Electrophysiology Flashcards
SA node
primary pacemaker of the heart
has highest rate of reaching threshold (70-80 APs/min)
failure–>bradycardia (because AV node would take over and it is slower)
Bachmann’s bundle
interatrial tracts that spread depolarization from RA to LA
AV node
allows signal to pass from atria to ventricles (only bridge b/w the two)
AN region: transitional zone, longer conduction path
N: midpoint of AV node, slower conduction velocity
NH: transition to bundle of His
—>delay before signal goes to ventricles
**allows for adequate ventricular filling
Wolff Parkinson White (WPW) syndrome
some individuals have alternate pathway for atrial–>ventricle conduction
faster AV nodal pathway
slower ventricular depolarization
—> can cause signal to conduct back up the normal pathway–>tachycardia
Purkinje fibers
arranged linearly like myocytes: have sarcomeres in the R and L ventricles
**larger diameter= increased conduction velocity
activated endocardial–>epicardial
apex–>Base
Functional Syncytium
cells contract in synchrony as a result of gap junction connections
if one cell depolarizes, the rest will follow suit
Extracellular Ca and Cardiac contraction
influx of EC Ca is required for additional Ca release from SR
**activates RYR
Relaxation
removeal of Ca
- 3Na1Ca antiporter–>ECF
- ATP Ca++ pump—>ECF (against ECF)
- SERCA back to sarcolemma
Pacemaker cell RMP
NO resting membrane potential
maximum diastolic potential only (slow depolarization)
Non-pacemaker cell RMP
RMP around -90mv (true RMP)
same ion distribution as normal AP
Hypernatremia
increased ECF Na increases CG during depolarization–>increased amplitude of AP depolarization
Slow response fibers
No RMP, lower threshold potential (-40mV)
- smaller amplitude depolarization
- Slower conduction velocity
slower upstroke (phase 0)
Fast response
have RMP, which is more negative threshold (-70mV), higher amplitude depolarization
very fast upstroke (phase 0)
Na current
phase 0 (rapid depol) in fast AP cells
Rapidly activate when membrane depolarizes
IG gates close at +30mV–>phase 1
but some channels remain open and prolongs plateau
Na current–.increased conduction velocity
Ca current
depolarization (phase 0) in slow AP channels
Small role in pacemaker phase (phase 4)
plateau in fast response cells
triggers contraction in all cardiomyocytes
*Slower conduction velocity due to smaller Ca current
K current
repolarization in all cardiomyocytes
In SA/AV K current decreased negative diastolic voltage to assist with pacemaker activity (phase 4)
pacemaker funny current
responsible for slow depolarization in SA and AV
-mostly Na influx–> pacemaker potential
Phase 4
Purkinje fiber
Normally a fast response fiber
but can also become pacemaker cells (very slow)
can have funny current
Conduction velocity
depends on
1) amplitude of AP (affected by Na ECF)
- -> increase amplitude= increase ability to depolarize adjacent membrane
2) Slope of depolarization
Hyperkalemia and conduction velocity
Small persistent depolarization (to -50)–> closes IG gates on may Na channels–> fewer channels able to respond–> smaller amplitude AP–> decrease conduction velocity
can be caused by CAD/MI ischemia–> decrease Na+K+ ATPase–> exs ECF Na and Exs ECF K–>rhythm disruption
-MI also releases K+
effective refractory period
aka absolute refractory
- IG gates closed after fast response depolarization
- phase 0–> midPhase 3
reopen after repolarization
relative refractory
can initiate another AP
mid-phase 3–> end phase 3
if a subsequent AP comes in, the later in the RP= greater amplitude of its upstroke
can limit ectopic beats
Ectopic foci
abnormal impulse that takes a different conduction path and setup its own pacemaker rhythm –> arrhythmias and fibrillation (circus movements)
ex: WPW syndrome
Long QT syndrome
prolonged action potential
still in some degree of refractory when another AP comes in–>causes oscillation of moderate depolarization/repolarization
Early afterdepolarization (EAD)
low slope, low amplitude
abnormal depolarization in late phase 2 or in phase 3
Long QT
more abnormal
Reentry
set up a new circuit that it completely out of order
generate APs that do not follow normal pathways (out of order)
cause premature contractions
–>prolonged QRS (PVCs)
Factors promoting reentry
***—>increase likelihood that you comeback to node by the time the cell has recovered
1) lengthened conduction pathway: dilated heart chambers, atrial enlargement etc
2) decrease conduction velocity: hyperkalemia, ischemia, Purkinje block
3) Shorten refractory period (drugs, epi)
Funny current
opens at more negative (hyperpolarized voltages)
causes Na influx
Hyperkalmeia and HR
slowes HR by affecting driving force for K efflux
–> slows phase 4 repolarization–>delay in reaching hyperpolarization
