Cardiovascular pharmacology II Flashcards
what are the four ways to decrease spontaneous activity in the heart?
- decrease phase 4 slope
- increase threshold
- increase maximum diastolic potential
- increase AP duration
what are the two ways to increase refractoriness? how do they work?
- sodium channel blockers - increases ERP by decreasing the % of sodium channels recovered from inactivation
- AP prolonging drugs (potassium channel blocker) - increase phases 2 and 3
what are the class Ia antiarrhythmic drugs?
- quinidine
- procainamide
- disopyramide
what are the class Ib antiarrhythmic drugs?
lidocaine
what are the class Ic antiarrhythmic drugs?
- propafenone
2. flecainide
what are the class II antiarrhythmic drugs?
beta blockers
what are the class III antiarrhythmic drugs?
amiodarone
what are the class IV antiarrhythmic drugs?
- verapamil
2. dilitiazem
what is the main function of the class I antiarrhythmics?
- block fast sodium channels in conductive tissues
- decrease max depolarization rate
- reduce automaticity, delay conduction
- prolong ERP - increased ERP/APD ratio
class I antiarryhtmics are good for what condition?
MI induced arryhthmia
what is unique about class Ia antiarrhythmics?
- block potassium channels - delay phase 3 - prolonged QRS and QT
- moderate sodium blocking
- 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?
- refractory patients
- convert Af or flutter
- prevent AF recurrence
- life threatening ventricular arrhtyhmias
what are the other effects of quinidine?
- block potassium channels - prolong APD
- block alpha receptors - lower BP
- block M receptors - increase HR in intact subjects
what are the adverse effects of quinidine?
- cinchonism - tinnitus, hearing loss, blurred vision
- diarrhea
- hypotension
- proarrythmic - torsades de pointes (prolongs AP due to sodium blocking - early afterdepolarizations)