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Procainamide

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143. Perioperative Beta Blockade in Noncardiac Surgery: A Systematic Review for the 2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery

was not deemed to be at high risk of bias for any assessed domain of study quality. Statistical Analysis Analyses were performed in STATA Version 13 statistical software (StataCorp LP, College Station, Texas). Statistical significance was defined by a 2-tailed p value 18 y of age undergoing major thoracic operation Prior beta-blocker use, asthma, HF, heart block, supraventricular tachyarrhythmias, prior specific drug use (digoxin, quinidine, procainamide, amiodarone, diltiazem, verapamil) Intrathoracic (100

2014 Society for Cardiovascular Angiography and Interventions

144. Boulware

: initially due to poor access to prompt testing, enrolment was on the basis of exposure to patients with pending test results. However, after March 23, the exposure had to be to a patient with confirmed PCR positive for SARS-CoV-2 Exclusion : <18 years Already taking hydroxychloroquine or chloroquine Already taking cardiac medicines: flecainide; amiodarone; digoxin; procainamide; or sotalol Already taking QT prolonging medicines hydroxychloroquine allergy Retinal eye disease G6PD deficiency CKD 4 or 5

2020 The Bottom Line

145. Geriatric Trauma Management

, Ic, III) z Amiodarone z Dofetilide z Dronedarone z Flecainide z Ibutilide z Procainamide z Propafenone z Quinidine z Sotalol Data suggest that rate control yields better balance of benefits and harms than rhythm control for most older adults Amiodarone is associated with multiple toxicities, including thyroid disease, pulmonary disorders, and QT interval prolongation Avoid antiarrhythmic drugs as first- line treatment of atrial fibrillation High Strong Disopyramide* Disopyramide is a potent

2013 American College of Surgeons

146. An unstable wide complex tachycardia resistant to electrical cardioversion

would have taken him to cath lab for temporary pacemaker and 'pace-termination' before considering procainamide (of course depending on hemodynamics at the moment)." -- Procainamide may work if the above do not, but is especially hazardous with decreased LV function and should be given very slowly, if at all. Give 20 mg/min to a total of 15 mg/kg until the arrhythmia terminates, the BP drops, or the QRS is prolonged by more than 50%. Procainamide slows the VT rate and though it often causes (...) like amiodarone, it is relatively contraindicated. And you can't measure the QT while the patient is still in VT! AHA guidelines: (Full text) Learning Points: 1. Learn to identify VT 2. Adenosine will not work for this VT. 3. Cardiovert unstable VT at 200 J biphasic 4. If no conversion, or if reversion, use amiodarone 5. If amio does not work, try lidocaine 6. Consider beta blockade. 7. Consider pacing termination 8. Only then consider procainamide, as it is particularly hazardous. Stable VT Here

2017 Dr Smith's ECG Blog

147. What happens when you give adenosine to a patient with this rhythm?

be anywhere between 240 and 360. The ventricular rate depends on AV node conduction and is usually half the atrial rate (2:1 conduction), but may become 1:1 (dangerous) or slow down to less than 2:1 in the presence of AV node blockers The atrial rate can be much slower in the setting of a sodium channel blocker such as flecainide, quinidine, or procainamide. Use of these medications without prior AV blockade is dangerous as it will lead to 1:1 conduction!! Atrial Flutter --Macro re-entrant loop just above (...) AV Node in right atrium --Atrial rate 240-360 without medications --2:1 block, vent rate 150 most common --Regular, fixed; or regularly irregular: RR interval an integer multiple of the atrial rate --Narrow if no aberrancy or bundle branch block --Flutter waves, sawtooth pattern--Nearly always visible in lead II --Adenosine can help to diagnose, not treat --Conversion vs. Ventricular slowing l50 Joules, Ibutilide/Amiodarone lDiltiazem slows at AV node Procainamide before Diltiazem is dangerous

2017 Dr Smith's ECG Blog

148. What is the cause of this patient's inferior ST depressions?

the ventricular rate of Aflutter with an agent like procainamide? It is ONLY in flutter that a rhythm control drug can paradoxically increase the ventricular rate. Is that what you are referring to? Would performing a Lewis Lead show the atrial activity more clearly? Lewis leads show sinus P-wave more clearly. Uncertain if they will show these flutter waves more clearly because the recording appears to already be at the optimal angle for highest possible amplitude. Dear colleague Could it be the same case

