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Samenvatting Human Anatomy & Physiology
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PHYSIOLOGY OF THEHEART
There are 2 circulations attached to the heart, the pulmonary circulation and the
systemic circulation. The pulmonary circulation pumps blood with low oxygen levels
from the right side of the heart to the lungs and the systemic circulation pumps
blood from the left side of the heart to the aorta, which provides all the organs of the
body with oxygen-rich blood. The pulmonary circulation is a very low-pressure
system and the systemic circulation is a high-pressure system. This means that the
left ventricle has a very thick muscular wall and the right ventricle had a thin wall,
because it doesn’t need to eject a lot of pressure. The function of the heart is pumping deoxygenated
blood to the lungs and oxygenated blood to all the organs in the body. Together with the blood vessels, it
provides adequate perfusion of all the organs and tissues of the body. Vital for the function of the heart
is that all the cardiomyocytes contract in unison. When contracting, the wall thickens, just like when
muscles contract. Otherwise, there will be not enough strength to eject the blood with a high pressure.
The contraction and relaxation of the heart determine the cardiac output.
Excitation-contraction coupling
Contraction of the heart follows the electrical stimulation of the cardiomyocytes. So, there is a way to
control the contraction of the cardiomyocytes, because they only contract when they are electrically
stimulated. The heart also has automation, it can beat independent of hormonal or neuronal input. This
means that it is spontaneous active and this is because it has pacemaker cells.
There are a couple of signals that are important for the electrical stimulation throughout the heart. 2
important structures of the heart are the SA-node (sinoatrial node) and the AV-node (atrioventricular
node). The SA-node is the site where the pacemaker cells are on top of the right atrium. This is where the
heartrate normally starts. The signal spreads to the atria and to pass to the ventricles, they have to go
through the AV-node. The AV-node is the only connection
between the atria and the ventricles. However, the AV-
node is a slow connection. It delays the signal from the atria
to the ventricles with 100 ms. This is important, because
the atria and the ventricles must not be contracted at the
same time. In that case, the filling of the ventricles will
become less sufficient. The Bundle of His and some bundle
branches are connected to the end of the AV-node. They
are important in the spreading of the signal throughout the
ventricle. Conduction happens from cardiomyocyte to
cardiomyocyte, but this conduction is very slow, so there are also cells in the heart with the specific task
to get the signal in the ventricles with high speed. This is needed to get the whole ventricle to contract all
at once and not the top part first.
The ventricular cells have an zero potential of about -85 mV. When an action potential is induced, the
mV rises to 20 and stays positive for a while. However, when there is no action potential induced, the
ventricular cells will stay at -85 mV. So, without a signal, nothing will happen. This is different in SA-node
cells. They have this prepotential, which slightly elevates the mV until it reaches the threshold of about
-60 mV. Then it undergoes an action potential and the mV becomes positive and goes back down until it
reaches its zero potential again, where another prepotential will start. This rhythm in which the cells
reach their threshold will determine the heartbeat. The ventricular cells have a stable zero potential, so
they aren’t leaky for positive ions (which go for the action potential to happen). SA-node cells don’t have
a stable zero potential, so they are leaky.
,The membrane potential is determined by the concentration differences of ions and the permeability to
ions. Normally, the cells will not let them go through, but there are specific channels for each ion. The
resting membrane potential (-85 mV) is largely determined by the K+ gradient (potassium). Normally, it is
very high inside the cell and very low outside the cell. In contrast, Na+ (sodium) and Ca+ (calcium) are
always high outside the cell and low inside the cell. In rest, the cells are only permeable to K+. There are
also negative charged particles in- and outside the cell (proteins, etc.), but there is a little surplus on the
inside, which makes the cells negatively charged. If the cell is negatively charged, K+ wants to go in.
During an action potential, ion channels open and close. The
sodium-channels open in response to an environmental
change in membrane potential. These are called volted-gated
signals. They notice that a neighbouring cell has undergone
an action potential and they open the channels. The sodium
ions go in the cell and the potential of the cell becomes
positive. Calcium channels do the same thing, however they
open up very slowly. The potassium channels close during an
action potential and only re-open in the end. They are called
channels and not pumps, because these processes do not
cost energy.
It works almost the same in the pacemaker cells, however, they have slightly different channels and
there is a spontaneous depolarization. Also, the channels are leak, so there will always be a flow of ions,
hence the prepotential. The spontaneous depolarization is important, because it determines the heart
rate. The slope of the prepotential determines the heart rate to a large extent, together with the resting
membrane potential of the SA-node cells. One of the things increasing the heart rate is exercise. This is
because there is an increase in the amount of blood going to the muscles needed. To increase the heart
rate with sympathetic stimulation, a lot of adrenaline and noradrenaline is released. One of the things
this does is opening the Ca2+ and Na+ channels in the pacemaker cells. This results in a quicker
depolarisation and a less negative resting potential. The counteracting partner is the parasympathetic
stimulation. Activation of the parasympathetic nervous system works through acetylcholine. This binds to
pacemaker cells and opens the K+ channels.
