In this class we’ll develop an anatomic-physiological description of the cardiovascular system. We will be interested in describing the cardiac cycle and the heart’s mechanical activity. Besides we will also introduce the concept of arterial pressure and related pathologies.

Heart’s Generalities
 

The heart possesses four compartments: 2 auricles (left and right) and 2 ventricles. At the center exists a structure of great importance, the septum which divides the heart in two compartments, the right or venous and the left or arterial heart. 

The right auricle receives venous blood from the Superior Cave Vein and the Inferior Vein Cave.
The left auricle receives 4 vessels from the lung veins, and these carry blood of the arterial type with a large oxygen saturation level.
The left ventricle expels blood towards the aorta while the right ventricle will do the same towards the lung artery.
The lung artery transports venous blood , or with a low oxygen saturation level, which means that is more correct to describe them as discarded elements than as Carbon Dioxide. This is a remark necessary so we may reach a conceptual look. When we talk about venous blood we prefer to describe it as blood with low oxygen saturation since Carbon Dioxide in reality exists in every structure just as the discarded elements are.
If we are to analyze this with a “large circulation” and “small circulation” criterion, the Superior and Inferior Cave Veins and the Aorta belong to the “large” one whereas the lung artery and the lung veins belong to the “small” or lung circulation.
Mainly, or using general concepts the Superior Vein Cave drains blood from the body’s superior half whereas the Inferior one will do the same with the inferior half.
The Aorta will be a great exit out of the heart towards the rest of the body, a great way of blood distribution towards the whole system.
Its diameter, thus, is very considerable and deals with very high pressures. In that sense it is important to remark a first difference between large and small circulation: the pressure difference. The left heart will expel blood through the aorta with a pressure which allows it to reach the toes while through the lung artery it will have to get out to reach the alveolus, to the lung. Pressure differences, in consequence, will be great between the lung artery and the aorta.
I will now offer to you some data about pressure differences. These are quite useful and some of them are very necessary to our knowledge. They are measured in mmHg which is a pressure unity.
 
 
 
Right Auricle
 
Left Auricle 
4.5
8.0 
Right Ventricle
 
Left Ventricle

4.5 a 10
 
9.5 a 125
 
Lung Artery
 
Aorta
 
10 a 25
 
80 a 120

 
 It is undoubted that the left heart requires a higher pressure and this is because it needs to propel blood into a larger surface thus requiring handling higher pressures.
 
 
 

Blood Circulation in the Heart.

 
The lung vein will receive oxygenated blood from the heart. The lung veins end in the left auricle. They pass to the left auricle through a valve, the mitral valve which corresponds to the right side tricuspid valve. Both are auricle-ventricle valves. The tricuspid separates right auricle from right ventricle and the mitral valve the left ones. We then find the Lung Artery (to the right) and the Aorta (to the left). Between both ventricles and these two great vessels we can find sigmoid valves named according to those vessels (lung valve and aortic valve). If we follow the path: blood arrives from the periphery. If it arrives from the inferior part of the body (inferior members, for example) it arrives through the Inferior Cave Vein, and if it comes from the superior parts (let us say head, superior members, thorax) it makes it through the Superior one.  It enters through the right auricle, passes through the tricuspid valve and it enters the right ventricle. It passes through the sigmoid valves that at this level are denominated lung valves.   It rises through the lung artery trunk and later on it divides itself into right and left lung artery which will end in the lung. These arteries will go to the lung, will oxygen themselves at the lung level and will return as lung veins. The lung veins will drain in the Left Auricle. They are 4 of them. Their names are right superior, left superior, right inferior and left inferior since they are disposed square-wise that way. The important thing is that now arterial blood enters the Left Auricle from the lung vein. This arterial blood goes through the mitral valve (auricle-ventricle) and will finally enter the Left Ventricle.
From the Left Ventricle passes through the aortic valves towards the Aorta describing a large curve named as aortic key. The aortic key will finally form the aorta and this formation will repeat in the whole body. The first aortic ramifications: those organs which receive blood from these ramifications will be organs receiving more oxygenated blood since this has just left the heart. They are the brain and the heart itself. This means that Anatomy is organized in such a way that takes care of those organs which might be sensible to any possible oxygen diminution thus giving them blood which recently left the heart and which possesses major oxygen saturation.  The brain, therefore, also forms part of the coronary vascular process. 
Being aware of this system, which are the names of the valves and what type of vessel comes out of each side of the heart we are now ready to continue with other topics.
 

