Anti-Arrhythmic Drugs Flashcards Preview

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Flashcards in Anti-Arrhythmic Drugs Deck (10)

What is the concept of use-dependence in Class I antiarrythmic drugs.


Recall: Class I is Na+ Channel blocker

Use-dependence:  Target the sodium channels that are more active - i.e. membranes more actively firing or depolarizing

  • Explained: This allows selective targeting (to a degree) of Na+ channels in the myocytes with abnormally high firing rates or abnormally depolarized membranes (which are the myocytes inducing the arrythmia)


What is the basis of use-dependent block of Na+ channels by class I antiarrythmics?

  • Channels must open before they can be blocked.
    • The channel must be open for the blocker to enter the pore, bind and thereby block the Na+ channel


How do Class I antiarrhythmetics increase the Na+ channel refractory period?


(regardless if they prolong phase 2 of the fast response)

Class I have a higher affinity for inactivated state of Na+ channel.

  •  Use-dependent blockers stabilize the inactivated state
    • i.e they prolong the refractory period

Alternative mechanism:

  • Prolonging phase 2: Myocyte membrane is depolarized for longer period of time -> more Na+ channels become inactivated -> refractory period longer


How do beta-adrenergic recepetor blockers help supress arrythmias?

Reduction of Ih, ICaL and IK reduces the rate of diastolic depolarization in pacing cells, reduces the upstroke rate and slow repolarization.

  • Refractory period is prolonged (reentry) in the SA and AV nodal cells


During what kind of arrhythmia's would one Rx a beta blocker?

Beta-blockers are used to terminate arrhythmias that involve AV nodal re-entry, and in controlling ventricular rate during atrial fibrillation.


How do Class III drugs increase the refractory period?

Blocking cardiac K+ channels

  • Consequences
    • Prolongation of fast response phase 2
    • Prominent prolongation of refractory period ( ̄ reentry)
      • Prolonged duration of phase 2 leads to an increased inactivation of Na+ channels.


What are the two ways in which antiarrhythmetics supress reentry?


*Hint*: Think about the two different requirements for a re-entry arrhythmia to occur.

  1. Terminating re-entry by slowing conduction velocity and upstroke rate -> slower conduction velocity
    • Slower conducting action potentials are more likely to fail to propagate through a depressed region.
  2. Terminating re-entry by prolonging refractory period

    • If tissue is still in refractory it cannot generate a new AP


How does reducing cardiac automaticity supress some arrhythmias?

Some arrhythmias arise from rogue myocytes that generate AP w/out direction from the AV/SA nodes.

  • Decreasing automaticity, ensures that cells do not generate their own “pacemaking” activity thereby suppressing these arrhythmias

  • Class II (beta blockers) and Class III (K+ channel blockers) drugs are particularly good at this.


What class antiarrhthmetic is adenosine described as?

TRICK QUESTION! It's unclassfied.


How does adenosine help supress arrhythmias?

Increases a K+ current, while also decreasing both L-type Ca2+ current and Ih in SA and AV nodes.

  • Adenosine induced changes cause a reduction in SA node and AV node firing rate as well as a reduced conduction rate in the AV node