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61. CRACKCast E108 – Neuromuscular Disorders

precipitants of a myasthenic crisis and describe 3 chronic therapies and 2 acute therapies General Precipitants: Infection Aspiration Medication changes Eg. stopping anticholinergics New medication that precipitates weakness Surgery Pregnancy Medications (Box 98.2) Cardiovascular Beta Blockers CCB’s Quinidine Lidocaine Procainamide Antibiotics Aminoglycosides Tetracyclines Clindmycin Lincomycin Polymyxin B Colistin Other Phenytoin Neuromuscular Blockers Thyroid Replacement Treatment: BiPAP +/- IPPV

2017 CandiEM

62. CRACKCast E091 – Pancreas

of GI bleeding Bowel obstruction correction Treatment of acute cholangitis / venous thrombosis Wisecracks Question 1) Specifically list 10 drug causes of pancreatitis. Cannabis Codeine Dapsone Enalapril Furosemide Isoniazid Metronidazole Pravastatin Procainamide Simvastatin Sulfamethoxazole Tetracycline Valproic acid These are some of the class Ia drugs – from Uptodate – where people have developed pancreatitis on a re-challenge of the drug and other causes of pancreatitis have been ruled out (e.g

2017 CandiEM

63. CRACKCast E079 – Dysrhythmias

: carbamazepine TCA neuroleptics citalopram, antihistamines cocaine pufferfish toxin shellfish toxin Class II: beta-adrenergic ANTagonists: suppress SA automaticity and slow AV node conduction Class III: prolong repolarization and refractory period (K+ channels) Other drugs: TCA’s, Antipsychotics Citalopram, Venlafaxine Antihistamines, Antimicrobials Class IV: Ca+ channel blockers (slow AV node conduction) for SVT’s Verapamil Diltiazem Other IA: >PROCAINAMIDE< 20-30 mg/min (total dose 12-20 mg) or ~1g. Risk (...) contraindicated Treatment 1st line: Procainamide, 2nd line: Amiodarone; then cardioversion if unstable. “Likewise, with a very rapid irregular tachycardia (i.e., atrial fibrillation with a ventricular rate exceeding 200) accompanied by a wide-complex QRS, the likelihood of accessory pathway conduction should be considered and nodal blocking agents again withheld. Procainamide is recommended any time an accessory pathway with wide QRS complexes or very rapid rates exists, with amiodarone as a secondary choice

2017 CandiEM

64. Management of Pregnancy in Patients With Complex Congenital Heart Disease: A Scientific Statement for Healthcare Professionals From the American Heart Association

MetoprololPropranololCarvedilolAtenolol CCCD None reported Association with fetal growth restriction in second and third trimesters (atenolol, propranolol), neonatal bradycardia (esmolol, nadolol) Consider serial fetal sonography to assess interval fetal growth in second and third trimesters Except for atenolol, probably safe Class 1A Quinidine Procainamide CC None reported Yes Class 1C Flecainide C None reported Yes Class III SotalolAmiodarone BD None reported Thyroid dysfunction NoNo WHO)/(AAP Yes) Purine nucleosides Adenosine C

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2017 American Heart Association

68. Atopic Dermatitis - Guidelines for Prescribing Topical Corticosteroids

, trifluoperazine Miscellaneous aminophylline, carbamazepine, chloral hydrate, cyanocobalamin, fluorouracil, idoxuridine, minoxidil, nitroglycerin, nystatin, procainamide, quinine, quinidine Patients with mild to moderate signs / symptoms of atopic dermatitis often do not require further investigation, however an assessment by the patient's primary care provider may be required in the following situations: Moderate to severe eczema on the face - a calcineurin inhibitor to avoid skin atrophy might be more

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2017 medSask

69. Arrhythmias in Congenital Heart Disease: A Position Paper of EHRA, AEPC, and ESC Working Group on Grown-up Congenital Heart Disease

, implantable cardioverter-de?brillator; LV, left ventricular; RV, right ventricular; SCD, sudden cardiac death; SVT, supraventricular tachycardia; VT, ventricular tachycardia. Table6 Recommendations for pharmacological therapy of ventricular tachycardia Recommendations Consensus statement References Electrical cardioversion is recommended for acute termination of haemodynamic stable/unstable VT. If not possible, intravenous amiodarone or procainamide may be considered. 155 For non-sustained ventricular

