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Wolff Pharmacology Review > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

refers to AV block where some beats are dropped (e.g., progressive prolongation of PR interval until a beat is dropped immediately followed by shortest PR interval (= Mobitz type 1 = Wenckebach heart block)); number, superscripted letters, word

A

2nd degree

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2
Q

therapy employed by cardiac electrophysiologists that has greatly decreased the need for chronic antiarrhythmic drug therapy

A

ablation

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3
Q

agonist at GPCR that hyperpolarizes the cell membrane and suppresses the rate of spontaneous depolarization in the SA and AV nodes, making it useful for aborting reentrant supraventricular arrhythmias in these structures

A

adenosine

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4
Q

receptors blocked by quinidine and procainamide but not disopyramide (2 words)

A

alpha adrenergic

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5
Q

classified as a class III antiarrhythmic but has range of effects that allow it to function as a “magic shotgun” for control of rhythm disturbances, in part because it lacks the anticipated reverse use dependence

A

amiodarone

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6
Q

effects associated with quinidine and disopyramide but not procainamide; reason disopyramide is selected to terminate vagally mediated atrial fibrillation

A

anticholinergic

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7
Q

less common form of AVRT where accessory pathway activates ventricles and AV node returns current to atria; treated acutely with procainamide and longer term with flecainide; class II and class IV drugs are contraindicated since their effects on the AV node could precipitate ventricular fibrillation

A

antidromic

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8
Q

risk factors for this include cardiovascular disease, diabetes, thyroid dysfunction, electrolyte imbalances, stimulants, alcohol and antiarrhythmic drugs

A

arrhythmia

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9
Q

transient form of this is the treatment objective when using adenosine to treat supraventricular tachycardia

A

asystole

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10
Q

treatment for bradycardia due to excessive parasympathetic tone

A

atropine

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11
Q

1s degree means PR interval is longer than normal, 3rd degree means there is a complete dissociation between atrial and ventricular action potentials

A

AV block

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12
Q

pausing the conduction signal here allows time for the atria to contract (abbr plus word)

A

AV node

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13
Q

abbr for atrioventricular nodal reentrant tachycardia, the most common cause of supraventricular tachycardia (especially young women)

A

AVNRT

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14
Q

abbr means there is an accessory pathway for atrioventricular communication (aka Wolff-Parkinson-White syndrome) which shows up as a delta wave during normal sinus rhythm; present in 1% of population and second most common cause of supraventricular tachycardia

A

AVRT

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15
Q

slow HR and AV conduction by decreasing cAMP levels that regulate the hyperpolarized cyclic nucleotide regulated (HCN) channels in the SA and AV nodes

A

beta blockers

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16
Q

seen in digoxin toxicity; a normal beat is followed by an ectopic ventricular beat

A

bigeminy

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17
Q

skin discoloration color associated with amiodarone

A

blue

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18
Q

responsible for the slow phase 0 depolarization in the SA and AV nodes, reason a drug like verapamil can slow the heart rate (abbr plus word)

A

Ca current

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19
Q

refers to the classic adverse/toxic effects of quinidine: decreased hearing, tinnitus, blurred vision, delirium

A

cinchonism

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20
Q

refers to a self-sustaining aberrant currents in the heart that occurs when timing is such that a wave of depolarizing current is able to pass in a retrograde direction through a one-way forward conduction block and encounters heart tissue that has already repolarized, and is therefore ready for another action potential

A

circus

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21
Q

class of sodium channel antiarrhythmic drugs that has little effect on phase 0 slope (i.e., rate of depolarization) but tends to shorten action potential duration by binding to channel and hastening/prolonging time that channel is in inactivated state; this decreases the frequency that an individual Na channel can be activated; rapid firing due to this effect causes the cell to desensitize as its population of receptors get stuck for longer periods of time in the inactivated state (word, roman num and letter)

A

class Ib

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22
Q

antiarrhythmic drug class that binds to the open state of voltage-gated sodium channels and dissociates very slowly; the loss of available Na+ channels can greatly decrease the rate of phase 0 depolarization and thereby the rate of signal conduction; action potential duration is relatively unaffected in a myocyte because the K+ channels are not directly affected and begin the normal repolarization process at a near normal time

A

class Ic

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23
Q

antiarhythmics that are beta blockers (word plus roman num)

