Physiology of Cardiovascular

System CVS
 Anatomy of the heart
Heart
The heart is a fist-sized organ that pumps blood throughout the body. It’s the circulatory system’s main
organ. Muscle and tissue make up this powerhouse organ. The heart contains four muscular sections
(chambers) that briefly hold blood before moving it. Electrical impulses make the heart beat, moving
blood through these chambers. the brain and nervous system direct the heart’s function.
Functions
1. The heart’s main function is to move blood throughout the body. Blood brings oxygen and
nutrients to the cells. It also takes away carbon dioxide and other waste so other organs can dispose
of them.
2. Controls the rhythm and speed of the heart rate.
3. Maintains the blood pressure.
The heart works with these body systems to control the heart rate and other body functions:
1. Nervous system: the nervous system helps control the heart rate. It sends signals that tell the heart
to beat slower during rest and faster during stress.
2. Endocrine system: the endocrine system sends out hormones. These hormones tell the blood
vessels to constrict or relax, which affects the blood pressure. Hormones from the thyroid gland
can also tell the heart to beat faster or slower.
The heart anatomy includes:
1. Walls.
2. Chambers
3. Valves that open and close
4. Blood vessels
5. An electrical conduction system
Heart walls
The heart walls are the muscles that contract (squeeze) and relax to send blood throughout the body. A
layer of muscular tissue called the septum divides the heart walls into the left and right sides.
The heart walls have three layers:
•Endocardium: Inner layer.
•Myocardium: Muscular middle layer.
•Epicardium: Protective outer layer.
The epicardium is one layer of the pericardium. The pericardium is a protective sac that covers the
entire heart. It produces fluid to lubricate the heart and keep it from rubbing against other organs.
Heart chambers
The heart has four separate chambers. You have two chambers on the top
(atrium, plural atria) and two on the bottom (ventricles), one on each side of the
heart.
1. Right atrium: Two large veins deliver oxygen-poor blood to the right atrium.
The superior vena cava carries blood from the upper body. The inferior vena
cava brings blood from the lower body. Then the right atrium pumps the
blood to the right ventricle.
2. Right ventricle: The lower right chamber pumps the oxygen-poor blood to
the lungs through the pulmonary artery. The lungs reload the blood with
oxygen.
3. Left atrium: After the lungs fill the blood with oxygen, the pulmonary veins
carry the blood to the left atrium. This upper chamber pumps the blood to the
left ventricle.
4. Left ventricle: The left ventricle is slightly larger than the right. It pumps
oxygen-rich blood to the rest of the body.
Heart valves
The heart valves are like doors between the heart chambers. They open and close to allow
blood to flow through. They also keep the blood from moving in the wrong direction.
1. Atrioventricular valves: the atrioventricular (AV) valves open between the upper and
lower heart chambers. They include:
• Tricuspid valve: Door between the right atrium and right ventricle.
• Mitral valve: Door between the left atrium and left ventricle.
2. Semilunar valves: open when blood flows out of the ventricles. They include:
• Aortic valve: Opens when blood flows out of the left ventricle to the aorta (artery that
carries oxygen-rich blood to the body).
• Pulmonary valve: Opens when blood flows from the right ventricle to the pulmonary
arteries (the only arteries that carry oxygen-poor blood to the lungs).
Blood vessels: the heart pumps blood through three types of blood vessels
1. Arteries carry oxygen-rich blood from the heart to the body’s tissues. The exception is the
pulmonary arteries, which go to the lungs.
2. Veins carry oxygen-poor blood back to the heart.
3. Capillaries are small blood vessels where the body exchanges oxygen-rich and oxygen-poor blood.
Coronary arteries
The heart receives nutrients through a network of coronary arteries. These arteries run along the heart’s
surface. They serve the heart itself and include the:
1. Left coronary artery: Divides into two branches (the circumflex artery and the left anterior
descending artery).
• Circumflex artery: Supplies blood to the left atrium and the side and back of the left ventricle.
• Left anterior descending artery (LAD): Supplies blood to the front and bottom of the left
ventricle and the front of the septum.
2. Right coronary artery (RCA): Supplies blood to the right atrium, right ventricle, bottom portion of
the left ventricle and back of the septum.
Electrical conduction system

The heart’s conduction system controls the rhythm and pace of the heartbeat. Signals start at the top of the heart
and move down to the bottom.

