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A/P > Lecture 10/30: EKG continued > Flashcards

Lecture 10/30: EKG continued Flashcards

Test 4

1
Q

Vetocardigrams were onces analyzed by ___________

A

Oscilloscopes

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2
Q

Why would we have an inverted T-wave?

A

Repolarizing the ventricular endocardium, and then the epicardium

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3
Q

What is a biphasic T-wave?

A

T-wave has both negative and positive deflections (a dip & a hill)

This indicates the tissue repolarizing in an abnormal way

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4
Q

L axis deviation could be:

A

BBB

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5
Q

R axis deviation could be:

A

Problem with atria

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6
Q

Long/Tall QRS in Lead I indicates:

A

Very long time to depolarize

usually d/t stretched out L ventricle

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7
Q

What do bunny ears represent?

A

BBB

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8
Q

What does Bunny ears in lead III mean?

A

L BBB

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9
Q

What happens in the ventricles when you have a bundle branch block?

A

If you have a R or L BBB it causes resistance in that side of the ventricle and the opposite side depolarizes faster.

This causes the vector to shift towards the tissues that is still resting (towards the block)

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10
Q

What causes large QRS complexes in lead III?

A

R ventricular hypertropy

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11
Q

If an area is chronically depolarized, where is the vector going to point at rest?

A

Towards the resting tissue

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12
Q

What is a COI?

A

Current of injury

shows current from injured area when there should be no current

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13
Q

Where is there no current in a healthy heart?

A

End of T-wave & beginning of P-wave

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14
Q

An area of injury is a piece of tissue that is stuck in a ___________ state

A

depolarized

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15
Q

What does a vector tell you?

A

Direction: where injury is

Magnitude: How big the injury is

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16
Q

When there is suppose to be no current & there is current, what does this mean?

A

There is an area of injury that is generating a current of injury

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17
Q

Where is the J-point?

A

End of S-wave

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18
Q

What does a positive (+) COI in V2 represent?

A

posterior injury

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19
Q

What does a negative (-) COI in V2 represent?

A

anterior injury

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20
Q

What lead tells us whether it is a posterior or anterior injury?

A

V2

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21
Q

If the beginning of the P wave is below the J-Point, what type of injury do you have?

A

(-) COI

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22
Q

If the beginning of the P wave is above the J-Point, what type of injury do you have?

A

(+) COI

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23
Q

What does the J-point represent?

A

End of S-wave
All of Ventricles depolarized

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24
Q

When plotting COI, the mean vector points _______ the injury

A

away from

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25
Q

A small area of injury in the ventricles is _________ . An area of injury that involves the entire wall ventricles is an_______. Both are more likely to originate in the ________ layer in the ______ ventricle due to high pressures.

A

Ischemia

Infarct

Subendocardium

Left

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26
Q

Where are Infarcts and Ischemia more likely to happen?

A

Subendocardium of L ventricle

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27
Q

Describe how ischemia would look in Lead II on an EKG? Why?

A

Ischemia is normally in the subendocardium in the L ventricle, which will still cause the vector to point to the L foot.

You will be able to see a (+) COI in lead II after the T wave and before the P-wave.

Since the T-P segment has RAISED UP, including the P-wave reference point. The J-point is low.
It will appear that the ST segment is lower

ST DEPRESSION

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28
Q

Describe how an infarct would look in Lead II on an EKG? Why?

A

Infarcts are large and are normally in the subendocardium in the L ventricle, which will cause the vector to point to the R arm.

You will be able to see a (-) COI in lead II after the T wave and before the P-wave.

Since the T-P segment has DROPPED DOWN, including the P-wave reference point. The J-point is high.
It will appear that the ST segment is higher

ST ELEVATION

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29
Q

What is the difference between ischemia and infarct?

A

Ischemia = blood obstruction to small part of heart

Infarct = blood obstruction to large part of ventricle wall

both normally orginiating in subendocardium L ventricle

30
Q

You will have a ______ vector in infarcts than ischemia

A

bigger

31
Q

A bigger vector means a ________ area is effected

A

bigger/larger

32
Q

In a L ventricle infarct, which way will the vector point?

A

R arm

33
Q

In L ventricular ischemia, which way will the vector point?

A

L foot

34
Q

ST elevation is associated with _______ and ST depression is associated with ________.

A

Infarcts

Ischemia

35
Q

What is your reference point when determining your point of injury?

A

J-point
isoelectric point

36
Q

Which 2 areas should always be on the same line in an EKG in a healthy heart?

A

J-point & T-P segment

37
Q

What is the bottom of the heart?

A

Apex

38
Q

If the mean COI vector is pointed up, what part of the heart is affected?

A

apex

39
Q

T/F: EKG machines can zero each lead to identify J-point?

