Samenvatting
Samenvatting van alle colleges van MG circulatory tract
Samenvatting van alle colleges van MG circulatory tract
[Meer zien]Voorbeeld 4 van de 69 pagina's
Voorbeeld 4 van de 69 pagina's
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Voorbeeld van de inhoud
Medicine groups: Circulatory tractLecture 1 Introduction
The heart is the transport system pump. It delivers blood to all organs and uses the blood as a
transport medium. Blood contains oxygen, nutrients, waste products and other substances. Blood is
composed of water, CO2, nutrients (e.g. glucose), hormones, ions and (immune) cells.
The veins contain blood with low oxygen levels. The
arteries contain oxygenated blood. Blood goes from
the veins into the heart into the right atrium then to
the right ventricle. The right ventricle pumps the
deoxygenated blood to the lungs via the pulmonary
arteries and in the lungs. There is the exchange of CO2
and O2. So CO2 is removed and oxygen is taken up by
the blood. Then the oxygenated blood is transported
via the pulmonary veins to the left atrium to the left
ventricle to the aorta. Via the aorta the blood will be
transported to various organs in the body. The heart
has its own blood supply by coronary arteries that
branch from the aorta. These arteries provide blood
to the heart. When oxygenated blood reaches the
organs, there are capillaries which are very small vessels that are permeable for nutrients, oxygen
and CO2. So there the exchange will happen. Then the deoxygenated blood will go back via the veins
to the heart. One important difference between the arteries and the veins is that the veins contain
valves that prevent returning of the blood flow. So they make sure that blood only goes from the
organs to the heart.
The superior and inferior vena cava transport the blood to
the right atrium. From the right atrium the blood goes to
the right ventricle. The heart contains valves to prevent
blood flowing back into the right atrium. Then when the
right ventricle contracts, the blood goes via the pulmonary
artery to the lungs. There the blood will get oxygenated
which will flow back via the pulmonary veins into the left
atrium to the left ventricle to the aorta. The muscle of the
left ventricle is much thicker than the muscle of the right
ventricle. This is because the left ventricle has to contract
much harder since from there the blood has to go to all
parts of the body. Whereas the right ventricle only has to pump the blood to the lungs. Most of the
time in pathologies, the left ventricle is highly affected.
Diastole is the phase during which the heart relaxes and fills again with blood.
Systole is the phase during which the heart’s atria/ventricles contract.
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,Heart rhythm:
1. Late diastole → both atria can fill with blood and the valves to the ventricles are open so also
these will fill up with blood.
2. Atrial systole → atria contract to force a small amount of blood into the ventricles.
3. Isovolumic ventricular contraction → first phase of ventricular contraction that pushes the
AV valves closed. But not enough pressure is created to open the semilunar valves. So the
blood volume in the ventricles remains the same.
4. Ventricular ejection → as ventricles are contracting the pressure increases until the
threshold is reached. The semilunar valves will open and the blood is pumped into the aorta
and pulmonary arteries.
5. Isovolumic ventricular relaxation → the ventricles and atria relax so that the heart can fill
with blood again.
Left ventricular pressure:
A. The diastole where the heart is relaxed with all valves open
so that it can fill with blood. There is no increase in pressure
but the volume is increasing.
B. The end-diastolic volume (EDV) is reached. So the heart has
completely filled and then the atria will contract. This causes
a little bit more blood to be pumped into the ventricles.
Thereby the pressure in the ventricles starts to increase.
C. Isovolumetric contraction. So the ventricles start to contract
so there is a rise in the ventricular pressure but no
difference in the volume. When the pressure is high enough, the valves will open. Blood goes
into the vessels. The pressure will increase but the volume will decrease.
D. Ventricular ejection into the vessels. So the end-systolic volume (ESV) is reached. The
pressure in the ventricle will drop completely going back to diastole.
Electrical conduction in the heart: The most important pacemaker cells are in the sinoatrial (SA)
node. These cells have an unstable membrane potential and they give rise to an electrical current
which is then spread to the heart to cause contraction. The cardiomyocytes are the contractile cells
of the heart. The electrical current goes from the SA node over to the cardiomyocytes. The
cardiomyocytes can propagate the electrical current to a next cell because they have intercalated
disks with gap junctions. When there is an electrical current, the membrane depolarizes which will
cause contraction and then the next cell will contract etc. If there is damage to the SA node, there
are also other pacemaker cells in the heart → atrioventricular (AV) node and the bundle of his and
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,Purkinje fibres. They all have pacemaker activity, so they can take over when there is a deficiency in
the SA node. However they have a lower frequency of firing, so the SA node is the main pacemaker.
