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Cardiovascular 3 > Electrophysiology and Arrhythmogenesis > Flashcards

Electrophysiology and Arrhythmogenesis Flashcards

1
Q

What is the normal resting membrane voltage of the cardiac myocyte?

A

-90mV

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2
Q

During the phase 0 of the ventricular myocyte action potential, which are the ONLY gates that are open from the threshold to -40mV?

A

Fast m Na gate

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3
Q

So which channels open at -40mV during phase 0?

A

L-type Ca++ channels

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4
Q

What causes the depolization to stop at a new + membrane potential in the ventricular myocyte AP?

A

Na+ h-gate closure

it’s slower and “h”ates positivity

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5
Q

During phase 1, the Ca++ are still open, allowing Ca++ into the cell, but which gates now open to repolarize the membrane?

A

K+

K is like the sober guy at the party who can’t directly control the drunken idiots. the whole time hes like “ok guys… come on… no… stop…” and once the drunken idiots pass out (Na and Ca), he cleans up the mess and gets everything back to normal.

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6
Q

However, there is a “Plateau” because of the flow of what ion into the cells, even though K is leaving? (phase 2)

A

Ca++

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7
Q

So after Ca++ channels close, there is only 1 channel open at this time, causing phase 3 of the AP and repolarization of the myocyte. Which is it?

A

K+

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8
Q

Since myocytes have a plateau phase, does it make the length of the refractory periods longer or shorter, as compared to neural APs?

A

Much longer

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9
Q

The long refractory period in cardiac myocytes allows for what physiological processes to occur?

A

ventricular emptying of blood and refilling b4 the next contraction

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10
Q

Why is there an “absolute” refractory period from periods 0-2 in the myocyte AP?

A

the h-gate is closed. no Na can come in.

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11
Q

If an AP occurs during the “relative” refractory in phase 3 period, why is the rate of AP slower?

A

Cuz some of the Na+ channels are still inactivated and K+ channels are open

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12
Q

THis is the refractory period when a less than normal (weaker) stimulus can trigger an AP.

A

Supranormal RP

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13
Q

What is the normal “resting” voltage of pacemaker cells?

A

-60mV

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14
Q

Since there is persistently less negative membrane voltage, which channels are inactivated?

A

fast Na+ channels

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15
Q

The automaticity of the pacemakers causes which phase to have a large slope?

A

Phase 4

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16
Q

During phase 4 of the pacemaker cells, which ion causes the leaky current?

A

Na+

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17
Q

During phase 0 of the pacemaker cells, which ion causes the upstroke?

A

Ca++

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18
Q

So in ischemia, the myocyte AP whill change. What will change in phase 0?

A

slope decreases as the rate of depolarization is decreased

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19
Q

Is peak voltage at the end of phase 0 in cardiac myocytes increased or decreased or unchanged in ischemia?

A

decreased

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20
Q

Is resting membrane potential for myocytes more hyperpolarized or depolarized or unchanged in ischemia?

A

depolarized

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21
Q

Is the slope increased or decreased or unchanged in phase 2 (plateau) in myocytes in ischemia?

A

increased

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22
Q

What causes the increased slope in phase 2 in ischemia in myocytes?

A

repolarization is quicker

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23
Q

If repolarization is quicker in ischemia, is the entire myocyte AP faster or shorter?

A

Faster.

For all of these, your cells are shitty. They’re not doing a good job at what they should be doing. RMP is high cuz your K leaks are shitty, AP height is small cuz your Na’s are shitty, plateau is short cuz Ca++ channels are shitty. EVERYTHING IS SHITTY.

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24
Q

Which channels can be activated by extracellular Ach or a decrease in intracellular [ATP] to shorten the AP?

A

Ligand-gated K+ channels (Ik)

25
Q

Ik channels are activated to shorten the AP in ischemia. But what’s the benefit of this?

A

reduces the amt of energy expended

26
Q

During phase 3 of the myocyte AP, which transporter restores the cell to normal physiological levels?

A

Na/Ca exhcanger

27
Q

So quick review, the h gate of the Na channel “h”ates positivity (negative nancy), so what causes it to close?

A

Depolarization

28
Q

And which gate opens when there is a depolarization above the threshold potential?

A

m gate

29
Q

So why can we have a depolarization to net positivity if the h gate hates postiivity and closes, yet the m gate is open?

A

h gate is slow to close

30
Q

When the h gate closes at the top of phase 0, which ion is still being efluxed?

A

K+

31
Q

And during phase 2 there is an INflux of which ion?