Capillary Concept

 
The vessels which we call arteries branch inside the body, they form arterioles and then smaller structures and at a capillary level these vessels begin to acquire every time weaker structures, thinner walls finally easing the gaseous exchange tissues need. This means that next to the heart, if we are to analyze a vessel’s structure, we will observe that they have a great amount of elastic fibers, of muscular walls, whereas as you reach the capillary the structure will be much thinner.  This is due to the gaseous exchange through which the capillary will yield Oxygen to the tissues and receive Carbon Dioxide and discarded elements from them. In order for this process to take place the vessels structure need to be small, thin and permeable to these gases. That is what we call capillary. Not always the organism keeps this model artery-capillary-vein. This very same thing happens in the lung: lung arteries which carry low oxygen saturation blood reach the alveolus and the capillary are finally created but in this case the capillary instead of yielding oxygen receive it and exactly the opposite takes place with carbon dioxide. It saturates with oxygen and returns as lung veins this time full of oxygen. However, this scheme of artery-capillary-vein continues, this time at a lung level.
 

Cardiac Innervations

Within the heart it is necessary to comprehend two systems: one is the vascular which we just have reviewed. There is a second one which we need to analyze which is the nervous system. We know that the heart is a pump which will contract in a synchronic, rhythmic way and that it will need some sort of nervous system able to regulate that type of contraction. If this fails to happen, pathologies appear. This system is denominated as cardio-connector system. It is an innervation’s intrinsic system which the heart possesses.   When we study sympathetic and Para-sympathetic we learn that there exists an extrinsic influence, which means that this happens out of the heart thus enabling to regulate the stress situations and other physiological situations as well.  The cardio-connector, however, is a heart intrinsic system which will regulate its contraction ability. We are going to find the Sino-auricular nodule and the auricle-ventricular nodule, which we will find on the floor of the right auricle within the separation between the auricle and the ventricle. We see haceks inter-nodules (its existence is still argued). We see the Has de hiss trunk with a left and a right branch.  Because we assert that the left heart is the one that is in charge of carrying all this blood, the left ventricle’s size is larger than the right and besides will have greater and more profuse innervations at the pirkinje fiber level.  It is notoriously larger, and that is why any pathology will concentrate at that level. The left ventricle’s wall is very important. The thickness will reach great importance in what is denominated cardiac hypertrophy and also regarding its contraction capacity. The cardio-connector will mainly gather the capacity of step-marker. Many organs in the body have that activity: within the digestive tube, the muscular fibers and also within some central structures.  In the heart there is a type of fiber with a special regulation which will discharge before the others and will mark the beat of discharge for the rest of the neurons.  Since its discharge rhythm is oldstronger, the rest will follow. This is the Sino-auricular nodule (san). And will mark the beat at a discharge frequency of 70 to a 100 discharges per minute. If san fails the rest of the cardiac system will follow the group of neurons which might have the second fastest rate: the auricular-ventricular nodule (avn) which will mark a frequency of 40 to 50 discharges per minute.  A failure at this level will provoke that the Has de Hiss trunk will lead the frequency at a 35 to 40 level, almost a life compatibility one.
Generally, before reaching these values the step-marker inactivity is tried to be substituted by an electrical one, introducing within the heart a devise which might produce a discharge more similar to the san’s one.  The important question here is to point out that each of the fibers will make its discharge in an independent fashion, with its own frequency, but will abandon that frequency to follow the one that might have a faster frequency. They will always mate that which might have a higher discharge speed. Any muscular cell, isolated, has its own discharge frequency, but when facing other cell stimulus it discharges sooner and produces a normal discharge cycle which would produce otherwise. However, it will mate in such a way that without getting into histological details we are going to comprehend the cells the same way we analyze the skeleton muscle ones, they are muscular cells, and conform the cardiac muscle. They have different characteristics but they will also develop as an outstanding particularity a high permeability between them because they are highly coordinated to one another since it is very important that the heart might contract in a synchronic and synergic manner in order to act as a pump and propel blood towards the periphery. 
Bradycardia: Slow rhythm.
Tachycardia: fast rhythm-
Arrhythmia: the heart rhythm does not keep regular intervals but it continues contracting generally in a collective manner.
 
