SACCM 168: Antiarrhythmic Agents Flashcards
What channel do Class I antiarrhythmics act and how do they generally affect the action potential (phase and shape change)?
fast Na-channel, decrease the slope of phase 0
Name 2 Class Ia antiarrhythmics
Procainamide
Quinidine
What other channels are blocked by Class Ia antiarrhythmics?
rectifier K current (IKr)
Which subclass of Na-channel blockers causes the strongest Na-channel blockage?
Ic - phase 0 experiences most shift
How do the different Na-channel blockers affect the cardiac action potential?
Ia - prolongs, by blocking K channels
Ib - shortens, by preventing late sustained Na release
Ic -no effect
What is the side effect of procainamide if given IV too fast?
hypotension
Why could procainamide IV worsen atrial tachyarrhythmias?
Class Ia agent
has anticholinergic effects –> increases the ventricular response rate
–> will worsen tachycardia from atrial tachyarrhythmia
give drugs that prolong the AV nodal conduction time (e.g., diltiazem)
What are the adverse effects of procainamide?
GI (vomiting, anorexia, nausea)
lupus erythematosus
How are Na channel blockers divided into their subcategories? (Ia, Ib, Ic)
according to their dissociation during the resting phase of the Na channel (i.e., during diastole Na-channel blockers should dissociate from the Na channels)
Ia: immediate dissociation
Ib: fast dissociation
Ic: slow dissociation
What state of the Na-channel do Class Ib antiarrhythmics primarily inhibit?
open and inactive state
with fast dissociation kinetics (fast onset/offset)
How do Class Ib antiarrhythmics shorten the action potential?
inhibition of the window sodium current, also called late sustained Na current
~2% of Na channels are not inactivated yet when action potential decrease –> usually prolong the action potential
How does the atrial action potential differ from the ventricular action potential?
- more depolarized resting membrane potential (slightly less negative)
- lack of plateau phase
Name 2 class Ib Na-channel blockers
- Lidocaine
- Mexiletine
What conditions increase lidocaine’s ability to block inward Na channels?
- acidosis
- hyperkalemia (increased extracellular potassium)
- partially depolarized cells
–> work well in ischemic and diseased ventricles
What does it mean that Class I antiarrhythmics are use-dependent?
work best on rapidly depolarizing tissues
If unsure whether a tachyarrhythmia is SVT or VT why is lidocaine safer than procainamide?
lidocaine has little atrial tissue or AV nodal conduction effects.
lidocaine has minimal hemodynamic effects
procainamide shortens AV nodal conduction and thus increases the ventricular repsonse rate
How is lidocaine cleared?
hepatic clearance –> determines serum cc –> increased toxicity risk with heart failure, hypotension, severe hepatic disease
What are the most common adverse effects of lidocaine?
- GI (vomting, nausea)
- lethargy
- tremors
- seizure activity
cats prone to bradyarrhythmias and sudden death
How is mexiletine used?
orally in dogs for VT and OAVRT
What state of the Na-channels do class Ic antiarrhythmics primarily inhibit?
open state
Name 2 examples of class Ic antiarrhythmics
propafenone (also has mild beta-blocking effects)
flecainide
Name examples of beta-blockers
- esmolol
- atenolol
- propranolol
- metoprolol
List contraindications for beta-blockers
- CHF
- pulmonary disease (bronchoconstriction)
- patients with sinus nodal dysfunction
- AV node conduction disturbances
what is the effect of dromotropic agents?
agents that affect the conduction speed in the AV node
