| The Heart - the Pumping
Function and its Regulation Research and development; addendum |
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The prevailing view is that the heart is pumping by squeezing motions. This view is relatively new. In fact, for almost 100 years (until the end of the Second World War), the heart was thought to carry out its pumping by a back and forth going motion of the valve plane. For example, this was the view of the German professors Henke and Böhme.
After the Second World War, first X-rays and later gamma camera and ultrasound investigation techniques gave a new interpretation of the pumping of the heart; the pictures was interpreted as if the heart carried out its pumping by squeezing motions.
Fig.11-1 The prevailing view, that the heart is pumping by squeezing motions.
Also, an uncovered heart, surrounded by air, changes its size while pumping. This was seen as another proof of the squeezing pumping motion of the heart.
In the beginning of 1980, M.D. Lundbäck rediscovered the pumping function of the heart. He also made a new discovery; the regulating function of the intra-ventricular septum. The investigations that lead to the discoveries was initiated by three patients with inexplicable and contradictionary observations.
(Explanations of the observations, see The inexplicable three observations, which led to the discovery of the true pumping and regulating function of the heart)
Those observations led to the discovery of the pumping and regulating functions of the heart. presented 1986 in the thesis 'Cardiac Pumping and Function of Ventricular Septum'. The thesis complemented with MRI (Magnet Resonance Imaging) describes why we have the impression/illusion that the heart is carrying out its pumping function with squeezing motions. It also introduce the heart as been a new kind of pump, which couldn't be incorporated into the existing pump-classes. That led to the introduction of a new pump-class we call Dynamic Displacement Pumps (DDP). The thesis also describes the importance of intra-ventricular septum, being the structure that regulate the blood flow through the pulmonary- and systemic- circulation system
There seems to be 5 'illusions' masking the real pumping and regulating function of the heart.
| Five illusions masking the pumping and regulating Function of the heart | ||
| Illusion | Method | Error |
| 1st | X-ray | Shows the motions of the inner contour |
| 2nd | Ultra sound | False reflection of a bent surface |
| 3rd | Isotope marking | Errors in the programming of the gamma camera and in treatment of the raw picture |
| 4th | Open chest | The heart changes to become a different type of pump |
| 5th | Magnet Resonance Imaging (MRI) | The power of the heart's way of working generated by shortening and thickening of the muscle. This shows a false picture of a volume displacement |
During open chest the heart behaves differently than when it is located in the intact chest. During surgery or in the animal laboratory, the support from the chest is lost, as is the apical fixation. The heart does change its pumping technique; it will transform into a displacement-pump. The displacement of the Atrio Ventricular(AV)-plane is therefore not obvious, and the myocardial contraction appears as a squeezing movement. Given an almost constant volume of the heart within the intact chest though, it is physically impossible for the myocardium to change the intra cavity volume to drive the blood flow.
With Magnet Resonance Imaging (MRI),not available 1986, one gets a different view of the pumping heart. In Fig.11-3A-B, one can easily see that the inner volume of the ventricles change drastically. The squeezing motion has been interpreted as being the mechanism for the pumping function of the heart. However, one can also make the following observations:
20 MRI-images from one heart cycle
These simple observations have strengthen us in our conviction; it is time to return to the earlier ideas of the pumping function being created by the moving valve plane. It is also time for a new way of explaining the regulation of the heart.
Using these new ideas of the function of the heart, hitherto inexplicable observations can be explained. Also, observations with X-ray, gamma camera and ultrasound technique as well as observations of uncovered hearts can be accounted for. This will not be further addressed here though (see Chapter 2 to 9).
Instead, we will present a new mechanical pump designed according to the same principles as we think apply to the heart. Using this mechanical pump as a model of the heart, a number of observations of the behavior of the heart can be accounted for.
In the following description, a distinction is made between two phrases. One is the actual stroke volume of a pump, which can be calculated from the geometry of the pump. The other is the apparent stroke volume, which can be calculated from the flow through the pump and the cycle frequency.
In some cases these phrases are the same, but in others they are not.
