Step 1 - Pharm - Antiarrhythmics (Lippencott)

Front 1

Treatment of choice for atrial flutter

Back 1

Propranolol, verapamil (act on AV node)

Front 2

Treatment of choice for atrial fibrillation

Back 2

Propranolol

Front 3

Treatment of choice for AV nodal reentry

Back 3

Propranolol, verapamil, digoxin (all of these slow AV node conduction)

Front 4

Treatment of choice for acute supraventricular tachycardia

Back 4

Adenosine, verapamil
(verapamil is also treatment of choice for atrial flutter)

Front 5

Treatment of choice for ventricular fibrillation refractory to electrical defibrillation

Back 5

Amiodarone, epinephrine, lidocaine

Front 6

This arrhythmia is a common cause of death in patients who have had an MI

Back 6

Acute ventricular tachycardia

Front 7

Treatment of choice for acute ventricular tachycardia

Back 7

Lidocaine, amiodarone

Front 8

How does hypoxia and potassium imbalance cause arrhythmia?

Back 8

They cause abnormal automaticity (vs. abnormal conduction, which is caused by bundle of Kent, scar tissue post-MI, etc.)

Front 9

What is the most common cause of arrhythmia?

Back 9

Reentry

Front 10

What are the two general means by which antiarrhythmics work?

Back 10

Suppression of automaticity (block Na or Ca channels to reduce the ratio of these ions to K); slow conduction and/or increase refractory period (thereby converting unidirectional block to a bidirection block, to treat reentry arrhtyhmias)

Front 11

This class of antiarrhythmics has the same mechanism of action as local anesthetics

Back 11

Class I (Na channel blockers)

Front 12

This class of antiarrhythmics blocks sodium channels

Back 12

Class I

Front 13

This class of antiarrhythmics blocks K channels

Back 13

Class III

Front 14

This class of antiarrhythmics is just beta-blockers

Back 14

Class II

Front 15

This class of antiarrhythmics is just calcium-channel blockers

Back 15

Class IV

Front 16

MoA of class IA

Back 16

Slow phase 0 depolarization in ventricular muscle

Front 17

MoA of class IB

Back 17

Shortens phase 3 repolarization in ventricular muscles

Front 18

MoA of class IC

Back 18

Like IA, but markedly (slows phase 0 depolarization, but does not affect AP duration)

Front 19

MoA of class III

Back 19

K channel blockers; prolong duration of AP by prolonging the effective refractory period; they do not affect phase 0 depolarization or resting membrane potention

Front 20

What does a prolonged QT interval correspond to?

Back 20

Slow repolarization (phase 3); caused by K channel blockers (class III)

Front 21

What causes torsades de pointes?

Back 21

Prolonged QT, eg, slow repolarization

Front 22

This class I drug can be used to maintain sinus rhythm following cardioversion of atrial flutter/fibrillation; and to prevent ventricular tachycardia

Back 22

Quinidine

Front 23

This is the prototype class IA drug

Back 23

Quinidine

Front 24

This class IA drug must have its dosages adjusted in patients with renal failure

Back 24

Procainamide

Front 25

This antiarrhythmic is associated with SLE-like syndrome

Back 25

Procainamide

Front 26

This antiarrhythmic is associated with CNS side effects (depression, hallucination, psychosis)

Back 26

Procainamide

Front 27

This class IA drug causes peripheral vasoconstriction, unlike others of its class

Back 27

Disopyramide

Front 28

This class of antiarrhythmics is useful in treating ventricular arrhythmias

Back 28

Class IB drugs (lidocaine, mexiletine, tocainide), which speed up rather than slow down HR

Front 29

These are oral version of lidocaine

Back 29

Mexiletine, tocainide

Front 30

This drug has littled effect on atrial or AV junction arrhythmias

Back 30

Lidocaine

Front 31

This antiarrhythmic is not use-dependent (eg, shows effects at normal heart rates)

Back 31

Flecainide (class IC)

Front 32

This drug is particularly useful in suppressing premature ventricular contractions

Back 32

Flecainide (class IC)

Front 33

This drug can aggravate CHF

Back 33

Flecainide (class IC)

Front 34

MoA of class II antiarrhythmics (beta blockers)

Back 34

Diminish phase 4 depolarization (Ca entry is controlled in part by catecholamine-dependent channels)

Front 35

This is a very short-acting drug used to treat acute arrhythmias that occur in surgical or emergency settings

Back 35

Esmolol

Front 36

This is the most widely used beta blocker in the treatment of cardiac arrhythmias

Back 36

Metoprolol (selective B1 blocker, therefore reduces risk of bronchospasm)

Front 37

This drug is structurally related to thyroxine

Back 37

Amiodarone

Front 38

This drug has both antianginal and antiarrhythmic activity

Back 38

Amiodarone

Front 39

This drug has a prolonged half-life of several weeks

Back 39

Amiodarone

Front 40

This drug distributes extensively in adipose tissue

Back 40

Amiodarone

Front 41

Effects of this drug may not be achieved until 6 weeks after initiation

Back 41

Amiodarone

Front 42

This drug can cause blue skin discoloration

Back 42

Amiodarone (due to iodine accumulation in skin)

Front 43

This antiarrhythmic is useless in prolonging survival in CHF patients

Back 43

Amiodarone

Front 44

This antiarrhythmic has the lowest rate of side effects

Back 44

Sotalol

Front 45

This drug can be used first-line to treat atrial fibrillation and heart failure, as well as CAD with impaired LV function

Back 45

Dofetilide

Front 46

These drugs are more effective against atrial than ventricular arrhythmia

Back 46

Calcium channel blockers (verapamil, diltiazem)

Front 47

This calcium channel blocker is not considered an antiarrhythmic

Back 47

Nifedipine

Front 48

This drug is notable for being extensively metabolized by the liver, and is therefore given carefully to patients with liver problems

Back 48

Verapamil

Front 49

How does digoxin treat arrythmias?

Back 49

Prolongs the effecitve refractory period; slows down AV node

Front 50

This drug is used to control ventricular response rate in a-fib and flutter

Back 50

Digoxin

Front 51

This drug has an extremely short duration of action (15 s), and is used to treat acute supraventricular tachycardia

Back 51

Adenosine

Front 52

These drugs prevent cardiac arrhythmias in post-MI patients, and are thus given prophylactically

Back 52

Beta blockers (esp metoprolol)

Front 53

These drugs are capable of producing bidirectional blocks (and thereby preventing reentry arrhythmias)

Back 53

Class I drugs (eg, lidocaine)

Front 54

This drug has as its side effects headache, dizziness and tinnitus

Back 54

Quinidine ("cinchonism")

Front 55

This drug can cause hypothyroidism

Back 55

Amiodarone