Lecture 2 Anti-arrhythmic drugs

Question 1

Classes of antiarrythmnics:
1 = \_\_\_ blockers
2 = \_\_\_\_ blockers
3= \_\_\_\_ blockers
4 = \_\_\_\_ blockers

Answer 1

sodium channel;
beta;
potassium (mainly) channel];
L-type calcium channel

Question 2

in general, class ___ arrythmics act on cardiac myocytes, while class ____ act on pace maker cells

Answer 2

1, 3;

2, 4

Question 3

which class decreases the phase 4 slope of pacemaker APs?

Answer 3

beta blockers (class 2)

Question 4

what configurations of receptor to class 1 AA (anti-arrhythmics) bind to?

Answer 4

open or inactive Na channels (not resting)

Question 5

in resting sodium channels, the ____ gate is closed, and class 1 AAs can’t bind. In inactivated sodium channels, the ___ gate is closed, but the ____ gate is open, so the class 1 AAs can bind

Answer 5

activation; inactivation, activation

Question 6

class 1 binding is described as ___ or ____ dependent. Rank the classes in order of most binding to least.

Answer 6

use, state;

C > A > B

Question 7

Class 1 AAs bind at a greater degree in tissues with an abnormally ____ frequency of depolarization, such as during ____

Answer 7

high;

tachycardia

Question 8

during ischemia, the resting membrane potential is ____, so there will be an increased number of ___ Na channels and thus ____ binding of class 1 AAs

Answer 8

depolarized; inactivated; greater

Question 9

class 1 AAs act on ___ channels, which are important in phase ____.

Answer 9

sodium; 0 (ie they change the slope of the upstroke)

Question 10

Class 1A effect on AP duration and ERP =

Answer 10

increase AP duration, prolong ERP

Question 11

Class 1B effect on AP duration and ERP:

Answer 11

decrease AP duration, shorter ERP

Question 12

Class 1C effect on AP duration and ERP:

Answer 12

no effect on AP duration, no effefct on ERP in purkinje or ventricular tissue; (prolong ERP in AV node and accessory bypass tract according to FA)

Question 13

what channel is affected that determines changing of the ERP? which class 1 subclasses affect these channels?

Answer 13

potassium;

1A and 1B

Question 14

What are the class 1A AAs?

Answer 14

procainamide, quinidine, disopyramide

Question 15

generally, class 1A AAs affect what location of arrhythmias?
What side effect do they all have?

Answer 15

supraventricular (atrial) and ventricular;

long QT, can cause torsades de pointes

Question 16

which of the class 1A AAs has metabolism via a P-gp efflux pump?

Answer 16

quinidine

Question 17

most notable side effect associated with quinidine:

what about procainamide?

Answer 17

cinchonism (headache, tinnitus);

lupus like syndrome

Question 18

disopyramide exhibits ____ side effects, which can cause or predispose patients to ____

Answer 18

anti-cholinergic; heart failure

Question 19

What are the 3 class 1B AAs?

Answer 19

mexilitine, lidocaine, plus tocainide (not mentioned in sketchy or FA)

Question 20

Class 1B AAs affect _____ purkinjke and ventricular tissue by blocking ____ channels. This _____ the refractory period

Answer 20

ischemic/depolarized;
potassium, decreases

not used for supraventricular things (ie not atrial afib)-IIB is “B”est post MI

Question 21

general side effects of class 1B antiarrythmics:

Answer 21

CNS effects, cardiovascular depression

Question 22

what are the two class 1C AAs?

Answer 22

flecainide, propanefone

Question 23

class 1C AAs markedly slow ____ ____ but have minimal effect on _____; the ECG shows a _____ QRS

Answer 23

conduction velocity;
action potential duration/Effective refractory period;
widened

Question 24

what part of the heart do class 1C AAs affect? (ie ventricles, atria etc)

Answer 24

both ventricular and supraventricular

Question 25

both class 1Cs are ____ and are contraindicated in patients with what?

