Mechanisms of dysrhythmias

Question 1

during which phases does the absolute refractory period occur?

Answer 1

phase 0 through end of phase 2

Question 2

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

Answer 2

potassium

Question 3

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

Answer 3

inner pore closed

inactivation gate open

Question 4

which part of the sodium channel is sensitive to voltage?

Answer 4

inner pore

Question 5

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

which refractory period does this correspond to?

Answer 5

inner pore open
inactivation gate closed

absolute refractory period

Question 6

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

Answer 6

resting

Question 7

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

Answer 7

duration

Question 8

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

Answer 8

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

Question 9

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

Answer 9

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

Question 10

how can you change activity of the myocyte?

Answer 10

changing calcium-ATPase pump

Question 11

which cells are sensitive to changes in automaticity?

Answer 11

cells that have a phase 4 depolarization

Question 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?

Answer 12

hyperpolarization-activated cyclic nucleotide-gated channels

(HCN gated funny channels)

Question 13

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

Answer 13

increase potassium current - reduce slope of phase 4

Question 14

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

Answer 14

increased calcium and funny current - increased slope of phase 4

Question 15

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

Answer 15

decreased potassium current, increases slope of phase 4

Question 16

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

Answer 16

increased maximum diastolic potential, increases slope of phase 4

Question 17

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

Answer 17

signifiantly depolarized membrane potential, cells become inexcitable

Question 18

what is the underlying theme of abnormal automaticity?

Answer 18

latent pacemakers generate impulse especially sensitive to phase 4 modulation

Question 19

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

Answer 19

cytosolic and/or SR calcium overload

phase 4

Question 20

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

Answer 20

altered ion flux during plateau phase - delayed plateau phase

end of phase 2, beginning of phase 3

Question 21

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

Answer 21

depolarization

activation of sodium channels

Question 22

prolonged AP duration can be related to what factors?

Answer 22

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

Question 23

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

can all lead to what effect on the AP?

Answer 23

prolonged duration

Question 24

why are early after depolarizations exacerbated by low Hrs?

Answer 24

APs are longer at lower HRs

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

Question 25

why are delayed after depolarizations exacerbated by high HRs?

Answer 25

Aps are shorter at higher HRs

cannot cycle calcium as effectively (excitation contraction coupling)

Question 26

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

Answer 26

impulses travel more than one pathway in the heart

radiofrequency ablation

Question 27

how are reentrant circuits defined functionally?

Answer 27

absence of defined anatomical pathway

Question 28

both anatomically and functionally defined reentrant circuits rely on what?

Answer 28

electrical anisotropy and tissue (spatial) inhomogeneities

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

Question 29

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

Answer 29

unidirectional

Question 30

what is the movement of a circus movement reentry?

Answer 30

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

Question 31

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

Answer 31

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

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

Question 32

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

Answer 32

shortened PR interval

no slowing down at AV node

Question 33

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

Answer 33

changes in gap junctions

changes in cellular structure

Question 34

how does tissue remodeling change conduction velocity?

Answer 34

source-sink relationship

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