Exam 4 Lecture 6 Flashcards
In a Current of Injury, which way does the tip of the arrow point?
Away from the injury
What is a current of injury?
While the rest of the heart is repolarized, the injured area is still depolarized
When are we most likely to see a current of injury?
During the T-P segment
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
ST-Segment Elevation
*(-) deflection
*Myocardial Infarct
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
ST-Segment Depression
*(+) deflection
*Subendocardial Ischemia
If Voltage of the TP segment is lower than the J-Point, ST _?
*What type of deflection
ST-Elevation and (-) deflection
Which has a larger deflection: Ischemia or Infarct
Infarct
At the J-Point, what should the ventricles be doing?
Fully depolarized, so should be getting ready for repolarization
If Voltage of the TP segment is higher than the J-Point, ST _?
*What type of deflection
ST-Depression
*(+) deflection
If the V2 Current is a (+) deflection, what type of injury is it
Posterior Current of Injury
If the V2 Current is a (-) deflection, what type of injury is it?
Anterior Current of Injury
If the MEA is pointed 270 degrees, what type of current of injury is it?
Injury at Apex of the heart
What part of the EKG does the machine have trouble calibrating?
J-Point
Where do vast majority of Infarcts happen?
L ventricle Wall
How does a Fast Na+ channel look at rest?
M Gate closed and H gate open
At rest, how does a Slow Ca++ channel look?
D gate closed and F gate open
Slow Ca++ and Fast Na+ channels Activation Gates
D and M
Slow Ca++ and Fast Na+ channels Inactivation Gates
F and H
In Phase 0, what are both ventricular myoctes and Nodal Tissue Permeable to
Na+, Ca++, K?
In order, rank different AP in terms of Ca++ permeability
SA, AV, Purkinje/Myocytes
What is Vrm for Ventricular Myocytes
-80mV
Why is it called a Fast AP in Phase 0?
B/c the slope is straight up and down
What is the slope of Phase 0 directly related to?
How many Fast Na+ channels we have involved
Ventricle Myocyte Phase 4: Slope
*Can it fire an AP on its own?
Slight slope above horizontal, due to leaky Na+ channels
*Yes, but takes a while
If the Vrm is increased, what happens to the Fast Na+ channels?
*Slope of Phase 0?
*Peak of Phase 1?
Less fast Na+ channels involved
*Slope of Phase 0 is shallower
*Peak of Phase 1 is less high
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?
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
If the Vrm is so high that the Fast Na+ channels and Slow L-Type Ca++ channels cannot repolarize, how does the AP look?
VFIB/Asystole
What phases are in a ventricular myocyte AP
Phases 4, 0, 1, 2, 3
Which is the fastest phase in the Nodal Tissues?
*Another name for this
Phase 4
*Diastolic Depolarization
What is the Vrm of the SA nodes?
*Threshold?
-55mV; -40 mV
What are the 2 theories for why there are no Fast Na+ channels in Nodal Tissues?
- There actually are no V-G Fast Na+ channels there
- There are V-G Fast Na+ channels, but do not function as Vrm is not (-) enough
Which Channel repolarizes at a more (+) number?
*Slow Ca++ or Fast Na+
Slow Ca++ [-55 mV]
How are Nodal Cells leaky to Ca++ at rest?
Thru Leaky Ca++ channels
What Phases are in a Nodal Tissues Cell
Phases 4, 0, 3
How does Lidocaine change the AP?
Reduces the Slope of Phase 0 by blocking Fast Na+ channels
If you have increased ACh or Vagal Tone, what happens to HR?
Increased K Perm = Reduced Vrm = reduced HR
What is the primary way nodal tissue adjusts Vrm?
Thru mACh-R and the attached K channels
3 Things that cause a more (+) Vrm
Hyperkalemia, Acidosis/Increased H, Increased Protons, MI
What happens if you give Atropine?
Decreased K permeability at the mACh-R sites, leading to increased Vrm = Increased HR
mACh-R 2nd set w/ Alpha Inhibitory Subunit: Effect on cell
Slows down AC when bound = decreased cAMP = decreased PKA
Beta-R subset that interacts w/ HCN channels: Effect on the cell
*How is it activated
Direct Stimulation and cAMP activation; when activated, HCN channels open and allow for more Na+ and Ca++ to influx during Nodal Cell Phase 4
What does HCN mean
Hyperpolarization Cyclic Nucleotide
What 3 things do PKA mainly phosphorylate?
L-Type Ca++ channels, Troponin I, Phospholamban
PKA Phosphorylation of L-Type Ca++ Channels
Makes them more sensitive and easier to open
PKA Phosphorylation of Phospholamban
Increase speed of Cell repolarization = allows for faster HR
Beta-R Alpha Subunit that is stimulatory: Effects on the cell
Increased AC = increased cAMP = increased PKA
At which part of the cell is Beta Adrenergic Stimulation most dangerous and why?
L-Type Ca++ channels, b/c more sensitive to PKA = increased AP firing when not supposed to [Arrythmias]
PKA Phosphorylation of Troponin I
Increased contractile protein sensitivity = increases CBC
Blocking Beta-R leads to what w/ HR, CBC, L-Type Ca++ channels
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
What does DAD stand for?
Delayed after depolarization
What does EAD stand for?
Early after depolarizations
Can cAMP fall apart on its own?
*What speeds up this process
yes, but slow
*Phosphodiesterase
What does PDE turn cAMP into?
AMP
What happens to cAMP/PKA if we give a PDE inhibitor?
Increases cAMP, PKA