The conduction system includes:

1. Sinoatrial (SA) node: Sends the signals that make the heart beat.

2. Atrioventricular (AV) node: Carries electrical signals from the heart’s upper chambers to its lower ones.

3. Left bundle branch: Sends electric impulses to the left ventricle.

4. Right bundle branch: Sends electric impulses to the right ventricle.

5. Bundle of His: Sends impulses from the AV node to the Purkinje fibers.

6. Purkinje fibers: Make the heart ventricles contract and pump out blood.
Layers and Structures of the Heart
There are three layers of the heart. They are:
•Epicardium (Outermost Layer of Heart)
•Myocardium (Middle Layer of Heart)
•Endocardium (Innermost Layer of Heart)

Visceral layer of serous pericardium

Epicardium
Comprised of mesothelial cells and fat and connective tissues
Muscle layer
Myocardium
Comprised of cardiomyocytes
Lines inner surface of heart chambers and valves
Endocardium Comprised of a layer of endothelial cells, and a layer of subendocardial
connective tissue
Functions of Epicardium
1. Its major function is to provide mechanical protection to the heart.
2. The serous layer secrets thin fluid called the pericardial fluid that lubricates the heart and
reduces friction during the pumping of the heart.
3. Being supplied with blood and lymph vessels, it also helps to distribute nutrients and
oxygen to the heart wall and collect and transport the wastes.
Myocardium (Middle Layer of Heart)
Myocardium is the middle thickest muscular layer made up of cardiomyocytes. It is
responsible for the contraction and relaxation actions of the heart. The SA (sinoatrial) and the
AV (atrioventricular) nodes of the heart conduction system are mostly located in this layer.
Location: It is the middle layer located between the epicardium and the endocardium.
Functions of Myocardium
1. Its major function is to contract and generate the force for the contraction of the heart wall.
2. The myocardium houses the Pacemaker cells and specialized cardiomyocytes that generate
and conduct the cardiac electric impulses.
Endocardium (Innermost Layer of Heart)
The endocardium is the innermost layer of the heart wall lining the internal chambers of the
heart and the heart valves. It provides a smooth surface for efficient blood flow inside the heart
chambers. It also houses capillaries to supply blood to the heart muscles, nerve fibers, and
heart conduction cells.
Location: It is found along the walls of the atria and the ventricles and as the outer covering of
the four heart valves.
Endocardium Structure
The endocardium is primarily composed of smooth endothelial and connective tissues and a
smaller fraction of smooth muscle cells. Anatomically, the endocardium can be divided into
three sub-layers, the endothelial layer, the subendothelial layer, and the subendocardial layer.
1. Endothelial Layer
It is the innermost layer composed of specialized flat and smooth endothelial cells. This layer
makes the surface smooth and allows easy blood flow without any friction, clotting, or
sticking.
2. Sub-endothelial Layer (fibro-elastic tissue layer)
It is the middle layer composed of connective tissue containing collagen, elastic fibers, and a
few smooth muscle cells. Due to its composition, it is also called the ‘fibro-elastic tissue
layer’. This layer provides structural support to the endocardium.
3. Sub-endocardial Layer
It is the innermost layer primarily composed of connective tissues. This layer is enriched with
capillaries, nerves, and cardiac conductive cells (Purkinje fiber).
Functions of Endocardium
1. It lines the chambers and valves of the heart and provides a non-adhesive surface for
efficient blood flow without adherence of platelets and blood clotting.
2. It acts as a blood-heart barrier.
3. It also allows smooth opening and closing of the heart valves.
4. It houses the Purkinje fibers and hence supports the heart’s conductive system.
 Electrical activity of the heart
1. Physiology of the cardiac muscle
2. Intrinsic conduction system
3. Extrinsic Cardiac Conduction System
4. Pacemaker potentials
5. Cardiac muscle action potentials
 PHYSIOLOGY OF CARDIAC MUSCLE