A

class II

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24
Q

antiarrhythmics that block voltage-gated Ca2+ channels in the heart

A

class IV

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25
Q

site of microdeposit accumulation during amiodarone therapy

A

cornea

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26
Q

abbr. for aberrant depolarization during phase 4 when a Ca2+-overloaded sarcoplasmic reticulum “burps”

A

DAD

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27
Q

prolongation of PR interval and ST ________ are associated with therapeutic levels of digoxin

A

depression

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28
Q

Na+ - K+ ATPase blocker and positive inotrope, its ability to increase the refractory period and slow conduction in the AV node means it can be useful for ventricular rate control in those with atrial fibrillation (problem is its proarrythmic actions in His-Purkinje fibers and ventricle)

A

digoxin

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29
Q

one of the Ca2+ channel blockers that is frequency/use dependent; often used for ventricular rate control in patients with atrial fibrillation or flutter

A

diltiazem

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30
Q

orally active class III drug requiring special training to prescribe due to risk of torsades de pointes, but useful for treatment of atrial fibrillation/flutter in those with heart failure

A

dofetilide

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31
Q

drug designed to maintain desirable properties of amiodarone while eliminating iodine and shortening half-life; unfortunately does not work as well and has been associated with increased mortality in those with severe heart failure or moderate heart failure after recent acute decompensation

A

dronedarone

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32
Q

increasing action potential _______ is a means of slowing heart rate

A

duration

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33
Q

abbr for aberrant depolarization during phase 3 of action potential; risk of this occurring is increased by drugs that block cardiac K+ channels and thereby increase the amount of time required for the myocyte to repolarize away from threshold potential down to the resting membrane potential

A

EAD

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34
Q

refers to a heart beat originating in the wrong place (e.g., damaged myocardium that has a “hair trigger” due to its inability to fully repolarize (i.e., can only repolarize to just below threshold potential)

A

ectopic

35
Q

short-acting class II antiarrhythmic useful for situations where immediate adrenergic blockade is needed (e.g., to slow HR because of rapidly conducted atrial fibrillation)

A

esmolol

36
Q

flecainide binds tightly to the open state of Na channels, and is use dependent meaning that it is most likely to find an open channel when the HR is ___

A

fast

37
Q

pulmonary _____ is an adverse effect of amiodarone

A

fibrosis

38
Q

class Ic antiarrhythmic drug used to control supraventricular and ventricular arrhythmias when structural heart disease is absent

A

flecainide

39
Q

name given to the sodium current responsible for the spontaneous depolarization during phase 4 of the action potential now known to be conducted by HCN (e.g., HCN4 channels); these channels are activated by Hyperpolarization (e.g., -50 mV) and conductance is increased by increased Cyclic Nucleotides (cAMP)

A

funny

40
Q

potentially problematic since it averages ~50 days for amiodarone

A

half-life

41
Q

suggested when HR is <60 bpm in patients receiving digoxin, reason to withhold dose

A

heart block

42
Q

refers to a resting membrane potential that is more negative than normal; this slows HR by increasing the distance to the threshold potential

A

hyperpolarized

43
Q

class III agent administered as a rapid infusion to convert acute onset (but not chronic) atrial fibrillation or flutter to normal sinus rhythm; can cause torsades de pointes

A

ibutilide

44
Q

gate in a voltage-gated channel that closes to terminate a cycle of channel conductance

A

inactivation

45
Q

molecular component of amiodarone, can cause thyroid dysfunction

A

iodine

46
Q

blocked by Vaughn-Williams class III antiarrhythmics (abbr plus word)

A

K channels

47
Q

increase is responsible for phase 3 repolarization of ventricular muscle (abbr plus word)

A

K current

48
Q

prototypical class IB antiarrhythmic; a major use was to treat ischemia-induced ventricular arrhythmias, but amiodarone is now first-line therapy

A

lidocaine

49
Q

treatment for torsades de pointes

A

magnesium

50
Q

orally active class Ib antiarrhythmic drug

A

mexilitine

51
Q

Vaughn-Williams class I antiarrhythmics block voltage-gated _____ (abbr plus word)

A

Na channels

52
Q

responsible for phase 0 depolarization in ventricular muscle (abbr plus word)

A

Na current

53
Q

property of class Ia, Ic, II and IV drugs, but not amiodarone and dofetilide (which is reason these latter drugs can be used in patients with heart failure) (2 words)

A

negative inotrope

54
Q

state of the voltage and inactivation gates of a voltage-gated channel when current is flowing

