RMP and AP Flashcards
What 3 properties give us consistency of the heart
automaticity, conduction system, functional syncytium
What structures are apart of conductions system
SA note, inter-atrial pathway, AV node, common AV bundle, R and L bundle fibers and the purkinje fibers
What cells are usually in charge of driving heart rate
SA nodes because reach threshold first
What would you expect to see if SA node fails
bradycardia
How does SA spread to AV node? left atrium?
AV node- internodal pathway
left atrium- brachmanns bundle or known as anterior interarterial myocardial band
3 functional regions of AV node
AN
N- nodal
NH
What paths slow conduction
AN and N
how does AN slow conduction
longer path
how does N region slow conduction
slower velocity
Why is there a delay between atria and ventricles
so we have time for filling of the heart during diastole
What is decremental conduction
effect dies out over time
Which node is common to have conduction blocks
AV
Once AV nodes fail what fibers take over
purkinje. 20-40 bpm
What do patients with Wolff-Parkinson-White Syndrome have
alternate path around AV node(bundle of kent). conducts directly atria to ventricle and is faster. but the ventricle depolarization is slower
Where does the right and left bundle branches go
R- down right IV septum
L- splits anterior and posterior
How are purkinje fibers arranged
linear like sarcomeres.
Which part of conduction system has fastest conduction velocity and how?
purkinje because they have a huge diameter
in which direction are purkinje fibers activated
endocardium- epicardium
apex- base
In ventricular m how are APs conducted
cell to cell
Which cells repolarize after depolarization
base- apex
epicardium- endocardium
What events are significant for ventricular depolarization
early contraction of IV septum(anchor)
early contraction of papillary m (prevent backflowto atria)
depolarization apex to base
Where is the slowest conduction velocity in the heart? and why?
AV and SA nodes
small diameter
how many nuceli are in cardiac m
mononucleated
Where is Ca stored in Cardiac m
ECF and SR
what is faster. rate of contraction of skel m or cardiac
skel m. cardiac is 1.5x slower
What are markers of myocardial injury
Troponin T and I markers and CK-MB
What accounts for the electrical syncitium of the heart
all cardiac m cells contract in syncrony
What allows for cell to cell communication
intercalated disks
If cell to cell communication is not working properly what do you see on the EKG
widened QRS complex
What is the all or none of the heart
either all cardiac cells contract or none
how do we alter contractility of cardiac m
increase Ca. sympathetic input
Why do we need Ca from ECF
to trigger release of Ca from SR
What do we need for relaxation of cardiac cells
Sarcolemmal 3Na/1Ca antiporter
and Sarcolemmal Ca pump using ATP
SERCA
Can cardiac m increase force of contraction through tetanus
no
Why can cardiac m not go under tetanus
AP is long (plateau)
How do we have a long AP in cardiac cells
VG L type Ca channels
and delayed K channel
Do pacemaker cells have RMP
no- maximum diastolic potential
What do we have instead of RMP in pacemakers
slow depolarizaiton phase
What is the RMP of fast conducting cells
-80 - -90
Ion distribution for RMP
Na and Ca high extracell
K high intracell
What is the RMP permeable to
K
effect of hyperkalemia
increase depolarization
Are AP constant thorughout all areas of cardiac cell conduction
no, initiation time shape and duration of APS changes depending on what cells.
2 main types of cardiac AP
fast response fibers and slow response fibers
Which RMP is more negative, fast or slow response AP
fast is more negative.
