Page images
PDF
EPUB

the arterial wall expands before the entering blood, the pressure rises, for more blood is entering the arterial system than is leaving it; when, at each cardiac diastole, the arterial wall recoils, the pressure falls, for blood is leaving the arterial system, and none is entering it. But before the fall has had time to become pronounced, while the arterial pressure is still high, the cardiac systole recurs, and the pressure rises again, as at the preceding fluctuation.

The Arterial Pulse. The increased arterial pressure and amplitude at the cardiac systole, followed by diminished pressure and amplitude at the cardiac diastole, constitute the main phenomena of the arterial pulse. They are marked in the manometric trace by those lesser rhythmic fluctuations of the mercury which correspond with the heart-beats. The causes of the arterial pulse have just been indicated in dealing with the causes of the arterial pressure. The pulse, in some of its details, will be studied further for itself in a later chapter. For the sake of simplicity, the respiratory fluctuations of the arterial pressure have not been dealt with in the discussion just concluded. The causes of these important fluctuations are very complex and are treated of under the head of Respiration.

The arterial pressure, then, results from the volume and frequency of the injections of blood made by the heart's contraction; from the friction in the vessels; and from the elasticity of the arterial wall.

The Capillary Pressure and its Causes.-When we studied the movement of the blood in the capillaries, we found the pressure in them to be low and free from rhythmic fluctuations. In both of these qualities the capillary pressure is in sharp contrast with the arterial. What is the reason of the difference? The work of driving the blood through as well as into the capillaries is done during the contraction of the heart's wall by its kinetic energy. During the repose of the heart's wall and the arterial recoil this work is continued by kinetic energy derived, as we have seen, from the preceding cardiac contraction. The work of producing the capillary flow is done in overcoming the resistance of friction. The capillary walls are elastic. The same three factors, then— the power of the heart, the resistance of friction, the elasticity of the wallwhich produce the arterial pressure produce the capillary pressure also. Why is the capillary pressure normally low and pulseless? The answer is not difficult. The friction which must be overcome in order to propel the blood out of the capillaries into the wider venous branches is only a part of the total friction which opposes the admission of the blood to the minuter vessels. The resistance is therefore diminished which the blood has yet to encounter after it has actually entered the capillaries. The force which propels the blood through the capillaries, although amply sufficient, is greatly less than the force which propels it into and through the larger arteries. In both cases alike the force is that of the heart's beat. But, in overcoming the friction which resists the entrance of the blood into the capillaries, a large amount of the kinetic energy derived from the heart has become converted into heat. The power is therefore diminished. As, in producing the high arterial pressure, much power is met by much resistance, and the elastic wall

is, therefore, distended with accumulated blood; so, in producing the low capillary pressure, diminished power is met by diminished resistance, outflow is relatively easy, accumulation is slight, and the elasticity of the delicate wall is but little called upon.

The Extinction of the Arterial Pulse.—But why is the capillary pressure pulseless, as the microscope shows? To explain this, no new factors need discussion, but only the adjustment of the arterial elasticity to the intermittent injections from the heart and to the total friction which opposes the admission of blood to the capillaries. This adjustment is such that the reçoil of the arteries displaces blood into the capillaries during the ventricular diastole at exactly the same rate as that produced by the ventricular contraction during the ventricular systole. Thus, through the elasticity of the arteries, the cardiac pulse undergoes extinction; and this becomes complete at the confines of the capillaries. The respiratory fluctuations become extinguished also, and the movement of the blood in the capillaries exhibits no rhythmic changes. This conversion of an intermittent flow into one not merely continuous but approximately constant affords a constant blood-supply to the tissues, at the same time that the cardiac muscle can have its diastolic repose, and the ventricular cavities the necessary opportunities to receive from the veins the blood which is to be transferred to the arteries.

A simple experiment will illustrate the foregoing. Let a long india-rubber tube be taken, the wall of which is thin and very elastic. Tie into one end of the tube a short bit of glass tubing ending in a fine nozzle, the friction at which will cause great resistance to any outflow through it. Tie into the other end of the rubber tube an ordinary syringe-bulb of india-rubber, with valves. Expel the air, and inject water into the tube from the valved bulb by alternately squeezing the latter and allowing it to expand and be filled from a basin. The rubber tube will swell and pulsate, but if its elasticity have the right relation to the size of the fine glass nozzle and to the amplitude. and frequency of the strokes of the syringe, a continuous and uniform jet will be delivered from the nozzle, while the injections of water will, of course, be intermittent.

