Flashcards in Cardiovascular pharmacology II Deck (30):
what are the four ways to decrease spontaneous activity in the heart?
1. decrease phase 4 slope
2. increase threshold
3. increase maximum diastolic potential
4. increase AP duration
what are the two ways to increase refractoriness? how do they work?
1. sodium channel blockers - increases ERP by decreasing the % of sodium channels recovered from inactivation
2. AP prolonging drugs (potassium channel blocker) - increase phases 2 and 3
what are the class Ia antiarrhythmic drugs?
what are the class Ib antiarrhythmic drugs?
what are the class Ic antiarrhythmic drugs?
what are the class II antiarrhythmic drugs?
what are the class III antiarrhythmic drugs?
what are the class IV antiarrhythmic drugs?
what is the main function of the class I antiarrhythmics?
1. block fast sodium channels in conductive tissues
2. decrease max depolarization rate
3. reduce automaticity, delay conduction
4. prolong ERP - increased ERP/APD ratio
class I antiarryhtmics are good for what condition?
MI induced arryhthmia
what is unique about class Ia antiarrhythmics?
1. block potassium channels - delay phase 3 - prolonged QRS and QT
2. moderate sodium blocking
3. calcium blocking at high doses - depressed phase 2 and nodal phase 0
what is unique about class Ib antiarrhythmics?
widened QRS complex
what are the clinical uses for quinidine?
1. refractory patients
2. convert Af or flutter
3. prevent AF recurrence
4. life threatening ventricular arrhtyhmias
what are the other effects of quinidine?
1. block potassium channels - prolong APD
2. block alpha receptors - lower BP
3. block M receptors - increase HR in intact subjects
what are the adverse effects of quinidine?
1. cinchonism - tinnitus, hearing loss, blurred vision
4. proarrythmic - torsades de pointes (prolongs AP due to sodium blocking - early afterdepolarizations)
how does procainamide differ from quinidine?
1. very little vagolytic activity
2. no hypotensive effect
3. does not prolong QT interval as much
what are the clinical applications for procainamide?
1. life threatening ventricular arrhythmias
2. reentry based SVT
4. AF associated with wolff-parkinson-white syndrome
what are the adverse effects of procainamide?
1. cardiac - arryhthmia aggravation, TdP,
2. extracardiac - SLE like syndrome, GI, nausea and vomiting
what are the effects of lidocaine?
1. weak sodium channel binding (blocks slow AND fast)
2. accelerated phase 3 repolarization - shortened APD and QT because it blocks late sodium channels - good use in digitalis and MI induced arrhythmia
3. lowers phase 4 slope
why is lidocaine more effective in ischemic tissues?
shortens AP and decreases ability of changes in calcium leading to arrhythmias in that way
which class of antiarrhythmics binds strongest to sodium channels?
what are the effects of propafenone?
1. strong inhibitor of sodium channels
2. moderate beta blocker
what are the clinical applications of propafenone?
1. atrial arrhythmias
2. heart function must be intact
what are the effects of flecainide?
1. potent sodium channel blockade
2. markedly slows interventricular conduction
what are the clinical applications for flecainide?
refractory life threatening ectopic ventricular arrhythmias
what are the effects of the beta blockers on antiarrythmias?
1. SA node automaticity
2. AV nodal conduction
3. ventricular contractility
what are the clinical applications of beta blockers?
1. supraventricular arryhtmias due to excessive sympathetic activity
2. prevention of sudden cardiac death in patients with prior MI
what are the effects of the class III antiarrythmia drugs?
1. main effect - prolong phase 3 repolarization - increased QT
2. blocks potassium channels - prolongs refractoriness and APD
3. blocks sodium channels in inactivated state
4. blocks calcium channels - slows AV node phase 4
5. noncompetitive blockade of a, B, M receptors
what are the clinical applications of amiodarone?
1. acute termination of VT or VF
2. conversion and slowing of AF
3. AV nodal reentry tachycardia
4. WPW syndrome tachycardias