Exam 4 - Lecture 6 Flashcards
If there is only a smart ischemia in the left ventricle on the endocardium, the MEA should be
Still pointing towards left foot
Where will we be able to see a current of injury with ischemia?
Where there should be no current, after T-wave before the P-wave
ST segment depression means
J-point/S-wave is below the T-P segment
Is the ST segment actually depressed?
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)
If the J-point is above the area after the T-wave, it is a
negative current of injury
If the J-point is below the area after the T-wave, it is a
positive current of injury
Why do we only pick out 2 of the 3 leads for the abnormal EKGs?
einthovens law, cause if we know whats in I and III, we know whats in II.
What does einthovens law need to hold true?
electrodes to be placed perfectly
It is basically impossible for the EKG equipment to find a a
zero point aka zero out the leads and find the J-point
The activation gate in fast Na+ channels is called what and where is it? What’s its status at rest?
M gate, on the outside. Closed.
The inactivation gate in fast Na+ channels is called what and where is it? What’s its status at rest?
H gate, inside. Open.
The activation gate in Ca++ slow channels is called what and where is it? What’s it’s status at rest?
D gate, outside. Closed.
The inactivation gate in Ca++ slow channels is called what and where is it? What’s it’s status at rest?
F gate, inside. Open.
outside of ca+ or na+ channel gate
activation gate, M/D gate. Closed at rest.
Inside of Ca++ or Na+ channel gate
Inactivation gate, H/F gate. Open at rest.
2 theories why there’s no fast sodium channels in nodal tissue
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.
Will the fast sodium channels or L-type channels need more repolarization to reset?
Fast sodium channels
The slope of phase 0 in ventricular myocytes is directly rated to
how many fast Na+ channels you have in heart
If you make the VRm more positive (higher), what can happen?
Lose fast Na+ channels, shallow out the slope of phase 0, shallow out the peak of phase 0
If you make the VRm too high, more positive, what can happen?
No fast Na+ channels, rely on slow Ca++ channels to propagate AP
Whats the one spot in the heart that doesnt have gap junctions?
AV node
What causes a high VRm?
Hyperkalemia, increased protons (Acidosis), myocardial infarction.
What does acidosis cause in the heart?
higher VRm, the enzymes in cells wont function properly, causing the cell to expand more energy, causing an energy deficit.
What does lidocaine or any other -caine drug do in the heart?
Shallow the slope of phase 0 of ventricular myocytes by blocking Na+ channels, slowing it down.
At rest, nodal tissue is significantly leaky to ________. In purkinje, theres not a lot of ______ during phase 4.
calcium through calcium leak channels. Calcium permeability.
SA node, AV node, purkinje fibers. List them in order from least to most permeable to calcium during phase 4.
Purkinje fibers, AV node, SA node (most)
mACh-r are attached to ____ channels in the cell wall of the heart cell
potassium
When an agonist binds to mACh-r, ___ will open up.
potassium channels
What is the primary way for nodal tissue maintain/adjusts VRm?
mACh-r with potassium channels
If we have lots of vagal tone, it would increase the ________, decreasing ________ and _________.
potassium permeability, decreasing VRm, decreasing heart rate.
If we block the mACh-r, it will ____, which gives us _________ VRm, resulting in ______.
decrease potassium permeability; higher; elevated heart rate
Adenylyl cyclase turns _____ into ____.
ATP into cAMP
An agonist of a secondary mACh-r that has an inhibitory alpha subunit attached, will bind to
Adenylyl cyclase and inhibit it, decreasing cAMP
Beta receptors in the heart have a ____ subunit and it is _____.
alpha; stimulatory in nature.
What happens when an agonist binds to a beta receptor in the heart?
activates alpha stimulatory subunits and speed up adenylyl cyclase, increasing cAMP.
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.
What comes in through HCN channels during phase 4?
Sodium and calcium
the more cAMP we have, the more activity we have of ____
PKA
PKA will
phosphorylate stuff
Target channel for PKA is
phosphorylate L-type calcium channels, making them more sensitive and easier to open, more calcium coming in during AP
Another target for PKA (non-channel) is
troponin-I.
Phosphorylates trop-I, which increases contractile protein sensitivity to calcium. Resulting in increased cross-bridge cycling rate.
Last major target for PKA is
Phospholamban
phospholamban
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
What are the 3 ways that PKA affects the heart rate?
-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.
The part that makes beta-adrenergic stimulation dangerous is the
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.
cAMP can ______ on its own.
fall apart
What if the speed of cAMP falling apart on its own is too slow?
heart will use phosphodiesterase (PDE), breaking down cAMP into AMP (removing cyclic connection), reducing cAMP, reducing all PKA activity.
What happens if you add a PDE inhibitor?
increases cAMP, increasing PKA activity.