Membrane potential of autorhythmic (pacemaker) cells: unstable membrane potential.
This is due to a sodium influx and a sharp rise (action potential) caused by calcium
influx. Repolarisation is due to potassium.
Membrane potential of contractile cells: due to sodium.
Electrical conduction in the heart: SA node
depolarises → electrical activity goes rapidly via
the internodal pathways to the AV node (there
is a small delay in the electrical conductance so
depolarization spreads more slowly across
atria) → depolarization moves rapidly through
the ventricular conducting system to the apex
of the heart (via bundle of His to bundle
branches to Purkinje fibres) → depolarization
wave spreads upwards from the apex. The
delay in the AV nodes prevents that the
ventricles already start to contract when the
atria are still full with blood. So it enables
emptying of the atria into the ventricles.
The action potential in the SA node is the first action potential. This is regulated by
calcium. Then there is an action potential in the atrium, AV node, Purkinje fibres and
ventricles. The action potential of the ventricles is very stable.
The heart has a long refractory period compared to the skeletal muscle. This is the period that the
ion channels are inactive, so no new action potential can be generated within this refractory period.
The skeletal muscle can be depolarized several times in a row causing accumulation of the force. But
the cardiac muscle has a much longer refractory period. This period is almost as long as it takes for
the muscles of the heart to contract and relax. So there is no accumulation possible of muscle
tension. So you can only have one contraction and only after this is finished, a new contraction can
happen. This is to protect the heart so that no muscle cramping can occur.
Types of muscle tissues are cardiac, skeletal and smooth muscle. These muscle types differ in action
potential mechanism and contraction mechanism.
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, Action potential of skeletal muscle: skeletal muscles are dependent on the somatic motor neurons
which can be activated voluntary. The resting potential is -70 mV. So an action potential goes over
the somatic motor neurons. The calcium channels will open causing ACh release. ACh is stored in
vesicles in motor neurons. These vesicles fuse with the neuronal membrane to secrete ACh into the
synaptic cleft. There ACh will bind to nicotinic receptors
(ligand-gated ion channels). This results in sodium influx.
When there is enough sodium, this will generate an
action potential which is then guided over the skeletal
muscle by T-tubules. The action potential can open the
DHP (dihydropyridine L-type) calcium channels which are
coupled to RyR (ryanodine receptor-channel) channels in
the SR. This can induce the release of calcium from the
SR. So calcium increases which will bind to troponin.
Troponin will displace tropomyosin on actin to allow
myosin to interact with actin and thereby cause a
contraction. This is voluntary control regulated via
neurones, not via hormones.
Action potential of pacemaker cells: Pacemaker cells initiate and conduct action potentials in the
heart. The resting membrane potential is usually negative. This means the cell is more negative on
the inside. At the resting state there are concentration gradients of several ions across the cell
membrane. More sodium and calcium are outside and more potassium is inside. These gradients are
maintained by several pumps. When the membrane voltage increases the cell is depolarized. For an
action potential to be generated, the membrane potential must decrease to the threshold.
Pacemaker cells fire about 80 action potential per minute, each representing a heartbeat. The resting
potential of pacemaker cells is -60 mV and this will spontaneously move up to a threshold of -40 mV.
This is called the pacemaker potential and is due to action of funny channels. Funny channels are
present in pacemaker cells and allow influx of sodium resulting in depolarization to -40 mV (when
sodium influx > potassium efflux). At threshold of -40 mV, calcium channels open and calcium will
flow into the cell to sharply depolarize the membrane. This is the action potential. At the peak of
depolarization, potassium channels open and calcium channels inactivate. Potassium ions will leave
the cell until the resting potential of -60 mV is reached again.
Action potential of contractile cells: Myocytes have a different set of ion channels. In addition their
SR stores a large amount of calcium. These cells have a stable resting potential at -90 mV. They
depolarize only when stimulated by e.g. neighbouring myocytes. When a cell is depolarised it has
more sodium and calcium inside the cell. This will bring up the potential to the threshold of -70 mV.
Then fast sodium channels open creating fast sodium influx and a sharp rise in voltage. This is the
depolarisation phase. As the action potential nears its peak, sodium channels close quickly and
voltage gated potassium and calcium channels open resulting in a steady decrease in membrane
potential (early repolarisation phase). Because of opening of the calcium channels, repolarization is
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