The Venous Pressure and its Causes.-The pressure in the peripheral veins is less than in the capillaries and declines as the blood reaches the larger veins. Very close to the chest the pressure is below the pressure of the atmosphere, and may sometimes vary from negative to positive, following the rhythm of the breathing. These respiratory fluctuations will be considered later. The low and declining pressures under which the blood moves through the venules and the larger veins are due to the same causes as those which account for the capillary pressure. It is still the force generated by the heart's contractions, and made uniform by the elastic arteries, which drives the blood into and through the veins back to the very heart itself. As the blood moves through the veins, what resistance it encounters is still that of the friction ahead. But the friction ahead is progressively less; the conversion of kinetic energy into heat is progressively greater. The venous wall possesses elas

ticity, but this is even less called upon than that of the capillaries; and, presently, in the larger veins, the moving blood is found to press no harder from within than the atmosphere from without.

Subsidiary Forces which Assist the Flow in the Veins.-There are certain forces which, occasionally or regularly, assist the heart to return the venous blood into itself. Too much stress is often laid upon these; for it is easy to see by experiment that the heart can maintain the circulation wholly without help. The origins of these subsidiary forces are, first, the contraction of the skeletal muscles in general; second, the continuous traction of the lungs; third, the contraction of the muscles of inspiration.

The Skeletal Muscles and the Venous Valves.-A vein may lie in such relation to a muscle that when the latter contracts the vein is pressed upon, its feeble blood-pressure is overborne, the vein is narrowed, and blood is squeezed out of it. The veins in many parts are rich in valves, competent to prevent regurgitation of the blood while permitting its flow in the physiological direction. The pressure of a contracting muscle, therefore, can only squeeze blood out of a vein toward the heart, never in the reverse direction. Muscular contraction, then, may, and often does, assist in the return of the venous blood with a force not even indirectly derived from the heart. But such assistance, although it may be vigorous and at times important, is transient and irregular. Indeed, were a given muscle to remain long in contraction, the continued squeezing of the vein would be an obstruction to the flow through it.

The Continuous Pull of the Elastic Lungs.-The influence of thoracic aspiration upon the movement of the blood in the veins deserves a fuller discussion. The root of the neck is the region where this influence shows itself most clearly, but it may also be verified in the ascending vena cava of an animal in which the abdomen has been opened. The physiology of respiration shows that not only in inspiration, but also in expiration, the elastic fibres of the lungs are upon the stretch, and are pulling upon the ribs and intercostal spaces, upon the diaphragm, and upon the heart and the great vessels. This dilating force at all times exerted upon the heart by the lungs is of assistance, as we shall see, in the diastolic expansion of its ventricles. In the same way the elastic pull of the lungs acts upon the venæ cave within the chest, and generates within them, as well as within the right auricle, a force of suction. The effects upon the venous flow of this continuous aspiration are best known in the system of the descending vena cava. This suction from within the chest extends to the great veins just without it in the neck. In these, close to the chest, as we have seen, manometric observation reveals a continuous slightly negative pressure. A little farther from the chest, however, but still within the lower portions of the neck, the intravenous pressure is slightly positive. The elastic pull of the lung, therefore, continuously assists in unloading the terminal part of the venous system, and thus differs markedly from the irregular contractions of the skeletal muscles.

The Contraction of the Muscles of Inspiration.-But some skeletal

muscles, those of inspiration, regularly add their rhythmic contractions to the continuous pull of the lungs, to reinforce the latter. Each time that the chest. expands there is an increased tendency for blood to be sucked into it through the veins. At the beginning of each expiration this increase of suction abruptly ceases.

