L11 Electrical activity of the Heart Flashcards Preview

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Flashcards in L11 Electrical activity of the Heart Deck (56):

What drives ion to move across membrane?

Different concentration of an ion on either side of a membrane:
Concentration gradient


What opposes further ion movement?

movement charge sets up electrical gradient


When does net movement stop?

Net movement ceases when electrical and chemical gradients are exactly balanced

At equilibrium potential for the ion


equilibrium potential for the ion can be calculated by?

Nernst equation: e.g. K
Ek = (RT/F) ln ([K0+]/[Ki+])

 EK = potassium equilibrium potential (= -90mV in heart)
 R = gas constant
 T = temperature (constant in body)
 F = Faraday constant
(RT/F= constant (in general))


Ions have same or diff equ potential?

different equilibrium potential


What is membrane potential? Vm

electrical gradient across the cell membrane (can change over time  action potential)


What does Vm depend on?

Depends on both:
1. Concentrations of ions on either side of the membrane; and
2. Permeability of the membrane to each ion


What is ture if Vm is close to one ion's equilibrium potential?

If much more permeable to one ion: that ion can easily cross the membrane to approach equilibrium potential)


If membrane is equally permeable to two ions, what would Vm be?

If equally permeable to two or more ions: VM close to average of the equilibrium potentials for those ions


How can rapid changes to Vm be induced?

Changing permeability of membrane to one or more ions (e.g. opening / closing of channels)

Takes very long to change concentration of ions


Which cells show fast response AP? Which ones slow?

Atrial muscle
Ventricular muscle
Purkinje fibres

Sinoatrial (SA) node
Atrioventricular (AV) node


Fast or Slow response AP cells show pacemaker activity?



Fast or slow response AP cells include rapid depolarization response



What is fast response AP initiated by? What is it depolarized by?

Initiated by electrical signal from adjacent cell

Voltage-gated (fast) Na+
channels opening (PNa increase)


When Voltage-gated (fast) Na+ channels open in fast AP cell membrane, what closes?

Inward-rectifier K+ channels close


When fast response AP cell is at rest, what maintains resting potential? At rest cell is impermeable to which 2 ions?

Inward-rectifier K+ channels open.
= highly permeable to K+ so resting Vm is close to EK (stable at ~-90 mV)

Highly impermeable to Na+ and Ca2+


At what Vm does V-gated Na+ channels open? What is the consequence of the opening?

When VM reaches -70 mV threshold

Rapid depolarization:
Membrane most permeable to Na+ >Vm approaches ENa


Fast AP.
What is Partial repolarisation?
Which 2 channels are involved?

Voltage-gated (fast) Na+
channels remain open only for a very short time and quickly close
decreased permeability to Na+ >Vm moves away from ENa

Transient outward K+ channels also open very briefly > help to partially
repolarise the membrane


What phase follows partial repolarisation in fast AP cells?

plateau ("slow inward current"


What is plateau ("slow
inward current") dependent on?

L-type Ca2+ channels


What triggers opening of L-type Ca2+ channels in fast AP cells?

Depolarisation to -40 mV triggers opening of voltage-gated Ca2+ channels (L-type:
long duration: slow to open and close)
VM remains close to ECa


What starts repolarisation after plateau?

1. Voltage-gated L-type Ca2+ channels close
2. Several K+ channels open:


Which K+ channels open during rapid repolarisation phase in fast response AP cells?

 1st : slowly-activated delayed rectifier K+ channels

 Then: rapidly-activated delayed rectifier K+channels

 Finally: inward rectifiers re-open (voltage-activated: when Vm is negative enough)


During rapid repolarisation in fast AP cells, what is the cell most permeable to?

Cell most permeable to K+
so Vm moves towards EK


In slow response AP cells, is there rapid depolarization?

No voltage-gated fast Na+
channels, so no


What is slow response AP DEPOLARIZATION started by? (remember slow tcells have pacemaker potential)

Initiation (spontaneous):
repolarization (from previous AP repolarisation ) to -40 mV triggers opening of “funny channels” Na channels
(gNa: permeable to Na+ so PNa increases)


What happens in slow AP cells when funny channels are opened and PNa increases?

Funny channels open and PNa increases, whilst K channels close so Vm moves further away from EK
Cell is further depolarized


When Vm in slow AP cells finally reach threshold of -40mV, what happens?

When VM reaches threshold (-40 mV), voltage-gated L-type slow Ca2+ channels open

Cell becomes most permeable to Ca2+ so Vm
moves close to ECa > AP


Is there partial repolarisation and plateau in slow AP cells?



