Unit IV - Circulatory System

Chapter 14

Anatomy and Physiology of the Veins

Aorta and Vena Cava

fig 227a,b. Aorta and Inferior Vena Cava

1. Structure of Veins:

     The veins have thinner walls than their corresponding arteries; and they are much larger in diameter. The appearance of a vein and artery in cross section is contrasted in Figure 227.

     The blood after passing through the capillaries is gathered into venules (small veins). These come together to make larger and larger veins which eventually fuse into two main veins. One, returning blood to the heart from the head and arms, is called the superior vena cava; the other, returning blood to the heart from the lower portions of the body, is called the inferior vena cava. These both enter the right atrium. A smaller vein, the axygos, which also enters the right atrium drains blood from the right side of the chest. Blood from the heart muscle also enters the right atrium via the coronary sinus.

2. Venous Anatomy:

     The veins of the chest are shown in Figure 247. Those of the neck are shown in Figure 248. The veins which drain the head are shown in Figure 249. Those which drain the brain are shown in Figure 250.

     Figure 251 shows the veins of the abdomen, except for those which drain the digestive organs. The arrangement of these is shown in Figure 252. Note that the veins which drain the intestines and spleen all go to the liver, where they break up into smaller vessels. These recombine and fuse with other veins originating in the liver. This type of circulation is called a portal circulation.

     The veins of the arms are shown in Figure 253. Those of the lower extremities are shown in Figure 254.

     The veins of the arms and legs are equipped with valves which control the blood so that it can flow only toward the heart. These valves are not present in the veins of the abdomen, chest, or head. The structure of valves is shown in a longitudinal section of a vein.

     In general the vein from any part returns to the heart along with the artery of that part. There are, however, notable exceptions.

     The veins of the brain drain by way of the jugular bulb. This is near the angle of the jaw and fairly superficial (Figure 250). Contrast this with the arterial delivery (Figure x).

     The veins which drain the heart have a separate course from its arteries. The arteries derive from the root of the aorta. The venous return from the heart (shown in Figure 247) enters the right atrium.

     The most striking difference between the venous and arterial pathway is shown in the blood supply of the liver, bowel and digestive organs. These organs are supplied by way of the superior mesenteric artery, the coeliac axis and the inferior mesenteric artery. (Figure x). The only branch which goes directly to the liver is a small branch of the coeliac axis--the hepatic artery. This supplies the liver with about one third of its blood.

     Practically all the rest of the digestive tract returns its venous blood to the liver (Figure 252). Here it breaks up again (as previously noted, this is called a portal circulation). Eventually the small vessels from the portal circulation fuse with the small vessels from the hepatic artery, and all are returned to the heart by way of the hepatic vein, which enters the inferior vena cava just above the diaphragm.

3. Control of Veins:

     The responses of veins like those of arterioles are controlled by physical, chemical, and nervous factors.

     Veins are extremely sensitive to temperature changes. Like arterioles they dilate when the temperature is high and constrict at low temperatures. This is especially true of the veins of the skin.

     The veins stretch very easily when the pressure of the blood in them is increased. On the other hand, external pressure tends to cause them to collapse and even to contract. These responses are often seen in introducing a needle into a vein. The vein is made to stand out by applying a loose tourniquet around the upper arm. Blood can enter the arm from the artery but cannot leave it. The vein therefore distends. If, now, an attempt is made to introduce a needle into the vein and the vein is touched externally before the needle has entered, the vein often disappears as the result of constriction due to external pressure. When this occurs, it is best to start over with a new vein since the contracted vein may remain contracted for a long time.

     Like the arterioles, the veins are affected by many chemical substances. Some of these are produced locally, some by glands secreting substances into the blood stream at a distance.

     Because any substance which dilates arterioles will increase the flow of blood into the corresponding vein, an arteriolar dilator may tend to be a venous dilator also. This is because the vein is so easily stretched by increasing its blood content. The opposite is true of arteriolar constrictors; they will act to narrow the veins.

     Though it is difficult to separate arteriolar and venous effects, it seems clear that veins are extremely responsive on their own to adrenaline and nor-adrenaline, both of which are strong constrictors in most veins. They respond also pitressin by vasoconstriction. It is highly probable that certain products of tissue activity and tissue injury dilate veins as well as arterioles.