In Fig. 11-4, the construction of the mechanical pump is shown. It consists of an inlet and an outlet tube with different diameters, d1 and d2, where d2 > d1. The inlet and outlet tube are joined by a third moving tube, that can move back and forth, sliding against the inlet and outlet tube. The moving tube has an inlet valve, which corresponds to the mitral (or tricuspid) valve of the heart.
Above the inlet valve, there is a volume A and below there is a volume V. The outlet tube has an outlet valve corresponding to the aortic (or pulmonic) valve of the heart.
There is a circular space between the outlet- and the inlet tube, that dynamically creates an external volume change DeltaV when the position of the sliding tube varies.
The external volume change DeltaV will effect the surroundings of the pump.
In an ordinary displacement pump (a piston pump), DeltaV is usually equal to the actual stroke volume. It means that the surroundings of the pump have to change its volume to the same extent as the actual stroke volume of the pump. This can cause severe problems when the surroundings of the pump is not air, or if the surrounding air volume is small.
For our pump model, the outer volume change DeltaV is small compared to the actual stroke volume. The latter can be calculated as 3.14*(d2 / 2)2 * * S, where S is the distance between the two end positions of the moving tube.
There is a power source (not shown in the Fig. 11-4) that can move the moving tube a distance S in the direction of the outlet valve. When the moving tube has reached its lower end position (closest to the outlet valve), the power source is disconnected and the moving tube can slide freely.
Fig. 11-5A-D shows the pump cycle at lower frequency. This case is explained first.
Starting from the upper end position (Fig. 11-5A), the moving tube is pulled towards the outlet valve by the power source, with closed inlet valve. This accelerates the fluid column on both sides of the inlet valve.
When the induced pressure exceeds the pressure in the outlet pipe, the outlet valve
opens and lets the fluid out of the pump (Fig. 11-5B). When the moving tube has reached its lower
end position, the acceleration of the upper and lower fluid column cease and the power
source is disconnected.
The upper and lower fluid column has now acquired its maximum kinetic energy (kinetic energy=mv^2/2 )
The kinetic energy of the lower fluid column will decrease rapidly because of the resistance in the circulatory system, and the outlet valve will close. (Fig. 11-5C).
The remaining kinetic energy of the incoming fluid column starts to push (when the lower fluid column slows down) the freely sliding moving tube back towards its upper end position. The moving tube will produce an internal redistribution of the fluid inside the pump and a volume increase, corresponding to volume difference DeltaV. The flow behind and through the inlet valve will create the pressure needed to close the inlet valve. The motion of the moving tube occurs because the moving tub has a larger surface, facing volume V, than the surface facing, volume A. When the surfaces are exposed to the same pressure, the force towards the upper end position will be stronger, due to the larger surface, facing volume V . This means that there is still an inflow to the pump, although the outflow has ceased.
If the kinetic energy of the incoming fluid column has not been consumed, by the time
the moving tube has reached its upper end position, the following will happen; the kinetic
energy will be consumed by an abruptly de-acceleration of the fluid column creating sounds
and maybe a small extra output from the pump (compare with the third sound of the heart
and the water hammer effect) (Fig.
11-5D).
This can only happen if the moving tube reaches its upper end position before the next
pump cycle has been started .
Note: the importance of the difference in volume DeltaV) between the upper and lower end positions of the moving tube. It is this DeltaV, that makes it possible to have a continuous inflow although the outflow is pulsating
The pump cycle at higher frequency, as demonstrated by Fig. 11-6A-D, the pump functions a bit differently.
Again starting from the upper end position (Fig. 11-6A), the pull towards the outlet valve of the moving tube, accelerates the fluid columns.
The kinetic energy of the fluid column is now, so large that when the sliding tube reaches its lower end position both valves will be open (Fig. 11-6B).
When the power source is disconnected, the moving tube can move freely. The flow through the outlet valve starts to decrease because of the resistance in the circulatory system but the inflow to the pump doesn't need to slow down. This occurs because of the possibility to fill the volume DeltaV, by pushing the moving tube back against its upper end position, in spite of both valves being open (Fig. 11-6C).
