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Arrhythmias Flashcards

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1
Q

class I

A

sodium channel blockers

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2
Q

class II

A

beta blockers

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3
Q

class III

A

potassium channel blockers

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4
Q

class IV

A

calcium channel blockers

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5
Q

class IA agents

A

quinidine, procainamide, disopyramide

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6
Q

class IB agents

A

lidocaine, mexiletine, phenytoin

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7
Q

class IC agents

A

flecainide, propafenone

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8
Q

class II agents

A

metoprolol, esmolol

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9
Q

class III agents

A

amiodarone, dronedarone, sotalol, dofetilide, ibutilide

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10
Q

class IV agents

A

verapamil, diltiazem

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11
Q

class I agents affect phase _ of the action potential

A

0

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12
Q

class IA cause Na channels to have a _______ recovery time

A

intermediate (intermediate potency)

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13
Q

class IA agents also inhibit _ channels

A

K+ (increasing action potential duration by prolonging repolarization)

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14
Q

class IB cause Na channels to have _____ recovery time

A

fast (low potency)

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15
Q

class IB ______ the action potential duration

A

decrease; shorten repolarization (opposite to IA agents)

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16
Q

class IC agents cause Na channels to have a ____ recovery time

A

slow (high potency)

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17
Q

effect of class IC agents on length of action potential duration

A

no effect

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18
Q

effects of quinidine on action potential

A

shifts phase 0 and phase 3 to the right, QT prolonged (torsades)

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19
Q

quinidine side effects that are mediated by blockade of autonomic nervous system receptors

A

anticholinergic effect (muscarinic receptors), increased HR, fast ventricular rate, hypotension (alpha receptor blockade)

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20
Q

therapeutic use of quinidine

A

limited, may be used for ventricular arrhythmias refractory to other therapies

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21
Q

other adverse effects of quinidine that lead to discontinuation

A

GI: diarrhea/n/v, cardiotoxicity, torsades, hypotension, cinchonism, increases plasma digitalis concentration and may precipitate digitalis toxicity

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22
Q

procainamide pearls

A

similar to quinidine but less anticholinergic effects, unique toxic effect: lupus erythematosus-like syndrome

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23
Q

disopyramide pearls

A

very anticholinergic, mostly used for a type of heart failure called hypertrophic cardiomyopathy

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24
Q

how is lidocaine administered

A

IV only (rapid first pass liver metabolism–> unsuitable for oral administration)