After the action potential, the cell goes back to its resting potential. This is called the refractory period.
This is the period in which cells are inexcitable. This is key to the contraction-relaxation behaviour of
cardiomyocytes. If this doesn’t happen, the heart keeps filling constantly and there is no flow.
A mutation in one of the ion channels causes an impaired repolarisation. If the potassium channel re-
opens very slowly, the repolarisation takes much longer, which results in long QT syndrome. The action
potential increases in length. Now, the cells that have a longer action potential can turn the cells with a
short action potential on again, resulting in ventricular defibrillation.
Excitation-contraction coupling is the link between membrane depolarisation and contraction. Ca2+ is the
signal that initiates contraction. This is because Ca2+ leads to the activation
of the contractile proteins, which initiates contraction. Humans have very
large cardiomyocytes and the amount of Ca2+ that can enter the cell is not
enough to get all these contractile proteins to contract. So, there is an
amplifier system, which is called calcium induced calcium release (CICR).
The sarcoplasmic reticulum (filled with Ca2+) releases Ca2+ once Ca2+ enters
the cell and binds to the receptor on the SR. About 90% of the Ca2+ in the
cell comes from the SR. To relax, the cell needs to get rid of the Ca2+, which
happens via a pump that pumps Ca2+ back into the SR. To contract, the
thick and thin filaments of the contractile proteins interact with each
other. The thick filament can pull the thin filament and the cell shortens.
This only happens when myosin (thick filament) interacts with the actin
(thin filament) and only when Ca2+ is present. When Ca2+ comes in, it binds to proteins on the thin
filament, causing a structural change that moves the tropomyosin filament out of the way. Now, myosin
can bind and hydrolysis of ATP happens. Then, the myosin is released and ADP is replaced with ATP. The
force depends on the amount of Ca2+ that is released. So, more Ca2+ leads to more force. But also the Ca2+-
sensitivity of the contractile apparatus.
, Action potential & ECG
An ECG doesn’t measure the action potential in the heart. Both
processes are linked, but they are separate events. An ECG measures
the differences in electro-activity between regions of the heart.
Before and after the spread of the action potential, the signal is zero.
The ECG only measures a signal when the action potential is
spreading. The signal starts in the SA-node (begin of P). The QRS-
complex is the spread of the depolarisation wave through the
ventricles. The delay between the atria en ventricles is caused by the
AV-node. However, the Q-wave is not always detected, so the PR-interval is the atrial-ventricular
conduction time. The T-wave is the repolarisation of the ventricles. The QRS-complex is short, because of
the fastened spread via the bundle branches and the bundle of His. The signal of the ECG is determined
by:
- Location of the electrodes
- Distance of electrodes to the heart
- Size of the heart muscle (mass = size of depolarisation wave)
When the depolarisation wave goes towards the positive electrode, there will
be a positive signal on the ECG. In the Einthoven’s triangle, there are 3 pairs
of electrodes measured. Number 1 is between right and left arm, number 2 is
between right arm and left leg and number 3 is between left arm and left leg.
This will give the directionality of the measured signal. Einthoven I will not
capture much activity, since the signal spreads from the atria to the
ventricles (top to bottom).
In Einthoven I, the signal that goes to the left is
captured as positive, since the positive electrode is
placed on the left arm. Once the signal enters the
ventricles, it spreads a little to the right, hence the
negative Q-wave. Then, the signal spreads
downwards, but since the heart is tilted to the left and
the left ventricle has more muscle mass, the signal
goes towards the positive electrode, so the signal becomes positive. When more and more cells become
polarised, the signal declines, until the whole heart is polarised and the signal reaches zero. The cells that
were polarised at the end (the outer layer) will also be the first ones to repolarise.
To capture every electrical signal, cardiologists use a
combination of 12 electrodes: Einthoven I, II and II,
and they also use the Goldberg’ leads and the
precordial leads. The precordial leads are placed
around the heart and the Goldberg’ leads are on the
most outer parts of the body.
An ECG shows a couple of heartbeats in each lead at
the top. At the bottom, it shows a rhythm stroke,
which shows some of the leads for a longer time.
The ST-segment is the area between the end of the QRS-complex and the beginning of the T-wave.
Normally, this would not show anything. However, in the case of a myocardial infarction, it does show a
signal. Now, there is no moment that all the cells are depolarised. A myocardial infarction is when one of
the coronary arteries is blocked and part of the heart doesn’t receive enough oxygen and nutrients. So, it
doesn’t have enough energy for action potentials. This means that one part of the heart has an action
potential and the other part doesn’t, that is why there is still a signal in the ECG.
One of the rhythm disorders an ECG can show are ectopic beats (extrasystole). This happens when an
action potential doesn’t originate in the SA-node. When it originates in the atria, it is called
supraventricular and when it originates in the ventricles, it is called ventricular. This gives an extra QRS-
complex in the ECG and width of the QRS-complex allows to determine the origin of the ES. When the
QRS-complex is normal, the ventricular conduction system still works the same, so this means that this
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