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Summary Human Anatomy and Physiology
- Instelling
- Vrije Universiteit Amsterdam (VU)
Human Anatomy and Physiology notes directly from the lectures and course material, integration with laboratory practicals and workgroups.
[Meer zien]Voorbeeld 4 van de 51 pagina's
Voorbeeld 4 van de 51 pagina's
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Voorbeeld van de inhoud
PHYSIOLOGY OF THE CARDIOVASCULAR SYSTEMPhysiology: learn how the heart beats and how its cardiomyocytes also do that.
Heart: two circulation, systemic is bigger and provides the organs of blood, and pulmonary.
These two circulations are the reason for two different pressures in the left and right parts
and different sizes of these two.
Function: the function of the heart is to pump blood, deoxygenated one to the lungs and
oxygenated to all the other organs.
Left atrium is where the lung vessels drain the oxygenated blood and it flows into the left
ventricle and pumps out to the aorta. This is also a matter of pressure. The ventricle walls
are thin and when they contract they thicken, thanks to a couple of billions of cardiomyocytes
and they all need to contract and relax at the same time in order to produce enough
pressure to eject that amount of blood. It has to fill with enough blood and eject it to the two
circulations, so there must be enough blood for the heart to contract and most of the time
diseases are a problem of filling and not pumping. The key to this is coordination of
relaxation and contraction. This is called excitation-contraction coupling, meaning that the
contraction of the heart follows electrical stimulation of cardiomyocytes, which is an action
potential, which you always need before contraction.
Automation: it doesn't need input from the nervous system, it contracts independently
because of pacemaker cells that set the rhythm, and we don’t need to think about heart beat.
Also, the heart can beat independent of neuronal input, meaning that if we remove it from
the body it keeps beating at its rhythm if given oxygen, but it doesn’t mean that it doesn’t
receive nervous inputs, which it does when for example the heart beat changes.
Right atrium: deox /Left atrium: ox
Sinoatrial node SA: on top of the right atrium, it contains pacemaker cells, muscle
specialized cells that generate action potentials. It needs to go through the whole RA and
then can go to the AV node.
Atrioventricular node AV: it allows the ventricle to receive the impulse from the atrium,
because the two are not connected, this is the only way the signal can pass between the
two. AV nodes are really slow conducting cells, because you want a delayed contraction,
100 ms delay, to allow the atrium to be filled a bit more before the ventricle starts
contracting, in order for the pumping to be efficient.
The left and right bundle branches allow the signal to pass through the right ventricle,
because the signal that passes through cardiomyocytes is quite slow, so these are used to
make it faster. It starts in the fibrous septum and then goes down to the Purkinje Fibers.
Action potential
Prepotential: outside of the cell membrane there are more negative ions, so this is negative,
we talk about the muscle cells, and this can change by opening up the sodium channels and
the ions go in, making the potential less negative. In the ventricular cells there are no leaky
channels, because there is a starting flat line, which is curved in the SA node.
SA node cell: pacemaker potential has a spontaneous depolarization because of leaky
channels. There is a threshold value that when reached (-55 mV) you set into motion an
action potential by opening the sodium channels, this is what a pacemaker cell does, and
after this it returns back to the starting point. It happens once a second if 60 beats per
minute, so it also decides the heart beat.
,Ventricular / atrium cell: there is a flat line that stays like this if nothing happens, so a
single cardiomyocyte wouldn’t do anything if it hasn't undergone action potential; then it goes
up quickly when received an action potential and they contract. They also have a plateau
phase, which is a longer period of action potential.
Ions: normally cells are not permeable to ions, but they have a number of channels specific
for certain ions. When the sodium goes inside, the channel is opened slightly allowing the
sodium to go in, the threshold is reached and the blue line is the prepotential; this allows
the calcium channel to be opened, because they are voltage gated, meaning that they
sense the change of potential, and it opens, reaching 35 mV and it closes again.
The potassium is higher inside and lower outside, so it exits and everything begins again.
Potassium is high inside and low outside, while Na and Ca are low inside and high outside.
This thing allows the ions to follow the concentration gradient when the channels are open.
Channel is passive and pump active, requiring energy.
There are other negatively charged ions inside the cell so there is a surplus and these are
the ones that determine the resting membrane potential. This causes the potassium to want
to go in because it is attracted to the positively charged ions, but also it wants to go out
because of homeostasis, so there is a concentration to which these two forces are in
equilibrium.
Action potential in cardiomyocytes: Everytime an SA node creates an electrical signal by
the pacemaker cells, the action potential happens. The action potential needs something
from the neighboring cells before happening. In fact, sodium and calcium channels are
voltage gated channels, meaning that they sense a change in the membrane potential and
open and the ions go in making the potential to become also positive at a certain point.
Sodium is very fast here and calcium is not, because there are different sodium channels in
our body. They react from the same signal, but calcium is very slow and sodium is way
faster. Na opens very quickly but also closes very quickly, instead calcium stays open a
longer time. Then, the K wants to go out, so K and Ca work at the same time (even though K
channels are more closed), and this is why the membrane potential never reaches a higher
level than with Na. Then, when Ca channels close, the potential becomes negative and
returns to the beginning, resting potential, and the K channel stays open. There is still more
inside than outside, but it doesn’t flow out all of it because of the equilibrium, meaning that it
wants to go out to follow K+ but also to follow negative charged ions.
K > Na > Ca
,Heart rate: blood flow goes up if this increases, when you need more oxygen, such as when
nervous or exercising. The threshold and lowest resting potential stay the same.
Heart rate during exercise increases and you could reach 12 liters per minute to your
muscles. This is determined by the heart rate because then it increases the amount of
pumped blood and given oxygen.