A pathology produced by imbalances is the fibrillation.  This is linked with channels that allow information permeability regarding what is going on in the previous cell discharge.
 
 
 
 
The Cardiac Properties

We will now name four or five heart properties. Traditionally only four properties were mentioned but relaxation became very fashionable in the last 20 years and it was included among them.
 
 

Automatism or Cronotropism

Excitability or Batomotropism

Conductivity or Dromotropism

Contractility or Inotropism

Relaxation or Lusitropism.

 
 
It is interesting to note that these five properties as simple phases within a normal contraction cycle. The muscular fibers have an automatic property. We have already stated that they have the ability to possess an endogenous rhythm so each of them could potentially contract in an autonomous fashion.  They are automatic; excitable (this autonomous rhythm will produce in them an excitation, an electric charge), they are able to conduct this charge , they are able to contract themselves because of  fibers such as the skeleton muscle and can also relax; which means they are simple phases.  These five characteristics are going to be modulated by the Autonomous Nervous System (ANS), and the sympathetic and Para-sympathetic nervous systems.
Which are the effects of the sympathetic and the Para-sympathetic on the cardiac properties?
The sympathetic system is going to stimulate the five cardiac properties whereas the Para-sympathetic system will inhibit them.   We link it to the concept of exercise. In the exercise is activated the sympathetic system and we link it with the tachycardia, or the rise of the cardiac frequency.
 
Useful Values
Volume per minute 5.5 liters
Fin de Diastole Volume: 130 ml
Residual Volume: 70/80 ml (these are variable data from the book)
Systolic Volume: 50 ml
Ejection Fraction: Systolic Volume / Diastole End Volume: 0.5 (relationship)

 
Cardiac Cycle

We are going to use these words on a trigger bases:  what is diastole and what is systole?
Diastole is a period of relaxation which will allow the filling.
Systole is a contraction which produces blood ejection in the heart. 
At the same time there is a rhythm of filling and emptying given by the san, which is of 70 to 100 hundred contractions per minute. This will generate a volume-minute of 5.6/6 liters which means that the blood volume that goes through the organism per minute is 5.5 liters.
Diastole End Volume: how much is there within each ventricle, in this filling relaxation phase, when the diastole ends?  Be careful, within each ventricle!! We draw our figure thinking in the left ventricle.  The left ventricle, when the diastole ends, when this filling phase ends will have some 130 ml inside. Afterwards, the contraction takes place (the systole) a 50 ml volume is going to be expelled from the ventricle. The residual volume is what remains within the heart after the systole. This means that we have to change the systole concept. Systole is a contraction which will not produce a total emptying of the ventricle, only a partial one.  There is a small blood volume which will remain in the heart and it will have its consequences. According to this analysis the diastole end volume (which means all the blood we find at the end of this process) is going to be equal to the volume expelled minus what is left: in other words, systolic volume plus residual volume. The ejection fraction shows clearly this relation, since 70 are more or less half of 130. What the heart ejects is more or less half of the volume there is when it is full. If a person has low contractility, if it has cardiac insufficiency, if someone has a small ejection capacity, the ejection fraction diminishes (minus 0.5). The cardiac frequency rises in all individuals when making exercise, in sportsman trained in aerobic activities. They will have a minor frequency and a major volume, and that major volume, depending on the activity they might develop, will correspond to a diastole end major volume or to a smaller residual volume. Very interesting is to analyze how a person can, modifying the activity also alter the cardiac properties. If you and your grandmother climb some steps, she will end puffing and blowing and you will not, and you won’t understand why. Since she does not make any physical activity her cardiac frequency will rise up a whole lot when making this exercise, whereas a person who is trained or practices any sport is much more used to effort. Thus, regarding that same effort his cardiac frequency is smaller. Probably his volume-minute is also higher depending upon the type and intensity of the exercise. The cardiac frequency, however, is the value in which this phenomenon can be better analyzed.
Let us study in a deeper way the cardiac cycle. Let us analyze -starting from the anatomy we have just seen- what the diastole and the systole are all about. Let us see some details about them. The chart we use to integrate the cycle with pressure normal values at the heart cavities’ level.  We call it Pressure Curve Volume. We first are going to comprehend this curve and then will understand its physiological variations.  This is a Chart where pressure is expressed in mmhg as regarding volume measured in ml. We have already expressed that the residual volume was of 50 ml. This is the smaller volume that the ventricle should carry. The diastole end volume is 130 ml, which is the maximum possibility for the ventricle. And 120-125 is the maximum we reviewed that systolic pressures can reach in the left ventricle as well the aorta. We will choose the 0.50 coordinates, which we will denominate Point One. At this “point one” the auricular-ventricular valves are going to open and the filling phase will start. We have to locate ourselves within the cycle: they are then in the second part of the diastole.  
 
