17 Mechanisms of anti-arrhythmic drugs

Question 1

mechanisms of propagation blocks

Answer 1

• *more positive resting membrane potential**
• less Na channels activated/slower conduction velocity/higher threshold

ischemia = decreased ATP

• Katp channels open/raised threshold/time from stimulus to phase 0 increased

Question 2

3 conditions for re-entry to occur

Answer 2

2 parallel conduction paths

unidirectional block in one path(extended refractoriness)

slow or delayed conduction in other path

Question 3

relavent class IA antiarrhythmics

mechanism, effect, use

Answer 3

”

quinidine, procainamid, disopyramide

block Na channels

increase length of AP, ERP and QT

procainamide is used acutely
“

Question 4

class IB antiarrhythmic drugs

mechanism, effect, use

Answer 4

“lidocaine

blocks Na channels

decrease length of AP

acute ventricular arrhythmias

”

Question 5

class IC antiarrhythmic drugs

mechanism

Answer 5

“flecainide, propafenone

strongly depress Na current(rate of rise of AP) strongly
“

Question 6

class II antiarrhythmic drugs

Answer 6

b-blockers

Propanolol(B1/2)

metoprolol, esmolol, atenolol (all B1 specific)

Carvedilol - B1/2/a1

Labetalol - B1/2/a

Reduced excitability and decreased conduction velocity in AV node

Question 7

class III antiarrythmic drugs

mechanism? effect?

Answer 7

amiodarone, dronedarone, sotalol, ibutilide, dofetilide

K+ channel blocker; prolong AP duration

Question 8

“describe ““reverse use dependence”” and which drug class these applyt o”

Answer 8

“K channel blockers work BEST when the channels are in resting state

therefore, these drugs produce long QT better at lower HRs

this is the opposite of ""use-dependent"" Na channel blockers(class I)
"

Question 9

class IV antiarrhythmic drugs

mechanism? effect?

Answer 9

verapamil, diltiazem

CCBs

increase refractoriness in AV node; harder for SA/AV to depolarize

Question 10

digoxin

Answer 10

Na-K exchange pump inhibitor

M2 agonist - vagal input activation

shortes refractory period; can be bad if there are aberrant pathways(enhanced excitability)

Question 11

antiarrhythmic drugs crossing the BBB; effect?

Answer 11

lidocaine - seizures

propanolol - nightmares, sedation

digoxin - cognitive/vision effects

metoprolol?

Question 12

adverse effects of amiodarone

Answer 12

high iodine content - propensity to cause hyper/hypothyroidism

pulmonary fibrosis

blue skin

photosensitivity

corneal deposits

Question 13

drug treatment for atrial flutter or afib

Answer 13

BBs or CCBs to slow AV excitability

anticoagulate if longer than 48 hrs

add class III drug to return to normal sinus rhythm

Question 14

difference between atrial fibrillation and flutter

Answer 14

flutter - excessive p waves; consistant/regugular QRS beats

fibrillation - irregularly irregular; QRS are not rhythmic; p waves are excessive/sporadic

Question 15

AVNRT treatment

difference for AVRT treatment?

Answer 15

• *acute**
• vagal maneuvers
• adenosine(IV) most effective; possibly verapamil to slow conduction/reentry

long term

• BBs or CCBs
• ablation

avoid CCBs and digoxin for AVRT since it can increase conduction down aberrant pathways(refractoriness is reduced on CCBs); otherwise, treatment is the same

Question 16

adverse effects of type III antiarrhythmics

Answer 16

tend to cause torsades at lower HRs