     In spite of their obvious importance in the regulation of the cardiac output, (see Part 4) the nervous factors which control the veins have not been investigated nearly as well as those which regulated the arterioles. The available evidence suggests that arterioles, venules, and veins behave in much the same manner with respect to nervous responses.

     A function of veins which is less certain than those described is in the regulation of blood volume. Most of the blood in the body is in the venous system. Estimates range from 60 to 90 percent. When blood is lost the veins "take up the slack." It is reasonable to assume that while they do so, they also relay information to those parts of the body concerned in the manufacture of new blood which causes these parts to make up the deficit. Many attempts have been made to demonstrate such a function for the veins. Some highly suggestive evidence is available, but the case cannot be considered proved.

4. Venous Regulation of the Cardiac Output:

     The veins, at first sight, appear to have only one function--the return of blood to the heart. Actually there are at least two functions.

     The first and most important function of the veins is, indeed, the return of blood to the heart. However, since the veins have a large capacity for blood--in fact, enough to contain all the blood volume when they are opened--by opening widely they can contain so much blood that very little will return to the heart. In the opposite way, when the veins become narrower they act to increase the return of blood to the heart. By varying the amount of blood which they move toward the heart the veins determine the cardiac output.

     This point, which is often neglected, may be clarified by considering Figure 256. This figure shows a model of a circulating system in which the pump which supplies the power for the circulation has the property that it will expel all the blood that is delivered to it. One part of this system has a relatively fixed capacity-this is the arterial part. The capacity of the veins is variable and so is the capacity of the small vessels. When ever the capacity of the veins for blood is increased less blood will return to the heart and the cardiac output will therefore be reduced. When the capacity of the veins is decreased as a result of contraction of the muscles in their walls, the displaced blood is forced toward the heart through channels which may have been previously closed. The cardiac output increases.

     Note that the changes in cardiac output produced by increased or decreased venous blood capacity are long lasting. The heart increases its output by that amount of extra blood supplied to it by the change in capacity of the veins. The blood when it has left the heart must find a place. Since there is no room for it in the arteries, the capillary bed must accomodate it. It will be recalled that only two billion capillaries of the 100 billion which exist are ordinarily open at any one time.

     Venous constriction thus is associated with an increased cardiac output and the opening of new capillaries. The newly opened capillaries together with the old permit the blood to flow more freely from the arteries to the heart, and the cardiac output, therefore, remains increased.

     The regulation of the cardiac output is only partially accomplished by venous constriction and dilation. The heart itself plays a very important role, as do the vessels between the arteries and veins. Furthermore, the cardiac output can be influenced by factors quite outside the circulatory system.

     It is convenient to describe the factors which influence the return of blood to the heart by dividing them into three forces. The first, the force from behind, describes the left over pressure from the heart which appears in the veins just after the capillaries. The second, the force from the side, is the sum of the forces which act on the vein wall. The third, the force from in front, is the force exerted by the organs of the chest in attracting venous blood.

     The most dramatic illustration of increased force from behind occurs when there is a so-called arteriovenous shunt. This is produced when a wound cuts an artery and vein together and in healing the artery and vein are re-united, so that blood flows without loss of pressure from the artery into the vein.

     The blood which passes into the affected artery is, so to speak, thrown back at the heart by way of the shunt, without having been slowed by the normal resistance. The heart must eject it over and over again, and the cardiac output becomes permanently elevated. In this condition, the work of the heart may be so much increased that it may fail. Location and repair of the shunt may be life saving.

     A more physiological type of increase in the force from behind occurs during pregnancy. The pregnant uterus, in growing, develops new blood vessels. These are something like a shunt in that they offer the blood a new avenue to return to the heart. The pregnant uterus (which needs blood) thus sets up an increased cardiac output (which supplies blood).

     In muscular exercise, as we have seen before, the resistance of the arterioles of the muscles is decreased. This again acts as a shunt. The increased flow of blood to the active muscles is accompanied by an increased force from behind, which by increasing the return flow to the heart increases the cardiac output enough to take care of the increased requirement by the muscles.

     This includes not only the forces exerted by the contraction or relaxation of the muscles of the vein wall, but also the forces exerted on the vein wall by external factors.

