Acecainide
Anti-Arrhythmia Agents
Quinidine
Disopyramide
Dynamic effects of intravenous procainamide infusion on the electrophysiological properties during atrial fibrillation. (1/188)
Although the mechanism of atrial fibrillation (AF) is still controversial, multiple wandering reentry is considered the primary mechanism in most AF. It has been suggested that prolongation of the wavelength would make it impossible for the reentry to continue and would lead to the termination of the AF. In the present study a dynamic fluctuation in the electrophysiological properties was observed with procainamide infusion during AF. In 12 patients, both the local electrogram and monophasic action potentials (MAP) during AF were recorded from the right atrium before, during and after infusion of procainamide (10 mg/kg). The minimum AF cyclelength (CLmin), MAP duration at 90% repolarization (MAPD90) and widths of the intraatrial potentials (WAP) were measured with custom-made computer software. The conduction velocity index (CVI) was determined from the WAP. The wavelength index (WLI=CVIxCLmin) and postrepolarization refractoriness (PRR= CLmin-MAPD90) were calculated. In 6 patients, AF was terminated by procainamide infusion (group A), but not in the other 6 patients (group B). Group A patients showed a biphasic change in the parameters following procainamide infusion. In phase I, the CLmin, MAPD90 and PRR increased, while the CVI decreased, and the WLI remained unchanged. In phase II, the PRR, CVI and WLI increased and the AF was terminated. No restoration of the CVI nor increase in the WLI were observed in group B. The biphasic fluctuation in the CVI and the remarkable increase of the PRR and WLI were observed before termination of AF by procainamide infusion. (+info)Amitriptyline and procainamide inhibition of cocaine and cocaethylene degradation in human serum in vitro. (2/188)
Amitriptyline (AMI) and procainamide (PA) have been reported to inhibit the activity of human plasma butyrylcholinesterase, an enzyme important in the metabolic degradation of cocaine (COC) and its ethyl analogue cocaethylene (CE). Because both AMI and PA may be used in the treatment of COC intoxication and abuse, the effect of high pharmacological concentrations of these compounds on the degradation of COC and CE in pooled human serum was studied. AMI (1.8 micromol/L) modestly inhibited the degradation of COC by 4.2% and of CE by 4.0%. PA (42.5 micromol/L) profoundly inhibited degradation of COC by 42.7% and of CE by 47.2%. In contrast, lithium carbonate (1 mmol/L, control) showed no inhibition of degradation of either COC or CE. These results suggest that AMI and PA may prolong the half-life of COC and CE in human serum. (+info)Doppler sonographic evaluation of left atrial function after cardioversion of atrial fibrillation. (3/188)
Restoration of sinus rhythm is not always followed by immediate return of effective atrial contraction. Left atrial mechanical function can be assessed by Doppler echocardiography; in the present study we measured the atrial ejection force, which is a noninvasive Doppler-derived parameter that measures the strength of atrial contraction. The aim of the present study was to evaluate the influence of clinical and echocardiographic parameters: duration and cause of atrial fibrillation, different modality of cardioversion, and left atrial size with respect to the delay in the return of effective atrial contraction after cardioversion. Seventy patients were randomly chosen to undergo cardioversion by either direct current shock or intravenously administered procainamide hydrochloride. The 52 patients who had sinus rhythm restored underwent a complete Doppler echocardiographic examination 1 h after the restoration of sinus rhythm and after 1 day, 7 days, and 1 month. The relation between clinical variables and atrial ejection force was tested. Atrial ejection force was greater immediately and 24 h after cardioversion in patients who underwent pharmacologic therapy compared to patients treated with direct current shock (11.3+/-3 versus 5+/-2.9 dynes; P<0.001). In both groups atrial ejection force increased over time. The mode of cardioversion was significantly associated with recovery of left atrial mechanical function by day 1 in univariate and multivariate analysis (odds ratio, 0.14; 95% confidence interval, 0.02-1.2). The other variable associated with the delay in the recovery of atrial function was a dilated left atrium (odds ratio, 0.16; 95% confidence interval, 0.12-1.6). Atrial ejection force is a noninvasive parameter that can be easily measured after cardioversion and gives accurate information about the recovery of left atrial mechanical function. The recovery of left atrial function was influenced by the mode of cardioversion and left atrial size. (+info)Electrical restitution and spatiotemporal organization during ventricular fibrillation. (4/188)