When the new pump cycle begins, the inlet valve will close and again accelerate the fluid column (Fig. 11-6D).
Note: that with higher inflow and thus higher frequencies, the importance of the outlet valve will cease, and the pump will have a continuous inflow and an almost continuous outflow. Also, since both valves are open at the same time, letting fluid pass through the pump, the apparent stroke volume will increase with increasing pump frequency.
The stroke length of the moving tube (compare with length S in Fig. 11-4) depends on the inflow to the pump.
With a constant frequency, the stroke length will vary with the inflow. A decrease of inflow gives a decrease in stroke length and an increase of inflow gives an increase in stroke length.
With a constant stroke length, the frequency has to vary with the inflow. A decrease of inflow gives a decrease in frequency and an increase of inflow gives an increase in frequency.
The Dynamic Displacement Pumps, is the only pump-technology where the inflow automatically controls the pump.
What are the similarities between the described mechanical pump and the human heart ?
The inlet and outlet tubes of the mechanical model correspond to the pericardium, which with support from the surrounding tissues prevents a change of the outer form of the heart. The shape of the pericardium is such, that the largest diameter is situated approximately 2-3 cm below the AV- plane in diastole; all diameters above this point are smaller. Thus, the prerequisites for a correct movement of the AV-plane exist.
The moving tube corresponds to the atrial- and ventricular muscles which, as observable with MRI, slide back and forth by stretching and shortening themselves inside the pericardium. This moves the AV-plane (with its valves) up and down.
As stated before, the inlet valve corresponds to the mitral (or tricuspid valve) and the outlet valve corresponds to the aortic (or pulmonic) valve.
The volume change DeltaV corresponds to the flexibility of surroundings of the heart (as observable with MRI). That the outer volume change should be small, can be understood by considering the fact that the heart is surrounded by tissues. These have to be moved for each pump cycle. Naturally, this waste of energy should be kept at a minimum.
In the mechanical model, only the movement of the moving tube contributes to the actual stroke volume of the pump. As previously stated, with MRI technique it is easy to see that the ventricular muscles of the heart gets much thicker in systole. Does the thickening of the muscles really contribute to the actual stroke volume of the heart? No, it does not!
In Fig. 11-7A-E, five models of the heart with a moving valve plane are displayed. In Fig. 11-7A and Fig. 11-7C, there is no significant thickening of the muscle walls, while in Fig. 11-7B, Fig. 11-7D and Fig. 11-7E the muscle walls get thicker in systole.
Consider the fact, that the outer contour change is minimal and that the total volume of the muscles does not change. The muscle volume is only distributed in a different way in Fig. 11-7B, Fig. 11-7D and Fig. 11-7E, compared to Fig. 11-7A and Fig. 11-7C.
Also, to make it easier to understand that there is no significant differences between the stroke volume in the five models, assume that the blood enters the heart models from the top and exits in the bottom. With this in mind, looking at Fig. 11-7C, it is fairly easy to realize that the actual stroke volume is determined by the movement of the valve plane, as shown in the third column. However, the same is true for all the models!
As is shown in Fig. 11-7E, DeltaV is divided in to parts, DeltaV1 andDeltaV2.
DeltaV1 is the part of DeltaV that is on the atrial side of the AV-plane, and is essential for the motion of the AV-plane. Even areas of the proximal aorta and pulmonary artery multiplied with the stroke length of the AV-plane gives a contribution to DeltaV1 .
DeltaV2 is the part of DeltaV that is on the ventricular side of the AV-plane. The outer volume change DeltaV2is very small, and do not contribute very little to the (actual) stroke volume. DeltaV2 doesn't contribute to the motion of the AV-plane. It exists due to some compliance in the myocard, pericardia and their surroundings, and is causing loss of energy.
In the mechanical model, there is nothing that corresponds to the atrial contractions of the heart, which contributes to the actual stroke volume. Atrial contractions are important at low frequencies, but the importance decreases with higher frequencies. If desired, this could be added to the mechanical model.
