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Procainamide

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81. 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

82. 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

83. 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

84. Atrial Fibrillation ? Diagnosis and Management

-threatening pulmonary fibrosis, hepatic dysfunction, and aggravation of arrhythmias Monitor transaminases and thyroid function every 6 months. Reduce dose of concurrently used beta-blockers, procainamide, quinidine, and warfarin by 50%. dronedarone Multaq® (IR tablet: 400 mg) 400 mg PO BID. $139 Limited Coverage Special Authority Diarrhea, dyspepsia, nausea, and hepatic dysfunction (rare) Slight increase in plasma creatinine related to inhibition of secretion Contraindicated in patients with severe heart

2015 Clinical Practice Guidelines and Protocols in British Columbia

86. HPLC-DAD Quantification of Flucytosine (5-Fluorocytosine)

Phenobarbital X 102 µmol/L 30 µmol/L Phenytoin X X 52 µmol/L 20 µmol/L Prednisolone X X Prednisone X Primidone 42 µmol/L Procainamide X 22 µmol/L 6 µmol/L Procarbazine X Prochlorperazine X Quinidine X 11.1 µmol/L 5 µmol/L Salicylate 1.4 mmol/L 300 µmol/L 23 DRUGS TESTED BURY ET AL., 1979 DIASIO ET AL., 1978 MINERS ET AL., 1980 NG ET AL., 1996 PETERSEN ET AL., 1994* SCHWERTSCHLAG ET AL., 1984 WARNOCK AND TURNER, 1981 Theobromine X Theophylline X 83 µmol/L 20 µmol/L Thioguanine X Thyroxine 175 nmol/L

2015 Canadian Agency for Drugs and Technologies in Health - Rapid Review

87. Classification of Anemias

deficiency high RDW, low-normal reticulocyte , Hemolytic anemia Drug induced Aplastic anemia: allopurinol, antithyroid meds , chemo, chloramphenicol, chlorpromazine, clopidogrel, corticosteroids, furosemide, gold, indomethacin, interferon a2a&2b , isoniazid, methyldopa, NSAIDs, penicillamine, phenothiazines, procainamide, sulfonamides & ticlopidine. Drug induced Hemolysis in G6PD Deficiency: ascorbic acid, benzocaine, chloroquine, dapsone, hydroxychloroqine, nitrofurantoin, phenazopyridine, primaquine (...) , sulfacetamide, sulfamethoxazole, sulfanilamide & sulfapyridine. Drug induced Hemolytic anemia: ACEI, acetaminophen, ASA/NSAIDs, cephalosporins, chlorpromazine, chlorpropamide, diclofenac, hydrochlorothiazide, interferon a2a&2b , isoniazid, levodopa, levofloxacin, mefenamic acid, methadone, methyldopa, penicillins, probenecid, procainamide, quinine, quinidine, ribavirin, rifampin, sulfonamides, & tetracycline. (Direct antiglobulin test-DAT or Coomb’s test is used to detect cause of hemolytic anemia) Drug

2014 RxFiles

88. Do you recognize this ECG yet?

R wave component in lead aVR. T HEREFORE : As per Drs. Gordon and Meyers — ECG #1 is completely consistent with any toxicity producing Sodium-Channel Blockade ( ie, tricyclic antidepressant overdose; proarrhythmia from antiarrhythmics such as flecainide or procainamide — or other agents, as listed by Dr. Burns at the above LITFL link ) . B eyond- t he- C ore : Returning for a moment to ECG #1 — I was not at all certain in my initial assessment of this tracing that there were P waves deforming

2019 Dr Smith's ECG Blog

89. Arrhythmogenic drugs can amplify spatial heterogeneities in the electrical restitution in perfused guinea-pig heart: An evidence from assessments of monophasic action potential durations and JT intervals. (PubMed)

with clinically proved proarrhythmic potential (dofetilide, quinidine, procainamide, and flecainide) and, if so, whether these effects can translate to the appropriate changes of the ECG metrics of ventricular repolarization, such as JT intervals. In isolated, perfused guinea-pig heart preparations, monophasic action potentials and volume-conducted ECG were recorded at progressively increased pacing rates. The APD90 measured at distinct ventricular sites, as well as the JTpeak and JTend values were plotted (...) as a function of preceding diastolic interval, and the maximum slopes of the restitution curves were determined at baseline and upon drug administration. Dofetilide, quinidine, and procainamide reverse rate-dependently prolonged APD90 and steepened the restitution curve, with effects being greater at the endocardium than epicardium, and in the right ventricular (RV) vs. the left ventricular (LV) chamber. The restitution slope was increased to a greater extent for the JTend vs. the JTpeak interval

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2018 PLoS ONE

90. Management of Electrical Storm

) Start an antiarrhythmic. My preference is procainamide, based on the . (Ortiz 2017) Procainamide 10 mg/kg over 20 minutes I think the benefit of amiodarone has been oversold for most conditions, but it is a reasonable second line option here. (Many authors list it as their first option, but with limited evidence). Chronic use of amiodarone has been shown to decrease the incidence of frequent ventricular dysrhythmias in these patients. (Connolly 2006) Boluses of 150mg, followed by an infusion of 1 mg (...) journal : official journal of the Japanese Circulation Society. 2010; 74(5):856-63. [ ] Nademanee K, Taylor R, Bailey WE, Rieders DE, Kosar EM. Treating electrical storm : sympathetic blockade versus advanced cardiac life support-guided therapy. Circulation. 2000; 102(7):742-7. [ ] Ortiz M, Martin A, et al. Randomized comparison of intravenous procainamide versus intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study. Eur Heart J. 2017 38;1329-1335. Patel