Despite recent advances in our understanding of the mechanism for ventricular fibrillation (VF), important electrophysiological aspects of the development of VF still are poorly defined. It has been suggested that the onset of VF involves the disintegration of a single spiral wave into many self-perpetuating waves. It has been further suggested that such a process requires that the slope of the electrical restitution relation be >/=1. The same theory anticipates that a single spiral wave will be stable (not disintegrate) if the maximum slope of the restitution relation is <1. We have shown previously that the slope of the restitution relation during rapid pacing and during VF is >/=1 in canine ventricle. We now show that drugs that reduce the slope of the restitution relation (diacetyl monoxime and verapamil) prevent the induction of VF and convert existing VF into a periodic rhythm. In contrast, a drug that does not reduce the slope of the restitution relation (procainamide) does not prevent the induction of VF, nor does it regularize VF. These results indicate that the kinetics of electrical restitution is a key determinant of VF. Moreover, they suggest novel approaches to preventing the induction or maintenance of VF. (+info)Procainamide inhibition of human hepatic degradation of cocaine and cocaethylene in vitro. (5/188)
Procainamide (PA), a cardioactive drug, inhibited the degradation of both cocaine (COC) and cocaethylene (CE) when either was incubated in human liver homogenates for 3 h at 37 degrees C. PA appeared to enhance the formation of CE when COC and ethanol (ETOH) were incubated together in liver homogenate. These observations are clinically significant because cardiotoxicity is common after COC abuse and because PA may be administered to individuals who use COC alone and with ETOH. (+info)Inhibitory effects of procainamide on rabbit platelet aggregation and thromboxane B2 production in vitro. (6/188)
AIM: To study the influences of procainamide (PA) on thrombin-induced rabbit platelet aggregation and thromboxane B2 (TXB2) production in vitro. METHODS: Turbidimetry and radioimmunoassay were used. RESULTS: PA 8.5, 34, 136, and 544 mumol.L-1 inhibited thrombin-induced platelet aggregation and TXB2 production, and the inhibitory rates were 45% +/- 37%, 48% +/- 32%, 88% +/- 23%, 92% +/- 15% and 53% +/- 24%, 65% +/- 26%, 90% +/- 6%, 95% +/- 6%, respectively. There was positive correlation between PA concentration and efficiency of inhibition of platelet aggregation and TXB2 production, and also between the inhibition % of platelet aggregation and that of production of TXB2. The three linear equations and main parameters were Y = 0.2075X-4.9157, r = 0.9985; Y = 0.9546X-34.6724, r = 0.9921; Y = 0.8202X + 19.7062, r = 0.9921. CONCLUSION: PA inhibited thrombin-induced platelet aggregation and TXB2 production in rabbits. (+info)Effect of procainamide on ultrastructure of blood platelet in rabbits. (7/188)
AIM: To study the effect of procainamide (PA) on the ultrastructure of blood platelets. METHODS: Arachidonic acid was added to PA-treated platelet-rich plasma to induce platelet aggregation. The 50-nm sections were examined with a transmission electron microscope. RESULTS: PA 8.5-136 mumol.L-1 markedly inhibited changes of pseudopods, alpha-granules, dense granules, glycogens, open canalicular system, and dense tubular system. CONCLUSION: PA markedly inhibited the changes of ultrastructure of blood platelet and releasing response. (+info)Mechanism of procainamide-induced prevention of spontaneous wave break during ventricular fibrillation. Insight into the maintenance of fibrillation wave fronts. (8/188)
BACKGROUND: Ventricular fibrillation (VF) is maintained by 2 mechanisms: first by reentry formation and second by spontaneous wave break or wave splitting. We hypothesized that spontaneous wave break results from a critical shortening of the action potential duration (APD) during VF and that its prevention by procainamide eliminates spontaneous wave break. METHODS AND RESULTS: The endocardial surfaces of 7 isolated, perfused swine right ventricles were mapped with a 3.2x3.8 cm plaque with 477 bipolar electrodes. Activation pattern during VF was visualized dynamically while simultaneously recording epicardial action potentials with a glass microelectrode. APD restitution curves were constructed during VF (dynamic) and during S(1)S(2) protocols. At baseline, VF was maintained by 5.3+/-1 wavelets. Procainamide (PA) at 10 microgram/mL decreased the number of wavelets to 3.5+/-1 (P<0.05). At baseline VF was maintained by spontaneous wave break and by new reentrant wave front formation. PA eliminated spontaneous wave break during VF while having no effect on reentry formation. PA increased the cycle length of the VF (148.5+/-41.2 ms vs 81+/-10 ms, P<0.01) and the core area of the reentry from 5.8 to 14.5 mm(2) (P<0.05). Dynamic APD restitution curve during VF showed that PA eliminated the initiation of activation with APDs shorter than 30 ms. The effects of PA on cellular properties and wave front dynamics were reversed during 60 minutes of drug-free perfusion. CONCLUSIONS: Critically short APDs during VF promote spontaneous wave break. Their elimination with PA, however, maintains VF by generating new reentrant wave front. (+info)Procainamide is an antiarrhythmic medication used to treat various types of irregular heart rhythms (arrhythmias), such as atrial fibrillation, atrial flutter, and ventricular tachycardia. It works by prolonging the duration of the cardiac action potential and decreasing the slope of the phase 0 depolarization, which helps to stabilize the heart's electrical activity and restore a normal rhythm.
