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Cardio Exam 2 > Lec 35 Anti Arrhythmic Pharm > Flashcards

Lec 35 Anti Arrhythmic Pharm Flashcards

1
Q

What is main determinant of conduction velocity [in ventricles]?

A

Ina

speed of upstroke = proportional to speed of conduction

slower upstroke –> also have longer delay between APs

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2
Q

What is physiology of the Na channel opening/closing?

A
  • channels open in response to increase in membrane voltage [depolarization]
  • channels automatically close [inactivate] even when voltage is maintained
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3
Q

What are the 3 states of Na channel?

A
  • closed but available
  • open
  • inactivated and unavailable
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4
Q

AT -80 mV what is probability of each of the 3 Na channel states?

A
  • 0% open
  • 85% closed
  • 15%
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5
Q

What is sequence of Na channel events during action potential?

A
  1. diastole: 85% of channels closed but available
  2. upstroke/plateau: transition to open then inacivated
  3. diastole: return to 85% closed but available [depending on how much time in diastole]
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6
Q

What is effect of time in diastole on Na channels?

A

determines whether there is time to redistribute back to mostly closed but available from mostly inactivated

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7
Q

What is most drug’s preference for the 3 channel states?

A
  • most preferentially bind at open and inactivated and have weaker binding at closed
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8
Q

What do atrial flutter/fib tell you?

A

only some atrial excitations are propagating into the ventricles

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9
Q

What are the 3 primary mechanisms of arrhythmia initiation?

A
  • early after depolarizations [EADs]
  • delayed after depolarizations [DADs]
  • reentry
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10
Q

What is an early after depolarization? What current?

A

second upstroke in the middle of the depolarization phase

due to reactivation of Ica –> can propagate and cause PVC

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11
Q

What puts at risk for early after depolarization?

A

longer action potential / slower rate

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12
Q

What is a delayed after depolarization? What current?

A

right after repolarization of AP

first phase = spontaneous release of intracellular Ca from SR –> slow depolarization due to NCX exchange [1 Ca out for 3 Na in]

second phase = if NCX high enough, activates Na channel and causes full AP

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13
Q

What puts at risk for delayed after-depolarization?

A
  • fast HR
  • B adrenergic stimulation
  • high intracellular Ca
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14
Q

What happens in reentry?

A
  • stimulus delivered late will propagate on both side and collide
  • if longer AP on R compared to L –> premature stimulus from will encounter refractory tissue and be blocked only be right; will propagate slowly on left –> by the time if propagates around the bottom, right side recovered

premature stimulus = EAD or DAD

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15
Q

What is the center “block” in the diagram model of reenty?

A
  • can be anatomically defined [e.g by AV node]

- can be functional block due to damaged tissue or temporary difference in refractory

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16
Q

What is mech of arrhythmias?

A
  • arrhythmia initiated by EADs/DADs and maintained by reentry
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17
Q

What is [are] theoretic place for blocking EAD?

A
  • EAD is from Ca channel –> block Ca current
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18
Q

What is [are] theoretical place for blocking DAD?

A
  • DAD is from spontaneous release of Ca then trigger of second AP

–> block B adrenergic signal to decrease HR and decrease likelihood of spontaneous Ca release

–> block Na channels to decrease likelihood of trigger

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19
Q

What is normal conduction velocity?

A

50 cm/s

20
Q

What is normal AP duration?

A

300 ms

21
Q

What is normal heart AP wavelength?

A

6 inches = same scale as heart itself

22
Q

What happens if wavelength < path length vs > wave length?

A

wavelength > path length –> reentry will spontaneously terminate

wavelength < path length –> reentry can continue indefinitely

23
Q

What is action of class I anti-arrhythmics?

A

block Na current

24
Q

What is action of class II anti-arrhythmics?

A

Block B-adrenergic receptors

25
Q

What is action of class III anti-arrhythmics?

A

Block K currents, prolong APD

26
Q

What is action of class IV anti-arrhythmics?

A

Block Ca currents

27
Q

What is strategy of class I anti-arrhythmics?

A

prevent spontaneous release of Ca and DADs from triggering action potential

28
Q

What is mech class II anti-arrhythmics?

A

block Beta –> decrease cAMP/protein kinase –> block positive inotropy + phosportylation of L type Ca channels that allows more Ca pumped into sarcoplasmis reticulum

slow or block conduction
–lower HR; prevent Ca overload and DADs

29
Q

What is mech of class III anti-arrhythmic?

A

block K channel –> increase wavelength/AP duration –> so reentrant arrhythmias self-terminate

30
Q

What is mech of class IV anti-arrhythmics?

A

block Ca –> slow conduction between AV node and longer delay between APs

–> suppress reentrant SVT dependent conduction through AV node

–> for AFib allow fewer atrial impulses to get conducted

31
Q

What are class IV anti-arrhythmics used to treat?

A
  • SVT

- AFib

32
Q

How do class IA, IB, IC drugs differ?

A

rate of Na channel unblock during diastole

block of other targets such as K channels

33
Q

For class IA drugs: [procainamide]

  • rate of unblock
  • K block
  • effects on APD, upstroke velocity
A
  • rate of unblock: medium
  • K block: strong

medium reduction in upstroke velocity
longer APD

34
Q

For class IB drugs: [Lidocaine]

  • rate of unblock
  • K block
  • effects on APD, upstroke velocity
A
  • rate of unblock: fast
  • K block: weak

small reduction in upstroke velocity
decrease in APD

35
Q

For class IC drugs: [Flecainide]

  • rate of unblock
  • K block
  • effects on APD, upstroke velocity
A
  • rate of unblock: slow
  • K block: weak

large reduction in upstroke velocity
little change in APD

36
Q

How do effects of Class I drugs change with depolarization?

A
  • bigger effect on depolarized [ischemic] cells
37
Q

What happens to membrane polarization, AP length in ischemia?

A
  • shorter AP

- membrane depolarized slightly

38
Q

What is pharmacokinetics of lidocaine?

A

metabolized quickly [1-2 hr 1/2 life] so have to administer as IV in the hospital

39
Q

What type of drug is lidocaine?

A

class IB anti-arrhythmic

use it for VT

40
Q

What type of drug is procainimide?

A

class IB

use it for WPW w/ AFib

41
Q

What are non-cardiac side effects specific to procainamide?

A
  • reversible lupus-like symptoms,

anti-nuclear antibodies

42
Q

What are non cardiac side effects common to all class IA drugs?

A

antimuscarinic activity

can cause fluid retention, dry mouth, constipation

43
Q

Which of the class I drugs are most dangerous?

A

Class 1C –> unbind so slowly –> most dangerous and used infrequently

44
Q

How are class I drugs pro-arrhythmic?

A

increase AP duration
BUT decrease conduction velocity

wavelength = APD * CV
overall they shorten wavelength –> promote reentry

45
Q

How are class III drugs pro-arrhythmic?

A

increase APD –> increase wavelength so prevent reentry

BUT –> increase APD encourages EADs

made worse b/c they prolong APs more at slower rates when it is most dangerous/least beneficial

46
Q

What is reverse rate dependence?

A

class III drugs are reverse rate dependent

–> prolong AP more at slow rate where this is bad; prolong AP less at fast rate where this could be beneficial

Cardio Exam 2 (19 decks)

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