Cardiac Action Potential, Animation.
Summary
TLDRThe heart is a self-regulating muscular organ that pumps blood through a series of electrical impulses. Its specialized cardiac myocytes initiate contractions via action potentials, which start at the SA node and spread via the conduction system. The SA node's pacemaker cells generate action potentials that synchronize atrial and ventricular contractions. The unique ion channels and calcium handling in cardiac cells ensure a prolonged plateau phase, allowing for efficient blood expulsion, while a longer refractory period prevents uncontrolled muscle responses.
Takeaways
- 💓 The heart is a muscle that pumps blood through contractions initiated by electrical impulses called action potentials.
- 🔌 Unlike skeletal muscles, the heart generates its own electrical stimulation, allowing it to beat independently of the nervous system.
- 🌀 The cardiac conduction system, starting with the SA node, controls the heart's rhythm and can continue to function even if the SA node is damaged.
- 🔥 The SA node's spontaneous firing of action potentials at about 80 per minute results in an average heart rate of 80 beats per minute.
- 🔄 The electrical signals propagate through the atria and ventricles via gap junctions, ensuring synchronized contractions.
- 🔮 Pacemaker cells have a unique action potential generation process involving 'funny' currents that lead to the pacemaker potential.
- 💥 The action potential in cardiac myocytes involves a rapid influx of sodium followed by a plateau phase due to a balance of calcium and potassium ions.
- 🏋️♂️ The influx of calcium ions is crucial for muscle contraction, with a significant amount released from the sarcoplasmic reticulum.
- 🔙 The repolarization phase involves the closing of calcium channels and the predominance of potassium efflux, returning the cell to its resting state.
- ⏱️ The cardiac muscle's absolute refractory period is much longer than skeletal muscle, preventing unwanted summation and tetanus that could disrupt the heartbeat.
Q & A
What is the primary function of the heart?
-The primary function of the heart is to contract and pump blood throughout the body.
What are cardiac myocytes and how are they involved in the heart's function?
-Cardiac myocytes are specialized muscle cells that contract to pump blood. They initiate contraction through electrical impulses known as action potentials.
How does the heart generate its own electrical stimulation?
-The heart generates its own electrical stimulation through a group of specialized myocytes called pacemaker cells, which are part of the cardiac conduction system.
What is the role of the SA node in the heart?
-The SA node, or sinoatrial node, is the primary pacemaker of the heart. It initiates all heartbeats and controls the heart rate.
How do the impulses from the SA node spread through the heart?
-The impulses from the SA node spread through the conduction system and to the contractile myocytes via gap junctions, which allow ions to flow from one cell to another.
What is the significance of the resting membrane potential in cardiac cells?
-The resting membrane potential, usually negative, indicates the cell's electrical state at rest. It is crucial for the generation of action potentials.
How does the action potential in cardiac cells differ from that in skeletal muscle cells?
-Cardiac cells have a plateau phase in their action potentials, which allows them to stay contracted longer than skeletal muscle cells, necessary for the expulsion of blood from the heart.
What is the role of the sarcoplasmic reticulum (SR) in cardiac muscle cells?
-The SR in cardiac muscle cells stores a large amount of calcium, which is crucial for the 'calcium-induced calcium release' process that triggers muscle contraction.
What is the significance of the absolute refractory period in cardiac muscle?
-The absolute refractory period in cardiac muscle is much longer than in skeletal muscle, ensuring that the muscle has relaxed before it can respond to a new stimulus, preventing summation and tetanus.
How does the nervous system influence the heart's beating?
-The nervous system can influence the heart's beating by making the heartbeats go faster or slower but cannot generate the heartbeats itself.
What happens if the SA node is damaged?
-If the SA node is damaged, other parts of the conduction system may take over the role of initiating heartbeats.