One important difference between the mechanical model and the heart though, is that the power source and the construction material in the heart are the same: the muscle. This is a unique construction, which have varying mechanical qualities depending on the state of muscle activity:
In conclusion, it seems as if the basic elements of the mechanical pump can be found in the heart. Using the mechanical pump as a model of the heart, a number of questions regarding the function of the heart can be answered. The following are examples of such questions and answers offered by the mechanical model:
How is it possible for the heart to be filled at high frequencies and at large flows ?
Answer 1
The major filling of the heart (except for the minor volume DeltaV ) occurs during systole. The prevailing view, that the major filling of the heart occurs during diastole is false.
During systole (when the AV-plan is moving in the direction of apex), the major part of the filling of the heart occurs
How can the right ventricle of the heart have a constant filling pressure, regardless of the frequency and the magnitude of the flow through the pump?
Answer 2
The heart is inflow controlled, like the mechanical pump. If the static inflow pressure should rise, baroceptors in the right atrium will immediately tell the heart to increase the frequency. Thus, the static pressure is almost constant, but the dynamic pressure (corresponding to the kinetic energy of the blood that passes through the heart) increases with increasing inflow and frequency. This is not possible to detect with the monitoring technology for medical purpose of today.
Why does not a person normally feel, that the heart is beating?
Answer 3
The outer volume change of the heart is limited to the very small volume DeltaV. That will not bring enough energy to feel the heart beating .
Why isn't there any back flow losses, when the valves are closing?
Answer 4
When the AV-plane has reached its lower end position (closest to the apex), the power from the contracting myocardium is interrupted and the acceleration of the fluid column cease.
The fluid column have now acquired an amount of kinetic energy. When the flow through the proximal aorta and pulmonic artery decreases.
The remaining kinetic energy of the incoming fluid column pushes the AV-plane back towards its upper end position consuming the volume difference DeltaV1. The motion of the blood behind and through the tricuspid- and mitral valves are closing those valves, and thus there will be no back flow losses..
The closing of the aortic- and pulmonic valves, can be achieved by the motion of the AV-plane catching up the speed of the outgoing blood stream, and thus there will be no back flow losses.
How can atrial contractions contribute to the pumping function when they lack inlet valves?
Answer 5
Because the force of inertia around and inside the heart. The contracting of the atrial muscles will bring the AV- plane away from apex (cf. Fig. 11-11). The atrial contraction thus contribute to the total stroke length.
What is the explanation of the auscultatory 3rd heart sound?
Answer 6
3rd heart sound appears, if the kinetic energy of the incoming fluid column has not been consumed by the time the AV-plane has reached its upper end position . The kinetic energy will be consumed by an acceleration of the entire pump and its surroundings. The sound comes from the pericardium, that suddenly stretches while consuming DeltaV. (It is well-known, that you can never hear a 3rd heart sound on a patient, who do not have a pericardium).
Why can you sometimes feel palpitations?
Answer 7
With the prevailing view (that the heart is pumping by squeezing motions), one can never answer this question. How could you feel the apex beating against the chest during systole, with the heart simultaneously getting smaller?
The explanation is, that the pulmonary artery and ascending aorta are attached to the anterior part of the AV-plane, and are relative fix to the surroundings of the heart. Therefore, when the AV-plane moves in the direction of apex during systole, the posterior part of the AV-plane will move more easily than the anterior part. This creates a momentum that can be felt, which causing the apex to beat against the chest wall .
The "rocking heart" phenomenon seen in pericardial effusion, can be due to the same momentum.
How is it possible, that there is an increase of the apparent stroke volume of the heart at high frequencies, although the heart size and the filling pressure to the right ventricle is unchanged ? (The filling pressure and the heart size can even decrease)
Answer 8
At high frequencies, the kinetic energy transferred to the blood by the ventricular muscles, will make both valves open at the same time . That will let more blood flow through the pump in systole, than can be calculated from the actual stroke volume and frequency. Compare the blood flowing through the heart, with a skier moving in a track. The skier continues to slide in the track, some seconds after pushing away with the sticks. In the same way, the blood continues to flow through the heart, some milliseconds after the mitral- and tricuspid valves have opened. Compare the pushing of the sticks, with mitral- and tricuspid valves gripping and moving the column of blood.