     Again, a rare but dramatic example will illustrate this force best. If a man were to stand up or sit up in a space craft during its launch, the blood would tend to accumulate in the lower part of his body. As he was accelerating upwards, the veins, unable to support the increased force exerted by the blood, would balloon out and no blood would return to the heart from the lower part of the body. The cardiac output would quickly become zero.

     Actually, something like this is observed in airplanes making a tight inside turn. The pilot of such a plane may lose consciousness, because, when his cardiac output fails, so does the blood flow to his brain.

     The remedy for this in space flight is to have as little of the venous system below the heart as possible. This is accomplished most easily by having the astronaut lie down during take off.

     More physiologically, the effect of the force from the side is seen after a hemorrhage. The loss of blood tends to diminish the pressure of the venous blood and therefore its return to the heart. The veins respond to this by constriction. This restores the force from the side, and, in fact after a small hemorrhage, the cardiac output remains quite normal.

     In muscular exercise, the contracting muscles squeeze the veins in or near them. This squeezing serves to increase the force from the side and aids in returning blood to the heart and increasing the cardiac output. This action supplements the one discussed previously, in which muscular activity increases cardiac output through increasing the force from behind.

     During breathing, the force from the side is increased in the veins of the abdomen by the downward movement of the diaphragm. The movement of the diaphragm during inspration is such that the abdominal organs are compressed. This compression applies equally to the veins. Blood is thereby "milked" into the chest and forced into the heart. This is obviously a very useful method for the adjustment of the cardiac output to the needs of the body; when increased activity results in increased respiratory activity, the cardiac output is increased automatically.

     During violent activity, adrenaline and nor-adrenaline are secreted into the blood stream. These act on all veins to cause contraciton of their walls. By so doing, they increase the force from the side and the cardiac output. The usefulness of this response is apparent.

     In lesser activity, the sympathetic nervous system is activated. This too has the effect of producing venous constricton.

     There are a number of diseases in which the force from the side is abnormally reduced. Only one will be considered here. When sympathetic nerves are cut or removed (sympathectomy) the vein walls do not contract very well. People who have had this operation are unable to make rapid circulatory adjustments by venous constriction. When, for example, a normal person sits up in bed after sleep, venous constriction supplies the necessary extra force from the side to deal with the increased force of the blood against the vein wall due to gravity. The sympathectomized person does not do this easily; when he sits up in bed, the increased pressure in the abdominal veins causes them to distend, uncompensated by venous constriction, this leads to reduction in cardiac output which may result in fainting or dizziness. Some normal people, with slowly responding sympathetic nervous systems, may feel the same effect (orthostatic hypotension)

     This is a combination of the forces produced by the muscles of respiration and the heart itself. Just as the downward movement of the diaphragm in inspriation produces a pressure in the abdominal organs which milks blood toward the chest, it also produces an area of lowered pressures in the chest. The blood displaced from the abdomen is thus sucked into the chest.

     A very interesting abnormality of this force is seen in normal people who attempt to breathe out while the airway is blocked. The pressure in the chest is raised by this proceedure; it may be raised so much that the veins of the chest will collapse and the cardiac output reduced to almost nothing. The procedure is called the Valsalva manuever. It is often carried out involuntarily in attempting to empty the bladder or the bowels by "bearing down." The performance of the Valsalva maneuver, whether deliberate or involuntary can lead to severe reduction in cardiac output and to loss of consciousness.

     The role of the heart itself in controlling the force from in front, and therefore its own output, was overlooked for many hundreds of years, since William Harvey, who discovered the circulation of the blood, stated that the heart did not suck.

     Actually, during ventricular systole, when the atrioventricular valves are pulled downward while closed, a potential space is created behind them. As long as blood is present, this space will be filled. Thus at the very same time as ventricular ejection occurs there is suction by the heart which, so to speak, pulls just as much as it pushes. Vigorous ejection is associated with vigorous filling; weak ejection results in impaired filling. Thus the heart cannot be considered only the servant of the circulation; to a certain extent it controls its own output by making venous blood available to itself.

     The "sucking" action of the heart may have an adverse effect on the circulation. This is particularly so after blood loss. The heart is usually stimulated to more vigorous action after hemorrhage. It may actually suck so hard on the great veins that it causes their collapse. This is something like what happens when one tries to drink a thick milkshake through a straw. Vigorous suction, instead of increasing the rate at which the milkshake can be sucked often results only in the collapse of the straw.

