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Flashcards in antiarrhythmia drugs Deck (22)
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Re-entry can be defeated by

1. slowed conduction velocity or
2. longer refractory period


Re-entry could be terminated by:

(1) converting uni- to bi-directional block
(2) or by prolonging refractory time


Unidirectional block can be converted to bi-directional block by:

(1) slowing action potential conduction velocity or
(2) by prolonging refractory period

Class I drugs generate both of these effects, and therefore these drugs may terminate re-entrant arrhythmias by either mechanism.


Steeper upstroke =

• Partial block of INa causes retrograde conduction to fail in a depressed region, which is the intent with the use of these drugs

1. faster propagation of action potential
2. steeper voltage gradient along the conduction pathway
3. This causes a larger flow of action current


Larger action current pushes

pushes adjacent regions to firing threshold sooner


Drug-induced ↓ in upstroke rate results in

↓ conduction velocity


Conduction velocity reports____

action current density

it is easier to measure conduction velocity than action current


Slower action potentials may not propagate through a _____ because ____

depressed region

Smaller action current fails to excite tissue beyond depressed region

Unidirectional block is converted to bi-directional block this way


↓ conduction velocity reports

drug-mediated block of Na+ channels


Prolonged refractoriness can suppress re-entrant arrhythmias because:

1. refractory tissue will not generate an action potential
2. and so the re-entrant wave of excitation is extinguished


One way to convert uni- to bi-directional block is by

slowing conduction velocity.


Yet slowing conduction velocity makes it less likely that

conduction time around the circuit will be shorter than the refractory period.


Paradoxically, the two fundamental means of terminating re-entry—

slowing conduction velocity and prolonging refraction—work via conflicting processes.


Class III antiarrhythmic drugs: function to

prolongers of phase 2


ibutilide and dofetilide specifically block

IKr channels


Class III: Prolongation of refractory period is due to ______, this leads to_______.

prolongation of phase 2

↑ inactivation of Na+ channels

↑ refractoriness is different from use-dependent class I action class IIIs are thus especially effective against re-entrant arrhythmias


Amiodarone mechanism

1. reduces conduction velocity (but not other class III drugs)
2. ↑ refractory period
3. ↓ rate of diastolic depolarization in automatic cells
thus reducing firing rate


how does amiodarone ↑ refractory period?

by blocking Na+ channels


Class 4 drugs are

are use-dependent blockers of L-type Ca2+ channels


Class 4 principle effects are on

Ca2+ channels in nodal cells also block Ca2+ channels in fast response myocytes


Ca2+ channel blockers function to

↓ upstroke rate in slow response tissue this in turn ↓ conduction velocity, particularly in the AV node


Just like class I blockers of Na+ channels, class IV Ca2+ channel blockers can:

prolong refractory period and thereby suppress re-entrant arrhythmias