Unit IV - Circulatory System
1. Similarities Between Systemic and Pulmonary Circulation:
The discussion of the circulation till now has been concerned with the supply of blood to the organs and tissues of the body. This is sometimes called the greater or systemic circulation.
The lesser, or pulmonary, circulation receives blood from the pulmonary artery, advances it through the lungs and returns it to the left atrium. From here it re-enters the systemic circulation.
Many features of the systemic circulation are duplicated in the pulmonary circulation. The motive force of the pulmonary circulation, like that of the systemic circulation, is gained from a ventricle. In the systemic circulation, the left ventricle is the prime source of power; in the pulmonary circulation, it is the right ventricle. The pulmonary artery, like the aorta, is guarded by semilunar valves; the right atrium is separated from the right ventricle by the same type of valve as exists between the left atrium and left ventricle.
The pulmonary artery subdivides into branches, which finally end in the pulmonary arterioles and capillaries. The capillary blood is collected by venules which combine to form veins.
2. Differences Between Systemic and Pulmonary Circulation:
The chief points of difference are concerned with the special function of the pulmonary circulation. This function is to bring the blood into effective contact with the respiratory structures of the lung, and thus to make possible gas exchanges with the outside air. These exchanges are primarily those of oxygen, which is taken into the blood, and carbon dioxide, which is lost from it.
In the systemic circulation, through arteriolar regulation, blood is usually directed toward active tissue and away from inactive ones. In the pulmonary circulation, in normal circumstances, all the arterioles are open at once. Since the passageways for the blood in the lungs are all wide open, the resistance to its flow is much less than in the systemic circulation. The pulmonary arterial pressure is, consequently, much lower than the systemic arterial pressure. A typical pulmonary arterial pressure is 30 / 10 mm Hg, about one-fifth of systemic arterial pressure.
The lower pressure against which the right ventricle works means that its power requirement is much less than that of the left. Correspondingly, its muscle is much thinner than the muscle of the left ventricle, although the chamber is of the same size. The special problems of the pulmonary circulation are these:
The forces concerned with water transfer in the pulmonary capillaries are of the same type as those of the systemic circulation. If everything were the same, this would mean that fluid left the pulmonary capillaries at their arteriolar end and was returned to them at the venular end. If this were so, the lung would be considerably wetter than it is, and the exchange of gases across the layer of fluid outside the capillary would be slowed.
This problem does not ordinarily exist in the healthy person, precisely because the pulmonary arterial pressure is so low. The hydrostatic pressure of pulmonary capillaries is about 10 mm Hg. The value is less than pulmonary arterial pressure since the blood has passed through the resistance of the pulmonary arterioles.
The balance of forces in the pulmonary capillaries is thus: outward pressure 5 - 10 rnm of Hg colloid osmotic pressure (directed inward) 25 mm Hg. The blood in the pulmonary capillaries therefore has no tendency at all to lose water to the outside, and the interior of the lung is, in the normal person, quite dry.There are many disorders in which this is not so. For example, when there is obstruction to the flow of blood from the pulmonary veins, the hydrostatic pressure in the pulmonary capillaries may increase considerably; when this happens, there is a leaking of fluid through the pulmonary capillaries into the lung tissue and the respiratory passages. This leads to defective gas exchange. Oxygen does not pass as easily through the wet tissue as through air, and the blood is insufficiently oxygenated. This is called pulmonary edema.
A common cause of this condition is a weakness of the left ventricle, that is to say chronic congestive left heart failure. The left ventricle becomes incapable of handling the blood delivered to it by the right heart, despite increases in its rate and modifications of its chemical environment. Failing to expel all the blood which came to it, the ventricle gets bigger and, so long as it does not pass its "best volume" on the Starling curve, somewhat stronger.
The price paid for this is that in order for the ventricle to distend, a higher pressure must be developed in it during diastole. This means that the entire lesser circulation, from the right ventricle to the pulmonary veins, must operate at a higher pressure than is normal. This includes the pulmonary capillaries. Thus, a weak left ventricle often results in the development of pulmonary edema.