5. Venous Collaterals:

     It was noted before that arterial collaterals could cause the blood to take roundabout routes to the parts supplied. Sometimes, however, the collateral develops too late; the part has already died.

     Parts of the body with obstructed veins usually find venous collateral with little difficulty. They are forced open more easily than arterial collaterals; they sometimes exist already.

     An example may be seen in the drug user who takes his drug by the venous route. Usually, the conditions under which the drug is taken are not the best. The vein may become infected and develop clots; it eventually closes off. Nevertheless, the blood return from the affected part (usually the arm) is unaffected. The blood simply circulates through deeper veins, which already have a collateral circulation with the areas drained by the superficial ones.

6. Disorders of the Veins:

     A remarkable example of the use of collateral venous circulation is seen in the treatment of varicose veins and hemorrhoids (which are varicose veins around the anus).

     Let us consider first the cause of varicose vein development. In the erect position, the veins of the legs must return blood to the heart against very high pressures (in a six foot man the pressure required to return blood from the foot veins to the heart is 1.3 meters of blood-almost 100 mm Hg). This force is broken up by the existence of valves; even so each segment of vein is exposed to enormous pressures.

     It will be recalled that the veins are thin walled. Pressure distends them easily; when the pressure becomes great enough the valve becomes incompetent. This can occur in all superficial veins of the legs and may be very disfiguring.

     Similarly the veins which drain the rectum and anus are subject to very high pressures and are not even protected by valves. These veins are prevented from ballooning out by the fact that they are surrounded by fairly tough tissues. In the course of time, however, they may, particularly if venous pressure is high, distend and become very painful. These are called hemorrhoids or piles. They may become so distended that they rupture and bleed.

     The treatment of varicose veins and hemorrhoids is surprising. It is only necessary to destroy them. This may be done by a variety of methods; one of the least obnoxious is the injection of a "sclerosing" solution. These solutions produce clotting in the affected veins; and they disappear. The parts which were drained by them are now drained by collaterals.

     One location of varicose veins where they are very difficult to treat and threaten life is the lower part of the esophagus. Usually, this part of the esophagus drains into the liver where it becomes part of the hepatic portal system.

     If this return is impeded in any way, the esophageal veins become dilated. They lack the supporting structures of the veins of the rectum and anus, and when they rupture, the bleeding is not only uncontrolled, but the bleeding site is virtually inaccessible. Rupture of such veins if untreated is almost invariably fatal. The results of surgical treatment are not particularly impressive (In a recent study 60% died within a year). Part of this unfavorable outlook results from the fact that the obstruction is usually a result of cirrhosis of the liver. When the obstruction comes about through other means, the results of surgery are much better.

     Many people think of cirrhosis of the liver as a disease of heavy drinkers; death from rupture of esophageal varicose veins seems to them just punishment for alcoholic excesses. Actually, alcoholic excess and dietary inadequacy together probably cause most of the cases of this disease seen in this country. This is not very comforting to the person who develops cirrhosis of the liver as the result of viral hepatitis, without alcoholic excess. Actually, the alcoholic cirrhotic is probably not very comforted either when he dies of cirrhosis of the liver, although he and his friends may feel that a rough kind of justice has been done.

     Regardless of these moral considerations, it is probable, once cirrhosis has occurred, that abstinence from alcohol is better than drinking it. Surgical correction should always be considered.

     The fact that veins are larger than arteries in cross section means that for an equal volume flow, the linear velocity of flow will be less. In a sense, venous blood is more stagnant than arterial. When clots form in veins, they are more like the clots of shed blood than the platelet accumulations of arteries.

     Sometimes these clots begin in an inflamed area of the vein wall. Such an inflammation is called phlebitis and when associated with a clot, thrombophlebitis. These clots may be quite large, but because they are very adherent to the vein wall at their base they rarely dislodge in one piece; usually, they dissolve slowly.

     Phlebothrombosis ordinarily occurs in a basically healthy vein. The clot may form at the wall, but it is not very adherent. It may reach immense size, and then suddenly dislodge. Passing to the heart and lungs it may produce fatal pulmonary embolism. Blood clots of this type are most often seen in elderly patients who have put at strict bed rest for another ailment. Characteristically such people while recovering from their ailment form a blood clot in the leg vein. They may recover from the original disease only to die when they are restored to health and normal activity.

Continue to Chapter 15.