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A&P 1 > Exam 4 Lecture 6 > Flashcards

Exam 4 Lecture 6 Flashcards

1
Q

In a Current of Injury, which way does the tip of the arrow point?

A

Away from the injury

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2
Q

What is a current of injury?

A

While the rest of the heart is repolarized, the injured area is still depolarized

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3
Q

When are we most likely to see a current of injury?

A

During the T-P segment

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4
Q

In a lead 2 current of injury, if the MEA points towards the Right Arm, what happens to the ST segment
*what type of deflection
*What type of cardiac injury

A

ST-Segment Elevation
*(-) deflection
*Myocardial Infarct

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5
Q

In a lead 2 current of injury, if the MEA points towards the Left Foot, what happens to the ST segment
*what type of deflection
*What type of cardiac injury

A

ST-Segment Depression
*(+) deflection
*Subendocardial Ischemia

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6
Q

If Voltage of the TP segment is lower than the J-Point, ST _?
*What type of deflection

A

ST-Elevation and (-) deflection

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6
Q

Which has a larger deflection: Ischemia or Infarct

A

Infarct

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7
Q

At the J-Point, what should the ventricles be doing?

A

Fully depolarized, so should be getting ready for repolarization

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8
Q

If Voltage of the TP segment is higher than the J-Point, ST _?
*What type of deflection

A

ST-Depression
*(+) deflection

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9
Q

If the V2 Current is a (+) deflection, what type of injury is it

A

Posterior Current of Injury

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10
Q

If the V2 Current is a (-) deflection, what type of injury is it?

A

Anterior Current of Injury

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11
Q

If the MEA is pointed 270 degrees, what type of current of injury is it?

A

Injury at Apex of the heart

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12
Q

What part of the EKG does the machine have trouble calibrating?

A

J-Point

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13
Q

Where do vast majority of Infarcts happen?

A

L ventricle Wall

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14
Q

How does a Fast Na+ channel look at rest?

A

M Gate closed and H gate open

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15
Q

At rest, how does a Slow Ca++ channel look?

A

D gate closed and F gate open

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16
Q

Slow Ca++ and Fast Na+ channels Activation Gates

A

D and M

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17
Q

Slow Ca++ and Fast Na+ channels Inactivation Gates

A

F and H

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18
Q

In Phase 0, what are both ventricular myoctes and Nodal Tissue Permeable to

A

Na+, Ca++, K?

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19
Q

In order, rank different AP in terms of Ca++ permeability

A

SA, AV, Purkinje/Myocytes

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20
Q

What is Vrm for Ventricular Myocytes

A

-80mV

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21
Q

Why is it called a Fast AP in Phase 0?

A

B/c the slope is straight up and down

22
Q

What is the slope of Phase 0 directly related to?

A

How many Fast Na+ channels we have involved

23
Q

Ventricle Myocyte Phase 4: Slope
*Can it fire an AP on its own?

A

Slight slope above horizontal, due to leaky Na+ channels
*Yes, but takes a while

24
Q

If the Vrm is increased, what happens to the Fast Na+ channels?
*Slope of Phase 0?
*Peak of Phase 1?

A

Less fast Na+ channels involved
*Slope of Phase 0 is shallower
*Peak of Phase 1 is less high

25
Q

If Vrm increases so much that Fast Na+ channels cannot be repolarized, how does the AP look?
*What is the cell relying on to propogate the AP thru the Gap Junctions?

A

Very similar to a slow L-Type Ca++ channel
*Ca++ to propagate the AP, but takes longer b/c it is slower and larger to fit thru

25
Q

If the Vrm is so high that the Fast Na+ channels and Slow L-Type Ca++ channels cannot repolarize, how does the AP look?

A

VFIB/Asystole

26
Q

What phases are in a ventricular myocyte AP

A

Phases 4, 0, 1, 2, 3

27
Q

Which is the fastest phase in the Nodal Tissues?
*Another name for this

A

Phase 4
*Diastolic Depolarization

28
Q

What is the Vrm of the SA nodes?
*Threshold?

A

-55mV; -40 mV

29
Q

What are the 2 theories for why there are no Fast Na+ channels in Nodal Tissues?

A
  1. There actually are no V-G Fast Na+ channels there
  2. There are V-G Fast Na+ channels, but do not function as Vrm is not (-) enough
30
Q

Which Channel repolarizes at a more (+) number?
*Slow Ca++ or Fast Na+

A

Slow Ca++ [-55 mV]

31
Q

How are Nodal Cells leaky to Ca++ at rest?

A

Thru Leaky Ca++ channels

32
Q

What Phases are in a Nodal Tissues Cell

A

Phases 4, 0, 3

33
Q

How does Lidocaine change the AP?

A

Reduces the Slope of Phase 0 by blocking Fast Na+ channels

33
Q

If you have increased ACh or Vagal Tone, what happens to HR?

A

Increased K Perm = Reduced Vrm = reduced HR

34
Q

What is the primary way nodal tissue adjusts Vrm?

A

Thru mACh-R and the attached K channels

34
Q

3 Things that cause a more (+) Vrm

A

Hyperkalemia, Acidosis/Increased H, Increased Protons, MI

35
Q

What happens if you give Atropine?

A

Decreased K permeability at the mACh-R sites, leading to increased Vrm = Increased HR

36
Q

mACh-R 2nd set w/ Alpha Inhibitory Subunit: Effect on cell

A

Slows down AC when bound = decreased cAMP = decreased PKA

37
Q

Beta-R subset that interacts w/ HCN channels: Effect on the cell
*How is it activated

A

Direct Stimulation and cAMP activation; when activated, HCN channels open and allow for more Na+ and Ca++ to influx during Nodal Cell Phase 4

37
Q

What does HCN mean

A

Hyperpolarization Cyclic Nucleotide

37
Q

What 3 things do PKA mainly phosphorylate?

A

L-Type Ca++ channels, Troponin I, Phospholamban

38
Q

PKA Phosphorylation of L-Type Ca++ Channels

A

Makes them more sensitive and easier to open

38
Q

PKA Phosphorylation of Phospholamban

A

Increase speed of Cell repolarization = allows for faster HR

38
Q

Beta-R Alpha Subunit that is stimulatory: Effects on the cell

A

Increased AC = increased cAMP = increased PKA

38
Q

At which part of the cell is Beta Adrenergic Stimulation most dangerous and why?

A

L-Type Ca++ channels, b/c more sensitive to PKA = increased AP firing when not supposed to [Arrythmias]

39
Q

PKA Phosphorylation of Troponin I

A

Increased contractile protein sensitivity = increases CBC

39
Q

Blocking Beta-R leads to what w/ HR, CBC, L-Type Ca++ channels

A

Decreased speed of cell repolarization [increased phospholamban = increased SERCA pump activity] = slower HR
*Slower CBC
*Makes L-Type Ca++ less sensitive and harder to open

40
Q

What does DAD stand for?

A

Delayed after depolarization

41
Q

What does EAD stand for?

A

Early after depolarizations

42
Q

Can cAMP fall apart on its own?
*What speeds up this process

A

yes, but slow
*Phosphodiesterase

43
Q

What does PDE turn cAMP into?

A

AMP

44
Q

What happens to cAMP/PKA if we give a PDE inhibitor?

A

Increases cAMP, PKA

A&P 1 (24 decks)

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