Procainamide is classified as a Class Ia antiarrhythmic drug, according to the Vaughan Williams classification system. It primarily affects the fast sodium channels in the heart muscle cells, reducing their availability during depolarization. This results in a decreased rate of impulse generation and conduction velocity, which can help to suppress abnormal rhythms.
The medication is available as an oral formulation (procainamide hydrochloride) and as an injectable solution for intravenous use. Common side effects of procainamide include nausea, vomiting, diarrhea, headache, and dizziness. Procainamide can also cause a lupus-like syndrome, characterized by joint pain, skin rashes, and other autoimmune symptoms, in some patients who take the medication for an extended period.
It is essential to monitor procainamide levels in the blood during treatment to ensure that the drug is within the therapeutic range and to minimize the risk of adverse effects. Healthcare providers should also regularly assess patients' renal function, as procainamide and its active metabolite, N-acetylprocainamide (NAPA), are primarily excreted by the kidneys.
Acecainide is a Class IC antiarrhythmic drug that was used to treat certain types of irregular heart rhythms (ventricular arrhythmias). It works by blocking the signals that cause the heart to beat irregularly. However, acecainide is no longer available in the market due to its potential to cause serious side effects, including a decreased survival rate in patients with heart disease.
Anti-arrhythmia agents are a class of medications used to treat abnormal heart rhythms or arrhythmias. These drugs work by modifying the electrical activity of the heart to restore and maintain a normal heart rhythm. There are several types of anti-arrhythmia agents, including:
1. Sodium channel blockers: These drugs slow down the conduction of electrical signals in the heart, which helps to reduce rapid or irregular heartbeats. Examples include flecainide, propafenone, and quinidine.
2. Beta-blockers: These medications work by blocking the effects of adrenaline on the heart, which helps to slow down the heart rate and reduce the force of heart contractions. Examples include metoprolol, atenolol, and esmolol.
3. Calcium channel blockers: These drugs block the entry of calcium into heart muscle cells, which helps to slow down the heart rate and reduce the force of heart contractions. Examples include verapamil and diltiazem.
4. Potassium channel blockers: These medications work by prolonging the duration of the heart's electrical cycle, which helps to prevent abnormal rhythms. Examples include amiodarone and sotalol.
5. Digoxin: This drug increases the force of heart contractions and slows down the heart rate, which can help to restore a normal rhythm in certain types of arrhythmias.
It's important to note that anti-arrhythmia agents can have significant side effects and should only be prescribed by a healthcare professional who has experience in managing arrhythmias. Close monitoring is necessary to ensure the medication is working effectively and not causing any adverse effects.
Quinidine is a Class IA antiarrhythmic medication that is primarily used to treat and prevent various types of cardiac arrhythmias (abnormal heart rhythms). It works by blocking the rapid sodium channels in the heart, which helps to slow down the conduction of electrical signals within the heart and stabilize its rhythm.
Quinidine is derived from the bark of the Cinchona tree and has been used for centuries as a treatment for malaria. However, its antiarrhythmic properties were discovered later, and it became an important medication in cardiology.
