the primary outcome of combined fatal coronary heart disease or nonfatal myocardial infarction among these therapies.|Serious adverse reactions requiring discontinuance of nifedipine therapy or dosage adjustment are relatively rare. An increase in the frequency, intensity, and duration of angina, possibly resulting from hypotension, has occurred rarely during initiation of nifedipine therapy. Additional serious adverse effects including myocardial infarction, congestive heart failure or pulmonary edema, and ventricular arrhythmia or conduction defects have reportedly occurred in 4%, 2%, and less than 0.5% of patients receiving conventional nifedipine capsules, respectively, but these have not been directly attributed to the drug.|Rarely, patients, usually receiving a beta blocker, have developed heart failure after beginning nifedipine. Patients with tight aortic stenosis may be at greater risk for such an event, as the unloading effect of nifedipine would be expected to be of less benefit to those patients, owing to their fixed impedance to flow across the aortic valve.|For more Drug Warnings (Complete) data for Nifedipine (32 total), please visit the HSDB record page.

Nifedipine is an inhibitor of L-type voltage gated calcium channels that reduces blood pressure and increases oxygen supply to the heart. Immediate release nifedipine's duration of action requires dosing 3 times daily. Nifedipine dosing is generally 10-120mg daily. Patients should be counselled regarding the risk of excessive hypotension, angina, and myocardial infarction.

A class of drugs that act by selective inhibition of calcium influx through cellular membranes. (See all compounds classified as Calcium Channel Blockers.)|Drugs that prevent preterm labor and immature birth by suppressing uterine contractions (TOCOLYSIS). Agents used to delay premature uterine activity include magnesium sulfate, beta-mimetics, oxytocin antagonists, calcium channel inhibitors, and adrenergic beta-receptor agonists. The use of intravenous alcohol as a tocolytic is now obsolete. (See all compounds classified as Tocolytic Agents.)|Drugs used to cause dilation of the blood vessels. (See all compounds classified as Vasodilator Agents.)

Sublingual dosing leads to a C_max of 10ng/mL, with a T_max of 50min, and an AUC of 25ng\*h/mL. Oral dosing leads to a C_max of 82ng/mL, with a T_max of 28min, and an AUC of 152ng\*h/mL. Nifedipine is a Biopharmaceutics Classification System Class II drug, meaning it has low solubility and high intestinal permeability. It is almost completely absorbed in the gastrointestinal tract but has a bioavilability of 45-68%, partly due to first pass metabolism.|Nifedipine is 60-80% recovered in the urine as inactive water soluble metabolites, and the rest is eliminated in the feces as metabolites.|The steady state volume of distribution of nifedipine is 0.62-0.77L/kg and the volume of distribution of the central compartment is 0.25-0.29L/kg.|The total body clearance of nifedipine is 450-700mL/min.|Approximately 90% of an oral dose of nifedipine is rapidly absorbed from the GI tract following oral administration of the drug as conventional capsules. Only about 45-75% of an oral dose as conventional capsules reaches systemic circulation as unchanged drug since nifedipine is metabolized on first pass through the liver. Peak serum concentrations usually are reached within 0.5-2 hours after oral administration as conventional capsules. Food appears to decrease the rate but not the extent of absorption of nifedipine as conventional capsules.|Plasma drug concentrations rise at a gradual, controlled rate after a nifedipine extended-release tablet dose and reach a plateau at approximately six hours after the first dose. For subsequent doses, relatively constant plasma concentrations at this plateau are maintained with minimal fluctuations over the 24-hour dosing interval. About a four-fold higher fluctuation index (ratio of peak to trough plasma concentration) was observed with the conventional immediate-release nifedipine capsule at t.i.d. dosing than with once daily nifedipine extended-release tablet.|At steady-state the bioavailability of the nifedipine extended-release tablet is 86% relative to immediate-release nifedipine capsules. Administration of the nifedipine extended-release tablet in the presence of food slightly alters the early rate of drug absorption, but does not influence the extent of drug bioavailability. Markedly reduced GI retention time over prolonged periods (ie, short bowel syndrome), however, may influence the pharmacokinetic profile of the drug which could potentially result in lower plasma concentrations.|The manufacturer states that relative oral bioavailability differs little if conventional nifedipine capsules are swallowed intact, bitten and swallowed, or bitten and held sublingually. However, some data indicate that the rate and extent of absorption of nifedipine following sublingual administration may be decreased substantially. Oral bioavailability of nifedipine may be increased up to twofold in patients with liver cirrhosis.|For more Absorption, Distribution and Excretion (Complete) data for Nifedipine (10 total), please visit the HSDB record page.

