Cardiac Action Potential, Animation.
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- เผยแพร่เมื่อ 23 ม.ค. 2017
- (USMLE topics, cardiology) Cardiac action potential in pacemaker cells and contractile myocytes, electrophysiology of a heartbeat.
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The heart is essentially a muscle that contracts and pumps blood. It consists of specialized muscle cells called cardiac myocytes. The contraction of these cells is initiated by electrical impulses, known as action potentials. The impulses start from a small group of myocytes called the PACEMAKER cells, which constitute the cardiac conduction system. The cells of the SA node fire SPONTANEOUSLY, generating action potentials that spread though the contractile myocytes of the atria. The myocytes are connected by gap junctions. This enables electrical coupling of neighboring cells. Pacemaker cells and contractile myocytes exhibit different forms of action potentials.
The pacemaker cells of the SA node SPONTANEOUSLY fire about 80 action potentials per minute, each of which sets off a heartbeat. Pacemaker cells do NOT have a TRUE RESTING potential. The voltage starts at about -60mV and SPONTANEOUSLY moves upward until it reaches the threshold of -40mV. This is due to action of so-called “FUNNY” currents present ONLY in pacemaker cells. Funny channels open when membrane voltage becomes lower than -40mV and allow slow influx of sodium. The resulting DE-polarization is known as “pacemaker potential”. Calcium channels open, calcium ions flow into the cell further DE-polarizing the membrane. This results in the rising phase. At peak, potassium channels open, calcium channels inactivate, potassium ions leave the cell and the voltage returns to -60mV. This is falling phase of the action potential.
Contractile myocytes have a different set of ion channels. Their sarcoplasmic reticulum, the SR, stores a large amount of calcium. They also contain myofibrils. The contractile cells have a stable resting potential of -90mV and depolarize ONLY when stimulated. When a cell is DE-polarized, positive ions leak through the gap junctions to the adjacent cell and bring the membrane voltage of this cell up to the threshold of -70mV. FAST sodium channels open creating a rapid sodium influx and a sharp rise in voltage. This is the depolarizing phase. L-type, or SLOW, calcium channels also open at -40mV, causing a slow but steady influx. Sodium channels close quickly, voltage-gated potassium channels open and these result in a small decrease in membrane potential, known as EARLY RE-polarization phase. The calcium channels remain open and the potassium efflux is eventually balanced by the calcium influx. This keeps the membrane potential relatively stable for about 200 msec resulting in the PLATEAU phase, characteristic of cardiac action potentials. Calcium is crucial in coupling electrical excitation to physical muscle contraction. The influx of calcium from the extracellular fluid triggers a MUCH greater calcium release from the SR, in a process known as “calcium-induced calcium release". Calcium sets off muscle contraction by “sliding filament mechanism”. Calcium channels close, potassium efflux predominates and membrane voltage returns to its resting value. The absolute refractory period is much longer in cardiac muscle. This is essential in preventing summation and tetanus.
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The heart is essentially a muscle that contracts and pumps blood.
It consists of specialized muscle cells called cardiac myocytes.
The contraction of these cells is initiated by electrical impulses, known as action potential (AP)
Unlike skeletal muscles, which have to be stimulated by the nervous system,the heart generates its own electrical stimulation.
In fant, a heart can keep on beating even when taken out of the body.
The nervous system can make the heartbeats go faster or slower, but cannot generate them.
The impulses start from a small group of myocytes called the pacemaker cells, which constitute the CARDIAC CONDUCTION SYSTEM.
These are modified myocytes that lose the ability to contract and become specialized for initiating and conducting action potentials.
The SA node is the primary pacemaker of the heart.
It initiates all heartbeats and controls heart rate
If the SA node is damaged, other parts of the conduction system may take over this role.(AV node , Bundle of His )
The cells of the SA node fire spontaneously generating action potentials that spread through the contractile myocytes of the atria.
The myocytes are connected by gap junctions, which form channels that allow ions to flow from one cell to another.
This enables the electrical coupling of neighboring cells.
An action potential in one cell triggers another action potential in its neighbor and the signals propagate rapidly.