The heart is composed of three major types of cardiac muscle—atrial muscle,

ventricular muscle, and specialized excitatory and conductive muscle fibers.
The atrial and ventricular types of muscle contract in much the same way as
skeletal muscle, except that the duration of contraction is much longer.
The specialized excitatory and conductive fibers of the heart, however, contract
feebly because they contain few contractile fibrils; instead, they exhibit
automatic rhythmical electrical discharge in the form of action potentials or
conduction of the action potentials through the heart, providing an excitatory
system that controls the rhythmical beating of the heart
Cardiac muscle composes of fibers arranged in a latticework, with the fibers dividing,
recombining, and then spreading again. Furthermore, cardiac muscle has typical myofibrils
that contain actin and myosin filaments almost identical to those found in skeletal muscle;
these filaments lie side by side and slide during contraction in the same manner as occurs in
skeletal muscle.
 Cardiac Muscle is a Syncytium.
The dark areas crossing the cardiac muscle fibers are called intercalated discs;
they are actually cell membranes that separate individual cardiac muscle cells
from one another. That is, cardiac muscle fibers are made up of many individual
cells connected in series and in parallel with one another. At each intercalated
disc, the cell membranes fuse with one another to form permeable
communicating junctions (gap junctions) that allow rapid diffusion of ions.
Therefore, from a functional point of view, ions move with ease in the
intracellular fluid along the longitudinal axes of the cardiac muscle fibers so that
action potentials travel easily from one cardiac muscle cell to the next, past the
intercalated discs. Thus, cardiac muscle is a syncytium of many heart muscle
cells in which the cardiac cells are so interconnected that when one cell becomes
excited, the action potential rapidly spreads to all of them.
 Functional syncytium
The heart actually is composed of two syncytia; the atrial syncytium, which
constitutes the walls of the two atria; and the ventricular syncytium, which
constitutes the walls of the two ventricles. The atria are separated from the
ventricles by fibrous tissue that surrounds the atrioventricular (A-V) valvular
openings between the atria and ventricles. Normally, potentials are not conducted
from the atrial syncytium into the ventricular syncytium directly through this
fibrous tissue. Instead, they are only conducted by way of a specialized
conductive system called the A-V bundle, a bundle of conductive fibers several
millimeters in diameter. This division of the muscle of the heart into two
functional syncytia allows the atria to contract a short time ahead of ventricular
contraction, which is important for the effectiveness of heart pumping
Intrinsic conduction system
Automaticity is basically the heart has its the intrinsic ability on its own to spontaneously deep
polarize itself and then Trigger action potentials to send it out to all the other parts of the heart.

The myocardium, or heart muscle, consists of two main types of cells:

1.Cardiomyocytes (Contractile cells):
These cells make up the bulk of the myocardium and are responsible for the heart's pumping
action. Cardiomyocytes are striated muscle cells with a single central nucleus and are rich in
mitochondria to provide the energy needed for continuous contraction. (Actin, myosin,
troponin, tropomyosin, sarcoplasmic reticulum).
2.Pacemaker cells (Conducting cells):
These specialized cells are part of the heart's electrical conduction system, which regulates
heart rate and rhythm. Pacemaker cells, such as those in the sinoatrial (SA) node and
atrioventricular (AV) node, generate and conduct electrical impulses.
Nodal cells are specialized pacemaker cells found in specific areas of the heart that play a
crucial role in regulating its rhythm and heartbeat. They are part of the heart's electrical
conduction system and are located mainly in two key structures:
1.Sinoatrial (SA) Node:
1. Often referred to as the natural "pacemaker" of the heart, the SA node is located in the
right atrium near the opening of the superior vena cava.
2. Nodal cells in the SA node generate spontaneous electrical impulses that set the pace for
the heart's rhythmic contractions. These cells have an intrinsic firing rate that typically