 
 
+filling   systolic iso-volumetric contraction    ejection    diastolic iso-volumetric relaxation       Active tension curve     Passive tension curve or distension ability
 
 
 
 
 
We are dealing with values of the left ventricle since from a physiological point of view they are more interesting to analyze. In the same way, when the auricular-ventricular valves close it is called medical clinic S1, and then the sigmoid ones close it is called S2. This is important regarding the blow diagnosis.  There has to be a fixed time between S1 and S2 and also between S2 and S1. If we find any alteration between those periods cardiac failures appear.

Filling
Passive Tension or Dis-sensibility
Systolic Iso-volumetric contraction
Ejection
Active Tension
Diastolic Iso-volumetric relaxation
 
We analyze pressure in mmHg over volume in ml. 50 is the residual volume, which is the blood volume remaining in the heart after the systole, and after the ejection and the  diastole end volume is of 130 ml which is equal to the blood total volume which the ventricle embraces before ejection takes place. Then, the diastole ends. Maximum volume is reached just before the systole begins.
We will review each point in this curve. We are now in point one; we will start with the ventricular filling. The auricle-ventricular valves need to open. Blood begins to enter the ventricle and its volume starts to rise, as we see, and its pressure also rises. The curve describes this trajectory up to point two. At point two a pressure of 10 is reached, equaling and surpassing the auricle’s pressure. What happened?  The auricular-ventricular valves closed because the ventricle’s pressure surpassed the auricular one.  That way begins the systolic iso-volumetric contraction phase. We should remember that the auricular-ventricular valve just happened to close.  After the ejection ended the sigmoid valves closed down. Since both valves are closed, it will be iso-volumetric, in such a way that the trajectory is going to be parallel to the axis. And no volume variation will be perceived. There is, nevertheless, a pressure rise due to the ventricle’s muscular fiber contractions.  An enormous pressure rise (10 to 80) will take place. The ventricle’s pressure rises up a lot during this stage. Point Three: The pressure rises up so much that the sigmoid valves open up. There is an opening of the aortic valve because the ventricular pressure was so high that surpassed the aorta’s pressure in diastole (which means before the ejection, 80-120, and an average aorta’s pressure during diastole). When reaching the ventricle, this pressure of eighty will allow the opening of the aortic valves. They open and the contraction continues to take place. In the beginning the pressure rise continues. We have already said that the ventricle’s pressure rises up to 120-125 which is the maximum figure that the ejection reaches during this first phase, really too fast. Then the diminishing phase starts, the ejection lowers which in turn also diminishes the ventricle’s pressure.  We see that during the ejection phase we go backwards, when analyzing this process, why? It is because the volume will be lowering. The ventricle’s volume if it is ejecting any blood then it will be diminishing. We finally reach the “point four”: the ventricle’s pressure diminishes so much that it will reach a point below the aortic pressure thus provoking the shut down of the aortic valves. At the ejection phase it lost volume in such a way, that its pressure lowered. When ejection begun, it was high, there existed a high pressure, and also a great difference which needed to be equilibrated. When we reach a certain stage, however, that strength reaches a maximum point, and that gap disappears and therefore the exit speed will lower, the ventricle’s pressure lowers and starts a reduced ejection phase. At point four, then, there is a close down of the aortic valves because the aortic pressure is larger than the ventricle’s pressure which went down a whole lot.  We now find a very interesting data. We had seen that the aorta’s pressure was 80 but here is closing at 100. Why is that so? Why is there a difference of 20 mmHg? At this point, the ventricle’s pressure (80 mm Hg) had surpassed the aorta’s one.  