What is the threshold potential in slow and fast AP
slow is -40
fast is -70
Which type of cardiac AP has faster upstroke
fast
Rank conduction veolocities of slow response, fast response in ventricles and fast response in purkinje
purkinje fastest
then fast response ventricle
slow response are the slowest
which fibers respond to greater AP firing rate
fast response fibers because recover fast from refractory period
What are the 4 main ion currents in cardiac AP
NA, Ca, K, and funny current
What phase is Ca responsible for in slow response fibers
slow depolarization- AV SA nodes
What phase is Ca responsible for in fast response fibers
plateau phase
What phase is the funny current responsible for in slow response AP
“pacemaker current” partialy helps the slow depolarization phase
What type of ion current is the funny current
Na
If the upstroke of a cardiac AP is solely due to Ca influx what type fiber is it
slow response AP
What two ions contribute to the rapid spike at the begining of a fast response cardiac AP
Na and Ca
Which type cardiac AP has a transient K current
fast response
What ions are still moving during the plateau phase in fast cardiac AP
K and Ca and tiny bit of Na
what ions are moving during the electrical diastolic phase of slow response cardiac AP
K Ca and the funny current
what ion impacts the conduction velocity
Na
what are the types of Ca channels in cardiac myocytes
L type Ca and T type Ca
When does Ca activate and inactivate in fast response AP
activate at more positive and inactivate slower than Na
What are the two K channels that contribute to respolarization
rapid and slow
describe K movement in SA and AV node
decreases efflux to promote depolarization
What would be the effect of a K channel blocker on AP in fast response
lose that little dip of repolarization after upstroke. Also prolonged AP
What AP is shorter, atrial AP or ventricl
AP because faster K efflux to repolarize
What are the 4 dependent currents in Purkinje fibers
Na Ca K and funny
What are the 2 factors that affect conduction velocity
AP amplitude
Rate or slope of the depolarization
When is there the greatest number of inactivation gates on Na channels
right after depolarization
How does hyperkalemia slow conduction velocity
decreases amplitude and slope depolarization because many of Na channels will be inactivated.
When do we see hyperkalemic states in cardio clinically
Ischemia- affects ATPase so ion [ ] not normal
Infarcted cells- cells release intracell K
When is the effective refractory period
after initiation of fast AP, locked Na gates
When is the relative refractory period
not fully excitable. before repolarization is complete
What does AP look like when happens during relative refractory
depends when it takes place/ if right before reached depolarization- looks normal.
if right when refractory begins, small amplitude
What is the purpose of refractory periods
avoid tetanus and gives time for adequate filling (diastole)
also can limit ectopic beats
What is an Ectopic foci
AP that do not follow normal conduction pathway
What does an EKG look like with ventricular ectopic foci? why?
wide QRS because takes longer for cells to communicate cell - cell
What are proarrhytmias
increased inward currents or decreased outward currents for repolarization
What do afterdepolarizations result in clinically
tachycardia
What will an early afterdepolarization look like
lower slope, lower amplitude, so slow conduction detrimental. Long QT syndrome– Torsades de pointes
What can cause a delayed afterdepolarization
elevated Ca
What is reentry of cardio
abnormal impulse that takes on own path. own pacemaker rhythm
What is a global rentry pathway
own curcuit
what is needed for reentry to occur
partial depolarization, unidirectional block, effective refractory period is shorter than necessary time (so new one during relative refractory)
Where does global reentry happen
between atria and ventricle
what can result clinically from global reentry
supraventricular tachycardia
where does local reentry occur
within atria. or within ventricles
What can result clinically from local reentry
atrial or ventricular tachycardia
What can cause reentry
autonomic input. sympathetic decreases ERP, vagal increases ERP
3 main factors promotin reentry
lengthened conduction pathway
decreased conduction velocity
reduced refractory period
What can cause lengthened conduction pathway
dilated heart chamber
What can cause decreased conduction velocity
hyperkalmeia, ischemia, purkinje system block
what drugs reduce refractory period
Epinephrine
What is the purpose of an external automated defibrillator EAD
alternating current promoting a reset by putting all cells into refractoriness at once- stopping fibrillation
How do we change HR in slow response
how quickly threshold reached, starting point RMP, or changing threshold itself
When is the inward funny current increased
the more negative membrane gets. hyperpolarization
What is moving through funny channel
Na influx, non specific
What results if decrease ECF Ca
small upstroke and amplitude of fast
Will hyperkalemia increase or decrease HR
decrease because changes driving form for K and slowing dow repolarization
Tetrodotoxin block
transitions from fast response to slow response fibers