Nifedipine is predominantly metabolized by CYP3A4. Nifedipine is predominantly metabolized to 2,6-dimethyl-4-(2-nitrophenyl)-5-methoxycarbonyl-pyridine-3-carboxylic acid, and then further metabolized to 2-hydroxymethyl-pyridine carboxylic acid. Nifedipine is also minorly metabolized to dehydronifedipine.|The drug is extensively metabolized in the liver (to highly water-soluble, inactive metabolites) by the cytochrome P-450 microsomal enzyme system, including CYP3A.|Nifedipine has known human metabolites that include Oxidized nifedipine.

The terminal elimination half life of nifedipine is approximately 2 hours.|In patients with normal renal and hepatic function, the plasma half-life of nifedipine is about 2 hours when administered as conventional capsules, and about 7 hours when administered as extended-release tablets (Adalat CC).

Nifedipine blocks voltage gated L-type calcium channels in vascular smooth muscle and myocardial cells. This blockage prevents the entry of calcium ions into cells during depolarization, reducing peripheral arterial vascular resistance and dilating coronary arteries. These actions reduce blood pressure and increase the supply of oxygen to the heart, alleviating angina.|The principal physiologic action of nifedipine is to inhibit the transmembrane influx of extracellular calcium ions across the membranes of myocardial cells and vascular smooth muscle cells, without changing serum calcium concentrations. Calcium plays important roles in the excitation-contraction coupling processes of the heart and vascular smooth muscle cells and in the electrical discharge of the specialized conduction cells of the heart. The membranes of these cells contain numerous channels that carry a slow inward current and that are selective for calcium. Activation of these slow calcium channels contributes to the plateau phase (phase 2) of the action potential of cardiac and vascular smooth muscle cells. The exact mechanism whereby nifedipine inhibits calcium ion influx across the slow calcium channels is not known, but the drug is thought to inhibit ion-control gating mechanisms of the channel, deform the slow channel, and/or interfere with release of calcium from the sarcoplasmic reticulum. By inhibiting calcium influx, nifedipine inhibits the contractile processes of cardiac and vascular smooth muscle, thereby dilating the main coronary and systemic arteries.|Nifedipine is a peripheral arterial vasodilator which acts directly on vascular smooth muscle. The binding of nifedipine to voltage-dependent and possibly receptor-operated channels in vascular smooth muscle results in an inhibition of calcium influx through these channels. Stores of intracellular calcium in vascular smooth muscle are limited and thus dependent upon the influx of extracellular calcium for contraction to occur. The reduction in calcium influx by nifedipine causes arterial vasodilation and decreased peripheral vascular resistance which results in reduced arterial blood pressure.

Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)pyridine-3,5-dicarboxylate|Dimethyl 2,6-dimethyl-4-(2_nitrosophenyl)pyridine-3,5-dicarboxylate|Methyl 2-(2-nitrobenzylidene)-3-oxobutanoate|Methyl 3-aminobut-2-enoate

SYMPTOMS: Symptoms of exposure to this compound via ingestion include diabetes mellitus, hallucinations, distorted perceptions, cardiac effects, nausea, vomiting, changes in regional blood flow, dermatitis, anaphylaxis and decreased blood pressure. Other symptoms via ingestion include headache, dizziness, flushing, hypotension, tachycardia, fatigue and edema. It also causes dilation of coronary arteries and arterioles, reduced oxygen requirements, decreased platelet aggregation, weakness, heartburn, muscle cramps, tremor, nervousness, mood changes, palpitation, dyspnea, wheezing, cough, nasal congestion, sore throat, chest congestion, diarrhea, constipation flatulence, muscle inflammation, joint stiffness, shakiness, blurred vision, difficulties in balance, jitteriness, sleep disturbances, pruritus, urticaria, fever, sweating, chills, sexual difficulties and syncopal episodes. It can cause bradycardia, lethargy and anginal pain. It can also cause improved contractility and segmental ventricular function, increased heart rate and cardiac output, and increased peripheral blood flow due to arterial dilation (with no change in venous tone). It can cause negative inotropy, excessive vasodilation, depression of the sinus nodal rate, A-V nodal conduction disturbances, digital dysesthesia, sedation and aggravation of myocardial ischemia. Somnolence may occur. ACUTE/CHRONIC HAZARDS: When heated to decomposition this compound emits toxic fumes of nitrogen oxides. (NTP, 1992)