The impulses reach the AV node, slow down a little to allow the atria to contract, then follow the conduction pathway and spread through the ventricular myocytes.
Action potential generation and conduction are essential for all myocytes to act in synchrony.
Pacemaker cells and contractile myocytes exhibit different forms of action potentials.
Cells are polarized, meaning there is an electrical voltage across the cell membrane.
In a resting cell, the membrane voltage, known as the resting membrane potential, is usually negative.
This means the cell is more negative on the inside.
At this resting state, there are concentration gradients of several ions across the cell membrane: more sodium and calcium outside the cell, and more potassium inside the cell.
These gradients are maintained by several pumps that bring sodium and calcium OUT, and potassium IN.
An action potential is essentially a brief REVERSAL of electric polarity of the cell membrane and is produced by Voltage-gated ion channels.
These channels are passageways for ions in and out of the cell,and as their names suggest are regulated by membrane voltage.
They open at some values of membrane potential and close at others.
When membrane voltage INCREASES and become LESS negative,the cell is LESS polarized, and us said to be depolarized.
Reversely, when membrane potential becomes MORE negative, the cell is repolarization.
For an action potential to be generated, the membrane voltage must depolarize to a critical value called THRESHOLD.
The pacemaker cells of SA node SPONTANEOUSLY fire about 80 potentials per minute, each of which sets off a heartbeat, resulting in an average heart rate of 80 beats per minute.
Pacemaker cells do NOT have a TRUE RESTING potential.
The voltage starts at about -60mV and SPONTANEOUSLY moves upward until it reaches the threshold of -40mV.
This is due to action of so-called "FUNNY" currents present ONLY in pacemaker cells.
Funny channels open when membrane voltage becomes lower than -40mV and allow slow influx of sodium.
The resulting depolarization is known as "pacemaker potential".
At threshold, calcium channels open, calcium ions flow into the cell further depolarizing the membrane.
This results in rising phase of action potential.
At the peak of depolarization, potassium channels open, calcium channels inactivate, potassium ions leave the cell and the voltage returns to -60mV.
This corresponds to the falling phase of the action potential.
The original ionic gradients are restored thanks to severy ionic pumps,and the cycle starts over.
Electrical impulses from the SA node spread through the conduction system and to the contractile myocytes.
These myocytes have a different set of ion channels
In addition, their sarcoplasmic reticulum, the SR, stores a large amount of calcium.
They also contain myofibrils.
The contractile cells have a stable resting potential of -90mV and depolarize ONLY when stimulated, usually by a neighboring myocyte.
When a cell is depolarized, it has more sodium and calcium inside the cell.
These positive ions leak through the gap junctions to the adjacent cell and bring the membrane voltage of this cell up to the threshold of -70mV
At threshold,fast sodium channels open creating a rapid sodium influx and sharp rise in voltage.
THIS IS THE DEPOLARIZING PHASE.
L- type or slow, calcium channels also open at -40mV, causing a slow but steady influx.
As the action potential nears its peak, sodium channels close quickly, voltage gated potassium channels open and these result in a small decrease in membrane potential, known as EARLY REPOLARIZATION PHASE.
The calcium channels, however, remain open and the potassium efflux is eventually balanced by the calcium influx.
This keeps the membrane potential relatively stable for about 200msec resulting in the PLATEAU phase, characteristic of cardiac action potentials.
Calcium is crucial in coupling electrical excitation to physical muscle contraction.
The influx of calcium from the extracellular fluid, however, is NOT enough to induce contraction.
Instead, it triggers a MUCH greater calcium release from the SR, in a process known as "calcium-induced calcium release".
Calcium THEN sets off muscle contraction by the same " sliding filament mechanism" described for skeletal muscle.
The contraction starts about half way through the plateau phase and lasts till the end of this phase.
As calcium channel slowly close, potassium efflux predominates and membrane voltage returns to its resting value.
Calcium is actively transported out of the cell and back to the SR.
The sodium/potassium pump then restores the ionic balance across the membrane.
