Chapter 14- Antiarrhythmic Drugs

Front 1

In what setting do cardiac arrhythmias commonly occur?

Back 1

the presence of preexisting heart disease

Front 2

Associations with antiarrhythmics?

Back 2

anesthesia, hyperthyroidism, electrolyte disorders, and digitalis toxicity

Front 3

What are the five main classes of antiarrythmic drugs?

Back 3

Group 1 (sodium channel blockers)
Group 2 (beta-blockers)
Group 3 (potassium channel blockers)
Group 4 (calcium channel blockers)
Group 5 (Miscellaneous)

Front 4

Esmolol is an example of what class of antiarrythmic?

Back 4

beta-blocker

Front 5

What are the two major mechanisms for arrhythmias?

Back 5

abnormal automaticity and abnormal conduction

Front 6

Name 6 clinically significant arrhythmias

Back 6

atrial flutter, atrial fibrillation, atrioventricular nodal reentry, premature ventricular beats, ventricular tachycardia, ventricular fibrillation

Front 7

What is torsade de pointes

Back 7

ventricular arrhythmia often induced by antiarrhythmic and other drugs that change the shape of the action potential and prolong the QT interval

Front 8

How does torsade de pointes present on an EKG

Back 8

polymorphic ventricular tachycardia, waxing and waning QRS amplitude; associated with long QT syndrome

Front 9

In the AV node, what current dominates the upstroke and the AP conduction velocity?

Back 9

calcium

Front 10

What is supraventricular tachycardia?

Back 10

a reentrant arrhythmia that travels through the AV node; may be conducted through atrial tissue as part of the reentrant circuit

Front 11

What is ventricular tachycardia?

Back 11

associated with MI; may involve abnormal automaticity or abnormal conduction; impairs cardiac output, may turn into V Fib (emergency)

Front 12

Effect of group 1A drugs on AP?

Back 12

prolong

Front 13

Class of procainamide?

Back 13

Group 1A

Front 14

Effect of group 1B on AP?

Back 14

shorten in some cardiac tissues

Front 15

Class of lidocaine?

Back 15

Group 1B

Front 16

Mechanism of action of group 1 antiarrhythmics?

Back 16

slow or block conduction in ischemic and depolarized cells;
slow or abolish abnormal pacemakers wherever they depend on sodium channels

Front 17

Very selective group 1 drugs work specifically on?

Back 17

ischemic or abnormal tissue

Front 18

How do certain group 1 drugs selectively block abnormal tissue sodium channels?

Back 18

-more effective when channel is open or in refractory period
-abnormal tissue ion channels spend more time in open state

Front 19

Effect of group 1C on AP?

Back 19

none

Front 20

quinidine and disopyramide class

Back 20

Group 1A

Front 21

Group 1A block which type of arrhythmias?

Back 21

both atrial and ventricular

Front 22

Full effects of group 1A drugs?

Back 22

slow conduction velocity and ectopic pacemakers, increase AP duration and effective refractory period

Front 23

Route of administration for lidocaine

Back 23

IV or IM

Front 24

Orally active 1B drug?

Back 24

mexiletine

Front 25

Lidocaine specifically affects?

Back 25

ischemic or depolarized Purkinje and ventricular tissue (little effect on atrial tissue)

Front 26

Phenytoin use as a cardiac drug?

Back 26

reverse digitalis-induced arrhythmias

Front 27

How does lidocaine work?

Back 27

Reduces AP duration in some cells, but slows recovery of sodium channels from inactivation which does not shorten the effective refractory period

Front 28

Prototype drug with group 1C actions?

Back 28

flecainide

Front 29

How do group 1C drugs work?

Back 29

depress sodium current and markedly slow conduction velocity in atrial and ventricular cells **visible on ECG as QRS elongation

Front 30

Toxicity of procainamide?

Back 30

increased arrhythmias, hypotension, lupus-like syndrome

Front 31

toxicity of quinidine

Back 31

cinchonism, cardiac depression, GI upset, autoimmune rxns

Front 32

Interaction of quinidine and digoxin?

Back 32

reduces clearance of digoxine and may increase the serum concentration

Front 33

What ionic state exacerbates cardiac tox of group 1A, 1B, and 1C drugs?

Back 33

hyperkalemia

Front 34

Treatment of overdose with group 1A drugs?

Back 34

sodium lactate and pressor sympathomimetics

Front 35

When are atrial arrhythmias responsive to lidocaine

Back 35

only if caused by digitalis

Front 36

Why is lidocaine not given orally

Back 36

high 1st pass effect and metabolites may be cardiotoxic

Front 37

Prototypic antiarrhythmic beta-blockers?

Back 37

propranolol and esmolol

Front 38

mechanism of action of group 2 antiarrhythmics?

Back 38

cardiac beta-adrenoceptor blockade, reduction in cAMP, results in reduction of both sodium and calcium currents and suppression of abnormal pacemakers

Front 39

Esmolol use exclusivity?

Back 39

acute arrhythmias

Front 40

Group 1B drugs used as prophylactics for MI patients?

Back 40

propranolol, metoprolol, timolol

Front 41

Five group 3 antiarrhythmics?

Back 41

dofetilide, abutilide, sotalol, amiodarone, dronedarone

Front 42

Mechanism of action of group 3 drugs?

Back 42

prolongation of the Ap duration; caused by blockade of potassium channels that are responsible for the repolarization of the AP **apparent use in ECG

Front 43

most important toxicity of group 3 drugs?

Back 43

torsade de pointes

Front 44

Most efficacios antiarrhythmic drug?

Back 44

amiodarone (broad spectrum)

Front 45

Amiodarone side effects?

Back 45

microcrystalline deposits in the cornea and skin, thyroid dysfunction, paresthesias, tremor, and pulmonary fibrosis

Front 46

Prototype of group 4 antiarrhythmics?

Back 46

verapamil (diltiazem also effective)

Front 47

Mechanism of group 4 drugs?

Back 47

-work in arrhythmias that must cross calcium-dependent cardiac tissue (AV node); cause a selective depression of calcium current in tissues that require L-type calcium channels

Front 48

Effect of group 4 drugs on AV conduction velocity, ERP, and PR?

Back 48

AV: decreased
ERP: increased
PR: increased

Front 49

In what cardiac clinical setting should group 4 drugs be avoided?

Back 49

ventricular tachycardias

Front 50

How does adenosine function as an anti-arrhythmic?

Back 50

blocks conduction in the AV node by hyperpolarizing tissue and reducing calcium current