Arteriosclerosis and Hypertension, with Chapters on Blood Pressure / 3rd Edition.

by Louis M. Warfield

Fig. 10.—Cross-section of a small artery in the mesentery. Note that the vessel appears capable of being much widened. The internal elastic lamina is thrown into folds somewhat resembling the convolutions of the brain. Note also that the middle coat of the artery is composed almost entirely of muscle. The enormous number of such vessels in the mesentery and intestines explains the ability of the splanchnic area to accommodate the greater part of the blood in the body. Universal constriction of these vessels would naturally render the intestines anemic. The vasomotor control of these vessels plays an important rôle in the distribution of the blood. Small arteries in the skin and in other organs, possibly the brain, have a similar function. (Microphotograph, highly magnified.)

It is conceivable that in one section of the body the vessels may be markedly contracted, but if there is dilatation in some other part there will be no increased work on the part of the heart, and theoretically, there should be no rise of blood pressure. The vascular system, however, while likened to a system of rubber tubes, must be regarded as a very live system, every subsystem having the property of separate control.

For blood tension to be raised all over the body, conditions must favor the generalized contraction of a large area of arterioles. Some authors consider that the so-called viscosity of the blood also is a factor in the causation of increased tension. The usual cause for the high tension is probably the presence in the blood of some poisonous substance.

It is held by some authors that the great splanchnic area is capable of holding all the blood in the body and in respect of its liability to arteriosclerosis, it is second only to the aorta and coronary arteries. The enormous area of the skin vessels could probably contain most of the blood. The tone of the vasoconstrictor center controls the distribution of blood throughout the body. The fact that the vessels in the splanchnic area are frequently attacked by sclerotic changes means, as a rule, increase of work for the heart.[1] The resistance offered to the passage of the blood must be great and signifies that, for blood to travel at the same rate that it did before the resistance set in, more power must be expended in its propulsion. In other words, the heart must gradually become accustomed to the changed conditions, and, as a result of increased work, the muscle hypertrophies. (See Fig. 11.)

Fig. 11.—Enormous hypertrophy of left ventricle probably due to prolonged increased peripheral resistance. Note that the whole anterior surface of the heart is occupied by the left ventricle. The right ventricle does not appear to be much affected. × ⅔.

In diffuse arteriosclerosis accompanied by chronic nephritis the heart is always hypertrophied. This is a result, not a cause of the condition. In the pure type, there is hypertrophy only of the left ventricle without dilatation of the chamber. The muscle fibers are increased in number and in size, and there are frequently areas of fibrous myocarditis due to necrosis caused by insufficient nutrition of parts of the muscle. In these cases the coronary arteries share in the generalized arteriosclerotic process. The openings of the arteries behind the semilunar valves may be very small. There is often thickening and puckering of the aortic valves and of the anterior leaflet of the mitral valve leading, at times, to actual insufficiency of the orifice. Later, when the heart begins to weaken, there is dilatation of the chambers and loud murmurs result, caused by the inability of the nondistensible valves to close the dilated orifices. Until the compensation is established, it is impossible to say whether or not true insufficiency is present.

In senile arteriosclerosis there is the physiologic atrophy of the media to be reckoned with. This change has already been referred to. When such degeneration has taken place, the normal blood pressure may be sufficient to cause stretching of the already weakened media with or without hypertrophy of the intima. The arteries may be so lined with deposits of calcareous matter that they appear as pipe stems. More frequently there are rings of calcified material placed closely together or irregular beading, giving to the palpating finger the impression of feeling a string of very fine beads. The arteries are often tortuous, hard, and are absolutely nondistensible. At times no pulse wave can be felt.

The larger arteries such as the brachials and femorals are most affected. The walls become thinned and show cracks, and areas apparently, but not actually denuded of intima. Yellowish-white, irregular, raised plaques are scattered here and there. Interspersed among these areas are irregularly shaped clean-cut ulcers having as a rule a smooth base, and frequently on the base is a thin plate of calcified matter. The color of these denuded areas is usually brownish red or reddish brown. White thrombi may be deposited on these areas. The danger of an embolus plugging one of the smaller arteries is great and probably happens more often than we think. The collateral circulation is able to supply the thrombosed area. Should the thrombus be on the carotid arteries, hemiplegia may result from cerebral embolism. On microscopic examination of the arteries there is seen extreme degeneration of all the coats, the degeneration of the media leading almost to an obliteration of that coat. On seeing such arteries as these one wonders how the circulation could have been maintained and the organs nourished. Senile atrophy of the internal organs naturally goes hand in hand with such arterial changes.