Antiarrythmics - PharmacologyofAntiarrythmics...

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Pharmacology of Antiarrythmics Dr. David Krummen, MD 08/11/2010 17:04:00 Cardiac Conduction System Anatomy Cellular APs and Surface ECG Only the His purkinje phase have the classical phase seen in textbooks o Phase 0,1,2,3,4 Cellular APs – Key points Phase 0 Na channels in most cardiac cells, except in AV node (Ca) SA/AV node upsloping phase 4 diastolic AP what allows them to have automaticity (fire on their own) Phase 0: Na rushes in Phase 2: Ca in Phase 3: K out Antiarrythmics best suited for tachyarrhythiasArrythmia suppression and rate control Pacemakers used to control slow HR (brady) Vaughn Williams classification Drugs classified by major effect A lot of drugs have actions in multiple classes (amiodarone acts in all 4 classes) Digoxin used very frequently, falls outside the classification system Class I- Na channel blockade Block Na current Slow conduction (phase 0 block) Suppress automaticity (phase 4 block) wherever these processes depend upon Na channels If have atrial fib due to increased automaticity in pulmonary veins, these agents can suppress abnormal automaticity in these pulmonary veins Ex) Quinidine – older med prev used to treat atrial fibrillation o No longer recommended b/c so much proarrythmia o Now used to suppress specific type of recurrent VF
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o Warning: SE QT prolongation and VT/VF EX) Procainamide – used in AF w/ rapid ventricular response due to atrioventricular bypass tract (i.e Wolf-Parkinson’s White Syndrom – rapid arrythmias in upper chambers conducted very rapidly down to ventricles ventricular fibrillation!!!) Procainamide blocks
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This note was uploaded on 09/14/2011 for the course PHARM pp taught by Professor Staff during the Spring '11 term at UCSD.

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Antiarrythmics - PharmacologyofAntiarrythmics...

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