Cardiology: Cardiac Action Potentials

Front 1

branches from different fibers in cardiac tissue connect to each other at

Back 1

intercalated disks

Front 2

what do intercalated disks contain

Back 2

gap junctions (which function as electrical synapses to transfer impulses from fiber to fiber)

Front 3

what initiates cardiac action potentials

Back 3

sinatrial node (SA) in the right atrium

Front 4

from the SA node, where does the action potential get sent to (and how does it get there)

Back 4

it goes to the AV (atrioventricular) node which is located at the top of the septum separating the right atrium and the right ventricle (and the most probable method of travel is via the atrial muscle fibers but this is up to debate)

Front 5

talk about the path the action potential takes on its way from the SA node to the ventricular muscle fibers

Back 5

SA node --> (via atrial muscle fibers) AV node --> bundle of His --> (via right and left bundle branches) to the ventricular muscle fibers

Front 6

why do action potentials look different in each part of cardiac muscle

Back 6

the differences (MOST LIKELY) enable the cardiac fibers to act in unison -- if there is a problem with this the blood cannot be circulated like in vfib

Front 7

what are the two general types of cardiac action potentials

Back 7

fast and slwo response action potentials

Front 8

when DEpolarizing which direction is the potential moving

Back 8

UP - MORE POSITIVE

Front 9

when re or hyper polarizing which direction is the potential moving

Back 9

DOWN - MORE NEGATIVE

Front 10

what is the main differnence between fast and slow response fibers in cardiac tissue?

Back 10

fast response = FAST depolarizing phase (STEEP)
slow response = SLOW depolarizing phase (LESS STEEP)

Front 11

what type of fibers are in the SA and AV node
what type of fibers are in the atrial and ventricular muscle fibers and the perkinje fibers

Back 11

SA / AV = SLOW (pacemaker fibers)
typical cardiac muscle = FAST

Front 12

phase 0: (fast response fiber)
where is it on the curve?
what channels are open?
what ions move around?
what is going on?

Back 12

- start of curve (from resting to +20mV) - SHARP RISE
- opening of voltage gated Na+ channels which allow for INWARD movement of na+ions
DEPOLARIZATION

Front 13

talk about the voltage gated Na+ channels
at rest which channels are open
when AP comes, what happens

Back 13

rest: fast gate = closed ; slow gate = open
AP --> fast gate opens fast and slow gate closes slow (bc of this difference in rate of opening/closing there is a brief moment where both gates are open --> na+ conductance incr's and Na+ ions move down their electrochemical gradient and MOST close (but not all - see phase 2) due to closing of slow gate

when the potential falls to resting (normal) value the Na channel gates return to their resting conformation and are capable of responding to another impulse

Front 14

phase 1: (fast response fiber)
where is it on the curve?
what channels are open?
what ions move around?
what is going on?

Back 14

the small decrease at the top of the peak (from +20 --> 0)
REPOLARIZATION is caused by closure of VG Na channels and opening of VG K channels (transient outward potassium channels) and thru these the K current that passes thru the channels is the transient outward K current (Ito or ito) --> positive charge goes out

this transient outward potassium is only open for a short time so it repolarizes rapidly but for a VERY short time (large slope, short distance)

Front 15

phase 2: (fast response fiber)
where is it on the curve?
what channels are open?
what ions move around?
what is going on?

Back 15

plateau - (bc there is a balance between inward andoutward ion movements)
Na (VG that havnt closed yet)and Ca (L-type ca channels open slowly and for a "L"ong time during polarization but no real effect until after phase 1) both enter
REPOLARIZATION
the main K channel responsible for outward movement of K in the plateau is the delayed rectifier K channel or channels (opens slowly = delayed ; and rectified = moves in ONE direction --> from INTRAcellular to EXTRAcellular)

outward movement is slightly greater than inward movement so this is why we have a slowly decreasing "plateau"

Front 16

phase 3: (fast response fiber)
where is it on the curve?
what channels are open?
what ions move around?
what is going on?

Back 16

RAPID repolarization
inward movement of Ca decr.
outward movement of K incr. (recovery phase)
the slow opening delayed rectifier K channel initiates phase 3 and when the potential goes below -30 --> inward rectifying K channel opens and incr. K EFFlux and it remains open at resting potential (unlike other K channels)

Front 17

talk about what is special about the inward rectifying K channel

Back 17

first of all its call INward even tho it permit K ions to go OUT of the cell --> promoting repolarization

when the membrane potential is more positive than the nernst equilibrium potential for K, the inward rectifying K channel will permit K ions to move out of the fiber ; the membrane potential is more negative than the nernst equilibrium potential forK --> inward rectivying K channel permits K ions to enter the fiber from the extracellular fluid (this is what happens during HYPERpolarization)

Front 18

phase 4: (fast response fiber)
where is it on the curve?
what channels are open?
what ions move around?
what is going on?

Back 18

RESTING MEMBRANE POTENTIAL
BACKGROUND INFO: Na-K pump pumps Na out and K into it and uses the energy of Na going DOWNhill across the membrane to fuel the pumping of Ca ion out of the fiber (which is uphill)

Front 19

what is the major contributor tothe resting membrane potential?

Back 19

K+ --> therefore the resting membrane potential in typical cardiac muscle fibers is close tothe nernst equilibrium potential for K --> -92.8mV

Front 20

what can hyperkalemia cause?

Back 20

abnormal arrhythmias, fibrilliation (due to the movement of the resting membrane potential to a more positive value) and cardiac arrest (which is due to the fact that the decreased K gradient leads to increased repolarization times and therefor arrhythmias and cardiac arrest!)

Front 21

what can hypokalemia cause?

Back 21

arrhythmias --> activates pacemaker channels which open when the membrane potential reaches its resting value (or becomes hyperpolarized which is the case in hypokalemia bc this decr. amount of K decr. the resting membrane potential...)