A

Ca++

32
Q

Wait so in nodal fibers, which sit at a more positive RMP, how the F can they depolarize if the h gate is always closing the Na channels?

A

By using Ca++

33
Q

If you block K channels in myocytes, will it increase or decrease the AP duration?

A

Increase

34
Q

If you block Ca++ channels in nodal cells, will it increase or decrease excitation?

A

Decrease

35
Q

Decreasing excitation in nodal tissues will cause which one: tachycardia or bradycardia?

A

Bradycardia

36
Q

Na-channel blockers will increase which factor in myocytes?

A. Action potential
B. Refractory period
C. Depolarization rate
D. Plateau period
E. My anus
A

E. My anus

37
Q

NE acts mainly on which receptors of the heart?

A

B1

38
Q

Are B1 receptors Gs, Gq, Gi, or Go?

A

Gs

39
Q

The Gs pathway causes increased cAMP, leading to the stimulation on protein kinases (PKA) and cause stimulation of which 2 channels to bring in Na+ and Ca++?

A
  1. Funny channels (Na)

2. T-type Ca++ channels

40
Q

So would NE cause a increase or decrease in nodal AP duration?

A

Decrease

41
Q

So would NE cause a increase or decrease in nodal depolarization rate?

A

increase (more Ca and Na flowin)

it’s like the dj who shows up to the party. gets the drunken idiots more drunk

42
Q

True or False: Ach works on both the ventricular myoctes and nodal fibers, opposing the actions of NE.

A

FALSE. It ONLY works on SA and AV nodal tissues

43
Q

What does Ach do to the conductance of K? Increase or decrease it?

A

Increase

sends in more sober guys to combat the drunken idiots

44
Q

Does Ach increase or decrease the slope of phase 4 depolarization?

A

decrease (more K leaving causes a bigger fight between +/- charges in the cell when depolarizing and the downrefulation of Na channels)

45
Q

If (funny channels) in nodal tissues allow the passive leakage of which ion to continually depolarize the membrane?

A

Na+

46
Q

We talked about “overdrive suppression” in EKG lectures, but why does it happen with higher automaticity foci?

A

THey cause hyperpolarization of downstream pacemakers

47
Q

Which ANS system is dominant at rest? PANS or SANS?

A

PANS

48
Q

The intrinsic HR is 100-110, but the PANS brings it down to which HR?

A

60-80.

49
Q

This is the problem when there is a block or slowing of conduction and it forces the current to go through another pathway.

A

Re-entry

50
Q

In order to cause tachyarrhythmias, the rate of retrograde conduction in the slowed (or blocked) limb must be LESS than what principle in the normal limb of the nodal tissues?

A

Refractory period

Otherwise a retrograde depol would just stop. It’s like you’re a kid and wana continually slide down a slide, but another kid is using it. The only way for you to not stop the process of sliding, running to the ladder, climbing up the ladder, and sliding again, is if the rate at which you climb up the ladder is slower than the rate at which the other kid slides down the slide in front of you. ya hear?

51
Q

Alteration in impulse formation can be from decreased phase 4 depolarization, leading to what type of HR?

A

Sinus bradycardia

52
Q

Ischemia, anatomic, or drugs can alter impulse conduction, leading to these arrhythmias.

A

AV blocks

53
Q

The SA node can cause tachycardia by increasing the slope of which phase in the nodal tissues?

A

4

54
Q

This is the condition where there is triggered activity and an early afterdepolarization from a prolonged AP duraton.

A

Torsades de pointes

55
Q

Digitalis toxicity can cause an intracellular Ca overload, leading to which tpye of abnormality?

A

Delayed afterdepolarization

56
Q

Atrial flutter, AV nodal reentrant tachy, and VT from scar tissue are examples of which type of re-entry abnormality?

A

Anatomical

57
Q

A. fib, polymorphic VT, and V fib are examples of which type of re-entry abnormality?

A

Functional

58
Q

Which channels re-open during phase 2 of the myocyte AP to cause early afterdepolarization?

A

Ca++

the drunken idiots wake up right away after passing out and party some more. your heart is like shitttttttttttttttttttttt

59
Q

High intracellular Ca++ can cause delayed afterdepolarizations by activating which exchanger, which creates a brief depolarization in the T wave?

A

Na+/Ca++ exchanger

(3 Na in for every 2 Ca out. The big influx of Na to try to get the Ca out causes a little blurp depolarization. your heart is like “fml”)

Cardiovascular 3 (8 decks)

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