When is gCa the highest in slow AP cells?

Peak of Vm


When is gNa the highest?

Small peak at the end of previous AP after complete repolarisation (funny channels are Na+ channels)


When is gK the highest and lowst in slow AP cells?

gK highest just before the end of complete repolarisation of previous AP

lowest at 40mV threshold just before depolarisation to AP


Which channel causes rapid repolarisation in slow AP cells?

Voltage-gated L-type slow Ca2+ channels close SPONTANEOUSLY
(opening = time-dependent)

Decrease in PCa cause Vm to move away from ECa


When slow AP cell is depolarized and PCa increases, what other channel also opens and increase said ions permeability?

K+ channels open (triggered by depolarization) and increase PK:
 1st: IKs:slowly-activated delayed rectifier K+channels

 Then: IKr:rapidly-activated delayed rectifier K+channels

 Finally: IK1:inward rectifiers re-open


Slope of which potential controls HR?

Slope of pacemaker potential controls heart rate (how long it takes to reach threshold to open gCa):

Steeper slope= faster heart rate


What is the intrinsic rate of pacemaker activity in SA node?

fastest intrinsic rate of
pacemaker activity (~ 100 beats/min)


How can electrical activity spread between cardiac cells? Where?

gap junctions = specialised areas of low electrical resistance

In longitudinal region of the extensive membrane folds
where 2 cells parallel each other


Where are muscle fibres (actin filaments) strongly joined? name, where in muscle

Intercalated disks
Always occur at Z-line
Attached to sacromere


Gap junctions are what?

Connexons = hemi-channels (6 subunits) on adjacent cells

connexons on each cell membrane dock >
connexin 43 channel


What happens when Connexin 43 channels are depolarized? What is the domino effect?

Ions flow from 1st depolarised cell to 2nd cell...etc

Lowers VM of 2nd cell to threshold level (depolarized)

Trigger action potential in 2nd cell

whole heart chamber
can depolarize and contract at the same time


Apart from the gap junctions, what other conducting pathways are there? (3) What are these for?

1. Anterior intermodal band
2. Middle intermodal band
3. Posterior intermodal band

For depolarization to spread to furthest part of atria so both atria contract almost


AV node conduction is slow. Why?

Atria finish contracting
before ventricular
contraction starts


Purkinje fibre network
How is it arranged?

 Arranged in right and left branches of Bundle of His
 Runs down interventricular septum
 Branches extensively throughout ventricles


Why is Purkinje fibre network necessary?

Action potential spread
quickly to all parts of


Rank the conduction speeds of nodes and fibres in ascending order (slowest first)

slowest= AV node (0.05m/s) > Atrial and ventricular muscle (0.5m/s) > Bundle of His (1m/s) > Purkinje network (5m/s)


How long does cardiac muscle AP last? How does this cycle divide?

Cardiac muscle action potential lasts ~250 msec:

First ~ 200 msec = absolute refractory period:

Remaining 50 msec = relative refractory period


What is refractoriness due to?

due to gates on Na+


Explain how Na+ channels cause refractoriness.

At rest:
Fast gates closed, slow gates open, channel cannot conduct

Fast gates open fast, slow gate close slow
For a limited time, both gates are open and Na+ passes through


Relate absolute refractory period to fast and slow Na+ gates.

First ~ 200 msec = absolute refractory period:

Slow gates are closed > cell is completely inexcitable when Vm is negative enough
> Impossible for another stimulus to produce another AP


Relate relative refractory period to fast and slow Na+ gates.

Remaining 50 msec = relative refractory period

When Vm becomes sufficiently negative again (-50mV):
 Fast gates quickly close
 Slow gates slowly open
** Slow gate partly open = relative refractory period


What happens if AP occurs during relative refractory period?

If AP occurs: slow gates close more quickly (because only partly opened)

Stronger stimulus can produce a smaller, shorter AP


What is contractile response due to? (which ion)

Ca2+ movement which takes time


What is contractile response latency?

10 msec


How long is total contractile response and when does it peak?

300msec total
Peaks before 200 msec (within absolute refractory period)


Why is there no tetanus occurring in relation to AP and contractile response?

AP lasts as long as contractile response (some rapid filling of ventricle has
already taken place)

only minimal summation of contractile responses

no tetanus can occur


Why is cardiac muscle unlike skeletal muscle in its contraction?

Cardiac muscle must always relax between contraction (unlike skeletal muscle)

so only minimal summation and no tetanus can happen

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