Because of the plateau phase, cardiac muscle stays contracted longer than skeletal muscle.
This is necessary for expulsion of blood from the heart Chambers.
The absolute refractory period is also much longer - 250 msec compared to 1msec in skeletal muscle.
This long refractory period is to make sure the muscle has relaxed before it can respond
to a new stimulus and is essential in preventing summation and tetanus,which would stop the heart from beating.
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so I thought lets be kind today and this is basically a summary of the video. you're welcome.
Action potential cardiac:
The contraction of cardiac myocytes (muscles in the heart) are initiated by electrical impulses, known as action potential. It generates its own electrical stimulation and the beats go faster or slower caused by nervous system, but the nerves don’t generate the contraction. The impulses start from a small group of myocytes (pacemakers cells). These are modified myocytes that lose the ability to contract and become specialized in initiating and conducting action potentials. SA node is the primary pacemaker of the heart it initiates all heart beats and controls heart rate. The cells of the SA node start spontaneously generating action potential that spread through the contractile myocytes of the atria. The myocytes are connected by gap junctions, which form channels that allow ions to flow from one cell to another. This enables electrical coupling of neighboring cells, an action potential in one cell triggers another action potential in its neighbor and the signals propagate rapidly.
- Cardiac myocytes; muscles that make up the heart
- Pacemaker cells; The cells that create these rhythmic impulses; heart rate
1. The impulses reach AV node
2. Slow down little to allow the atria to contract
3. Follow the conduction pathway and spread through the ventricular myocytes
- Action potential generation and conduction are essential for all myocytes to act in synchrony.
Polarized: there is an electrical voltage across the cell membrane
Resting membrane potential, resting voltage, meaning that the cell is more negative on the inside.
- More sodium and calcium outside the cell and more potassium inside the cell
- Maintained through pumps
- When membrane voltage increases and becomes less negative cell is less polarized depolarized. When cell gets more negative cell gets repolarized
80 action potentials/beats per minute
Pacemaker cells do not have true resting potential.
Action potential in pacemaker cells
• The voltage starts at -60 mv and spontaneously goes up to -40mv (threshold) Pacemaker potential
- Due to funny currents, only present in pacemaker cells, open when membrane voltage gets lower than -40mv, allows slow influx of sodium (inside the cell)
• At threshold calcium channels open calcium ions flow in to the cell, further depolarizing rising (depolarizing)
• At the peak of depolarization potassium channels open calcium channels inactivate, potassium ions leave the cell ant the voltage returns to -60mv. falling (repolarization)
Electrical impulses from the SA nodes go to the contractile cells. Contractile cells store a large amount of calcium.
Action potential in contractile myocytes
- A stable resting state of -90mv and depolarize only when stimulated, usually by a neighboring myocyte.
- When is cell is depolarized it has more sodium and calcium ions inside to cell, these positive ions leak through the gap junctions to the adjacent cell and bring the membrane voltage up to -70 mv (threshold)
- At threshold: fast sodium channels open creating a rapid Sodium influx inside the cell and get a sharp rise in voltage. depolarizing phase
- Slow calcium channels opene at -40 causing a slow but steady influx, as the action potential nears its peak sodium channels close quickly, voltage-gated potassium channels open and these resolve in small decrease in membrane potential early repolarization phase
- the calcium channels remain open and potassium efflux is eventually balanced by the calcium influx this keeps the membrane potential relatively stable for about 200 milliseconds plateau phase
- the calcium inside the cell is not enough to trigger a muscle contraction, instead it releases calcium induced calcium release which sets off muscle contraction
contraction starts at half of the plateau phase and lasts until the end.
- Calcium channels close, potassium efflux predominates and membrane voltage goes back to it resting value. The sodium potassium pump then restores the ionic balance across the membrane. repolarization
Because of the plateau phase cardiac muscle stays contracted longer than skeleton muscle, which is important for pumping blood. Absolute refractory (state after and before resting) state is 250 millisecond compared to 1millisecond in a skeleton muscle. the cardiac muscle has a longer absolute time so it can rest before it starts contracting again, which is important.
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