Antiarrhythmic Drugs - part 3 Flashcards
Class 3 antiarrhythmics increase …
the effective refractory period
–this abolishes the re-entry circuit and terminates arrhythmias that arise from it
Amiodarone
- activity
- use
- half life
- adverse effects
Activity like all 4 anti arrhythmic drug classes, but Ikr block is the most important
SHOT GUN DRUG
Commonly used to suppress emergency ventricular and atrial arrhythmias
-#1 for suppression of post MI vent arrhythmias
Prevention of a fib
Very long half life (weeks)
Adverse
- hypothyroidism
- pulmonary fibrosis
- photosensitivity
Dronedarone
An analog of amiodarone that was designed to have fewer toxicities and a shorter half life
Used in a fib
Ibutilidine
Selective blocker of HERG channel
Effective at rapidly converting a fib or a flutter to normal sinus rhythm
Sotolol
Has both K+ channel blocking activity and B-bloacker activity
Used for life threatening ventricular arrhythmias or maintenance of normal sinus rhythm after a fib/flutter
–main use is prevention of a fib recurrence
Dofetilide
High risk for Torsades de Pointes (10%)
Use infrequently
For atrial arrhythmias
Torsades de Pointes
–this is a severe toxicity of which drugs?
Ikr block induces EADs and triggered upstrokes
Multifocal/polymorphic ventricular tachycardia
Can degenerate into ventricular fibrillation
Severe toxicity of class III drugs which block the HERG K+ channel
Congenital Long QT syndrome
- -what causes this?
- -what does this condition put people at risk for?
- -what are most treated with?
Mutations in one of several channel genes
Have higher risk for
- torsades
- syncope
- sudden cardiac death due to V fib
Most are treated with a B-blocker
With congenital long QT syndrome, what may contribute to the production of torsades?
The mutation alone may not be sufficient to cause TdP under normal states, but it can be induced by stress, exercise, or other situations where catecholamine levels are elevated
What are the three main mutations of congenital LQTS?
SCN5A
KCNQ1
KCNH2
Acquired long QT syndrome?
-how?
Drug induced
Electrolyte imbalances
Block of HERG channel
Drug induced – most drugs capable of pro ducting TdP do so by blocking the HERG channel which gives risk to the Ikr current during depolarization phase of the cardiac AP
Digoxin
Direct inhibition of AV node
Useful in A fib pts who also have heart failure
Orally available, long half life
Magnesium chloride
Treat hypomagnesemia
Convert TdP
Prevent MI and digoxin associated arrhythmias
Potassium chloride
Hypokalemia reduces Ikr current, which can prolong action potentials and be pro-arrhythmic
Atropine
Blocks M2R, opposes pro-vagal action of ACh on heart
Increases HR
Given IV in emergency situations
