L11: Electrical Activity Of Heart Flashcards
Equilibrium potential for the ion
- electrical gradient (due to charge difference) = chemical gradient (due to concentration difference)
- calculated from Nernst equation: E = RT/F x ln [outside]/[inside]
Membrane potential
- electrical gradient across the whole cell membrane
- depend on:
1. Concentration of ions (smaller effect)
2. Permeability of membrane to each ion (much greater effect, major factor —> rapid changes in membrane potential)
Vm = RT/F x ln (P[outside]/[inside] + P[outside]/[inside] + …)
Two ions equally permeable: membrane potential = average equilibrium potential of 2 ions
5 phases of Cardiac action potential
0: Rapid depolarisation
1: Partial repolarisation
2: Plateau
3: Rapid repolarisation
4: Gradual depolarisation to threshold / Pacemaker potential
SA node, AV node:
- slow response action potential (lack rapid depolarisation phase)
- prominent gradual depolarisation / pacemaker potential
Atrial, Ventricular muscle, Purkinje fibre:
- fast response action potential (rapid depolarisation phase by fast Na channel)
- no pacemaker activity
Fast response action potential (phase 0, 1, 2, 3, 4)
- At rest
- highly permeable to K at rest due to Inward-rectifier K channel
- highly impermeable to Na and Ca
—> membrane potential ~ EK:-90mV - Rapid depolarisation
- depolarisation initiated by electrical signal from adjacent cell through gap junction
- Voltage-gated Na channel open when reach -70mV
- Voltage-gated Inward rectifier K channel close
- membrane potential approach ENa - Partial repolarisation
- Voltage-gated Na channel open for very short time —> close
- permeability to Na ↓
- membrane potential move away from ENa
- Transient outward K channel open very briefly - Plateau
- Depolarisation to -40mV open Voltage-gated L-type Ca channels (slow to open/close)
- membrane potential approach ECa - Rapid repolarisation
- closure of Voltage-gated L-type Ca channels and opening of K channel (slowly-activated delayed-rectifier K channel, then rapidly-activated delayed-rectifier K channel)
- membrane potential approach EK
- finally Inward-rectifier K channel reopen
Sequence of channels:
Inward rectifier K channel —> voltage gated fast Na channel —> L type Ca channel + transient outward K channel —> slowly activated delayed-rectifier K channel —> rapidly activated delayed-rectifier K channel —> Inward rectifier K channel
Slow response action potential (phase 0, 3, 4)
- Gradual depolarisation
- no fast Na channel
- funny Na channel open —> increased Na permeability —> depolarisation
- K channels are closed —> membrane potential move away from EK —> further depolarisation - Action potential
- L-type Ca channel open when threshold -40mV is reached
- most permeable to Ca —> membrane potential approach ECa - Repolarisation
- L-type Ca channel close spontaneously after a while (time-dependent)
- Depolarisation also cause K channel to open (slowly-activated delayed-rectifier K channel —> rapidly-activated delayed-rectifier K channel)
- membrane potential approach EK
Sequence of channels:
Funny Na channel —> inward-rectifier K channel (close) —> L-type Ca channel (action potential) —> slowly activated delayed-rectifier K channel —> rapidly activated delayed-rectifier K channel —> Funny Na channel
Spread of electrical activity
- SA node: intrinsic rate pacemaker activity ~100 beats/min
- electrical activity spread from cardiac to another through gap junction in longitudinal region of membrane folds (low electrical resistance)
- one muscle fibre linked to another at intercalated disk (at Z line, jump over several Z line —> increase strength of anchoring)
- connexons on adjacent cell dock —> Gap junction: connexin 43
- connexin channels are voltage gated —> depolarisation open connexin —> ions flow from depolarised cell to the other
- membrane potential lowered to threshold —> action potential triggered
- repeat until depolarisation spread to all cardiac muscle cell
- whole heart chamber to depolarise and contract at the same time
3 rapidly conducting pathways:
- anterior, middle, posterior internodal bands
- depolarisation to spread rapidly to furthest parts of atria
- simultaneous contraction of both atria
- internodal band merge before AV node (only electrical connection between A and V)
- Conduction through AV node is slow (allow atria to finish contraction before ventricular contraction)
- action potential pass rapidly through Purkinje fibre network to all parts of ventricles
- left and right branches Bundle of His running down interventricular septum
- branches extensively through Purkinje fibres throughout ventricles
Conduction velocity in the heart
Conduction velocity: A + V muscle: 0.5m/s Internodal band: 1m/s AV node: 0.05m/s Bundle of His: 1m/s Purkinje network: 5m/s
Timing of electrical and mechanical events
Cardiac muscle action potential: ~250 ms
First 200ms: absolute refractory period (impossible for another stimulus to trigger action potential)
Final 50ms: relative refractory period (stronger-than-normal stimulus can trigger smaller-than-normal, shorter-than-normal action potential)
Contractile latency: 10ms, peaks before 200ms, lasts 300ms
Overall: contractile response only marginally longer than cardiac action potential (50ms) —> very short relative refractory period —> no tetanus/minimal summation of contractile responses —> allow the heart to be filled with blood before next contraction
Refractoriness
Due to Na channels
At rest:
fast gates closed, slow gates open
Depolarisation:
fast gates open, slow gated close slowly
Absolute refractory period:
fast gates open, slow gate CLOSED
(cardiac cell must repolarised to -50mV to reopen slow gate, otherwise remain closed —> hyperkalaemia —> prevent repolarisation of membrane potential)
Relatively refractory period:
fast gate closed, slow gate OPEN SLOWLY (partly open —> another stimulus can only trigger smaller-than-normal, shorter-than-normal action potential)
Effect of hyperkalaemia
- Lower threshold for depolarisation —> but inactivate Na channels for action potential —> cell cannot be depolarised
- Hyperkalaemia prevent repolarisation of membrane —> does not allow inactivating slow gate to open —> cell cannot be repolarised