2017 Dr Smith's ECG Blog

149. Wide Complex Tachycardia: is the patient stable or unstable?

reccurr but if it did what would be the drug of choise ?? Procainamide would be supported by the currently held physiology and the AHA/ACC guidelines in this case. Ibutilide is also listed with the same level of recommendation in our guidelines (Class I, Level C-LD: very low level of evidence, but supposedly more than just expert opinion), but unless I'm mistaken this drug is more expensive and less commonly used. Electricity is clearly not going to be effective long term if the rhythm is re

2017 Dr Smith's ECG Blog

150. A Healthy 50-something with new dyspnea on exertion and an interesting ECG

antidysrhythmics such as procainamide, quinidine, disopyramide and also type 1c such as flecainide. d. Myocardial infarction, acute or old . ----When anterior MI, then it is below the AV node (bundle branch or fascicle) and more dangerous. ----When inferior MI, it is the AV node that is ischemic. It is less likely to progress to complete AV block and more likely to be sensitive to atropine. e. Underlying AV nodal structural abnormalities f. Infiltrative diseases such as sarcoidosis, amyloidosis

2017 Dr Smith's ECG Blog

151. Wide complex tachycardia at a rate of 270

, increased sympathetic tone also increases AV conduction (makes it more "slick," or "greasy"). This could counteract the faster atrial rate and prevent the slowing of the ventricular rate. Why is this concept important for us? If you see a patient with atrial flutter with 2:1 conduction and you want to convert the atrial flutter chemically with, for instance, procainamide (or any other type 1 antidysrhythmic), you could convert to 1:1 conduction. How? Procainamide is used to convert flutter to sinus (...) , but before conversion (or if it is ineffective), it will cause the atrial flutter rate to slow to a rate that makes 1:1 AV conduction possible. You will have made the situation worse. Therefore : If you ever want to convert atrial flutter by giving procainamide or any other Type 1 antidysrhythmic, you MUST give an AV nodal blocker first , or you will make the patient worse. I always use electricity to convert atrial flutter. It is safer. Similarly : Any patient who is started on a Type 1 antidysrhythmic

2017 Dr Smith's ECG Blog

152. Test almost all of your most important ECG rhythm interpretation skills with this case.

with management that is based on acknowledging both possibilities simultaneously. Options for this patient with wide complex regular tachycardia and some signs of hemodynamic compromise but not peri-arrest include: Immediate attempted intervention on the rhythm: - Synchronized electrical cardioversion - Adenosine and/or vagal maneuvers - Medical cardioversion (procainamide, amiodarone, etc) These options all incur some small risk (sedation for cardioversion, very small risk of deterioration in rhythm (...) with adenosine, hypotension or rhythm deterioration with amiodarone/procainamide), while having the potential benefits of cardioversion (if the rhythm is not Sinus Tach) and further diagnostic information for the rhythm. Observe the patient on NTG drip and BiPAP for a short time (~10 minutes at bedside): Observe for improvement with the current ongoing interventions, more historical or EMR information, serial ECGs, and bedside features that help differentiate the rhythm including variation in rate

2017 Dr Smith's ECG Blog

154. Guidelines for Responsible Opioid Prescribing in Chronic Non-Cancer Pain

) Pseudoephedrine Methamphetamine d-Methamphetamine d-Amphetamine Chloroquine (Aralen) Desoxyephedrine MDMA (Ecstasy) Methamphetamine (Desoxyn) Bupropion (Wellbutrin & Zyban) Chloroquine (Aralen) Chlorpromazine (Thorazine, Largactil) Desipramine (Norpramin) Dextroamphetamine (Dexedrine) Ephedrine (Ephedra and Ma Huang) Fenfluramine (Fen Phen) Labetalol (Labetalol) Mexiletine (Mexitil) n-acetyl procainamide (Procainamide) Phenylephrine (Neo-synephrine) Propranolol (Inderal) Pseudoephedrine (Claritin-D

2012 American Society of Interventional Pain Physicians

155. A Phase 2A Evaluation of the Safety, Tolerability, Pharmacokinetics, Efficacy of Clofazimine (CFZ) in Cryptosporidiosis

