Introduction to Cardiac Electrophysiology Flashcards
Are AP in atria longer/shorter than in ventricles?
shorter AP and refractory period–> don’t need to generate high pressures, but can lead to development of rapid atrial rhythms
Where is the AV node located?
low in the R atrium
The property of some specialized cells to spontaneously depolarize and reach threshold to trigger an action potentail
automaticity
What is the difference between phase 4 depolarization in purkinje and SA node?
purkinje automaticity is driven mostly by If whereas Ik and Ica play the main role in the SA node
How does the SA node stay “in charge”?
faster intrinsic rate of firing + overdrive suppression–> overrides the other pacers except in emergencies
What is overdrive suppression?
activation of the na/k pump leads to hyperpolarization in non-sa pacers that opposes automaticity –> automaticity returns when SA overdrive suppression disappears
Open or closed at upstroke? Na channel: M gate and H gate
M gate open, H gate open
Open or closed at plateau? Na channel: M gate and H gate
M gate open, H gate closed (inactivated)
Open or closed at resting? Na channel: M gate and H gate
M gate closed, H gate open (excitable)
3 factors that determine conduction velocity
- how large the inward sodium current is
- how fast does the inward sodium current activate
- how much resistance there is
How does fibrosis lead to slow conduction after an MI?
separation of fibers by fibrosis reduces number of gap junctions –> increases resistance to axial current flow
How does an acute infarction affect conductance?
reduced gap junction conductance
How do Na blockers affect conductance?
blockade of sodium channels reduces conduction
How does a local elevation of K in an acute infarct or elevated serum K in renal failure affect conduction?
depolarization of resting potential leads to Na channel inactivation resulting in slow conduction
What does safety factor for propagation mean and how does it differ between sodium/calcium current mediated cells?
the term suggests how much the excitation can be reduced before inhibiting the given cell–> Na current is more resistant/higher safety factor/would have to reduce Na current a lot to make the cell inexcitable whereas calcium dependent cells are inhibited by smaller changes in calcium current
How do kinetics for recovery of excitability post repolarization differ between sodium/calcium current mediated cells?
slow response AP has a delayed recovery (calcium mediated) vs. cells that are sodium mediated
What is the effective refractory period?
time following depolarization when a stimulus cannot elicit a propagating action potential
How does ERP compare in fast/slow response cells (aka sodium/calcium mediated)
slow response have a longer ERP because need to wait for calcium channels to reactivate (happens slower than na channel reactivation)
What is the main determinant of ERP in fast response cells?
action potential duration aka rate (in atria and ventricles)
What is the main determinant of ERP in slow response cells?
things that boost the calcium current reduce ERP
What do we expect will happen to ERP in the AV node as heart rate increases?
longer- -> fewer calcium channels reactivated each time
Short/long APD and ERP in atria allow fast atrial rhythms
short
short/long ERPs in AV node and bundle branches protect ventricles during fast atrial rhythms
long
Genetically abnormal Na and K channels can produce very long/short APDs in ventricles
long