In addition to its use in treating arrhythmias, quinidine may also be used off-label for other indications such as the treatment of nocturnal leg cramps or myasthenia gravis. It is available in various forms, including tablets and injectable solutions.
It's important to note that quinidine has a narrow therapeutic index, meaning that there is only a small difference between an effective dose and a toxic one. Therefore, it must be carefully monitored to ensure that the patient is receiving a safe and effective dose. Common side effects of quinidine include gastrointestinal symptoms such as nausea, vomiting, and diarrhea, as well as visual disturbances, headache, and dizziness. More serious side effects can include QT prolongation, which can lead to dangerous arrhythmias, and hypersensitivity reactions.
Disopyramide is an antiarrhythmic medication that is primarily used to treat certain types of irregular heart rhythms (arrhythmias), such as ventricular tachycardia and atrial fibrillation. It works by blocking the activity of sodium channels in the heart, which helps to slow down and regulate the heart rate.
Disopyramide is available in immediate-release and extended-release forms, and it may be taken orally as a tablet or capsule. Common side effects of this medication include dry mouth, blurred vision, constipation, and difficulty urinating. More serious side effects can include dizziness, fainting, irregular heartbeat, and allergic reactions.
It is important to take disopyramide exactly as directed by a healthcare provider, as improper use or dosing can lead to serious complications. Additionally, individuals with certain medical conditions, such as heart failure, kidney disease, or myasthenia gravis, may not be able to safely take this medication.
Propafenone is an antiarrhythmic medication used to treat certain types of irregular heartbeats (such as atrial fibrillation, paroxysmal supraventricular tachycardia). It works by blocking certain electrical signals in the heart to help it beat regularly. Propafenone belongs to a class of drugs known as Class IC antiarrhythmics.
It is important to note that this definition provides an overview of what propafenone is and how it is used, but it does not cover all possible uses, precautions, side effects, and interactions related to the drug. For more detailed information about propafenone, including its specific indications, contraindications, and potential adverse effects, consult a reliable medical reference or speak with a healthcare professional.
Procainamide
Disopyramide
Sodium channel blocker
Kamala Balakrishnan
Cardioversion
Acecainide
Ebstein's anomaly
Ventricular tachycardia
Drug-induced lupus erythematosus
Bernard Beryl Brodie
Wolff-Parkinson-White syndrome
N-acetyltransferase
Aconitum carmichaelii
Aconitum
Aconitum coreanum
Aconitum napellus
Management of atrial fibrillation
Sergio Erill
Boxer cardiomyopathy
Cimetidine
Loading dose
Antinuclear antibody
Diltiazem
Lupus
Atrial fibrillation
Torsades de pointes
Tachycardia-dependent bundle branch block
Myotonia congenita
Cardiology
Adverse drug reaction
Procainamide - Wikipedia
Procainamide (Intravenous Route) Description and Brand Names - Mayo Clinic
Trimethoprim alters the disposition of procainamide and N-acetylprocainamide
PROCAINAMIDE HYDROCHLORIDE - Books - NCBI
procainamide, Pronestyl; Procan-SR; Procanbid Side Effects - Hdkino.org
Procanbid, Pronestyl (procainamide) dosing, indications, interactions, adverse effects, and more
Anti-Procainamide Antibody (16709) - QED Bioscience Inc
Procainamide : Overview, Uses, Side Effects, Precautions - illness.com
Procainamide Hydrochloride | CartPharmacy.Com
Procainamide - SPS - Specialist Pharmacy Service - The first stop for professional medicines advice
Procainamide (Pronestyl) | Davis's Drug Guide
APO-PROCAINAMIDE 375MG - ADV Pharmacy
Procainamide in Horses (Equis) | Vetlexicon
emDOCs.net - Emergency Medicine EducationAmiodarone vs Procainamide for Stable VT - emDOCs.net - Emergency Medicine Education
Atrial Tachycardia Medication: Beta Blockers, Intrinsic Sympathomimetic, Beta-Blockers, Beta-1 Selective, Beta Blockers,...