, Bepridil, Chloroquine, Chlorpromazine, Cisapride, Clarithromycin, Cyclobenzaprine, Darunavir, Delamanid, Disopyramide Dofetilide, Domperidone, Droperidol, Erythromycin, Fosamprenavir, Halofantrine, Haloperidol, Ibutilide, Indinavir, Levomethadyl, Lopinavir, Mesoridazine, Methadone, Nelfinavir, Pentamidine, Pimozide, Procainamide, Quinidine, Ritonavir, Simiprinivir, Sotalol, Sparfloxacin, Thioridazine, or Tiprinivir Pregnant and lactating women (screening pregnancy test for females and pregnancy test

2017 Clinical Trials

156. Trial to Evaluate the Efficacy, Safety and Tolerability of BPaMZ in Drug-Sensitive (DS-TB) Adult Patients and Drug-Resistant (DR-TB) Adult Patients

of their components is contra-indicated, including but not limited to drug allergy. Use of any drug within 30 days prior to randomisation known to prolong QTc interval (including, but not limited to, amiodarone, amitriptyline, bepridil, chloroquine, chlorpromazine, cisapride, clarithromycin, disopyramide dofetilide, domperidone, droperidol, erythromycin, halofantrine, haloperidol, ibutilide, levomethadyl, mesoridazine, methadone, pentamidine, pimozide, procainamide, quinacrine, quinidine, sotalol, sparfloxacin

2017 Clinical Trials

157. Dysregulation of miR-155-5p and miR-200-3p and the Anti-Non-Bilayer Phospholipid Arrangement Antibodies Favor the Development of Lupus in Three Novel Murine Lupus Models Full Text available with Trip Pro

Dysregulation of miR-155-5p and miR-200-3p and the Anti-Non-Bilayer Phospholipid Arrangement Antibodies Favor the Development of Lupus in Three Novel Murine Lupus Models Systemic lupus erythematosus (SLE) is characterized by deregulated activation of T and B cells, autoantibody production, and consequent formation of immune complexes. Liposomes with nonbilayer phospholipid arrangements (NPA), induced by chlorpromazine, procainamide, or manganese, provoke a disease resembling human lupus when

2017 Journal of immunology research

158. A High-Performance Liquid Chromatography Assay Method for the Determination of Lidocaine in Human Serum Full Text available with Trip Pro

A High-Performance Liquid Chromatography Assay Method for the Determination of Lidocaine in Human Serum Here we report on the development of a selective and sensitive high-performance liquid chromatographic method for the determination of lidocaine in human serum. The extraction of lidocaine and procainamide (internal standard) from serum (0.25 mL) was achieved using diethyl ether under alkaline conditions. After liquid-liquid extraction, the separation of analytes was accomplished using

2017 Pharmaceutics

159. Direct Comparison of Derivatization Strategies for LC-MS/MS Analysis of N-Glycans Full Text available with Trip Pro

different properties that affect both glycan retention on LC columns and MS analyses. To provide guidance for the proper selection of derivatizing reagents and LC columns, herein, we describe a comprehensive assessment of 2-aminobenzamide, procainamide, aminoxyTMT, RapiFluor-MS (RFMS) labeling, reduction and reduction with permethylation for N-glycan analysis. Of the derivatization strategies examined, RFMS provided the highest MS signal enhancement for neutral glycans, while permethylation

2017 The Analyst

160. Antimicrobial activity and acetylcholinesterase inhibition by extracts from chromatin modulated fungi Full Text available with Trip Pro

to promote the expression of genes commonly silenced. For such finality, five filamentous fungal species (Talaromyces funiculosus, Talaromyces islandicus, Talaromyces minioluteus, Talaromyces pinophilus, Penicillium janthinellum) were grown or not with DNA methyltransferases inhibitors (procainamide or hydralazine) and/or a histone deacetylase inhibitor (suberohydroxamic acid). Extracts from T. islandicus cultured or not with hydralazine inhibited Listeria monocytogenes growth in 57.66±5.98% and 15.38 (...) ±1.99%, respectively. Increment in inhibition of acetylcholinesterase activity was observed for the extract from P. janthinellum grown with procainamide (100%), when compared to the control extract (39.62±3.76%). Similarly, inhibition of acetylcholinesterase activity increased from 20.91±3.90% (control) to 92.20±3.72% when the tested extract was obtained from T. pinophilus under a combination of suberohydroxamic acid and procainamide. Concluding, increases in antimicrobial activity

2017 Brazilian Journal of Microbiology

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