Sympathetic: innervates the organs, release of the noradrenaline and epinephrine.
Sodium channels are opened a bit more thanks to noradrenaline, so more sodium goes in,
starting with a more positive negative potential as a starting point, and you don't go to the
lowest level that negative anymore, and also the prepotential line is more still and shorter,
leading to a faster reach of the threshold and a faster heart beat.
Parasympathetic, rest and digest, lowers, innervates the atria and it releases acetylcholine.
Acetylcholine: it opens the potassium channels, so K goes out and there is a
hyperpolarization reaching a lower negative membrane potential, so a slower reach of the
threshold, in order to make the heart beat slower.
If someone has received a donor heart, their sympathetic and para nerves are cut and they
cannot be connected, so they would have the innate heart rate of 100 times per minute
because there is no connection with the brain. During rest your parasympathetic system
rules. If a person with a donor heart gets scared, there is a delay in its increase in heart rate.
Cardioplegic solution for transport heart, meaning that the heart doesn’t beat anymore and
you want this because of the health of the heart because if the heart beats, using energy
without supplying energy then you get ischemia meaning cell death, so you prevent action
potential from happening, by lowering sodium low calcium or high potassium.
Contraction
Calcium is the key regulator in muscle cells, increasing the Ca inside the cells is the thing
that needs to happen before starting the contraction. Here, we mean the calcium that goes
inside the cell as the second ion. When inside, it leads to the activation of contraction. But to
do this, we need a higher concentration of calcium and we use the calcium induced
calcium release system. This starts in the sarcoplasmic reticulum, a calcium storage
organelle, which releases Ca when the Ca enters the cell and binds to the SR via a receptor,
which opens and lets the Ca outside into the cytoplasm. Ca enters the cells and it goes
inside the SR thanks to the RyR enzyme and it opens the channels (receptor) that release
the storage of calcium. From the SR into the cytosol and then into the SR again to lower the
calcium concentration to make the muscle cell relax, via the SERCA ATPase. 10% of Ca
comes from the outside, while 90% comes from the SR, there must be homeostasis.
Myosin and actin, thick and thin, and the contraction consists in shortening the filaments by
myosin dragging actin towards the middle of the bundles, the power stroke. So, when Ca
comes in, it binds to actin leading to a conformational change in the tropomyosin, connected
to actin, which moves up and allows the myosin to bind to the actin and contracts. ATP is
already bound to myosin and when this binds to actin, it becomes ADP and during the
relaxation another ATP binds to myosin. To release myosin and actin bonds it needs ATP,
because the two really want to stay bound to each other. When ATP runs out, it only
happens when you die, the muscles stay contracted.
, Electrocardiogram: it measures electrical differences between regions in the heart,
measuring actually the spread of the action potential throughout the heart. Two electrodes,
and heart muscle in the middle whose cells are depolarized and resting, so there is no
potential difference, all negatively charged. When the action potential starts, there is a signal
and a difference between negatively and positively charged, white ones and red cells, at the
end all are red so you don’t measure anymore differences, you don’t measure action
potential, but differences, and when they are all red or white there is none, (polarized and
not).
P wave is the start, then QRS wave, then T wave: PR is from SA node to AV node.
At the SA node point is when the pacemaker cells have reached the threshold and spread
the action potential to the atria. At the start of the P wave not all atrium cells are depolarized,
while at the end of the wave all of them are (straight line again). The right atrium is
depolarized earlier than the left one.
Then there is the spread of the depolarization through the ventricle, the QRS wave, after
which all the ventricular cells are depolarized. The delay between the spread from atria to
ventricles is due to the AV node.
T wave is the repolarization starting, not again all cells at the same time, so a little wave.
There are timings used to see if people have something wrong.
PR time checks if the AV node works well, it usually is between 0.12 - 0.20 s, and if it takes
longer it means that it doesn’t work properly. It measures signals between atrium and
ventricle, so measures the health of the AV node and its conduction.
QRS time: through the ventricles, very quickly, 0.07 - 0.10 s. If it’s longer than this, the
conduction is also abnormal and something might be wrong in the ventricle branches or you
might also have a larger ventricle size.
QT time: this measures the time of depolarization and repolarization of the ventricles.
between 0.3 - 0.4 s, it can show if something is wrong with the repolarization.
The signal depends on where you place the electrodes, the distance from the heart and the
distance between them. Also, if the heart is bigger, it’ll measure a higher electroactivity. You
never measure the ECG with one pair of electrodes, but many, and it never goes vertical.
RA-LA I, difference between right and left, horizontal, so with the lead I you won’t measure
the whole depolarization wave; RA-LL II, LA-LL III. The signal goes septum way.
It’s convention that the depolarization wave travels towards the positive electrode, so II and
III show both positive signals.
QRS complex Lead I, signals to the left positive and to the right negative: Q goes up first but
sometimes you might not have it cause it can go straight up right away, signal goes down the
septum to the AV node and starts at the left and then goes to the right (a bit); then, it goes
down the septum and spreads to the ventricles on the inside down and then outside, and
since the left ventricle is thicker than the right so there is more signal going to the left than to
the right, so this is why most people have a positive QRS complex in Lead I.
T wave in lead I, when cells start to repolarize, and the signal travels the same, but the cells
on the outside are the ones that depolarize first and then the ones on the inside,
endocardium, which stays depolarized longer.
12 combinations to be able to check every possible angle.
Myocardial infarction: ST-segment changes: normally should stay the same straight line,
here there is no rest but a signal after the QRS before T, and this is because not all cells are
depolarized anymore, since one of the coronary artery is blocked so a part of the heart does
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