The nature has, by the motion of the inter-ventricular septum and the pumping function of the heart, created a double auto regulation function, that exactly balance the stroke volumes to the systemic- and pulmonic circulation. This is made by using the passive (non-rigid) and active (rigid) phases of the muscles in the following way.
In order to have a circulatory balance with no regulation, the intra-ventricular septum needs to keep its systolic shape even in diastole. This is why ,normally, the left ventricle always has a higher diastolic pressure than the right ventricle. This pressure difference is always generated by the heart itself , because it has to overcome the elastic forces in septum .
An increased inflow to the right side of the heart will during the first few heartbeats, generate an increased static filling pressure to the right ventricle. By the balancing action of the inter-ventricular septum, the stroke volume from the right ventricle is increased. Accordingly, the stroke volume will decrease during the first few beats from the left ventricle.
An increased inflow to the the pulmonic circulation, will soon produce an increase in filling pressure to the left side of heart. An increase in filling pressure on the left side. By the balancing action of the inter-ventricular septum, the stroke volume from the ventricle will increase. The stroke volume from the right ventricle will decrease accordingly and the total static pressure within the heart has increased.
The baroceptors in the right atrium, and to some instant the automation within the muscle itself , will sense the increase in static filling pressure, and increased the heart frequency. Due to the pumping function of the heart, the increase of the heart rate enables the heart, to take care of the increased inflow and convert the increased static pressure to dynamic pressure. Within a few heart beats, balance has been attained again and flow rate has increased and the static flow pressures are the same, as before the change of inflow to the heart .
The inter-ventricular regulating function is in fact the key for the transplanted heart, which have to cope with regulation in spite of all external nerves cut off.
A decrease of the inflow to the heart, will during the first few heart beats generate a decrease in the static filling pressure to the right side of the heart. Consequently the pressure on the left side, will be relatively higher. This means that intra-ventricular septum during a few beats, will be pushed towards the right ventricle. Compared with Example I, septum now has to be stretched out, which requires extra work-load, this work-load cannot be generated due the fact that the stroke volume from the right side will decrease. This means that the total heart volume will be smaller.
The baroceptors in the right atrium ,and to some instants the automation within the muscle itself , will sense the decrease of the filling pressure and decrease the heart rate. The dynamic pressure into the heart will go down, and the static pressure to the right ventricle will go up, and bring back the heart to its 'normal' size. The balancing act of the ventricular septum and the pumping function of the heart, has within a few heart beats adapted to the new inflow. Compare this with the change of stroke volumes and heart size during breathing.
The pumping function of the heart can roughly be compared with an ordinary garden pump (see Film: Cardiac Pumping and function of ventricular septum). The outer cylinder made of steel or polymeric material can be compared with the pericardial sack. The inner tube, made of the same material, can be compared with the atrial- and ventricular-muscles. The artificial valves can be compared with the valves in the heart. The power needed to create a back and forth movement of the inner cylinder is powered by external forces, like manpower or an electrical motor. In the heart the power is generated by the atrial and ventricular muscles. The produced back and forth movement is gripping/catching the fluid column, when the inner cylinder is reaching its highest position and with the valves closing the inner cylinder will displace the fluid column when going forth again .
If the power supply in the garden pump would change, it wouldn't change the mechanical construction of the garden pump. Instead the change of power supply would alter the capacity of the garden pump.
Example: 50% change of power would result in 50% in capacity.
If the power supply in the heart would change, not only the capacity but also the construction of the heart would be altered. This is due to that the muscle is both the energy source and the construction material, where the construction material varies very much if it is in an active or passive phase. If the part of the heart muscle that is leaning against the pericardial sack for some reason can't stiffen (be rigid), this part of the heart muscle will then be supported (during systole, when high pressure occurs) by the rigid pericardial sack and the surrounding tissues. Other parts e.g. the intra-auricular- and intra-ventricular septum has only its own rigidity in the inactive phase and the difference in blood pressure between the chambers to lean on. This is what the intra-auricular- and intra-ventricular septum has to rely on when it shall withstand the blood pressure that is generated during systole.
