Antiarrhythmics pt 2 Flashcards
(50 cards)
what phase is being prolonged, what channels, and what class of drugs cauase this?
phase 0: fast action depoloarization in the myoctes
Na blocking drugs
class I (abc)+class III drugs
Left to right
A. class 1a: QRS increased; QT increased ; AP increased; ERP increased
B. class 1b: QRS no change; QT decreases; ERP+AP both decrease
c. class 1c: QRS increases; QT no change; ERP+AP no change
red line = after drug administration
which class 1 drug effects sodium channels largely during their depolarized state?
class 1b: bind above 0mv
RAPIDLY unbinds- unbound by the time the next impulse arrives; therefore works better in fast heart rates
which drug can be used to treat re-entry and what is the MOA of this induced state?
Re-entry occurs when there is an accessory route refracting a depolarizing wave back to the atria: lidocaine inhibits this “two way” electrical route and permits only unidirectional electrical flow.
re-entry pathways look like this
unidirectional (normal)–> bidirectional (pathological)
which class 1 causes CNS toxicity? what is its bother AE?
class1b: tremor and agitation
class 1b also causes heart block, bradycardia
MI-associated arrhythmia and Ic drugs
CAST trial showed almost 4x mortality in patients using class 1c antiarrhythmics following MI: DONT USE THEM
therefore ONLY USE DRUG IN NORMAL HEARTS
Monitor patient so QRS does NOT PROLONG
bradycardia vs tachycardia: which of these conditions will class 1 drugs be beneficial?
tachycardia for class 1 drugs: they all have USE-dependence but especially class 1c drugs, meaning they only act when the channels are open/activated
which drug class causes these changes?
K+ (repolarization) channel blockers: class III: amidarone, sotalol, dofetilide, ibutilide
torsade de pontes
may be induced by class III and Class 1a because these drugs prolong AP, therefore QT interval
prolongs QRS, slows AV conduction, slows HR
Amiodarone: has class I (prolonged class I character), class II+IV (delays HR and AV conduction) characteristics.
Amiodarone is the class III drug with the lowest risk of TDP induction torsade.
half life of amiodarone
58 days; lipid soluble, so accumulates in tissues
amiodarone: photosensitivity to sun is the most common affect of amiodarone
least common side effect of amidarone: blue man syndrome
pulmonary fibrosis- SE of amiodarone, “honeycombing” cxr: foamy macrophages fllled with phospholipids
tests needed for px on amiodarone
LVTs, TFTs, PFTs
class III drugs for cardiomyopathy
sotalol, dofetilide: they have reverse use dependence; this permits them to bind during the potassium resting state, when they aren’t in use. They have the greatest effect in bradycardic patients
Ibutilide
Class III drug, Intravenous (Ibut..), 2-4 hr half life, used predominantly for cardioversion
terminates arrhythmia but can induce torsades
Class II drugs (beta blockers)
class II drugs (BB): blue is before red is after
AV block drugs
Class II BB and Class IV CCBs: decrease AV conduction –> type 1 AV block or type II (Mobitz 1; wenckebach)
used soley for anti-arrhythmic rates
VTac/Vfib–>SCD. which drug would decrease rates of SCD among antiarrhythmics?
beta blockers: they not only slow AV conduction down but also work on ventricular myocytes as well, so they improve outcomes for patients.
adenosine
adenosine receptors, use, and mode of delivery, SE
located in the AV node and blood vessels
used for AVNRT (most common SVT)
used via IV
because of vascular receptors–> vasodilation, flushing
