Class I antiarrhythmics

Question 1

Definitions

Answer 1

Local anesthetics
Slow or block conduction (esp in depolarized cells)
Decrease slope of phase 0 depolarizatoin
Increase threshold for firing an abn pacemaker cells

Are state dependent: selectively depress tissue that is frequently depolarized (tachycardia)

Hyperkalemia causes increases toxicity for all class I drugs.

Question 2

Class IA:

Names

Answer 2

Quinidine,
Procainamide
Dispyramides

“The Queen Proclaims Diso’s Pyramid”

Question 3

Class IA: MOA

Answer 3

Increase AP duration
Increase effective refractory period (ERP)
Increase QT interval

Affect both atrial and ventricular arrhythmias, esp reentrant and ectopic supraventricular and VT.

Question 4

Class IA: toxicity

Answer 4

Quinidine: cinchonism (HA, tinnitus)
Procainamide: SLE
Dispyramide: Heart failure

All can cause thrombocytopenia and torsa de pointes due to increase QT interval

Question 5

Class IB: names

Answer 5

Lidocaine,
Mexiletine,
Tocainide

Phenytoin can also fall into this category

“I’d Buy Lidy’s Mexican Taco’s”

Question 6

Class IB: MOA

Answer 6

Decrease AP duration
Preferentially affects ischemic or depolarized Purkinje and ventricular tissue

Useful in acute ventricular arrhythmias (esp post MI)
digitalis induced arrhythmias.

“IB is Best post-MI”

Question 7

Class IB: toxicity

Answer 7

Local anesthetic,
CNS stimulation/depression
CV depression

Question 8

Class IC: names

Answer 8

Flecainide

Propafenone

Question 9

Class IC: MOA

Answer 9

No effect on AP duration
Useful in ventricular tachy that progress to VF and in intractable SVT.

Usually used only as last resort in refractory tachy.
For pts without structural abn,

“IC is Contraindicated in structural heart disease and post MI”

Question 10

Class IC: toxicity

Answer 10

Proarrhythmic, esp post MI (contraindicated)

Significantly prolongs refractory period in AV node.