Another condition in which pulmonary edema develops as a result of increased pressure is seen in stenosis of the mitral valves. In this condition, blood does not flow easily from the left atrium into the left ventricle, because of the narrowed opening between the valve leaflets. Left atrial pressure rises, and with it the pulmonary venous pressure and the pulmonary capillary pressure. Pulmonary edema may result.
In many ways mitral stenosis produces the symptoms of left heart failure (See Chapter 16). It is very important to distinguish between them. Mitral stenosis is best treated by surgical repair of the affected valve. Left heart failure may be treated in a variety of ways, depending on its cause, but these treatments will not usually benefit mitral stenosis.
Pulmonary edema may also develop in inflammatory diseases of the lung. In lobar pneumonia, the pulmonary capillaries become permeable to blood proteins. The low hydrostatic pressure in the pulmonary capillaries is not countered by an adequate osmotic pressure. The affected part of the lung quickly fills up with fluid and becomes useless in oxygen exchange.
Some war gases may act in the same way. Chlorine gas, phosgene, and some others, act to increase the permeability of the lung capillaries to protein, which results in the development of the same picture.
The second problem of the pulmonary circulation is concerned with the adjustment of pulmonary resistance to cardiac output. Why this is important can be seen by considering what happens to the circulation in exercise.
Muscular exercise may increase the cardiac output four times above normal. The left heart must do four times as much work as normal to keep up with circulatory demand. If this blood were being passed through a normal resistance, the pressure would also be four times as great as normal, and the work of the heart would be increased four times as much again--a total of sixteen times over resting level.
In the systemic circulation, however, the very same factors that increase the return of blood to the heart also operate to reduce the peripheral resistance. Actually, in exercise, the mean blood pressure is not appreciably elevated.
This also applies to the pulmonary circulation. The right heart, receiving the blood from the exercising body, must put it through the pulmonary circulation. If the right heart is not to fail from overload, the pulmonary resistance must fall as much as the cardiac output rises.
In fact, it does. During exercise, there is very little change in pulmonary arterial pressure. Evidently, there is a dilation of the pulmonary arterioles in response to exercise, so that the lungs can accept the extra volume flow of blood without imposing a strain on the right heart.
Very surprisingly, the factors which bring about this effect are not known. Physical, chemical, and nervous effects have all been suspected, but the actual cause of the vasodilation of the pulmonary arterioles in exercise has not been found.
The third special problem of the pulmonary circulation is very intimately related to the second: not all parts of the lung are equally effective at exchanging gases with the outside. If the circulation to the lungs were distributed so that small amounts of blood passed through the lung areas which were best ventilated and large amounts through the poorest ventilated areas of the lungs, the exchange of gases in the lung would be very poor. The best exchange would be accomplished if the amount of blood which reached any part of the lung were always in proportion to the ventilation of the lung. This is probably what happens in healthy persons. The ventilation-perfusion ratio is said to be optimal.
The manner in which this adjustment is made is completely unknown, but it is usually very effective. For example, if a part of a lung collapses and becomes useless as a respiratory organ, it will also stop accepting blood. The oxygenation of the blood is, therefore, not impaired at all. This is not true in lobar pneumonia, where useless lung still receives blood.
An interesting and important condition in which the mechanism which controls blood distribution in the lung goes wrong occurs in babies who have respiratory difficulties at birth. In these babies, the blood is shunted away from inactive areas of the lung, but, unfortunately, this is the whole lung. Thus the mechanism which normally operates to direct the blood away from those areas where the lung is not functioning well, now operates to keep blood away from almost all of the lung. Obviously, this situation is not compatible with life, and in fact, with the best medical treatment the mortality rate in these babies is over 25 percent. It might be possible to do better if we understood how the lung arterioles were adjusted to the respiratory activity of the lung. This important area of research is going on in many places.
Continue to Chapter 16.