A

F

40
Q

In L-type V-G Ca++ , where is the activation & inactivation gate?

A

Activation = outer

Inactivation = inner

41
Q

What is the top of the heart called?

A

The base

42
Q

What is the activation gate called in V-G Ca++ channels?

A

D-gate

43
Q

What is the inactivation gate called in L-type V-G Ca++ channels?

A

F-gate

44
Q

V-G L-type Ca++ channels work similar to which channels? And how are they different?

A

V-G Na++ channels

The gates have different nicknames
Na+: inactivation-h
activation-m
Ca++: activation-d
inactivation-f

L-type Ca++ is slow to open & slower to close (therefore stays open longer)

45
Q

T/F: L-type V-G Ca++ channels can inactivate themselves

A

T

46
Q

In order to use a cell again, what do we need to happen?

A

The gates need to be reset, cells need to be repolarized

47
Q

What is a slow AP? Why?

A

SA node AP

The slope in phase 0 is not steep compared to fast AP in ventricular conduction system caused mostly by fast Na+ channels

48
Q

Phase 4 in________ AP is steeper and fastest. It is also called __________.

A

SA node

Diastolic Depolarization

49
Q

Describe Na+ involvement in SA node AP?

A

Phase 4: a small amount of Na+

Phase 0: No Na+

50
Q

What is the theory about V-G Na+ channels in SA nodal tissue?

A
  1. There are none
  2. Vrm doesnt get low enough to activate them
51
Q

At what voltage can L-type Ca++ channels reset?

A

-55 mV

52
Q

What happens when we increase Vrm in ventricular conduction system AP?

A

Lose Fast Na++ channels
Slope of phase 0 tapers
Peak of phase 1 wont be as high

if very high
No fast Na+ channels will be involved & will look like SA node AP

53
Q

What happens if your Vrm is so positive that you lose VG Ca++ channels?

A

“AP becomes a squiggly line”

Asystole/Afib

54
Q

What are the top reasons that your Vrm becomes so positive that you lose fast Na++ channels and VG L-type Ca++ channels?

A
  1. High levels of K+
  2. Acidosis (Increase H+; pH less than 7.4)
  3. MI (ischemia/infarct)
55
Q

How does acidosis increase Vrm?

A

Prevents enzymes from catalyzing chemical reactions at optimal speeds for resetting cells needed for provind energy to cells

56
Q

In SA node: What does increasing Ach does?

A

Bind to mAch-R –> increase K+ permeability –> decrease Vrm –> decrease HR

57
Q

In SA node: What does decreasing Ach does?

A

decreases K+ permeability –> increases Vrm –> increases HR

58
Q

In SA node: what effect does the mAch inhibitory-R have?

A

Inhibits Adenylyl cyclase –> decreases HCN channels –> decreases Vrm –> increases phase 4 –> decreases HR

59
Q

In SA node: what effect does a Beta-R have?

A

With agonist: increases adenylyl cyclase

With antagonist: decreases adenylyl cyclase

60
Q

In SA node: What channel can be attached to a Beta-R?

A

HCN channel

61
Q

Increasing cAMP increases _________

A

PKA (Protein kinase A)

62
Q

In SA node: What does PKA phosphorylates? How does this work?

A
  1. L-type Ca++ channels: makes them more sensitive & easier to open; increasing HR
  2. Phospholamban: inhibits SERCA pump in cardiac myocyte; increases speed of SERCA pump; increases HR
  3. Troponin I: Increases contractile sensitivity to Ca++; increases crossbridge generating filaments; increases HR
63
Q

In SA node: How does HCN channels effect HR?

A

Increase permeability to Na+/Ca+ during phase 4 –> makes slope steeper –> increases HR

64
Q

cAMP =

A

Cyclic Adenosine Monophosphate

65
Q

In SA node: Which Beta stimulation in reference to increasing PKA and phosphorylation is more dangerous? Why?

A

Phosphorylating L-type Ca++ channels

This causes heart attacks.

If too sensitive, will open & generate an AP when there should be one.

66
Q

What is DAD and EAD? What contributes to this? Why is this relevant?

A

Delayed after depolarization
Early after depolarization
This is present in some arrhythmias

L-type Ca++ channels contribute to this

67
Q

T/F: cAMP falls apart on its own

A

T

68
Q

What breaks down cAMP?

A

PDE (Phosphodiasterase)

69
Q

What happens when we give PDE?

A

Decrease cAMP –> decreases PKA –> decreases HR

70
Q

What happens if we inhibit PDE?

A

Increase cAMP –> increase PKA –> increase HR

71
Q

What is a normal QT interval?

A

0.25 - 0.35 seconds

A/P (25 decks)

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