Outlines
🫀 Heart's Electrical Conduction System
The heart is a muscular organ that contracts to pump blood, composed of specialized cells known as cardiac myocytes. These cells contract due to electrical impulses called action potentials. Unlike skeletal muscles, the heart generates its own electrical stimulation, allowing it to continue beating even when removed from the body. The nervous system can influence the heart rate but does not create the heartbeats. The cardiac conduction system, starting with the pacemaker cells, initiates these impulses. The SA node, as the primary pacemaker, controls the heart rate. If damaged, other parts of the system can take over. The action potentials spread through gap junctions, electrically coupling neighboring cells. The conduction system ensures synchronized contraction of all myocytes. The SA node cells have a unique way of generating action potentials, with no true resting potential and a spontaneous depolarization due to 'funny' currents. The action potential involves the flow of ions through voltage-gated channels, leading to the contraction of the heart muscle.
🔬 Cardiac Action Potential and Muscle Contraction
The second paragraph delves into the specifics of the cardiac action potential and how it differs from that of skeletal muscles. The contractile myocytes have a stable resting potential and depolarize only upon stimulation. The depolarization leads to the opening of fast sodium channels, causing a rapid rise in voltage. L-type calcium channels open subsequently, contributing to the depolarization. The action potential reaches a plateau phase, unique to cardiac cells, where calcium influx from the extracellular fluid and the sarcoplasmic reticulum triggers muscle contraction. The plateau phase allows for a longer contraction time, essential for blood expulsion from the heart. The refractory period in cardiac muscle is significantly longer than in skeletal muscle, preventing unwanted summation and tetanus, which could halt heart function. The restoration of ionic balance is facilitated by pumps and the sodium/potassium pump, ensuring the muscle can relax and prepare for the next contraction.
Mindmap
Keywords
💡Cardiac Myocytes
💡Action Potentials
💡Pacemaker Cells
💡Cardiac Conduction System
💡Resting Membrane Potential
💡Depolarization
💡Repolarization
💡Threshold
💡Voltage-gated Ion Channels
💡Calcium-induced Calcium Release
💡Refractory Period
Highlights
The heart is a muscle that pumps blood through contraction.
Heart contractions are initiated by electrical impulses called action potentials.
The heart generates its own electrical stimulation independently of the nervous system.
Pacemaker cells are specialized myocytes that initiate and conduct action potentials.
The SA node is the primary pacemaker, controlling the heart rate.
If the SA node is damaged, other parts of the conduction system can take over.
Action potentials propagate through gap junctions connecting myocytes.
The AV node slows impulses to allow atrial contraction before ventricular contraction.
Action potential generation and conduction synchronize all myocytes.
Pacemaker cells and contractile myocytes have different action potential forms.
Resting membrane potential is negative, indicating the cell is more negative inside.
Ion concentration gradients are maintained by pumps moving sodium and calcium out, potassium in.
An action potential is a brief reversal of the cell membrane's electric polarity.
Pacemaker cells of the SA node fire about 80 times per minute, correlating to an average heart rate.
Pacemaker cells lack a true resting potential and spontaneously depolarize to threshold.
The influx of calcium ions is crucial for the rising phase of the action potential.
The plateau phase of the cardiac action potential is unique to heart muscle cells.
Calcium-induced calcium release from the sarcoplasmic reticulum triggers muscle contraction.
The absolute refractory period in cardiac muscle is much longer than in skeletal muscle.
Transcripts
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.
Unlike skeletal muscles, which have to be stimulated by the nervous system, the heart
generates its own electrical stimulation.
In fact, 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.
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, 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.
The impulses reach the AV node, slow down a little to allow the atria to contract, then
follow the conduction pathway and spread though 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 becomes LESS negative, the cell is LESS polarized,
and is said to be depolarized.
Reversely, when membrane potential becomes MORE negative, the cell is repolarized.
For an action potential to be generated, the membrane voltage must depolarize to a critical
value called the THRESHOLD.
The pacemaker cells of the SA node SPONTANEOUSLY fire about 80 action 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 the rising phase of the 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 several 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 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.
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 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, 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 channels slowly close, potassium efflux predominates and membrane voltage returns
to its resting value.
Calcium is actively transported out of the cell and also 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 1 msec 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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