2017 Heart Rhythm Society

70. Medications in Adult Advanced Life Support

), amiodarone, lidocaine (lignocaine), procainamide, bretylium, magnesium (magnesium sulfate heptahydrate), buffers, calcium, hormones or fibrinolytics) during human CPR increases survival to hospital discharge. 4 3 Specific Resuscitation Drugs 3.1 Adrenaline (Epinephrine) This is a naturally occurring catecholamine with alpha and beta effects. It is administered in cardiac arrest to cause peripheral vasoconstriction via its alpha-adrenergic action (directing available cardiac output to myocardium and brain

2016 Australian Resuscitation Council

71. Management of drug-induced immune and secondary autoimmune, haemolytic anaemia

IVIg can also cause acute haemolysis related to passive transfer of antibodies e.g. to ABO or Rh antigens. Some drugs (e.g. fludarabine, cladribine, levodopa, mefenamic acid and procainamide) cause drug-independent DIIHA that can be serologically indistinguishable from warm AIHA while others can only be detected in vitro in the presence of the drug or its metabolites (drug-dependent DIIHA). Patients can present within hours of exposure to drug with severe complement- mediated intravascular

2016 British Committee for Standards in Haematology

72. CRACKCast E010 – Pediatric Resuscitation

) adenosine 0.1 mg/kg rapid IV push, max 6mg, second dose 0.2 mg/kg rapid IV push, max 12mg 4b) amiodarone 5mg/kg IV/IO over 20-50 minutes OR procainamide 15mg/kg IV/IO over 30-60 minutes 5) narrow complex – probable SVT 5a) consider vagal maneuvers – ice bath, carotid sinus massage, or any Valsalva (REVERT trial?) 5b) adenosine as above or synchronized DCCV if no vascular access 6) If probable sinus tachycardia: search for and treat the cause NOT the HR 3) Describe the PALS septic shock algorithm Rosen’s (...) 0.05 – 2 mcg/kg/min – for shock (septic particularly) Procainamide 15 mg/kg for stable wide complex tachycardia Sodium bicarbonate 1-2 mEq/kg – for profound metabolic acidosis or Na channel blocker overdose (e.g. TCA) Two more medications that Rosen’s lists: Alprostadil (PGE1) – Prostaglandin used for ductal dependent congenital heart disease infusion: start at 0.05 – 0.1 mcg/kg/min can cause apnea Milrinone for bad cardiogenic shock to decrease SVR and PVR 5) What are 8 risk factors for Sudden

2016 CandiEM

75. A Middle-Aged Man with Chest pain, Hypotension and Tachycardia

records. We did know he was on a beta blocker, so it could have been the case that he is in chronic atrial fib/flutter. However, he was in shock and we had to take the risk of cardioversion. 3. Chemical cardioversion. Without first giving an AV nodal blocker, chemical cardioversion with agents such as procainamide can paradoxically increase the ventricular rate by slowing the atrial flutter rate enough for the AV node to conduct every beat; 1:1 conduction would result in a much faster ventricular rate

2018 Dr Smith's ECG Blog

76. Idiopathic Ventricular Tachycardias for the EM Physician

regular tachycardia according to our ACC/AHA guidelines as an option, assuming you do not think it's SVT. I would say in general that, if you do not suspect a particular SVT with aberrancy or a particular idiopathic VT on the differential, then just revert back to your classic strategy for wide complex regular tachycardia. For many people, this includes drugs like amiodarone or procainamide (if you can get it easily), all vs. elective cardioversion. Remember, these idiopathic VTs are really only (...) procainamide. For SVT with aberrancy, amiodarone does have AV nodal blocking effects, so that may break and suppress the rhythm. For IVT, I do not know which particular rhythms would respond to amiodarone (I don't think anyone knows this), but I could imagine that sometimes it may work. Just as long as the rhythm is not irregular and polymorphic (like AF with WPW would be) then I don't see any clear downside to amiodarone, except that it might simply not work in many scenarios. Subscribe to: Recommended

2018 Dr Smith's ECG Blog

77. 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

78. 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

79. 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

80. 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

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