In this condition the air vesicles are over-distended, and, by partial atrophy of their walls, to some extent coalesced, but without any actual tearing of them.

Causation Of Emphysema

There have been differences of opinion as to the exact manner in which the over-distension is brought about. On the one hand, Gairdner asserted that it was produced during inspiration, while Jenner held that it was due to the expiratory force. Probably each of these has its influence, and the cases may be divided according as they are due to repeated and severe expiratory efforts as in coughing (Substantial emphysema), or to inspiratory distension, acting especially on one part in consequence of another part being uninflated (Complementary or Vicarious emphysema). In the former case we have a more generalized and in the latter a more localized emphysema.

Substantial or Substantive emphysema is due to over-distension during expiration. When the glottis is closed, and Expiration violently performed, the air in the vesicles will be at an increased pressure. The expiratory effort is produced by the muscles causing the movable walls of the chest to be pressed against the lung. The contraction of the abdominal muscles presses the diaphragm upwards, while the ribs are depressed. The lung is thus compressed, but at the same time it is supported by the structures which compress it, and the same force that increases the pressure helps the lung tissue to resist it by increasing the support. When the glottis is closed the whole lung may be regarded as one cavity, and the pressure will be universally diffused. It may be expected, therefore, that if any part of the lung be insufficiently supported the distensile force will tell especially there. The question therefore arises, Are there any parts where the lung is not fully supported by the chest walls 1 If a deep breath be taken, the glottis closed, and the act of expiration vigorously performed for a few seconds, we find in our own feelings indications that the lungs are over-distended, mainly in the anterior parts and the parts above the clavicles. We can easily understand how this should be. The anterior part of the chest, by reason of the flexibility of the costal cartilages, is more movable than the rest of it, and the anterior edges of the lungs, as we can see in an animal whose chest is laid open while artificial respiration is carried on, have very free play. Then, above the clavicle the lung is obviously less supported than where the chest has bony walls. We shall see afterwards that these, with one or two other parts, are those in which emphysema, when due to frequent expiratory efforts, occurs most typically.

It will be obvious that, if the lung tissue has lost in elasticity, permanent dilatation of the air vesicles will occur more easily, and will readily extend to parts more fully supported than those mentioned. In Senile Emphysema, to be afterwards referred to, there is a loss of elasticity from the atrophy of old age. But there seems to be in some cases a general loss of elasticity, and it appears as if such a condition were hereditary to some extent. It is true that frequent overdistension will cause atrophy of the elastic tissue of itself, but it is quite apparent that in many individuals there is, to begin with, less elastic tissue, or it is less resistant, andso we have a predisposition to emphysema, sometimes inherited. A similar loss of elasticity may be induced by disease, as in a case by Hertz in which a cornet player developed a marked emphysema after an attack of pneumonia.

Emphysema is liable to occur when frequent and violent expiratory efforts are made with closed glottis. Coughing implies such efforts, and it is chiefly in diseases where coughing is a prominent feature that we are to look for emphysema from this cause. It is met with pre-eminently in bronchitis. It also occurs in whooping-cough, occasionally in croup, and even in the violent expiratory efforts of parturition. As chronic bronchitis is specially a disease of more advanced life, we may expect that a preliminary atrophy of the lung tissue, implying a loss of elastic tissue, plays an important part in the production of emphysema in a large number of cases.

Complementary or Vicarious emphysema arises in consequence of over-distension during inspiration. If a part of the lung does not distend fully in inspiration, there must either be a falling-in of the chest to a corresponding extent, or else an over-distension of another part of the lung in order to fill up the space. To what extent one or other or both of these will occur is determined by circumstances, chiefly by the situation of the insufficiently distended part and the time occupied in the occurrence of the lesion.

If a portion of the lung is collapsed, the neighbouring part often undergoes emphysematous distension. It occurs thus in bronchitis, and the wedges of collapse, already referred to, are often fringed with emphysema. We see it also around cicatrices in phthisis, or along with bronchiectasis in fibroid phthisis. Emphysema occurs sometimes to a remarkable extent in connection with general adhesions of the lung, and the emphysema is often very marked at the anterior parts. In this case the adhesions prevent the forward movement and expansion of the lung during inspiration, and there is thus an over distension in this direction. The opposite lung may project so as to partly fill the space, and its edge may be also emphysematous.