The Respiratory Pulse in the Veins near the Chest, and its Limitation. In quiet breathing the movements of the chest-wall produce no very conspicuous effect. If, however, deep and infrequent breaths be taken, the pressure within the veins close to the chest becomes at each inspiration much more negative than before; and at each inspiration the area of negative pressure may extend to a greater distance from the chest along the veins of the neck, and perhaps of the axilla. As the venous pressure in these parts now falls as the chest rises, and rises as the chest falls, a visible venous pulse presents itself, coinciding, not with the heart-beats, but with the breathing. At each inspiration the veins diminish in size, as their contents are sucked into the chest faster than they are renewed. At each expiration the veins may be seen to swell under the pressure of the blood coming from the periphery. If the movements of the air in the windpipe be mechanically impeded, these changes in the veins reach their highest pitch; for then the muscles of expiration may actually compress the air within the lungs, and produce a positive pressure within the vena cava and its branches, with resistance to the return of venous blood during expiration, shown by the swelling of the veins. These phenomena are suddenly succeeded by suction, and by collapse and disappearance of the veins, as inspiration suddenly recurs. The respiratory venous pulse, when it occurs, diminishes progressively and rapidly as the veins are observed farther and farther from the root of the neck—a fact. which results from the flaccidity of the venous wall. Were the walls of the veins rigid, like glass, the successive inspirations would produce obvious accelerations of the flow throughout the whole venous system, and the contractions of the muscles of inspiration would rank higher than they do among the causes of the circulation. In fact, the walls of the veins are very soft and thin. If, therefore, near the chest, the pressure of the blood within the veins sinks below that of the atmosphere, the place of the blood sucked into the chest is filled only partly by a heightened flow of blood from the periphery, but partly also by the soft venous wall, which promptly sinks under the atmospheric pressure. This is shown by the visible flattening, perhaps disappearance from view, of the vein. This process reduces the visible venous pulse, where it occurs, to a local phenomenon; for, at each inspiration, the promptly resulting shrinkage of all the affected veins together is nearly equivalent to the loss of volume due to the sucking of blood into the chest. Therefore the flow in the more peripheral veins remains but slightly affected, and the pressure within them continues to be positive and without a visible pulse. During expiration the swelling of the veins near the chest, the return of positive pressure within them, may be simply from the return of the ordinary balance of forces after the effects of a deep inspiration have

disappeared. But, if expiration be violent and much impeded, the positive pressure may rise much above the normal. Here again, however, regurgitation will meet with opposition from the venous valves, though the flow from the periphery may be much impeded.

The "Dangerous Region," and the Entrance of Air into a Wounded Vein. Quite close to the chest, then, the normal venous pressure is always slightly negative; and in deep inspiration it may become more so, and this condition may extend farther from the chest along the neck and axilla, throughout a region known to surgeons as "the dangerous region." It is important to understand the reason for this expression. It has already been mentioned that the wounding of a vein in this region may cause intermittent bleeding. It now will easily be understood that such bleeding will occur only when the pressure is positive-that is, during expiration. During deep and difficult breathing, indeed, the venous blood may spring in a jet during expiration instead of merely flowing out, and may wholly cease to flow during inspiration. The cessation is due, of course, to the blood being sucked into the chest past the wound rather than pressed out of it.

It is not, however, the risks of hemorrhage that have earned the name of "dangerous" for the region where intermittent bleeding may occur. The danger referred to is of the entrance of air into the wounded vein and into the heart, an accident which is commonly followed by immediate death, for reasons not here to be discussed. Very close to the chest, where the venous pressure is continuously negative and the veins are so bound to the fascia that they may not collapse, this danger is always present. Throughout the rest of the dangerous region, the entrance of air into a wounded vein will take place only exceptionally. In quiet breathing the venous pressure is continuously positive throughout most of this region; and then a wounded vein will merely bleed. It is only in deep breathing that a venous pulse becomes visible here, and that the venous pressure becomes negative in inspiration. But even in forced breathing it is rare for a wounded vein of the dangerous region to do more than bleed. The cause of this lies in the flaccidity of the venous wall. At each expiration the blood may jet from the wound; but at the following deep inspiration the weight of the atmosphere flattens the vein so promptly that the blood is followed down by the wounded wall and no air enters at the opening. It is only when, during deep breathing, the wounded wall for some reason cannot collapse, that the main part of the "dangerous region" justifies its name. Should the tissues through which the vein runs have been stiffened by disease, or should the wall of the vein adhere to a tumor which a surgeon is lifting as he cuts beneath it, in either case the vein will have become practically a rigid tube. Should it be wounded during a deep inspiration, blood will be sucked past the wound, but the atmospheric pressure will fail to make the wall collapse; air will be drawn into the cut, and blood and air will enter the heart together, probably with deadly effect.

Summary. It appears from what has gone before that the elasticity of the lungs and the contractions of the muscles of inspiration regularly assist in

VOL. I.-7

« PreviousContinue »