Lecture 6 Test 4 Flashcards
When should you not see any electrical activity on your EKG?
Before the P wave and after the T wave.
If you have a current of injury on your left ventricle sub endocardium what would you see on the EKG?
Positive deflections before the P wave and after the T wave.
What can the TP segment tell you?
If there’s a depression or elevation.
If you have an infarct on the left wall thickness of the ventricle what would you see?
A bigger vector, going towards the right arm. Negative deflection on Lead II
What does a negative deflection on the ST segment tell you?
ST elevation = infarct
If you’re looking at leads V2 with a negative deflection?
This is an anterior injury
If your axis is pointed straight up what does it mean?
You have an infarction on the Apex of the heart
What does it mean if V2 has a positive deflection?
Posterior injury
Positive deflection on V2 with the Mean axis pointed straight up means?
Posterior apex injury.
General rule of thumb, ischemia is usually on the ……… and infarct
- little sliver on the left side
- Whole left wall
Fast Na channel: at rest
Inactivation gate
Activation gate
- H gate (inside) open
-M gate (outside) closed
Fast Na channel: depolarization
- M gate (activation) opens
- H gate (inactivation) open for a brief time and closes
Fat Na channel: repolarize
- M gate closes
- H gate opens
T/F: you need repolarization before being able to do another Fast Na Channel depolarization
True
L-type Ca Channel gates:
inactivation gate (inside)
Activation gate (outside)
- F gate
- D gate
resting Fast Na channel gates are
M gate is closed and H gate is open
resting L-type channel gates are
D gate is closed and F gate is open
What causes the L type channel to open?
Voltage dependent and when threshold is reached but opens and closes slower than fast Na channels
L Type channel: depolarized
D gate opens while F gate is open but closes slowly
L type channel: repolarized
D gate is closed, F gate is closed
SA node resting Vrm and threshold Vrm
-55 Vrm
-40 Vrm
SA node AP speed is dependent on the ______ slope of the phase 0
L type
are there Na leaky channels and HCN on the SA node phase 4
yes
Are there any fast Na leaky channel on the phase 0 slope of the SA node?
No
Are there any VG or fast Na channels on the nodal tissues?
No
What’s another theory in regards to VG Na channels on the SA node?
The Vrm is -55 (not negative enough) so maybe it is not able to function
Purkinjie:
Fast Na channel phase 4 is…..
pretty much horizontal
Purkinjie:
Fast Na channel phase 0 slope is
straight up and down
Purkinjie:
What happens when the Vrm is more positive? from -80 Vrm to -60Vrm
You start to lose some fast Na channels and the slope decreases and the height decrease
Purkinjie:
What happens if the Vrm is more positive than the fast Na channels can handle?
the AP will look more like a slow AP because there’s no Na channels involved
What happens when we have no Na involved in the AP?
the heart won’t pump as well but we tend to rely on the Ca channels.
Purkinjie:
If we have a really positive Vrm……
maybe due to?
NA and Ca channels won’t work = no AP
Hyperkalemia
Acidosis
MI
What does lidocaine (-caine) do for our APs?
decreases the slope of phase 0
What’s the difference with phase 4 of the purkinjie fibers and SA node?
Phase 4
- SA node is leaky to Ca channels
- AV node is 2nd leaky to Ca channels
- Purkinjie has no leaky Ca channels
T/F: Fast Na channels can trigger Ca channels to open.
True
mACh-R in a (SA) heart cell when activated
causes K+ to efflux to reduce Vrm
SA node:
we have a second set of mACh-R that has an a-subunit that’s inhibitory and attached to?
adenylyl cyclase that turns ATP to cAMP.
What happens to the secondary mACh-R when the main mACh-R is activated?
it is inhibited
SA node:
Beta receptors with an a-subunit (stimulatory)
activates alpha stimulatory subunits to increase adenylyl cyclase > increase cAMP
SA node:
Beta receptors with HCN channels are activated by?
increase cAMP > increase Na and Ca influx to the pacer cells in phase 4
SA node:
increase in cAMP, you get an increase in pKA that activates (phosphorylates)….
- L-type Ca channels
- Troponin I > increases contractile sensitivity to Ca++
- Phospholamban > inhibits SERCA > reset faster > increase hr
If you have too much Beta adrenergic receptors causing > increase cAMP > increase pKA > L type Ca channel influx > MI
Ex. Grandpa shoveling snow > EAD (early after depolarizations) / DAD (delayed after depolarizations) > arrhythmia
cAMP can fall apart on its own. But our body has PDE that leads to?
increase cAMP conversion to AMP > reduce pKA > reduce L type Ca influx > reduce hr
PDE inhibitor > pKA
Second beta receptor attached to HCN channel has unknown reason but it does per Schmidt!