Procainamide Level: Reference Range, Interpretation, Collection and Panels
Procainamide: Uses, Interactions, Mechanism of Action | DrugBank Online
The EKG in the patient treated with procainamide - wikidoc
Procainamide Hydrochloride Suspension 50 mg/mL in: Extemporaneous Formulations
procainamide Hydrochloride Injection, USP () Dosage and Administration | Pfizer Medical Information - US
Nexus Pharmaceuticals Receives FDA Approval for Procainamide HCL Injection | Nexus Pharmaceuticals
Procainamide - SPS - Specialist Pharmacy Service - The first stop for professional medicines advice
Anti-Arrhythmics - GlobalRPH
MiraLAX: Dosage, side effects, uses, and more
Table of Pharmacogenetic Associations | FDA
Foscarnet Injection: MedlinePlus Drug Information
Protocols for E0577 | NEB
Pharmacokinetics and pharmacodynamics of procainamide1
- The steady-state pharmacokinetics and pharmacodynamics of procainamide and its active N-acetyl metabolite (NAPA) were assessed alone and in combination with trimethoprim. (nih.gov)
Sustained-release procainamide2
- Eight healthy men received oral sustained-release procainamide, 500 mg every 6 hours for 3 days, alone and with oral trimethoprim, 200 mg daily for 4 days. (nih.gov)
- For this reason, patients on sustained-release procainamide get a complete blood count test ( CBC ) every 2 weeks for the first 3 months of treatment. (hdkino.org)
Arrhythmias11
- Procainamide (PCA) is a medication of the antiarrhythmic class used for the treatment of cardiac arrhythmias. (wikipedia.org)
- Procainamide is used for treating ventricular arrhythmias: ventricular ectopy and tachycardia and supraventricular arrhythmias: atrial fibrillation, and re-entrant and automatic supraventricular tachycardia. (wikipedia.org)
- Description Procainamide is an antiarrhythmic used to treat cardiac arrhythmias. (qedbio.com)
- Procainamide Hydrochloride is a tablet medication used for the treatment of supraventricular and ventricular arrhythmias. (cartpharmacy.com)
- Procainamide is a class 1a antiarrhythmic that is used to treat various ventricular and atrial arrhythmias. (medscape.com)
- Procainamide is a medication used to treat life threatening ventricular arrhythmias. (drugbank.com)
- Procainamide Hydrochloride Injection is useful for arrhythmias which require immediate suppression and for maintenance of arrhythmia control. (pfizermedicalinformation.com)
- Oral procainamide dosage forms are preferable for less urgent arrhythmias as well as for long-term maintenance after initial parenteral PA therapy. (pfizermedicalinformation.com)
- Procainamide hydrochloride injection is indicated for the treatment of documented ventricular arrhythmias, such as sustained ventricular tachycardia, that, in the judgement of the physician, are life-threatening. (nexuspharma.net)
- Because of the proarrhythmic effects of procainamide, its use with lesser arrhythmias is generally not recommended. (nexuspharma.net)
- Procainamide is a medication for cardiac arrhythmias. (fingerlakes1.com)
Amiodarone vs Procainamide1
- Ortiz and colleagues [ 2 ] sought to compare the efficacy of amiodarone vs procainamide in patients with hemodynamically stable, regular WCT. (medscape.com)
Concentration of procainamide2
- With increasing concentration of procainamide, the frequency of long blockage becomes less without the duration of blockage being affected. (wikipedia.org)
- The therapeutic concentration of procainamide is 4-8 µg/mL. (medscape.com)
Quinidine3
- The mode of action of the antiarrhythmic effect of Procainamide appears to be similar to that of procaine and quinidine. (drugbank.com)
- Patients with ongoing proarrhythmic conditions such as uncorrected hypokalemia or hypomagnesemia, clinically significant bradycardia, and in patients receiving Class IA (quinidine, procainamide) or Class III (dofetilide, amiodarone, sotalol) antiarrhythmic agents. (cdc.gov)
- Currently, with the exception of ciprofloxacin, each of these quinolones contains labeling guidance in the form of a warning (gatifloxacin, moxifloxacin) or a precaution (levofloxacin), and concurrent use with class IA (e.g., quinidine, procainamide) or class III (e.g., amiodarone, sotalol) antiarrhythmics should be avoided to reduce the risk of torsades de pointes per current product labeling. (cdc.gov)
Torsade de poin1