triggers about 60-100 beats per minute in a healthy adult.
3. The electrical impulses generated by the SA node spread through the atria, causing them
to contract and pump blood into the ventricles.
2.Atrioventricular (AV) Node:
1. The AV node is located at the junction between the atria and the ventricles, near the
center of the heart.
2. Nodal cells in the AV node receive the electrical impulses from the SA node and delay
them slightly before passing them to the bundle of His and the Purkinje fibers, which
conduct the impulses into the ventricles.
3. This delay ensures that the atria have time to contract fully and push blood into the
ventricles before the ventricles themselves contract.
Properties of Nodal Cells:
•Automaticity: Nodal cells have the unique ability to generate electrical impulses without
external stimulation.
•Rhythmicity: They fire in a regular, rhythmic manner, ensuring a steady heartbeat.
•Conductivity: These cells can transmit electrical impulses throughout the heart to coordinate
the contractions of the atria and ventricles.
SA node spreads the action potential from the right atrium
to the left atrium through Bachmann's bundle. these
electrical potentials through Bachmann's bundle to activate
and depolarize the atria. SA node connects to other parts of
the atria that can come and supply different parts of the atria
here through the inter-nodal pathway. So all of these guys
will come out and stimulate different parts of the atria.
So SA node to Bachmann's bundle is going from the right
atrium to the left atrium to supply the left atrium
myocardium.
From the SA node to these inter-nodal pathways, this will
supply all the other parts of the right atrium. But eventually,
all of this inter-nodal pathway will converge onto this
second important structure, which is
Called the AV node.
The AV node is so important because runs from the actual
right atrium into the interventricular septum. So it's acting
as a connection, the gateway between the atria and the
ventricles.
So some of the actual potentials from the Bachmann's bundle can make their way over to the
AV node. So either way, all of the action potentials that are coming from the SA node that are
being spread out for the internodal pathway or the Bachmann's bundle are converging onto the
AV node.
Once the AV node receives these signals, it's going to take a little bit of time.
The actual action potentials here take about 0.1 seconds. About 0.1 seconds, which is a little
bit longer than how much it takes for them to move through the SA node cells, the Bachmann
bundle cells, the internodal pathway cells. The AV node to take a 0.1 second delay before it
sends the action potentials down through the interventricular septum to the bundle of his is
because it wants to give time for atria to contract before the ventricles contract.
0.1 second delay, it gives the time enough adequate time for the atria to contract and push their
blood into the left ventricle.
Because if the AV node were to fire, not have that 0.1 second delay, it would be depolarizing
the myocardium while the left atrium and right atrium are trying to empty their blood into the
ventricles. If that's the case then, as the ventricles are going to be polarized, they might start
contracting at the same time that the atria is contracting.
We want: contract, squeeze all the blood into the ventricles, then let the ventricles attain
the blood and then squeeze the ventricles to push it out through the aorta and the
pulmonary circulation.
Now, the question is, why does it take 0.1 second?
1. It gives the time for the atria to contract before the ventricles contract.
2. There's two microscopic reasons: These nodal cells are filled with a ton of gap junctions,
which are just basically channels that allow for ions to pass from cell to cell. However, the
AV node, which consists of a bundle of those nodal cells, it has a lot fewer gap junctions
than these other nodal cells. So a lot less gap junctions. So a lot less ions can flow from
cell to cell. That decreases the actual speed at which it's moving.
3. Another one is because they have a smaller diameter. So the actual fibers are actually a lot
smaller in diameter. And if you know a little bit about conduction, we know that the larger
the diameter of the structure, the faster the velocity of the conduction is going to move.
So the smaller the diameter, the slower the conduction speed.
 The pacemaker of the actual cardiovascular center:

