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Flashcards in Arrhythmias Deck (29)
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1

Almost all arrhythmias are ____

acquired= myocardial infarction (MI), ischemia, acidosis, alkalosis, electrolyte abnormalities.

Drug toxicity is a common cause of arrhythmia

2

when are antiarrhythmic drugs used

1) treating some arrhythmias (e.g., supraventricular
2) used with ICDs- decr arrhythmic episodes, decr discharges

3

Familial Long QT

cardiac AP is extended

prolonged phase 2 --> too much Ca2+ entry --> afterdepolarizations --> torsades --> v-fib and sudden death

4

which phase is prolonged in familial long QT

phase 2 --> too much Ca2+ entry

5

how do mutations in K+ channels lead to long QT

mutations = decr expression of K+ channels so less K+ current to end Phase 2

6

how do mutations in Na+ channels lead to long QT

prevent Na+ channels from inactivating completely --> continued flow of Na+ --> prolong phase 2

7

Triggered afterpolarizations are a cause of _____

inappropriate impulse initiation --> abnormally depolarized diastolic membrane potential triggered by an AP

8

when do Early afterdepolarizations arise

late phase 2 or phase 3

9

what causes Early afterdepolarizations

1) prolonged phase 2
2) reactivation of Ca2+ channels so more Ca2+ enter into cytoplasm
3) allows 2nd AP to fire releasing more Ca2+ from SR

10

when do delayed afterpolarizations arise

phase 4

11

what causes delayed afterpolarizations

NCX exchanger working fast enough to trigger depol

1) elevated cytoplasmic Ca2+
2) causes NCX to pump out Ca2+
3) but NCX leads to net positive charge inward
4) depolarization

12

Criteria for re-entry arrhythmia

1) unidirectional conduction block in a functional circuit
2) conduction time around circuit is longer than refractory period

13

what triggers re-entry arrhythmia

triggered by afterpolarizations

14

what happens in re-entry arrhythmia

block in normal conduction --> prevents current from flowing in norma pathway

current cirumvents block and excites damaged area on other side of block not in refractory (due to incr conduction time)

15

what does use-dependent block mean for class 1

channel must be open before it is blocked by drug
drug enters pore --> binds, and blocks ions from crossing

more a channel open, more chance drug has to bind

16

what do class 1 drugs preferentially target with use dependent block

abnormally high firing rates or abnormally depolarized membranes

17

2 effects of class 1 antiarrhythmics

increase Na+ channel refractory period by (2)

1) use dependent mechanism
2) prolonged phase 2

18

class 1 use dependent mechanisms

class 1 have high affinity for inactive state of channel --> stabilizes in inactive state and prolong refractory period

19

class 1 prolonged phase 2 duration

during phase 2, more Na+ channels inactivated --> prolongs refractory period

ONLY CLASS 1A AND 1C (CLASS 3 EFFECT BY BLOCKING K+ CHANNELS)

20

which class 1 prolong phase 2

CLASS 1A AND 1C

21

how do beta blockers help suppress arrhythmias?

reducing If, ICa-L and IKs

decreasing
1) diastolic depolarization
2) upstroke rate
3) refractory rate

--> decr HR and prolong refractory period in SA and AV cells

22

which cells are beta blockers effective against

AV node

used to treat arrhythmias with AV nodal re-entry
control ventricular rate during a-fib

23

how do class 3 drugs increase refractory period

increasing fast response phase 2

inactivation of more Na+ channels and extended refractory period

24

how do class 4 reduce re-entry ?

decreasing conduction velocity

prolonging refractory period (especially AV node)

25

how do class 4 decrease conduction velocity

blocking of L-type Ca2+ channels in upstroke (phase 0) of slow AP

therefore, slower and less likely to cross cardiac tissue in re-entry

26

how do class 4 increase refractory period

use-dependent block of calcium channels (stabilize inactive state) --> refractive cells can't conduct AP

27

how does increasing refractory period help decrease re-entry arrhythmias

refractory tissue can't generate AP

AP that reaches refractory tissue is extinguished.

28

why is decreasing cardiac automaticity good for treating arrhythmia?

rogue cardiomyocytes generating AP independent of AP node (ectopic foci)

29

which antiarrhythmic drugs treat arrhythmias by decr cardiac automaticity?

class 2, 3, 4, and adenosine