Mechanisms of dysrhythmias Flashcards Preview

Year 2 Cardiovascular > Mechanisms of dysrhythmias > Flashcards

Flashcards in Mechanisms of dysrhythmias Deck (34):
1

during which phases does the absolute refractory period occur?

phase 0 through end of phase 2

2

the refractory period of the AP is related to which ion?

potassium

3

in the resting state, what is the configuration of the sodium channel gating?

inner pore closed
inactivation gate open

4

which part of the sodium channel is sensitive to voltage?

inner pore

5

in the inactivated state, what is the configuration of the sodium channel gating?

which refractory period does this correspond to?

inner pore open
inactivation gate closed

absolute refractory period

6

the relative refractory period corresponds to which configuration of the cardiac sodium channel?

resting

7

changing which feature of the AP will change the refractory period?

duration

8

what are the steps of calcium movement during contraction in excitation contraction coupling?

1. calcium entry through VOCC
2. calcium release from SR (RyR2)
3. calcium interacts with troponin
4. contractile shortening of sarcomere

9

what are the steps of calcium movement during relaxation in excitation contraction coupling?

1. calcium dissociates from troponin
2. calcium is taken back up into store via SERCA
3. calcium is bound to proteins within SR (calsequestrin)
4. calcium is pumped out of cell at membrane

10

how can you change activity of the myocyte?

changing calcium-ATPase pump

11

which cells are sensitive to changes in automaticity?

cells that have a phase 4 depolarization

12

diastolic depolarization underlies a major difference in channel expression between nodal and non-nodal cells. what ions are not present in non-nodal tissue?

hyperpolarization-activated cyclic nucleotide-gated channels

(HCN gated funny channels)

13

what is the effect of Ach on phase 4 diastolic depolarization of nodal cells?

increase potassium current - reduce slope of phase 4

14

what is the effect of NE on phase 4 diastolic depolarization of nodal cells?

increased calcium and funny current - increased slope of phase 4

15

what is the effect of hypokalemia and ischemia on phase 4 diastolic depolarization of nodal cells?

decreased potassium current, increases slope of phase 4

16

what is the effect of mild hyperkalemia on phase 4 diastolic depolarization of nodal cells?

increased maximum diastolic potential, increases slope of phase 4

17

what is the effect of severe hyperkalemia on phase 4 diastolic depolarization of nodal cells?

signifiantly depolarized membrane potential, cells become inexcitable

18

what is the underlying theme of abnormal automaticity?

latent pacemakers generate impulse especially sensitive to phase 4 modulation

19

delayed after depolarizations are related to changes in what ion and in what compartment? during which phase does it occur?

cytosolic and/or SR calcium overload

phase 4

20

how do early after depolarizations occur? during which phase(s) do they occur?

altered ion flux during plateau phase - delayed plateau phase

end of phase 2, beginning of phase 3

21

depolarizing the intracellular environment enough will lead to what? how?

depolarization

activation of sodium channels

22

prolonged AP duration can be related to what factors?

reduced potassium current
increased calcium
increased sodium-calcium exchanger activity
increased late sodium current

23

reduced potassium current
increased calcium
increased sodium-calcium exchanger activity
increased late sodium current

can all lead to what effect on the AP?

prolonged duration

24

why are early after depolarizations exacerbated by low Hrs?

APs are longer at lower HRs

anything that extends AP duration could contribute to an early after depolarization

25

why are delayed after depolarizations exacerbated by high HRs?

Aps are shorter at higher HRs

cannot cycle calcium as effectively (excitation contraction coupling)

26

how are reentrant circuits defined anatomically? how are they treated?

impulses travel more than one pathway in the heart

radiofrequency ablation

27

how are reentrant circuits defined functionally?

absence of defined anatomical pathway

28

both anatomically and functionally defined reentrant circuits rely on what?

electrical anisotropy and tissue (spatial) inhomogeneities

(there are difference between cells - electrical properties or how they are spaced)

29

a circus movement reentry is caused by what type of block?

unidirectional

30

what is the movement of a circus movement reentry?

wave propagates along distinct pathway, returning to point of origin and then following same path again

31

what is wolff parkinson white syndrome? what is the result?

accessory pathway links atrial tissue to ventricular tissue, bypassing AV node

AV node functions to slow conduction, therefore the accessory pathway is abnormally fast

32

how does wolff parkinson white syndrome manifest on ECG? why?

shortened PR interval

no slowing down at AV node

33

what are the general mechanisms of arrhythmogenesis, on a cellular level?

changes in gap junctions
changes in cellular structure

34

how does tissue remodeling change conduction velocity?

source-sink relationship

shortened AP duration AFTER the impedance because more signal converges on a smaller group of cells