Introduction to Cardiac Electrophysiology Flashcards

1
Q

Are AP in atria longer/shorter than in ventricles?

A

shorter AP and refractory period–> don’t need to generate high pressures, but can lead to development of rapid atrial rhythms

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2
Q

Where is the AV node located?

A

low in the R atrium

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3
Q

The property of some specialized cells to spontaneously depolarize and reach threshold to trigger an action potentail

A

automaticity

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4
Q

What is the difference between phase 4 depolarization in purkinje and SA node?

A

purkinje automaticity is driven mostly by If whereas Ik and Ica play the main role in the SA node

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5
Q

How does the SA node stay “in charge”?

A

faster intrinsic rate of firing + overdrive suppression–> overrides the other pacers except in emergencies

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6
Q

What is overdrive suppression?

A

activation of the na/k pump leads to hyperpolarization in non-sa pacers that opposes automaticity –> automaticity returns when SA overdrive suppression disappears

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7
Q

Open or closed at upstroke? Na channel: M gate and H gate

A

M gate open, H gate open

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8
Q

Open or closed at plateau? Na channel: M gate and H gate

A

M gate open, H gate closed (inactivated)

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9
Q

Open or closed at resting? Na channel: M gate and H gate

A

M gate closed, H gate open (excitable)

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10
Q

3 factors that determine conduction velocity

A
  1. how large the inward sodium current is
  2. how fast does the inward sodium current activate
  3. how much resistance there is
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11
Q

How does fibrosis lead to slow conduction after an MI?

A

separation of fibers by fibrosis reduces number of gap junctions –> increases resistance to axial current flow

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12
Q

How does an acute infarction affect conductance?

A

reduced gap junction conductance

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13
Q

How do Na blockers affect conductance?

A

blockade of sodium channels reduces conduction

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14
Q

How does a local elevation of K in an acute infarct or elevated serum K in renal failure affect conduction?

A

depolarization of resting potential leads to Na channel inactivation resulting in slow conduction

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15
Q

What does safety factor for propagation mean and how does it differ between sodium/calcium current mediated cells?

A

the term suggests how much the excitation can be reduced before inhibiting the given cell–> Na current is more resistant/higher safety factor/would have to reduce Na current a lot to make the cell inexcitable whereas calcium dependent cells are inhibited by smaller changes in calcium current

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16
Q

How do kinetics for recovery of excitability post repolarization differ between sodium/calcium current mediated cells?

A

slow response AP has a delayed recovery (calcium mediated) vs. cells that are sodium mediated

17
Q

What is the effective refractory period?

A

time following depolarization when a stimulus cannot elicit a propagating action potential

18
Q

How does ERP compare in fast/slow response cells (aka sodium/calcium mediated)

A

slow response have a longer ERP because need to wait for calcium channels to reactivate (happens slower than na channel reactivation)

19
Q

What is the main determinant of ERP in fast response cells?

A

action potential duration aka rate (in atria and ventricles)

20
Q

What is the main determinant of ERP in slow response cells?

A

things that boost the calcium current reduce ERP

21
Q

What do we expect will happen to ERP in the AV node as heart rate increases?

A

longer- -> fewer calcium channels reactivated each time

22
Q

Short/long APD and ERP in atria allow fast atrial rhythms

A

short

23
Q

short/long ERPs in AV node and bundle branches protect ventricles during fast atrial rhythms

A

long

24
Q

Genetically abnormal Na and K channels can produce very long/short APDs in ventricles

A

long