The nature has made use of the muscle being a nonrigid material in diastole and a rigid material in systole in the following way: the back going motion of the valve plane in diastole, and the regulating function of the ventricular septum.
The nature has to some instant compensated a malfunction (infarction) of the muscle as
construction material (the muscle leaning on the pericardial sack) with the rigidity of
the pericardial sack and the surrounding tissues.
However a malfunction (infarction) of the intra-ventricular septum, can bring the
mechanical functions of the heart to a lethal outcome, although the power supply is good
enough for a healthy normal life. The reason for this is that the inactive parts
(infarcted area) has not enough support from the surroundings (as is the case with the
muscle leaning on the pericardial sack). Its only support is the low pressure in the right
ventricle and its own passive rigidity. Therefore the pressure and the pumping function
generated by the healthy part of the left ventricle, will create a membrane pump like
function of the injured part (that cannot stiffen) of intra-ventricular septum. This
membrane pump function together with the healthy part of the right ventricle will pump all
blood into the lungs and within seconds kill the patient.
As a well-known cyclist. The sportsman came for an investigation of his heart, because he had suddenly had some unspecified, unpleasant feeling in his heart and thorax, especially during rest.
ECG and auscultation of his heart did not show anything unusual. In stress test on a bicycle with 50 W steps every 5 minutes, he went up to 450 W and cycled for 2 minutes with this load.
With ultrasound monitoring, one could see unusually large movements back and forth of the inter-ventricular septum (see Part Two - the regulation of the heart) indicating a large aortic insufficiency.
The cyclist continued to complain. When he was catheterised, it was discovered that he had a complete rupture of two of the three aortic leaflets. It was more or less no pressure gradient over the aortic valve in diastole.
He was operated and got an artificial aortic valve. His career as a cyclist was over.
In those days, the fact that his heart worked so well in spite of the ruptured aortic valve was a mystery.
With the new pump-technology modelling the heart, it is quite obvious that the importance of the aortic valve decreases with inflow and frequency high enough (cf. Fig. 11-6A-D). I.e. when the bicyclist was active the heart didn't need the aortic valves, because the valves never have to close due to the high kinetic energy of the blood. But at rest the aortic valves has time to close, and then it becomes obvious that the aortic insufficiency has a major impact on his well-being.
The concrete worker explained, that he one year before the investigation had acquired a heavy flue, during that flue he got severe chest pains but thought this was caused by the flue and never visited a doctor. He went back to his work after two weeks, but felt a little tired for a few months. Later during an ordinary health control they discovered a 'strange ECG'.
The concrete worker had an intact function of the intra-ventricular septum but a total infarction on the rest of the left ventricle. That meant that the infarcted area was about 50% of the left ventricle. The infarcted area had a total support of the pericardial sack and surrounding tissues, and thus had time to stabilize, and the regulating function of intra-ventricular septum was in order and so also the force to bring the Atria Ventricular-plane (AV-plane) towards apex. By a higher frequency and training, the heart could perform an ordinary workload.
Lundbäcks father had four years earlier with good result gone through a coronary bypass operation. Some months before his death, his angina pectoris returned. The angina pectoris this time was also accompanied with the feeling of not having enough air to breathe (dyspnoe). He ended up in the intensive care unit with pre-infarction syndromes. After three weeks at the intensive care unit, and with many attacks of angina pectoris and pulmonary oedema, he was going to a new coronary bypass operation. A few hours before the surgery was due, he died in pulmonary oedema.
During the attacks of angina pectoris and the resulting pulmonary oedemas, one could easily see, with ultrasound registrations, that the intra-ventricular septum couldn't withstand the pressure within the left ventricle when the rest of the healthy heart pulled the AV-plane towards apex.
Septum acting like a diaphragm pump contributed by its pumping function, creating an overflow of blood into the lungs and thereby causing pulmonary oedema and death.
An infarction in septum will not only create a loss of power, but also a loss of the very important regulating function of the heart. If the heart looses its regulating function it more or less doesn't matter how good the pumping function of the heart is.
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