- Procainamide is contraindicated in conditions with preexisting QT prolongation, torsade de pointes, second- or third-degree heart block without pace maker placement, or history of hypersensitivity reaction to procainamide. (medscape.com)
Hydrochloride Injection1
- If daily total fluid intake must be limited, a 4 mg/mL concentration (1 g of Procainamide Hydrochloride Injection in 250 mL of 5% Dextrose Injection, USP) administered at 0.5 to 1.5 mL/minute will deliver an equivalent 2 to 6 mg per minute. (pfizermedicalinformation.com)
Atrial fibrillation2
- Some indications for the use of procainamide include atrial premature contractions, premature ventricular contractions, ventricular tachycardia, paroxysmal atrial tachycardia, and maintenance of a normal sinus rhythm after conversion from atrial fibrillation/flutter. (medscape.com)
- [ 7 ] For treatment and conversion of stable narrow complex atrial fibrillation as well, procainamide has received strong support and is commonly used in Canada. (medscape.com)
Drugs4
- Which drugs or supplements interact with procainamide? (hdkino.org)
- tell your doctor and pharmacist if you are allergic to procainamide, anesthetics, aspirin , or any other drugs. (illness.com)
- Some drugs (eg, hydralazine , procainamide , isoniazid , anti-tumor necrosis factor [TNF] drugs) cause a reversible lupus-like syndrome. (merckmanuals.com)
- None were taking bolic pathway in the biotransformation of drugs that would interfere with acetylation a number of drugs such as procainamide, nor were any on any drugs known to be hydralazine, sulphonamides, isoniazide and polymorphically N-acetylated. (who.int)
Antiarrhythmic drug2
- It was also detected that the antiarrhythmic drug procainamide interferes with pacemakers. (wikipedia.org)
- Procainamide is an injectable antiarrhythmic drug that is used to correct disturbances in the heart 's rhythm. (hdkino.org)
Acetylation2
- Most of these side effects may occur due to the acetylation of procainamide. (wikipedia.org)
- After trimethoprim coadministration, there was also a trend toward a decrease in the apparent acetylation clearance of procainamide (19%, p = 0.057). (nih.gov)
Concentrations3
- We conclude that trimethoprim increases the plasma concentrations of procainamide and NAPA by decreasing their renal clearances and allowing more conversion of procainamide to NAPA. (nih.gov)
- Amiodarone ( Cordarone ) increases the blood concentrations of procainamide by either decreasing the kidneys or the liver's abilities to remove procainamide. (hdkino.org)
- It is advisable to dilute either the 100 mg/mL or the 500 mg/mL concentrations of procainamide hydrochloride prior to intravenous injection to facilitate control of dosage rate. (pfizermedicalinformation.com)
Dofetilide1
- procainamide, dofetilide. (medscape.com)
Sodium2
- Procainamide is also known to induce a voltage-dependent open channel block on the batrachotoxin (BTX)-activated sodium channels in cardiomyocytes. (wikipedia.org)
- Procainamide is sodium channel blocker. (drugbank.com)
Ventricular tachycardia1
- Procainamide is an agent indicated for production of local or regional anesthesia and in the treatment of ventricular tachycardia occurring during cardiac manipulation, such as surgery or catheterization, or which may occur during acute myocardial infarction, digitalis toxicity, or other cardiac diseases. (drugbank.com)
Mechanism of act1
- What is procainamide, and how does it work (mechanism of action)? (hdkino.org)
Medication1
- Procainamide Hydrochloride is an FDA-approved medication that works by lessening the sensitivity of heart muscle cells to electrical impulses. (cartpharmacy.com)
Conduction3
- A toxic level of procainamide leads to decrease in ventricular conduction velocity and increase of the ventricular refractory period. (wikipedia.org)
- Procainamide slows the conduction velocity and increases the refractory period, such that the maximal rate of depolarization is reduced. (wikipedia.org)
- Procainamide decreases the speed of electrical conduction through the heart muscle, prolongs the electrical phase during which the heart's muscle cells can be electrically stimulated, and prolongs the recovery period during which the heart muscle cells cannot be stimulated. (hdkino.org)
Trimethoprim3