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25
therapeutic use of lidocaine
ventricular arrhythmias only
26
adverse effects of lidocaine
it is lipophilic so crosses BBB so CNS effects-- drowsiness, slurred speech, tremors, seizures
27
lidocaine effects on fast fibers
blocks Na channels--> channels unresponsive to stimulation for longer time--> channels in damaged tissue are in inactivated state longer--> decreases responsiveness/slows conduction in damaged tissue
28
what is mexiletine essentially
PO version of lidocaine
29
mexiletine therapeutic use
ventricular arrhythmias
30
mexiletine side effects
significant GI effects
31
flecainide mech
blocks sodium and some potassium channels
32
flecainide therapeutic use
atrial arrhythmias like AF/AFl
33
propafenone mech
blocks sodium and some potassium channels, some beta-blocking properties (structurally similar to propranolol)
34
propafenone therapeutic use
atrial arrhythmias like AF/AFl
35
what did the cardiac arrhythmia suppression trial demonstrate about flecainide and propafenone
they may actually exacerbate arrhythmia and worsen outcome in patients with structurally abnormal hearts (post-MI)
36
how do beta blockers have antiarrhythmic action
they block effects of endogenous norepinephrine on beta-one receptors
37
what are the actions of norepinephrine that lead to arrhythmia
increase the automaticity of normal and abnormal pacemaker cells, increase conduction velocity in the AV node
38
what do you see on the ECG after beta-blocker administration
prolongation of PR interval
39
beta blockers ____ the effective refractory period of AV node
increase
40
how are beta blockers able to prevent fatal arrhythmias after MI
the presence of norepinephrine may lead to augmented automaticity of cardiac muscle cells, allowing them to generate abnormal rhythms, but beta blockers block the effects of norepi
41
therapeutic use of beta blockers for arrhythmias
supraventricular arrhythmias: AF, AFl, paroxysmal atrial tachycardia
42
what causes "sudden death" after MI
ventricular arrhythmia, ventricular tachycardia, ventricular fibrillation
43
esmolol pearls
short acting beta blocker given IV, can be used in a clinical situation to suppress arrhythmias related to excess norepi
44
class III mech
block K+ channels, prolong refractory period (repolarization)
45
amiodarone has mechanistic properties of which classes
ALL: blocks inactivated Na channels, blocks Ca channels, blocks K channels, blocks beta receptors
46
amiodarone therapeutic uses
oral therapy for severe ventricular arrhythmias (recurrent V tach or fib), also used for a fib and a flutter
47
PK profile of amiodarone
variable absorption and hepatic metabolism (CYPA3A4) to active metabolite, very long half-life of approx. 50 days, highly lipophilic with extensive volume of distribution
48
toxicity with amiodarone
PK profile explains multi-organ adverse effects: pulmonary fibrosis or pneumonitis, microdeposits in the cornea, thyroid toxicity (iodine-related, hypo or hyperthyroidism), skin blue-grey discoloration (smurf syndrome), photosensitivity, many others
49
dronedarone therapeutic uses
paroxysmal or persistent AFib or AFL
50
dronedarone is a derivative of _____
amiodarone; but it is free of iodine and less lipophilic than amio (less ADE but less effective)
51
sotalol mech
prolongs action potential by blocking K channels, non-selective beta blocker with class III effect
52
sotalol therapeutic uses
AFib/AFL, sometimes for ventricular arrhythmias
53
dofetilide therapeutic uses
AFib/AFL
54
what does dofetilide require
inpatient initiation with monitoring of QTc interval, creatinine clearance (renal dose adjustment), and screening for drug-drug interactions
55
dofetilide pearls
PO only, pure class III K channel blocker
56
Ibutilide pearls
pure class III K channel blocker, only available IV, higher risk of causing torsades
57
ibutilide therapeutic uses
cardioversion of AFib/AFL
58
calcium channel blockers mech for arrhythmias
decrease Ca current by blocking a fraction of the Ca channels participating in upstroke of AP--> slows conduction of AV node (slow response fibers). block activated and inactivated channels
59
electrophysiologic effects of calcium channel blockers
decrease AV node conduction velocity, increase AV node refractory period
60
effect of CCBs on ECG
prolongation of PR interval
61
therapeutic uses of CCBs
slows ventricular RATE to supraventricular arrhythmias: treatment of reentrant supraventricular tachycardia when reentry circuit involves AV node, reduces ventricular response in AFib and AFL
62
do not use CCBs in patients with ____
AV conduction problems, or severe ventricular dysfunction
63
other antiarrhythmic agents
adenosine, digoxin, magnesium
64
adenosine is a naturally occurring ____
nucleoside
65
adenosine acts on ____
specific adenosine receptors (A1)
66
why is adenosine's use limited to the clinical setting
ultrashort half-life: given by rapid IV bolus administration, rapidly metabolized with a half-life of seconds
67
the adenosine A1 receptor is a ______ receptor
G-protein coupled receptor
68
adenosine therapeutic uses
acute termination of supraventricular tachycardia (SVT)
69
what is digoxin used for
controlling ventricular response to AFib (common in heart failure)
70
what is the mechanism of digoxin
increases vagal tone, slows conduction through AV node, decreases ventricular rate
71
what is magnesium used for
Torsades first line, used to manage a variety of arrhythmias that occur in the setting of hypomagnesemia
72
mech of magnesium
slows the rate of SA node impulse formation, prolongs conduction time. magnesium is necessary for movement of Ca, Na, and K and membrane stabilization

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