Exam 4 - Lecture 6

Question 1

If there is only a smart ischemia in the left ventricle on the endocardium, the MEA should be

Answer 1

Still pointing towards left foot

Question 2

Where will we be able to see a current of injury with ischemia?

Answer 2

Where there should be no current, after T-wave before the P-wave

Question 3

ST segment depression means

Answer 3

J-point/S-wave is below the T-P segment

Question 4

Is the ST segment actually depressed?

Answer 4

No, it just looks that way because the time after T-wave before p-wave is elevated abnormally due to ischemic tissue causing extra depolarization during a time where there should be no current (current of injury)

Question 5

If the J-point is above the area after the T-wave, it is a

Answer 5

negative current of injury

Question 6

If the J-point is below the area after the T-wave, it is a

Answer 6

positive current of injury

Question 7

Why do we only pick out 2 of the 3 leads for the abnormal EKGs?

Answer 7

einthovens law, cause if we know whats in I and III, we know whats in II.

Question 8

What does einthovens law need to hold true?

Answer 8

electrodes to be placed perfectly

Question 9

It is basically impossible for the EKG equipment to find a a

Answer 9

zero point aka zero out the leads and find the J-point

Question 10

The activation gate in fast Na+ channels is called what and where is it? What’s its status at rest?

Answer 10

M gate, on the outside. Closed.

Question 11

The inactivation gate in fast Na+ channels is called what and where is it? What’s its status at rest?

Answer 11

H gate, inside. Open.

Question 12

The activation gate in Ca++ slow channels is called what and where is it? What’s it’s status at rest?

Answer 12

D gate, outside. Closed.

Question 13

The inactivation gate in Ca++ slow channels is called what and where is it? What’s it’s status at rest?

Answer 13

F gate, inside. Open.

Question 14

outside of ca+ or na+ channel gate

Answer 14

activation gate, M/D gate. Closed at rest.

Question 15

Inside of Ca++ or Na+ channel gate

Answer 15

Inactivation gate, H/F gate. Open at rest.

Question 16

2 theories why there’s no fast sodium channels in nodal tissue

Answer 16

Either there’s no channels there, or there is, but they dont function because the VRm only gets down to -55, and that is not negative enough to activate fast sodium channels.

Question 17

Will the fast sodium channels or L-type channels need more repolarization to reset?

Answer 17

Fast sodium channels

Question 18

The slope of phase 0 in ventricular myocytes is directly rated to

Answer 18

how many fast Na+ channels you have in heart

Question 19

If you make the VRm more positive (higher), what can happen?

Answer 19

Lose fast Na+ channels, shallow out the slope of phase 0, shallow out the peak of phase 0

Question 20

If you make the VRm too high, more positive, what can happen?

Answer 20

No fast Na+ channels, rely on slow Ca++ channels to propagate AP

Question 21

Whats the one spot in the heart that doesnt have gap junctions?

Answer 21

AV node

Question 22

What causes a high VRm?

Answer 22

Hyperkalemia, increased protons (Acidosis), myocardial infarction.

Question 23

What does acidosis cause in the heart?

Answer 23

higher VRm, the enzymes in cells wont function properly, causing the cell to expand more energy, causing an energy deficit.

Question 24

What does lidocaine or any other -caine drug do in the heart?

Answer 24

Shallow the slope of phase 0 of ventricular myocytes by blocking Na+ channels, slowing it down.

Question 25

At rest, nodal tissue is significantly leaky to ________. In purkinje, theres not a lot of ______ during phase 4.

Answer 25

calcium through calcium leak channels. Calcium permeability.

Question 26

SA node, AV node, purkinje fibers. List them in order from least to most permeable to calcium during phase 4.

Answer 26

Purkinje fibers, AV node, SA node (most)

Question 27

mACh-r are attached to ____ channels in the cell wall of the heart cell

Answer 27

potassium

Question 28

When an agonist binds to mACh-r, ___ will open up.

Answer 28

potassium channels

Question 29

What is the primary way for nodal tissue maintain/adjusts VRm?

Answer 29

mACh-r with potassium channels

Question 30

If we have lots of vagal tone, it would increase the ________, decreasing ________ and _________.

Answer 30

potassium permeability, decreasing VRm, decreasing heart rate.

Question 31

If we block the mACh-r, it will ____, which gives us _________ VRm, resulting in ______.

Answer 31

decrease potassium permeability; higher; elevated heart rate

Question 32

Adenylyl cyclase turns _____ into ____.

Answer 32

ATP into cAMP

Question 33

An agonist of a secondary mACh-r that has an inhibitory alpha subunit attached, will bind to

Answer 33

Adenylyl cyclase and inhibit it, decreasing cAMP

Question 34

Beta receptors in the heart have a ____ subunit and it is _____.

Answer 34

alpha; stimulatory in nature.

Question 35

What happens when an agonist binds to a beta receptor in the heart?

Answer 35

activates alpha stimulatory subunits and speed up adenylyl cyclase, increasing cAMP.

Question 36

Subset of beta receptors in the heart that are able to interact with HCN channels, directly activated by beta-adrenergic receptors, which increase cAMP through increased speed of adenylyl cyclase, that opens HCN channels, allowing more sodium and calcium to come into the pacemaker cells during phase 4.

Question 37

What comes in through HCN channels during phase 4?

Answer 37

Sodium and calcium

Question 38

the more cAMP we have, the more activity we have of ____

Answer 38

PKA

Question 39

PKA will

Answer 39

phosphorylate stuff

Question 40

Target channel for PKA is

Answer 40

phosphorylate L-type calcium channels, making them more sensitive and easier to open, more calcium coming in during AP

Question 41

Another target for PKA (non-channel) is

Answer 41

troponin-I.

Phosphorylates trop-I, which increases contractile protein sensitivity to calcium. Resulting in increased cross-bridge cycling rate.

Question 42

Last major target for PKA is

Answer 42

Phospholamban

Question 43

phospholamban

Answer 43

inhibitor of SERCA pump, so if we phosphorylate (inhibit) phospholamban, it will increase the speed of the SERCA pump.

Inhibiting the inhibitor!

increases speed of resetting the cell.

Results in faster heart beat

Question 44

What are the 3 ways that PKA affects the heart rate?

Answer 44

-Phosphorylating L-type calcium channels to increase calcium influx.
-phosphorylating phospholamban, which will allow the SERCA pump to work faster, increasing heart rate.
-phosphorylating troponin-I, increasing contractile protein sensitivity to calcium, increasing cross-bridge cycling rate.

Question 45

The part that makes beta-adrenergic stimulation dangerous is the

Answer 45

phosphorylation of calcium channels in cell wall.

Results in too much heart activity, causing things like heart attacks. Open at the wrong time and generating APs when they shouldnt.

Shoveling snow when youre 80 years old in wisconsin in the water.

Question 46

cAMP can ______ on its own.

Answer 46

fall apart

Question 47

What if the speed of cAMP falling apart on its own is too slow?

Answer 47

heart will use phosphodiesterase (PDE), breaking down cAMP into AMP (removing cyclic connection), reducing cAMP, reducing all PKA activity.

Question 48

What happens if you add a PDE inhibitor?

Answer 48

increases cAMP, increasing PKA activity.