- Concomitant trimethoprim significantly increased the plasma AUC(0-12) of both procainamide and NAPA (63% and 52%, respectively), with concurrent decreases in their renal clearances (47% and 13%, respectively) and a 39% increase in the mean urinary recovery of NAPA (as percentage of procainamide and NAPA recovery). (nih.gov)
- The change in procainamide and NAPA renal clearances after trimethoprim coadministration strongly correlated with their baseline renal clearances (r = 0.84 and r = 0.74, respectively, p less than 0.0001). (nih.gov)
- There was small but significant increase in the corrected QT interval with procainamide administration, which increased further with trimethoprim coadministration. (nih.gov)
Precautions1
- What are the precautions in taking Procainamide Hydrochloride? (cartpharmacy.com)
Hydroxylamine3
- Many symptoms resemble systemic lupus erythematosus because procainamide reactivates hydroxylamine and nitroso metabolites, which bind to histone proteins and are toxic to lymphocytes. (wikipedia.org)
- These leukocytes release myeloperoxidase and hydrogen peroxide, which oxidize the primary aromatic amine of procainamide to form procainamide hydroxylamine. (wikipedia.org)
- Procainamide hydroxylamine has more cytotoxicity by hindering the response of lymphocytes to T-cell and B-cell mitogens. (wikipedia.org)
Intravenous dose1
- A period of about three to four hours (one half-time for renal elimination, ordinarily) should elapse after the last intravenous dose before administering the first dose of Procainamide Hydrochloride tablets or capsules. (pfizermedicalinformation.com)
Leukopenia2
- Procainamide could initiate leukopenia and/or agranulocytosis, which are serious hematologic disorders, and is also known for causing gastrointestinal disturbances and aggravating pre-existing abnormalities in impulse initiation and propagation. (wikipedia.org)
- Procainamide should be discontinued if leukopenia is noted. (medscape.com)
Increases2
- fingolimod increases effects of procainamide by pharmacodynamic synergism. (medscape.com)
- goserelin increases toxicity of procainamide by QTc interval. (medscape.com)
Adenosine1
- In the United States, there are 5 readily available options in every hospital's formulary - amiodarone, procainamide, lidocaine, adenosine, and propofol (i.e. electricity) . (emdocs.net)
Ranitidine1
- Procainamide and ranitidine have a negative interaction that can worsen procainamide's side effects. (fingerlakes1.com)
Dosage1
- What is the dosage for procainamide? (hdkino.org)
Toxic1
- As with procainamide, the toxic concentration of NAPA is 16 µg/mL or greater, although symptoms may develop at 8-10 µg/mL. (medscape.com)
Interval3
- amiodarone and procainamide both increase QTc interval. (medscape.com)
- haloperidol and procainamide both increase QTc interval. (medscape.com)
- In normal procainamide typically produces a 10% to 20% increase in the HV interval. (wikidoc.org)
Adverse3
- The risk or severity of adverse effects can be increased when Procainamide is combined with Acetylcholine. (drugbank.com)
- This RCT of patients with tolerated wide complex tachycardia found that IV Procainamide (10 mg/kg IV over 20 minutes) was better than IV Amiodarone (5 mg/kg over 20 minutes): less major cardiac adverse events, more efficacious in terminating tachycardia, and more efficacious in both endpoints in patients with structural heart disease. (emottawablog.com)
- In the following 24 hours, adverse events occurred in 31% of the amiodarone group vs 18% of the procainamide group. (medscape.com)
Injection7
- Procainamide injection is used to treat irregular heartbeats and to slow an overactive heart. (mayoclinic.org)
- b) Alternatively, a loading infusion containing 20 mg of Procainamide Hydrochloride per mL (1 g diluted to 50 mL with 5% Dextrose Injection, USP) may be administered at a constant rate of 1 mL per minute for 25 to 30 minutes to deliver 500 to 600 mg of PA. (pfizermedicalinformation.com)
- To maintain therapeutic levels, a more dilute intravenous infusion at a concentration of 2 mg/mL is convenient (1000 mg procainamide HCl in 500 mL of 5% Dextrose Injection, USP), and may be administered at 1 to 3 mL/minute. (pfizermedicalinformation.com)
- Vernon Hills, Ill., Oct. 19, 2017 - Nexus Pharmaceuticals announced today the immediate availability in the United States of Procainamide HCL Injection, USP. (nexuspharma.net)