A

open

55
Q

common form of AVRT with AV node conducting current to ventricles and accessory pathway returning current to atria; treated by vagal maneuvers, adenosine, class II or class IV drugs

A

orthodromic

56
Q

reason resting HR < 100 bpm, (i.e., ~spontaneous rate of SA node), too much causes bradycardia (2 words)

A

parasympathetic tone

57
Q

means the arrhythmia begins and ends abruptly

A

paroxysmal

58
Q

name given to the phase 2 portion of a ventricular action potential during which there is Ca2+ influx through voltage-gated Ca2+ channels

A

plateau

59
Q

major intracellular cation, resting membrane potential is due to its inability to exit from the cell down its concentration gradient (i.e., anion cannot follow), thereby creating the resting charge separation across the membrane

A

potassium

60
Q

condition during which digoxin–rather surprisingly– has a long history of safe use as treatment for supraventricular tachycardia

A

pregnancy

61
Q

class Ia drug now typically selected for IV administration if needed to treat paroxysmal atrial tachycardia or recurrent ventricular tachycardia; poorly tolerated when used chronically with side effects that include drug-induced lupus and agranulocytosis

A

procainamide

62
Q

a class Ic antiarrhythmic drug

A

propafenone

63
Q

EKG portion widened by class Ia and class Ic drugs due to slowing of Na conduction in conduction pathway myocytes

A

QRS

64
Q

EKG interval increased by class Ic agents and even more so by class Ia agents due to their additional blockade of K+ channels (2 words)

A

QT interval

65
Q

prototypical class Ia blocker, has a moderate affinity for open Na+ channels that slows the rate of impulse conduction ; other effects include K+ channel blockade to prolong action potential duration and anticholinergic and alpha-blocking effects

A

quinidine

66
Q

type of tachycardia caused by accessory pathways; class Ic drugs are especially effective at treating this

A

re-entrant

67
Q

increasing or decreasing this period can disrupt the timing of recirculating currents in the myocardium

A

refractory

68
Q

this is delayed by K+ channel blockade

A

repolarization

69
Q

refers to the sodium channel state in which its voltage gate is closed (i.e., triggerable) and its inactivation gate is open

A

resting

70
Q

refers to fact that K+ channel blockers bind to the channels during the resting state, meaning that adverse proarrhythmic consequences are more likely when HR is slow (3 words)

A

reverse use-dependence

71
Q

calcium release channels in the sarcoplasmic reticulum also blocked by flecainide; mutations here can cause catecholamine triggered sudden death

A

RYR2

72
Q

cells here have the fastest rate of spontaneous depolarization and therefore control HR; first to get “bingo” causes others in region to respond (abbr plus word)

A

SA node

73
Q

with a half-life of ~10 ____, adenosine must be administered IV to cause its desired short-lived effect

A

seconds

74
Q

syndrome means that SA node is failing to originate a heart beat

A

sick sinus

75
Q

decreasing this during phase 4 in the SA node occurs with drugs such as propranolol or ivabradine

A

slope

76
Q

typical form of AVNRT, initiated when a premature beat reaches the slow pathway through the AV node that has recovered/repolarized more rapidly after having been extinguished by the previous beat (2 words)

A

slow-fast

77
Q

occurs in the cells of the SA and AV nodes, triggers the transmission of the action potential (2 words)

A

slow potential

78
Q

major extracellular cation, has both electrical and concentration gradients favoring cellular influx, but approximately no functioning influx pathways in the resting state of excitable cells

A

sodium

79
Q

beta blocker with class III antiarrhythmic effects, can cause torsades de pointes, useful for recurrent atrial fibrillation or ventricular tachycardia related to an old myocardial infarction(i.e., coronary artery disease)

A

sotalol

80
Q

contraindication for use of class Ic antiarrhythmic drugs (3 words)

A

structural heart disease

81
Q

refers to the voltage at which depolarization causes voltage-gated sodium channels to open in ventricular muscle, thereby causing phase 0 in the action potential

A

threshold

82
Q

potentially lethal ventricular tachycardia associated with drugs that prolong the QT interval (e.g., quinidine and dofetilide)… and later found for many other drugs already on the market

A

torsades de pointes

83
Q

maneuver that increases parasympathetic tone; can cause bradycardia or treat tachycardia

A

valsalva

84
Q

a frequency/use dependent Ca2+ channel blocker that can therefore be used as an anti-arrhythmic agent to control supraventricular tachycardias

A

verapamil

Wolff Pharmacology Review (12 decks)

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