The valves opened, it surpassed it, but when it lowered down to 100 then the aortic valves did close. Why did this take place? This takes place because the ventricle is emptying towards the aorta in such a way that at the same time the ventricle’s pressure lowers the aorta’s rises.  We should remember that not only the heart has a diastolic and systolic pressure (or a relaxation and contraction pressure). Also the vessels (in this case the aorta) will register a diastolic and systolic pressure as well. We have already stated that the aorta has a diastolic pressure of 80, which means that before receiving the heart blood flow its diastolic pressure almost reached 120. At approximately 100 equilibrium and closing take place.  One more clue: when you measure your arterial pressure, two figures are given to you.  These figures correspond to a diastolic and a systolic value.  The same way the heart will carry on this biphasic cycle of diastole and systole, retaining or freeing blood towards the vessels, which in a certain way are elastic, distensible, they in turn will respond to this diastole and systole process. At a moment they do not receive anything and all of a sudden they do receive. When we measure a person’s pressure, then, it will reflect this alteration of the cardiac cycle. When we reach 100 mmHg the aortic valves close down. What stage is left?  The diastolic iso-volumetric relaxation. Relaxation:  the ejection has just taken place and the ventricle is relaxing. Iso-volumetric: the aortic valve is closed and the auricular-ventricular valves are closed two stages behind. This blood inflow and outflow ceases and thus, during relaxation pressures diminishes and its volume remains unaltered.  During this stage, as we see, the residual volume is the same. Residual volume does not change since the auricular-ventricular valves shut down. And we reach again the Phase Number One where pressures lowers and reaches a point where the auricle and ventricle pressure difference is zero and once again the opening of the auricular-ventricular valves and the filling process takes place.  This means that the heart is always changing between this residual volume and the diastole end volume. We always find it between these two stages, or in the iso-volumetric one or going into the other one. The heart is constantly equaling, surpassing or just below the pressures of the surrounding compartments (auricles or vessels). And that is how the cardiac cycle regulates. Thus, physical processes, time coordination are involved and we will understand the importance of this cardio-connector system we referred to before. If this system is not perfectly coordinated this cycle does not work out. And we now comprehend how steps coordinate one another.
 
.
 
Some Variables
Volume-minute equals Cardiac frequency (quantity of discharges per minute) times Systolic Volume (blood amount leaving the heart)
When we state volume-minute we refer to the amount of blood that leaves the heart every minute. If we take into account normal values, the cardiac frequency in normal physiology is 70 beats per minute.  Systolic Volume: we had stated a 70 ml figure. 70 times 70 is 4900 (almost five liters and we had mentioned 5.5). These figures never match since each author publishes its own, but the normal volume-minute figure varies from 5 to 6. This is the accepted concept we have to deal with.
 
Diastole End Volume: Systolic Volume plus Residual Volume, which is what remains in the heart when diastole ends. When filling ends it will be equal to what ejected plus what is left.
Arterial Pressure: is equal to arterial tension. They are considered the same thing. Physically speaking, pressure equals strength against surface. That is pressure, a strength made in a normal direction, perpendicular to any surface. What is tension, then? Strength made not in a perpendicular way, but rather embracing that surface. That is the difference between pressure and tension. The “tension” concept is useful to comprehend that we are dealing with vessels, but in the daily chat there is no difference between them. 

