Anti-arrhythmics Flashcards
Which conformation of the fast Na channel does each subtype of Class I block?
IA - Blocks the activated form
IB - Blocks the inactivated/refractory form
IC - Blocks the resting form (in reality can block all of them; fairly nonspecific)
Why do we prefer to use Class IB after an MI?
Class IB is selective for inactivated/refractory form of Na channel (i.e. tissue that is already depolarized) - this will select for the hypoxic or damaged tissue that we are worried about post-MI
What is the effect of Class IA channel blockers on the action potential?
Increases AP duration (decreases the slope of phase 0; slows down the AP) and effective refractory period
What are 3 class IA drugs?
Mnemonic: The queen proclaims Diso’s pyramid.
Quinidine, Procainamide, Disopyramide
Why is there a risk of tachycardia with quinidine?
- Muscarinic antagonist (antagonizes M2)
2. Alpha blocker
What do we really like to use quinidine for?
Atrial fibrillation
What do we often give with quinidine and why?
Digoxin - to slow AV conduction (mitigate the potential risk of tachycardia)
What is cinchonism and what drug is associated with it?
Cinchonism - side effects from the ANS activity
Quinidine
In the case of quinidine we get: GI distress, ocular dysfunction, tinnitus, CNS excitation
Why is there a risk of Torsades de Pointes with quinidine?
Anti-muscarinic effect (tachycardia causes prolongation of QRS and increased QT interval)
What enzyme is used to metabolize procainamide?
N-acetyltransferase
What 3 drugs are associated with producing SLE like syndrome?
Procainamide, hydralazine, isoniazid
What hematologic side effect are you concerned about with procainamide?
Thrombocytopenia
Which antibody is more specific for drug-induced SLE vs. general SLE?
Antihistone
How does Class IB affect action potential?
Decreases action potential duration by blocking the slow Na “window currents (this reduces the K/Ca plateau phase which also have some influence from Na)
What is the one Class IB drug to remember?
Lidocaine
When do we use lidocaine?
Think: depolarized tissue (has more inactivated/refractory sodium channels)
- Post-MI
- Open heart surgery
- Digoxin toxicity
What is the least cardiotoxic drug of the anti-arrhythmics?
Lidocaine
What toxicity do we worry about with lidocaine?
CNS (e.g. seizures)
How do we typically give lidocaine?
IV use (first pass metabolism)
What is different about mexiletine and tocainide from lidocaine?
They can be given orally
Give 2 examples of Class IC drugs.
Flecainide, propafenone
When do we use class IC?
Last resort in refractory ventricular tachycardia
What is the effect of class IC on AP duration?
Minimal effect
What do Class II antiarrhythmics act on?
Beta blockers that work on NODAL cells (SA, AV nodes)
By decreasing cAMP in the cells, it leads to decreased phosphorylation of all the channels which means closed Na and Ca channels and open K channels (slowed depolarization)