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

Generally, overdosage with nifedipine leading to pronounced hypotension calls for active cardiovascular support including monitoring of cardiovascular and respiratory function, elevation of extremities, judicious use of calcium infusion, pressor agents and fluids. Clearance of nifedipine would be expected to be prolonged in patients with impaired liver function. Since nifedipine is highly protein bound, dialysis is not likely to be of any benefit; however, plasmapheresis may be beneficial.|/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/SIGNS AND SYMPTOMS/ Generally, overdosage with the drug would be expected to produce toxic effects that are extensions of the usual adverse effects of the drug, including pronounced hypotension. ... Other symptoms associated with severe nifedipine overdosage include loss of consciousness, heart rhythm disturbances, metabolic acidosis, hypoxia, and cardiogenic shock with pulmonary edema.|/SIGNS AND SYMPTOMS/ The use of the selective serotonin reuptake inhibitor fluoxetine is associated with only minor cardiovascular effects. However, due to a possible inhibitory effect on the metabolism of calcium channel blockers it may potentiate the activity of nifedipine, causing profound adverse cardiovascular effects. This report describes the appearance of profound weakness, orthostatic hypotension and tachycardia following the initiation of fluoxetine treatment in a nifedipine-treated 80-year-old patient.|/SIGNS AND SYMPTOMS/ Several cases of profound hypotension, cerebrovascular ischemia or stroke, myocardial ischemia or infarction, and/or death have been reported when conventional short-acting preparations of nifedipine were used for the management of hypertensive crises, and therefore, the manufacturers currently warn that short-acting preparations should not be used for acute reduction in blood pressure. However, profound hypotension, myocardial ischemia or infarction, and/or death also have been reported occasionally in patients receiving conventional short-acting preparations of the drug for other uses (e.g., angina, pulmonary hypertension). The manufacturers also warn that short-acting preparations of nifedipine should not be used for the chronic management of hypertension.|/CASE REPORTS/ In one lactating woman who received 10, 20, and 30 mg of the drug every 8 hours as conventional capsules, peak milk concentrations of nifedipine occurred within 1 hour after a dose and ranged from about 13-53 ng/mL; the drug generally was not detectable during the hour prior to a dose.|For more Human Toxicity Excerpts (Complete) data for Nifedipine (30 total), please visit the HSDB record page.

Adalat

Adalat|Bay 1040|Bay A 1040|Citilat|For more Formulations/Preparations (Complete) data for Nifedipine (9 total), please visit the HSDB record page.

Analyte: nifedipine; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards|Analyte: nifedipine; matrix: chemical identification; procedure: ultraviolet absorption spectrophotometry with comparison to standards|Analyte: nifedipine; matrix: chemical identification; procedure: retention time of the major peak of the chromatogram with comparison to standards|Analyte: nifedipine; matrix: chemical purity; procedure: liquid chromatography with ultraviolet detection at 235 nm and comparison to standards|For more Analytic Laboratory Methods (Complete) data for Nifedipine (8 total), please visit the HSDB record page.

Analyte: nifedipine; matrix: pharmaceutical preparation (capsule); procedure: thin-layer chromatography with comparison to standards (chemical identification)|Analyte: nifedipine; matrix: pharmaceutical preparation (capsule): procedure: liquid chromatography with ultraviolet detection at 265 nm and comparison to standards (chemical purity)|Analyte: nifedipine; matrix: pharmaceutical preparation (capsule); procedure: retention time of the major peak of the liquid chromatogram with comparison to standards (chemical identification)|Analyte: nifedipine; matrix: pharmaceutical preparation (extended-release tablet); procedure: retention time of the major peak of the liquid chromatogram with comparison to standards (chemical identification)|For more Clinical Laboratory Methods (Complete) data for Nifedipine (9 total), please visit the HSDB record page.

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