 
Properties of the Vessels and Pressure

Elasticity is the capacity to recover a former condition. I take something stretchable, I stretch it, then I loosen it up and the object recovers its former condition.  Distensibility, on the other hand, is the capacity to modify a certain condition, its `physical conditions. I stretch a chewing gum and changes. Conceptually speaking, thus, elasticity and distensibility are opposite. Elasticity is the ability to recover a former condition, and distensibility the capacity to modify a physical condition. In general, when dealing with physiological concepts we are taken as equals. In order to make a first approach, however, we need to analyze both. When the heart ejection phase takes place, a great amount of blood is liberated towards the aorta, how will the vessels react? They will distend. They will modify their previous condition so they are able to receive blood. This also does not alter the vessel volume too much, avoiding its rupture. Finally they are not very oldstrong structures. They will reach this ability to distend themselves and adapt their volume capacity to the blood that might arrive.  But this process takes place through a tension rise. In order to widen its volume, to receive this new content, pressure will necessarily rise.
 
 
If I take a spring and I distend it, I feel the tension that structure receives. Same thing happens with vessels. When the blood went through, during that second diastole took place, the vessel will recover its former condition. That is exactly what stretching ability means: the capacity to recover its former condition. Both concepts are equal to us since one affects the other.  If a vessel is hard it is not able to distend nor can return to its former condition. However, we need to distinguish between distension and elasticity.
Now, arteriosclerosis is basically this: fat agglutinates (especially cholesterol) in the vessels’ walls, they harden up and they loose they elastic capacity. When blood arrives they are not able to distend. Therefore they will be more susceptible to ruptures (ischemia, internal hemorrhages). This is why people affected by arteriosclerosis suffer from pressure rises. Their vessels volume is unable to change thus provoking a rise in the arterial pressure.  We are now able to comprehend why we have a minimum and a maximum pressure. The first movement will carry the blood of the ejection phase of the cardiac cycle. The vessels will distend in order to receive this tension but the last will be higher so that when we register it, we will find it in its maximums peak. Once the blood went through, the vessel will recover its former condition, its volume will diminish and pressure against its wall will also be lower.  Thus, when we measure this pressure it will be lower (“minimum”) than before.
Let us write down the usual pressure figures. This is important.
Pressure equals strength against surface. That is the most usual one. Therefore we will find a diastolic and a systolic arterial pressure.  I want everybody now to feel their own pressure. Are you able to feel how blood passes through? What are you measuring now? Is it Systolic or diastolic arterial pressure? It is important to point out which is the zero point.  Differential pressure is systolic arterial pressure minus diastolic arterial pressure and that is why you are not measuring any of them. This happens because you do not have a zero point.
When blood arrives you feel systolic arterial pressure and when that blood impulse is not present you do not feel a zero value, what you then measure is diastolic arterial pressure which is what we normally consider as a zero value. Thus, when you measure that pressure you measure a pressure difference, systolic minus diastolic.  A value frequently used is the medium arterial pressure and to reach it we use the diastolic arterial pressure plus a third of differential pressure. It looks like a complicated formula, but it is a simplified manner of expressing a planimetric integration of a somehow strange curve.  The important thing to comprehend is that medium arterial pressure is not an average between the diastolic and the systolic arterial pressures. It is closer to the diastolic one, which is a lower figure and this is related to physical values. It is important to note that when you read medium arterial pressure do not think in a media between diastolic and systolic, is just a separate figure: diastolic arterial pressure plus a third of differential pressure.
 
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Peripheral Vascular Resistance