The SA node can transmit impulses to the left atrium via the Bachman's bundle. Eventually all
of those fibers converge onto the AV node though. The AV node takes about a 0.1 second
delay because of the fewer fibers and less gap junctions, and offer the atria to contract, and
then the ventricles to contract. Then from the AV bundle to the bundle of his. Or we call it the
AV bundle. Then it goes into the right and left bundle branches. into the right and left bundle
branches. If it's the right one, it's going to the right myocardium. If it's the left bundle branch,
it's going to the left myocardium. Then going to go into the last one, which is going to be the
Purkinje system, so the Purkinje fibers.
• I can say that if I have this nodal cell here, this nodal cell could be connected to many other
nodal cells by gap junctions. And because of the gap junctions, this can allow for ions to
pass from one cell to next cell……ect.
• funny sodium channels. There's actually funny sodium channels. These channels that are
within this nodal cell are very leaky, and they allow for a little bit of sodium to leak into the
cell very, very slowly. slow flow of this sodium into this nodal cell.
• Now generally, nodal cells don't have a stable resting membrane potential. Normally resting
membrane potentials like negative 70 to negative 90 millivolts. It depends upon the cell.
But these nodal cells don't really have a stable resting membrane potential. So their
membrane potential fluctuates. But in general, before these funny sodium channels open,
they generally are going to have a membrane potential around negative 60 millivolts. That's
approximately where it's at. These funny sodium channels start actually causing the inside
of the cell to become a little bit more positive because we're bringing positive ions into the
cell. Sodium.
• As the sodium starts coming into the cell to start approach the threshold potential.
• Bringing some positive charges with it. This happens around negative 60 millivolts. But
then what happens is these other channels, they're called t-type calcium channels. These are
called t-type calcium channels. These calcium channels open up approximately around
negative 55 millivolts. So these positive ions are bringing it from negative 60 millivolts to
Negative 55 because it's a really slow flow of sodium.
• When they stimulate, these t-type calcium channels start opening and calcium starts
flowing in slowly also. As these calcium ions start accumulating with the sodium ions will
lead to become even more positive. They hit threshold potential.
• Generally within the cell, the threshold, these actual nodal cells, is around negative 40
millivolts. Normally it's like negative 55 in most cells, but in this one it's about negative 40.
Once we hit that negative 40, another type of channel opens up. When this channel opens
up, it blasts open a lot of calcium.
• It rises up very, very quickly, and it happens in just a second, these channels are called L-
type calcium channels. They're very, very sensitive to voltage. Once this happens, it gets to
around -40 millivolts and guess who starts flowing in very powerfully. Calcium starts
flowing in very, very powerfully. As the calcium starts flowing in very, very aggressively,
and the inside of the cell become super, super, positive.
• it goes up to negative 40 and It generally goes up to approximately in this cell because the
calcium is coming in very, very, very aggressively. It generally comes in to approximately
around positive 40 millivolts.
• As you start bringing tons and tons and tons of positive ions into the cell, what is it going to
do to the inside of the cell? It's going to depolarize the cell.
• depolarized the cell. It didn't require any nervous system functioning.
• gap junctions. Lots and lots of positive charges. Lots of cations. As a lot of these cations are
being loaded into these actual nodal cells, what can happen? These beautiful gap junctions
are connecting. They're acting as the communication gateway between the nodal cells and
other nodal cells, or the nodal cells, and contractile cells. So what are these gap junctions
actually made up of? Another made up of what's called proteins, specifically called
connexins. So they're called connexin proteins. So basically a whole bunch of different
types of connexins. Now, these cations, they actually move through these gap junctions into
the other cells. They can go from cell to cell to cell to cell to cell. Now, because of that,
positive ions over into this cell through the gap junctions.
• How do we keep these cells so tightly close together, so that the gap junctions aren't
separating whenever the heart's being stretched? Because we don't want these actual gap
junctions to get separated because it's actually two different proteins between the cells
connecting together.
• To keep the cells so tightly together, we have these special structural proteins here, which is
called Desmosome.
• the lot of cations, sodium and calcium ions are flowing through these Gap junctions into
this other cell, this contractile cell. How does this help the contractile cell?
• The cell starts becoming a little bit more positive, Positive ions come over into this cell.
When the positive ions come over into this contractile cell, the actual resting membrane
potential of this cell around negative 85 to negative 90 millivolts. So its resting membrane
potential is in between like negative 85 to negative 90 millivolts. those positive ions that are
leaking into the cell via the gap junctions. They start trying to bring the actual membrane
potential closer towards the threshold. They're trying to bring this closer towards threshold.
That's their purpose. But what happens is along that way, what's the threshold potential
within these cells? Threshold potential is approximately right around negative 70 millivolts
within these cells. see how different cells can have different resting membrane potentials
and threshold potentials. It depends upon the movement of potassium ions.
• As it does that, we reach threshold and these specialized voltage-gated sodium channels
blast open. This stimulates these voltage-gated sodium channels. These voltage-gated
sodium channels start opening. When they open, who starts flowing in?
• Sodium. And when sodium flows in, the flows in very, very fast. As the sodium ions start
flowing into the cell, the inside of the cell starts becoming very, very positive. this positive
charge starts moving across the actual cell membrane, or in this case, It's called the
sarcolyma. So these positive charges start moving in like a wave around the actual
sarcolyma of the muscle cell membrane.
• it gets to about positive, around positive 10 millivolts. So it gets to approximately around