- Nexus Pharmaceuticals' Procainamide HCL Injection, USP is available as a multi dose vial containing 1,000 mg per 2 mL (500 mg/mL) or as a multi dose vial containing 1,000 mg per 10 mL (100 mg/mL) and is an AP Rated generic equivalent. (nexuspharma.net)
- Procainamide HCL Injection, USP is currently listed on the FDA Drug Shortage Database. (nexuspharma.net)
- The introduction of Procainamide HCL Injection, USP further illustrates Nexus Pharmaceuticals' commitment to meeting market needs and shortages in the short term, while broadening the availability of effective generic products for the long term," said Mariam Darsot, President of Nexus Pharmaceuticals Inc. (nexuspharma.net)
Lupus1
- A syndrome resembling lupus erythematosus, including fever , chills , joint pain , chest pain , and/or skin rash can occur with procainamide. (hdkino.org)
Antibodies1
- Application Instructions These antibodies have been qualified for use in ELISA to detect procainamide. (qedbio.com)
Dose1
- levels of both procainamide and NAPA are typically checked before the administration of the second dose. (medscape.com)
Side effects5
- There are many side effects following the induction of procainamide. (wikipedia.org)
- What are the side effects of procainamide? (hdkino.org)
- Procainamide may cause side effects. (illness.com)
- When procainamide levels become supratherapeutic, the risk of the drug's side effects becomes increased (see Background). (medscape.com)
- When the level of procainamide or NAPA becomes supratherapeutic, the risk of the drug's side effects becomes increased. (medscape.com)
Decrease1
- Abacavir may decrease the excretion rate of Procainamide which could result in a higher serum level. (drugbank.com)
Allergic1
- Procainamide may also lead to drug fever and other allergic responses. (wikipedia.org)
Generic1
- Is procainamide available as a generic drug? (hdkino.org)
NAPA2
- Procainamide and its breakdown product, N-acetylprocainamide (NAPA), are both powerful antiarrhythmics that necessitate careful monitoring. (medscape.com)
- Procainamide is converted by the liver to its breakdown product N-acetylprocainamide (NAPA), which is also an active antiarrhythmic compound. (medscape.com)
Abnormal1
- Procainamide is used to treat abnormal heart rhythms. (illness.com)
Infusion1
- 8. Subjects who are anticipated to receive infusion of blood or blood products, chemotherapeutic agents, hypertonic solutions, caustic agents or any agents known to harm bone marrow or cause bone marrow suppression such as azathioprine, procainamide, sulfasalazine via the test device. (who.int)
Drug4
- Anesthesia Central , anesth.unboundmedicine.com/anesthesia/view/Davis-Drug-Guide/51633/11.0/procainamide. (unboundmedicine.com)
- The administration of procainamide known to impair the HPS can unmask extraordinary sensitivity to the usual therapeutic doses of the drug, which can itself indicate poor HPS reserve. (wikidoc.org)
- The most recent study [ 2 ] of amiodarone vs the older drug procainamide has perhaps added one more nail in amiodarone's coffin. (medscape.com)
- Admittedly, procainamide is not a perfect drug either. (medscape.com)
Increase2
- Procainamide may increase the arrhythmogenic activities of Acebutolol. (drugbank.com)
- Acetazolamide may increase the excretion rate of Procainamide which could result in a lower serum level and potentially a reduction in efficacy. (drugbank.com)
Typically1
- When procainamide is given in a hospital setting, it is typically given either intravenously or intramuscularly. (medscape.com)
Prospective2
- Unfortunately, there are no prospective, randomized, head-to-head trials comparing amiodarone to procainamide. (emdocs.net)
- Although this is the first controlled prospective trial comparing procainamide vs amiodarone, this is not the first study that has cast doubt on the effectiveness of amiodarone in WCTs. (medscape.com)
Class2
- Currently, the AHA has it riding shotgun (with procainamide driving) with a Class IIb recommendation (1). (emdocs.net)
- Procainamide is a Class Ia antiarrhythmic agent. (emdocs.net)
Brand Names1
- What brand names are available for procainamide? (hdkino.org)
Works2
- Procainamide works as an anti-arrhythmic agent and is used to treat cardiac arrhythmia. (wikipedia.org)
- Procainamide works by slowing the nerve impulses in the heart and reducing the sensitivity of heart tissues. (mayoclinic.org)