B4.017 - Anti-arrhythmic Drugs Flashcards

1
Q

what are the extracardiac effects of amiodarone

A

peripheral vasodilation especially after IV administration

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2
Q

what is lidocaine used for

A

ventricular arrhythmias most effectively associated with MI ischemia or digoxin toxicity

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3
Q

which drug is used for acute tachicardias during surgery

A

esmolol

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4
Q

harmful effects of beta blockers

A

negative inotropy may worsen HF in patients with acute myocardial infarction or decompensated heart failure

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5
Q

how is lidocaine given and why

A

IV, high first pass metabolism

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6
Q

what is Procainamide used for and why

A

it increases refractory period so can help treat atrial and ventricular tachycardia

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7
Q

extracardiac effects of quinidine

A

blocks alpha adrenergic receptors to cause vasodilation which can lead to marked hypotension and reflex tachycardia

also has antimuscarinic effects

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8
Q

what is disopyramide approved in US to treat

A

ventricular arrhythmias

not used often because of antimuscarinic effect

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9
Q

what is the least cardiotoxic antiarrythmic drug

A

lidocaine

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10
Q

does procainamide elevate digoxin levels?

A

no

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11
Q

how do class 1 sodium channel blockers work

A

decrease HR by elevating threshold for excitation and decreasing phase 4 depolarization in SA node

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12
Q

Lidocaine is rarely effective for what

A

normally polarized tissues like atrial flutter or fibrillation

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13
Q

which drug class prolongs action potential duration in addition to being a sodium channel blocker and what can that cause

A

Class 1A

Procainamide, Quinidine, Disopyramide

QT prolongation

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14
Q

Class 1C drugs

A

Flecainide, propafenone, moricizine

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15
Q

which drug releases NO from endothelial cells

A

amiodarone

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16
Q

cardiac effects of amiodarone

A

prolongs AP duration by blocking K channels

decreases rate of firing in pacemaker cells by blocking inactivated Na channels

blocks alpha and beta adrenergic receptors and calcium channels and thus inhibits AV node conduction to produce bradycardia

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17
Q

what is the half life of amiodarone

A

short 3-10 days

slower - several weeks, toxicity long after it is discontinued

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18
Q

what is sotalol used for

A

life threatening ventricular arrhythmias

maintainging sinus rhythm in a fib

treatment of supraventricular and ventricular arrhythmias in pediatrics

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19
Q

what are the 2 most frequently used beta blockers and what are they used for

A

propranolol and atenolol

rate control

to treat supraventricular and ventricular arrhythmias caused by sympathetic stimulation or to prevent ventricular fibrilation

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20
Q

what can procainamide cause due to a prolonged QT interval

A

life threatening arrythmias

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21
Q

what are toxicities of quinidine

A

precipitates digoxin

thrombocytopenia

syncope due to torsade de pointe

chinchonism (headahce, dizziness, tinnitus)

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22
Q

beneficial effects of beta blockers

A

diminished sympathetic activation of heart and blood vessels and thus diminished workload