positive 10 millivolts. Now, along the way, throughout this process, some other channels
open up a little bit and allow for a little bit of calcium to start trickling in. as the sodium is
starting to approach and start causing the cell to depolarize, some of these calcium channels
start slowly opening, only a little bit often. So now the sodium channels are closed. But what
else, what other channels open a little bit? A little bit of calcium channels are open. Very,
very little though, not too many. But what else decides to open up at the same time? Another
channel that decides to open up at the same time over here is going to be potassium.
• The cell is super, super depolarized.
• these potassium channels open up and they allow for potassium to start coming out. Now
the potassium ions start coming out a little bit more than the calcium ions are kind of
slowly, slowly trickling in.
• So a lot of potassium ions are going to go out here for a moment of time. As that starts
happening, what starts happening to the inside of the cell? It's losing positive charges,
becoming a little bit more negative. What happens then? Because the potassium leaks out of
the cell for a moment, it drops down a little bit. At positive 10, sodium channels close,
potassium channels open, and potassium starts slowly leaking out. A tiny, tiny bit of
calcium is coming in and it causes it to drop down to around zero millivolts.
• When it hits zero millivolts, the calcium channels, those actual voltage, the calcium
channels, become even a little bit more active. They become even a little bit more active
now. So once you hit about positive zero, That becomes a very powerful stimulus for these
L-type calcium channels.
• L-type calcium channels. calcium starts flowing in very powerfully. These positive ions
from the calcium start coming into the cell. These potassium ions are also leaving the cell.
So because of that, we're having potassium ions leave the cell at the same time cations,
calcium ions are coming into the cell. So if you think about it, positive ions are leaving and
positive ions are coming in. So really, there's no change in the membrane potential. And it's
going to plateau actually for a decent amount of time, about 250 milliseconds. That's a
pretty decent long time for a cell.
• These positive ions, these actual calcium ions can also flow in through this area too. What
is this little invagination here called? That invagination is called a T-tubule. So from these
invaginations, sodium ions can flow into the cells and trigger the calcium to be released
here also from the actual T-tubules. The reason this is because these calcium ions, when
they're coming in, they're going to go to this special area within the cell, special organelle.
This organelle is called the sarco-plasmic reticulum.
• What happens is these calcium ions have these special, special calcium-sensitive channels.
Calcium comes over binds onto a protein. One of the proteins is called chalmodulin. Now
what happens is calcium and chalmodulin or just calcium can come over here and bind onto
this receptor, a very sensitive receptor to calcium. This receptor is called a ryanidine
receptor type2. Whenever there's increase in calcium levels, this ryanidine receptor opens
up a channel. Now calcium is going to be really concentrated inside of the sarco-plasmic
reticulum
• calcium binds onto a special protein. This protein here is called troponin. It's actually
consisting of three components. Troponin I, troponin T, and troponin C. Troponin C is
where the calcium binds. Troponin T is where the tropomycin is binding to the troponin.
And troponin I is where the troponin is bound to actin. So quickly here, it's bound to actin.
It's bound to tropomycin, or it's bound to calcium. So calcium binds onto the troponin C
site, which changes the shape of the troponin. calcium binds onto the troponin, which
changes the shape of the tropomycin. If it changes the shape of the tropomycin, what
happens then? So calcium coming to this area increases cross bridges. Cross bridges
between the actin and the myosin. It's representing the contraction. So more cross bridges
means more contraction. And then that's going to help to be able to create that pump to
squeeze the blood. So increasing the cross bridge interaction increases the contraction,
which is going to cause the heart to. Pump action.
• how we actually get this cell to rest.
• at positive 40 millivolts, because these voltage-gated calcium channels, these L-type
calcium channels were open. When we get positive 40, they shut off. When they shut off,
another channel starts opening. Very, very, very powerfully. This is actually going to be
called a potassium channel. And this potassium channel opens and potassium starts exiting
the cell. As you start losing tons and tons and tons of potassium, you lose positive ions.
• What starts happening to the inside of the cell? You start losing positive ions, and the cell's
going to start becoming a little bit more negative. And it's going to become negative, and
more negative, and more negative. And then what starts happening to the inside of the cell?
It's starting to repolarize. So you're going to see this actual line going down on the graph.
Phase 0 (Rapid Depolarization)
•Trigger: Initiated when the cardiac muscle cell reaches the threshold potential.
•Ionic movement: Rapid influx of sodium ions (Na⁺) through voltage-gated sodium channels.
•Effect: This results in a rapid depolarization, with the membrane potential quickly rising to a
positive value (+20 to +30 mV).
2. Phase 1 (Initial Repolarization)
•Ionic movement: Sodium channels close, and transient outward potassium (K⁺) channels
open, allowing a brief efflux of potassium.
•Effect: Causes a slight decrease in membrane potential (early repolarization), forming a
small dip after the peak of the action potential.
3. Phase 2 (Plateau Phase)
•Ionic movement: Slow influx of calcium ions (Ca²⁺) through L-type calcium channels and
continued efflux of potassium ions. The calcium influx balances the potassium efflux.
•Effect: This creates a prolonged plateau in the membrane potential, maintaining
depolarization. This phase is crucial for sustaining the contraction of the cardiac muscle.
4. Phase 3 (Repolarization)
•Ionic movement: Calcium channels close, and potassium efflux continues through delayed
rectifier potassium channels.
•Effect: The membrane potential gradually returns to the resting state as the cell repolarizes.
5. Phase 4 (Resting Membrane Potential)
•Ionic movement: The cell returns to its resting state with a stable membrane potential,
maintained by the continuous efflux of potassium and the activity of the sodium-potassium
pump (Na⁺/K⁺ ATPase).
•Effect: The membrane potential stabilizes around -90 mV, ready for the next action potential.