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Antiarrhythmic Drugs
Stack #28608
| Question | Answer |
|---|---|
| Class 1a | quinidine, procainamide, disopyramide |
| Class 1a Benefit | Increase duration of Action Potential and intermediate onset and off set |
| Class 1a SE | Muscaranic antagonism (block Para), Ca blockade, adrenoceptor blockade |
| Quinidine class | Ia |
| Procainamide class | Ia |
| disopyramide class | Ia |
| Quinidine SE | cardiotoxicity, atrial Fib, ventricular Tach, syncope, SA block, AV block, increase vasodialation |
| Procainamide SE | Cardiotoxic, No Atrial Fib, or Vent Tach, but induce SEL, arthraliga, arthritis, limits long term use |
| disopyramide SE | Negative inotropic, cardiotoxic |
| disopyramide Contra | HF |
| Class Ib MOA | decrease duration, rapid onset and offset |
| Class Ib Agents | Lidocaine, mexilitine |
| Class 1a MOA | Na & K channel block, |
| Class Ib MOA | Block activated & inactivated Na channels, Increase activation of K channels, decrease slope of phase 0 |
| Lidocaine SE | CNS sym-dissociation, drowness, agitation |
| Mexilitine SE | CNS sym, dizzy, tremor, lightheaded |
| Class Ib interactions | Hyperkalemia decreases rate of depolarization or hyperkalemia increases depressant effects |
| Class 1c Benefits | No change in duration of action potential but a slow onset and off set. |
| Class Ic Agents | flecainide, profenone |
| Most potent antidysrhythmics | Class Ic |
| Class Ic SE | Prodysrhythmics (esp vent tach) |
| Class 1c contra | Benign or potentially malignant vertricular dysrhythmias |
| Flecainide SE | visual distrubances(10-15%) |
| Propafenone SE | Granulocytopenia, SLE like syndrome |
| Antirrhythmic Drugs MOA | Depolarize cells more affected than polarized cells, Decrease conduction and excitibility in tissues, and prevent re-entrants |
| Propranolol | K channel activation of purkinje fibers |
| Propranolol | membrane stabalizing |
| esmolol | cardiac depression, non-selective (watch asthmatics)sudden withdraw dysrrhythmias |
| propranolol, esmolol | b adrenoceptor antagonist- decrease slope phase 4 |
| propranolol, esmolol | increase ERP, decrease autmatocity of purkinji fibers, decrease afterdepolarizations |
| amidarone SE | pulmonary fibrosis, prodysrrhythmic, photo dermititis, corneal deposits |
| Sotolol SE | prodysrrhythmic, less effective with increasing rate |
| Bretylium SE | prodysrrhythmic, less effective with increasing rate |
| Verapamil, Diltilazem, Bepridil SE | hypotension, cardiac depression, sinus arrest, AV block, torsades de point |
| Adenosine SE | flushing, SOB |
| Adenosine contra | dipyramole, theophylline |
| Digoxin-SE | Dysrrhythmias |
| Digoxin- Interactions | Amidarone, proferenone, verapamil, bepridil, dilitizem |
| Ibutilide class | III |
| Amidarone | non-competitive B antagonist and in all groups |
| Sotolol | competitive b antagonist |
| bretylium | adrenergic neuron blocking drug |
| Bretylium SE | orthostatic hypotension |
| Block AP in pacemakers | Class IV |
| Adenosine half life | 6 seconds |
| adenosine | induces cardiac effects via A1 and A2 vasodialitation |
| adenosine location | Acts in SA and AV nodal cells to promote K activation decrease phase 4 |
| Digoxin location | Increase Parasympathic and increase K channel activation in SA and AV nodes decrease phase 4 |
| MgSo4 | modulates Ca currents into cell and decrease overloading of Ca great for torsades de point |
Created by:
liza001
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