Answer 25

pro-arrythmic;

ischemic heart disease;typically last resort drugs

Question 26

class 1 AAs:
which prolongs the QT? which shortens it?Which widens the QRS?

Answer 26

prolong = class 1a
shorten = class 1b
widen QRS = 1a and 1c

Question 27

Class 2 AAs cause a decrease in ____ at the nodes which closes ___ channels. this causes a prolonged phase ____

Answer 27

cAMP, Calcium;4

Question 28

beta blockers cause a ____ in pacemaker activity, a ___ in conduction time through the AV node, and a ____ ERP

Answer 28

decrease, increase, increased

Question 29

some beta blockers are membrane ____, such as propanolol. these ____ the QRS

Answer 29

stabilizers, prolong

Question 30

which of the class 2 AAs is especially short acting and can be used in emergency?

Answer 30

esmolol (ie supraventricular arrythmias)

Question 31

class 1 AAs help control the _____ in Afib. class 2 AAs help restore the ____.

Answer 31

rhythm; rate

Question 32

name 4 class 3 AAs mentioned in FA/sketchy:

Answer 32

AIDS: amiodarone, ibutilide, dofetilide, sotalol

also bretylium

Question 33

class 3 AAs prolong the ____ by increase phase ___ repolarization without affecting the depolarization phase (phase __)

Answer 33

action potential duration, 3;

0

Question 34

class 3 AAs have the most effect at ____ rates. thus they are ____ dependent

Answer 34

low, reverse-use

Question 35

all class 3 AAs have what side effect? What can occur do to this side effect?

Answer 35

prolong QT –> torsades

Question 36

amiodarone has a ____ onset and ____ duration of action. is it a fun drug?

Answer 36

slow, long; no (hella side effects)

Question 37

what class properties does amiodarone have ? what about sotalol?

Answer 37

amiodarone = class 1, 2, 3, 4;
sotalol = classes 2 and 3

Question 38

do class 3 AAs affect myocytes or pacemaker cells? do they help with control of rhythm or rate in Afib?

Answer 38

myocytes, rhythm

Question 39

side effects of amiodarone:

pulmonary ____, _____ toxicity, acts as a hapten causing ____ deposits in the ____ and ____

Answer 39

fibrosis, hepatic;

grey-blue, cornea, skin (photodermatitis)

Question 40

side effects of amiodarone continued:
it is 40% ___ by weight so it can cause ____, CNS effects, GI effects such as ____, cardiovascular effects such as ____ cardia and heart block

Answer 40

iodine hypo/hyperthyroidism; constipation, brady

Question 41

to top it all off, amiodarone inhibits ____

Answer 41

CYP450 = drug interactions

Question 42

class 4 AAs work by blocking ___ ____ channels. what are the 2 ones to know?

Answer 42

L-type calcium; verapamil and diltiazem

Question 43

class 4 AAs depress phase ___ and ___ depolarization in the (nodes or myocytes?). they lengthen phase ___ repolarization and the ERP.

Answer 43

0, 4;
nodes;
3

Question 44

Adenosine binds ___ receptors, causing an increase in ___ efflux out of cells. this hyperpolarizes the cell and decreases inward ____.

Answer 44

A1, potassium;

calcium

Question 45

adenosine is first line treatment in what? what drug drug interactions does it have?

Answer 45

SVT; inhibited by theophylline and caffeine (aka methylxanthines)

Question 46

what does binding of A2 receptors with adenosine cause? clinical use of this?

Answer 46

coronary vasodilation; used in cardiac stress test

Question 47

side effects of adenosine:

____, ___tension, chest pain, sense of ___ ____, broncho____

Answer 47

flushing, hypo; impending doom, spasm

Question 48

digoxin directly inhibits the ____ node. this increases the ____ and decreases conduction velocity

Answer 48

AV, ERP