 
Résistance is everything that impedes the blood stream, in this case, evidently related to the pressure concept.  What is usually expressed is that since there are several vessels resistance is parallel.  Evidently, total resistance will always be minor than every one of the individual resistances.
Peripheral Vascular Resistance: the cardiovascular system has the capacity to control and regulate the contraction at the arterioles level.  The arterioles will be the body’s maximum resistance point.  At that level the cardiovascular system will regulate the peripheral vascular resistance. Already knowing that the volume-minute is equal to the arterial pressure divided by the peripheral vascular resistance we will be able to comprehend its importance.  The body, foe example, will regulate the arterial pressure through the arteriole’s resistance.  Resistance is the resistance to blood pass. Volume-minute is the amount of blood which will leave the heart. If the peripheral vascular resistance raises then the blood able to leave the heart will lower. This will picture what’s going on. If resistances contract at a certain level, then the amount of blood able to pass will lower. Example: during an exercise there will be blood redistribution through the whole body and the sympathetic will guarantee that this blood reaches the places which will need it. In this case will be a certain muscle. There will then exist a rise in the peripheral vascular resistance in other organs (digestive, immunologic, renal too).  Those organs do not need blood at that moment, certain muscles need it the most and their volume is important. How ensuring that blood does not reach the unwanted organs? This is done through the vessel-constriction and the vessel-dilatation which will regulate the peripheral vascular resistance. Its rise will be given by the vessel-constriction and, on the contrary, its diminution will be related to dilatation.  Which system contracted the vessel, the sympathetic or the Para-sympathetic? The sympathetic.  Generally speaking the sympathetic effect is vessel-contracting. When explanations are needed, simplified schemes are useful. Most of the processes will require sympathetic and Para-sympathetic.  Thus sympathetic will produce vessel-constriction and a rise in the peripheral vascular resistance. Imagine a vessel: if you squeeze it resistance will rise and volume allowed to pass trough will lower. Vessel-dilatation, on the other hand, will be given by the Para-sympathetic. Peripheral vascular resistance will then diminish. This will acquire some importance when we analyze stress. And we also can perceive how these concepts are able to regulate arterial pressure. Example: In persons who suffer hypertension, very probably, the medicines they receive are inhibitors of vessel contraction.  If we inhibit such contraction we do not allow the rise of the peripheral vascular resistance thus provoking a pressure lowering and maintaining the body’s activity. We will se how these three variables (arterial pressure, peripheral vascular resistance and volume-minute) interact between them and we will now use an old formula. Later on when we analyze stress we will perceive how these variables interact between themselves.
The same way we said there is a cardio-connector system, a nervous system that will intrinsically regulate the heart; we will also find an exogenous system, an outside system which will oldstrongly influence it and changes the scale, the scheme of this cardio-connector system. The sympathetic alters its base time. Following other base rhythm will change the scale, the fundamentals.  The cardio-connector system will hierarchically place itself below this autonomous system in such a way that both the Para-sympathetic and the sympathetic will act at the heart’s level.
 
 
When we talked about the sympathetic we said that it uses acetylcholine as neuronal transmitter.   The heart uses a receptor named M2, or better yet muspharinical 2. As for the sympathetic we have referred to noradrenalin and we found the receptors Beta 1 within the heart. The Para-sympathetic diminished the cardiac properties, it inhibits them and the sympathetic, on the contrary, rises and stimulates them. Now, in spite of the fact that the Para-sympathetic generally influences the vessels, once we refer to vessels we will talk about the sympathetic effects. I do not want to confuse you but that is the way it is. Some other thing I do want to explain to you. If this confuses you even more, just try to forget it buy for me it is very important to explain this concept. The sympathetic will act in a vessel level. Which will be the neuronal transmitter? Noradrenalin. At vessels level the last will have two basic receptors. Beta 2(vessel dilatation) and Alfa 1 (vessel constriction). What does this mean?  Was not the sympathetic the one that provoked the vessel constriction? What are you saying to me right now? That the Para-sympathetic just makes the opposite than the sympathetic? Yes, of course, but they are just simplified schemes. This is the only thing I do want to explain to you. We are watching at a unified system that with the same neuronal transmitter provokes two effects: vessel constriction and dilatation. Why? What will decide which of the opposites will be the effect?  The receptor.  If noradrenalin interacts with Alfa 1 the effect will be constriction and if the receptor happens to be Beta 2 dilatation will take place. The same signal, when interacting with two different receptors will provoke two completely different signals. What is this saying to us? That the receptor chooses the effect and that if I introduce any other substance within the organism which may carry something that the receptor recognizes or provokes its interaction, then the receptor will follow its path towards constriction or dilatation. Anything that might correctly stimulate the receptor will produce an effect. This means that the effect depends upon the receptor, not the neuronal transmitter, the signal. That is the concept of drugs, medicines. How can we introduce substances that the body may have never been in touch with and produce any effect? Simple, we can copy the molecular composition of noradrenalin or any other substance. The last, new to the body,   interacts with receptors. And these just have to follow the previewed plan.