Exam 2 Flashcards
MOA Anti-Arrhythmias CLAS ONE
Na+ Channel Blockers
Class 1A Anti-Arrhythmias
Quinidine
Procainamide
Disopyramide
Class 1B Anti-Arrhythmias
Lidocaine
Mexilietine
Tocainide
Class 1C Anti-Arrhythmias
Flecainide
Propafenone
Moricizine(Ethmozine)
What phase of action potential do Class one Anti-Arrhythmia’s effect?
Phase 0
Class 1 Anti-arrhythmic Acronym
Double Quarter Pounder
Lettuce Mayo Pickle
Fries Please
Contraindication for the entire class one
- 2nd/3rd degree block unless pt has functional pacemaker
- Increased QT
What is preload?
End diastolic volume (EDV) at the BEGINNING of Systole
What is afterload?
Ventricular pressure at the END OF SYSTOLE
What determines the End-Systolic-Volume?
The Afterload
Glyceryl Trinitrate
Nitroglycerin
Glyceryl Trinitrate is metabolized by what if it is administered orally?
Glutathione-S-transferase
to produce active NO
Isosorbide is metabolized to what two metabolites?
Isosorbide-2-mononitrate
Isosorbide-5-mononitrate
Which isosorbide metabolite has the longest half life?
Isosorbide-5-mononitrate
What are the 3 ways that ON’s cause their effect?
1-Dilation on venous capacitance vessels(decrease Preload)
2-Mildly dilate arteriolar resistance vessels(decrease afterload)
–These 2 decrease myocardial oxygen demand
3-Dilate large epicardial arteries (Increase Myocardial O2supply)
IN SHORT-ON’s do what?
Decrease Demand, Increase Supply
ON’s exert the majority of their effect by doing what…
Dilating the Venous Capacitance Vessels
MOA of CCBs
Inhibit voltage gated L-type Ca2+ channels that lead to a decrease in Ca2+ influx causing relaxation of the vascular smooth muscle.
Amlodipine
Norvasc
Nifedipine
Procardia
Nicardipine
Cadene
Diltiazem
Cardizem
Verapamil
Isopten
CCBs that act on the HR
Diltiazem, Verapamil