Antiarryhthmics Flashcards
action Class 1A Na channel blockers
(quinidine, procainamide, dispyramide)
moderate 0 deepression
slowed conduction (+2)
shorten repol
phase 2 =
plateau phase
blanced inward Ca and outward K
action of Sotalol
block IKr channel
B block
Ic na channel blockers
flecainide
action class IV drugs
verapamil, diltiazem
Ca channel blockers
side effects Lidocaine
dizziness
seizures
side effects Beta blockers
negative ionotropic
heart block,
bradycardia
bronchospasm
catecholamine impact on depolarization
enhance depl in slow response cells (no impact in fast response cells)
specific side effects, diltiazem (less so in other Ca blockers )
interact with digitalis to slow AV conduction > heart block (and verapamil)
compete for digitalis renal excretion (and verapamil)
indications sotalol
VF VT
supravent tachycardia
a fib
impact, flecainide
threshold
vmax
increase threshold
decrease Vmax
main physiological effect of fleccainide
strongest change in depol (slight in duration)
side effects amiodarone
triggered arrhythmias (torases de pointes rare)
altered thyroid fxn (inhibts T4>T3) > hypothyroidism
pulmonary fibrosis (reversible)
impact, Na channel blockers (Class I)
membrane responsiveness
threshold
Vmax
Refractory
reduce mem responsiveness
increase threshold
decrease Vmax
increase refractory
indirect effects QUinidine, class Ia na blockers
block K channels early after depol (EAD)
Vagolytic effect - enahnce communication across AV > Vtach
phase 3 =
rapid repolarization
(L type close while K still open)
indications flecainide
approved in life-threatenign when supraventricular and ventricular arrhythmias are resistant to other drugs
action of class II drugs
Propanolol, esmolol
beta adrenergic blockers
class III K channel blockers
amiodarone
sotalol
dofetilide
class IV Ca channel blockers
verapamil
diltiazem
since beta blockers do not _____, they are safe for pt with Long Qt
prolong repolarizaation
indications Adenosine
supraventricular tachycardia (slows AV conduction and heart rate)
1-4-dihydropyridines are not used as antiarrhythmics because,
they are used, however, to relieve
primarily target vascular cells (vs cardiac)
used to relieve angia pectoris to relieve chest spasms
Class IV Ca blockers (Diltiazem and Verapamil) act primary on ___ cells
which are dependent on ___ for AP depol
act primarily on slow response cells (AV and SA nodes) which are dependent on Ca influx for AP
action 1C Na blockers
flecainide
Marked 0 depression
slow conduction (4+)
little impact on repol
triggered automaticity after repolarization excerbated by
fast rates
high intracellular Ca
class IA Na Channel blockers
quinidine
procainamide
disopyramide
action 1b Na blockers
(lidocaine)
minimal phase 0 depression
slow conduction (0- 1+)
shorten repol
indications lidocain
Vtach
Digitalis - induced arrhthmias
Safe for pts with long QT syndrome
indications Ca blockers
Atrial tachycardia
paroxysmal supraventricular tachycardia
mechanism DIoxin
enhances vagal parasympathetic activity > slow conduction at AV node
mechanism Adenosine
rapidly activates K channels to slow phase 4 depol at AV node
blocks cAMP enhance Ca channel activity at AV node
nifedipine specific side effects (weaker in other Ca blockers)
peripheral edema
side effects felcainide
pro-arrhtyhmic (CAST trial)
all actions of amiodarone (class III)
**K blocker **
Modest Na, Ca blocker
modest B adenoreceptor blocker
ach impact on depolarization
significantly depresses depol in slow response cells (no effect inf ast)
indications, Beta blockers
arrhythmias
VF vT with high catecholamine
(SA and AV node highly innervated)
action calsss III drugs
amiodarone, sotalol, dofetilide
K channel blockers
triggered automaticity, intterupted repolarization exacerbated by
long QT syndrome
phase 1
inactivation of fast Na chennels (or closure of L-type Ca)
Torsade de Pointes in pt on sotalol
U wave likely due to long repol of purkinje fibers
post ectopic pause + long QT
phase 4 =
resting membrane potential
(mostly K)
4 ways antiarrhythmic drugs reduced spontaneous discharge
1 decrease phase 4 slope (slow rate)
- increase max diastolic potential (more negative, further from threshold)
- Increase threshold
- increase AP duration > increase refractory period
phase 0
rapid depol of AP phase (Na in fast cells, Ca L-type in slow cells)
impact, lidocaine
threshold
AP
refractory rate
increase threshold
decrease AP duration
decrease refractory
Class II beta adrenergic blockers
propanolol, esmolol
class IB Na channel blockers
Lidocaine
verapamil side effects (less so in other Ca blockers )
constipation
interaction with digitalis to slow conduction velocity in AV > hear block (and verapamil)
increase plasma digitalis levels by competing for renal excertion (and verapamil)
short, long acting B blockers
propanolol - long, oral
esmolol - short, IV
indications Digoxin
Afib and supravent tachycardia
(to control ventricular response rate)
major side effects Ca blockers
Negative chronotropic effect - decreases automaticity of SA (brady)
Negative ionotropic (decrease Ca influx)
hypotension (decrease Ca into smooth muscle)
indication amiodarone (class III)
VF VT
prevention of reccurent paroxysmal a fib or flutter
most common target of Class III (amiodarone, sotalol)
IKr channel (increases Refractory peirod) (possible arrhytmias)
indications quinidine
atrial flutter
A fib
prevent VF VT
action of beta blockers in presence of catecholamines
slow rate of diastolic (phase 4) depolarization)
major side effects QUinidine
Severe GI
Vagolytic
inhibits p450s
Proarrhythmic,
reduced renal clearance of digitalis
metabolized by liver (renal failre pt OK)