2019 First10EM

91. Drug-induced systemic lupus: revisiting the ever-changing spectrum of the disease using the WHO pharmacovigilance database. (PubMed)

≥0 were extracted. The median age at DIL onset was 49 years and the female to male sex ratio was 4.3. The median delay between start of suspected treatment and DIL occurrence was 172 days. DIL was reported as serious adverse event in 55.4%. Among the 118 suspected drugs, 42 had not been previously reported in association with DIL. The drugs associated with the highest number of DIL cases were infliximab, adalimumab, etanercept, procainamide and hydralazine.This study enables the identification

2019 Annals of the Rheumatic Diseases

92. A Multicenter Randomized Trial to Evaluate a Chemical-first or Electrical-first Cardioversion Strategy for Patients With Uncomplicated Acute Atrial Fibrillation. (PubMed)

18 to 75 with uncomplicated symptomatic AF of less than 48 hours and CHADS2 score of 0 or 1 were randomized using concealed allocation in a 1:1 ratio to one of the following strategies: 1) chemical cardioversion with procainamide infusion, followed by electrical countershock if unsuccessful; or 2) electrical cardioversion, followed by procainamide infusion if unsuccessful. The primary outcome was the proportion of patients discharged within 4 hours of arrival. Secondary outcomes included ED

2019 Academic Emergency Medicine

94. Funtabulously Frivolous Friday Five 197

. The boy’s chest was surgically opened, and manual cardiac massage was undertaken for 45 minutes until the arrival of the defibrillator. The use of procainamide and defibrillation successfully reverted the boy into a sinus rhythm. [ ] Last update: [last-modified] Share this: Filed Under: Tagged With: , , , , , , , , , About Neil Long Emergency Physician working in Vancouver. Loves the misery of alpine climbing and working in austere environments. Supporter of FOAMed, tox, sim, ultrasound and any other

2017 Life in the Fast Lane Blog

95. Chest Tightness and Asthma in a Young Man

V1-V2 was positive and diagnostic. If not, we do refer those type II patients for procainamide testing (not to be done in the ED, our electrophysiologists team said this could lead to refractory VF). It's also funny that some years ago, we did learn much from... one of the three Brugada brothers, who were working in research and clinical at Montreal Heart. He did a lot of reinforcement, especially to the ECG techs, about how to do those high V1-V2. It would have been interesting to see the result

2016 Dr Smith's ECG Blog

96. Wide Complex Tachycardia

that convert atrial fibrillation to sinus, such as procainamide or ibutilide (and others), but when you have a wide complex very fast tachycardia, it is best to use electrical cardioversion. It is the safest, and keeps you from having to make a definite diagnosis. As long as you can manage procedural sedation, which is very easy in the case of cardioversion because you only need seconds of sedation and amnesia, then cardioversion is the safest method. Even in the ED, the pattern was not recognized (...) guidelines, but it remains in the European guidelines (although I question it's safety due to the partial AV nodal blocker effect). Where I work we don't have neither procainamide nor ibutilide. 2. Do you think vernakalant would work and would it be safe? 3. How would you manage a stable patient with preexcited Afib that you've decided to sedate and DC cardiovert, in a situation where the patient just had a meal. Is it safe to wait a couple of hours with the patient closely monitored (thereby limiting

2016 Dr Smith's ECG Blog

98. Task Force 5: Pediatric Cardiology Fellowship Training in Critical Care Cardiology

inhibitors, calcium channel antagonists, beta-adrenergic antagonists, nitric oxide donors) • Commonly used antiarrhythmic agents (eg, digoxin, adenosine, esmolol/propranolol, procainamide, lido- caine, amiodarone) • Pulmonary vasodilators (eg, inhaled nitric oxide, prosta- cyclin, PDE5 inhibitors) • Prostaglandin E 1 • Neuromuscular blocking agents (eg, pancuronium, vecuronium, rocuronium, succinylcholine) • Analgesics and sedatives (eg, opiates, ketamine, benzo- diazepines, dexmedetomidine

2015 American Heart Association

99. Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 9: Arrhythmias and Conduction Defects

if the syncope raises concern for arrhythmic causes, contrast-enhanced magnetic resonance imaging, cardiac computed tomography, coronary angiography, and invasive electrophysiological testing may be indicated. Provocative testing with stress testing, epinephrine, procainamide, or isoproterenol should be considered to identify otherwise concealed cases of long-QT syndrome, catecholaminergic polymorphic VT, and Brugada syndrome. Genetic testing may be clinically useful in selected cases. Neurally mediated

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2015 American Heart Association

100. A 12 year old with Wide Complex Tachycardia

was always taught, if it's wide, treat it wide. Even though there is no sign of delta wave, or irregularity (afib with wpw), my general inclination would be to avoid av nodal blocking agents or ccb's. Perhaps just go straight to procainamide? That said faced with this case in front of me, I could see myself convincing myself it's probably just svt with abberancy and giving adenosine x 2. I think my personal preference would have been amiodarone or procainamide, any reason NOT to use those?...verapamil

2016 Dr Smith's ECG Blog

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