Anti-Arrhythmia Med Mech

Question 1

what are the 2 ways arrhythmia originate

Answer 1

1. inappropriate impulse initiation

2. disturbed impulse conduction

Question 2

two major sources of inappropriate impulse initiation?

Answer 2

ectopic foci

triggered afterdepolarizations

Question 3

ectopic focus can be due to (2)

Answer 3

Pacing (i.e. SA node slow, or focus fast)

Infarct (Na/K pump failure)

Question 4

triggered afterdepolarzations
early due to
late due to

Answer 4

both are due to increased intracellular calcium

early are dependent of re-activation L-type calcium channel

later are dependent of NCX

Question 5

long qt –>

Answer 5

early afterdepolarization –> TdP –> V-fib

Question 6

2 causes of disturbed impulse conduction

Answer 6

conduction block

re-entry

Question 7

Two requirements for re-entry circuit

Answer 7

unidirectional block

conduction time longer than refractory period

Question 8

what underlies atrial flutter, fibrillation, TdP, and V-fib?

Answer 8

re-entry!

Question 9

Class I AA?

Answer 9

Block voltage gated cardiac Na+ channels

Question 10

Class II AA

Answer 10

B-adrenergic receptor blockers

Question 11

Class III AA

Answer 11

prolong phase II of fast response

Question 12

Class IV

Answer 12

Block V gated Ca2+

Question 13

Adenosine

Answer 13

works via GCPR –> increase cAMP to decrease funny HCN current and ICa-L influx and Gby to open Ik-ado (=Ik-ach)

Thus decreases automaticity at nodes
Decreases conduction at AV

Question 14

Amiodarone

Answer 14

Offical Class III (i.e. prolong phase II of fast)
However!
Also reduces conduction velocity and increases refractory period via blocking Na+ channels
Also reduces rate of diastolic depolarization in automatic cells - reducing firing rate

Question 15

Class I drugs effect

Answer 15

selective Na+ channel blockers
Good for re-entry block
slow phase 0 upstroke (decrease conduction velocity)
increase refractory period

Question 16

Lidocaine

Answer 16

Class IB
pure Na+ blocker
slow upstroke (conduction velocity)
shorten AP / repolarization 
Increase refractory period

Question 17

Beta blockers mechanism

Answer 17

by blocking beta-adrenergic receptor 
do not make cAMP
decrease funny current
decrease PKA-p of L-Ca
decrease PKA-p of K current 

decreasing diastolic depolarization of pacers
decreasing upstroke decreasing repolarization

PARTICULARLY AV NODE

Question 18

Effect of Class II

Answer 18

Decrease automaticity (phase 4 slope)
Prolong repolarization/effective refractory period (Phase3) --> decrease re-entiry

Question 19

Class III mechanism

Answer 19

Prolong phase II of fast
Usually via K+ channel block –> prolongs refractory period owing to increased Na+ inactivation form prolonged depolarization
SO

Question 20

Effect of Class III

Answer 20

Decrease re-entry

Question 21

Effect of Amiodorone

Answer 21

Decrease re-entry 
Decrease automaticity (nodal) 
Decrease conduction velocity

Question 22

Class IV

Answer 22

Use dependent L-type Ca2+ blockers
Decrease conduction velocity
Prolong refractory period (fewer K+ activated)
NODAL CELLS

Question 23

Class IV effect

Answer 23

suppress re-entry arrhythmia involving nodal cells via decreased velocity and increased effective refractory (via fewer K+ channel activation due to reduced amp AP from L-channel block)

Question 24

Effect of adenosine

Answer 24

decrease SA node and AV node firing
(due to closure of funny current and opening of K1)
decrease conduction rate (via inhibitory GPCR of AC so no cAMP so no PKA)

Question 25

Drug of choice for PSVT

Answer 25

Adenosine

Question 26

Drug of choice for Afib

Answer 26

AV node blockers (acute)

Amiodorone (chronic)

Question 27

Drug of choice for v-tac / v-fib

Answer 27

Amiodorone