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23
Q

which drug can cause SA and AV node depression directly

A

Procainamide

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24
Q

what does moricizine do

A

potent sodium channel blocker that does not prolong APD

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25
what are the class 1A drugs
Procainimide, Quinidine, Disopryramide
26
what drug has a very narrow therapeutic window
digoxin
27
what is teh difference between mexiletine and lidocaine
lidocaine has to be given IV because of first pass system Mexiletine can be given orally Mexiletine can also be used for relief of chornic pain especially in diabetic neuroathy and nerve injury
28
what are amiodarone toxicities
asymptomatic bradycardia and AV block pulmonary fibrosis abnormal liver function and hepatitis grayish blue skin corneal microdeposits thyroid function needs to be evaluated before treatment blocks T4-T3 hypothyroidism or hyperthyroidism
29
how is amiodarone given and why
orally or IV to maintain normal sinus rhythm in patietns with a fib or prevent recurrent ventricular tahcycardia
30
what will enhance toxicity of digoxin
hypokalemia
31
what effect do Class 1B drugs have on APD
shortened APD
32
what is the main therapeutic use of adenosine
IV injection to convert paroxysmal supraventricular tachycardia to sinus rhythm, very short half life
33
what drug type causes this
Class 1A Procainamide, quinidine, disopyramide moderate Na+ channel block; prolong APD
34
what effect do class 1C drugs have on APD
minimal effect on APD
35
magnesium is used for what
to prevent torsade de pointes
36
what drug has a metallic taste
propafenoe
37
what does digoxin do to heart rate
stimulates vagus nerve and decreases heart rate can be used in atrial fibrillation to decrease the rate
38
why is digoxin more toxic in hypokalemic patients
K and digoxin compete for bidning to Na/K ATPase so if theres less potassium to compete its effects will be too strong
39
what does adenosine do
opens inward rectifier K+ channels leading to hyperpolarization and inhibits L type calcium channels to inhibit calcium entry and conduction velocity in AV node
40
digoxin toxicities
GI - nauseal vomiting, diarrhea, abdominal discomfort cardiac - can lead to almost all arrhythmias
41
what is flecainide very effective in suppressing
premature ventricular contractions
42
what are oral class IV antiarrhythmics used for treatment of
supraventricular arrhythmias and for rate control in a fib
43
what drug class causes this
Class 1B Lidocaine, Mexiletine Shorten APD
44
what does quinidine precipitate
digoxin toxicity
45
what are the extracardiac effects of procainamide
ganglion blocking activity which reduces peripheral resistance and can lead to hypotension
46
which effect do class 1A drugs have on APD
prolonged APD
47
cadiotoxic effects of procainamide
QT prolongation inducing torsades de pointes
48
class 1B drugs
Lidocaine, Mexiletine
49
50
does flecainanide have antimuscarinic effects
no
51
what is flecainide used to treat
supraventricular arrhythmias
52
what is the similarity of class 1A antiarrhythmics
all block Na andK channels and induce torsade de pointes
53
what does Flecainide do
blocks Na+ and K+ channels with no QT prologation
54
procainamide long term adverse extra cardiac effects
reversible lupus like syndrome (rash, arthralgia, arthritis, pericarditis)
55
what are the anti arrhythmic drugs that are not part of the 4 classes
Adenosine Digoxin Magnesium
56
therapeutic use of procainamide
most atrial and ventricular arrhythmias short hlaf life so less useful for long term oral treatment
57
what is dronedarone
structural analogue of amiodarone but no iodines
58
what does digoxin do
potent and selective inhibitor of Na/K ATPase --\> increased intracellular calcium concentration --\> positive inotrope
59
what drug has modest muscarinic effects
quinidine
60
how are all class 1 C antiarrhythmics administered
orally
61
what is sotalol
class 3 antiarrhythmic used as beta blocker and potassium channel blocker
62
how is amiodarone metabolized
CYP3A4 --\> drug drug interactions
63
what drug class causes this
Drug class 1C Minimal effect on APD Flecainide, propafenone, moricizine
64
what drug has a black box warning and what is it for
dronedarone amiodarone analogue increased risk of death, stroke and heart failure in patients with decompensated heart failure or a fib
65
what are toxicities of disopyramide
more antimuscarinic effects than quinidine Atropine like activity: Urinary retention Dry mouth, blurred vission, constipation worsening glaucoma
66
what are the 4 classes of anti arrhythmic drugs
Class 1 - sodium channel blockers Class 2 - beta blockers Class 3 - potassium channel blockers Class 4 - calcium channel blockers
67
what do verapamil and dilitiazem
block L type Ca channels in myocardium and vascular smooth muscle decreases contractility reduces SA node automaticity slow AV node conduction
68
how does adenosine inhibit pacemaker current
decreases heart rate
69
which drug is withdrawn from US market
moricizine
70
what are common side effects of dofetilide adn ibutilide
prolonged QT and torsade de pointes
71
compare and contrast the antimuscarinic, lupus like syndrome, plasma digoxin and alpha adrenergic block of the class 1A drugs
72
propafenone blocks what well and what weakly
blocks Na well, beta blocking activity weakly because its a propranolol analogue