The lungs entirely fill the pleural sacs when completely distended, but only partly so in quiet, ordinary respiration. They are encased in a bony cage that is open below, on account of which, when the lungs distend, they expand mostly downward. To a less extent they expand, in forced respiration, both laterally and anteroposteriorly, due to the elevation of the ribs owing to the traction of the muscles upon them. Ordinary breathing is performed mainly by the diaphragm. It acts like the piston of a cylinder and as it descends the air is drawn into the trachea and lungs. As the diaphragm falls a negative pressure is produced within the chest and were it not for its bony framework, it would collapse. The framework is sufficiently strong to retain its shape in spite of this pressure if the breathing is normal and the chest-walls are healthy. When, however, obstruction of the air-passages is present, perhaps from enlarged pharyngeal or faucial tonsils or nasal hypertrophies, then the deformities known as funnel-breast, pigeon-breast, etc., already described, arise. They are also produced if there is no obstruction to the breathing but only a weakness in the bony thorax, as occurs in rickets.

Fig. 215.   Posterior surface relations of the lungs and pleurae.

Fig. 215. - Posterior surface relations of the lungs and pleurae.

Two of the most common of the diseases of the lungs produce changes in the shape of the thorax; they are emphysema and phthisis. Pneumonia, though a frequent enough disease, does not produce any changes, as it is too short in its duration.

In emphysema the lungs are in a state of hyperdistention, hence they fill the chest to its greatest capacity and tend to make the soft parts bulge between the ribs. In phthisis the lungs are contracted, hence the intrathoracic pressure becomes a negative one and the soft parts sink in between their bony support. In emphysema the anteroposterior diameter increases and the chest assumes the barrel-form already described. In phthisis it becomes lessened in its anteroposterior diameter and we have the flat chest. Enlargement of the chest posteriorly is impossible on account of the support of the ribs, vertebrae, and strong back muscles. Enlargement downward is allowed by a descent of the diaphragm; hence the fulness of the abdomen in those affected with emphysema and conversely the flatness of the abdomen in those having phthisis. In the region of the apices the thorax is closed by the deep fascia, which spreads from the trachea, oesophagus, muscles, and great vessels and blends with the pleura to be attached to the first rib. In the normal condition this is level with the plane of the first rib and rises little if at all above it. Even in disease it is not materially altered. This is certainly so in phthisis and probably so in emphysema. The apparent fulness of the supraclavicular fossae and intercostal spaces in emphysema and the increased depth of these hollows in phthisis are not due so much to a bulging or to a retraction of the lungs at these points as to the atrophy of the fatty and muscular tissue in phthisis and to the muscular tension in emphysema.

In coughing, the apex of the lung does not jump up into the neck above the clavicle as it appears to do, but remains nearly or quite below the plane of the top of the first rib. The appearance of bulging is caused by the movements of the trachea in the median line and the muscles laterally. This is noticeable particularly in the case of the platysma and omohyoid muscles. In quiet breathing the posterior belly of the omohyoid lies about level with the clavicle, but in coughing it rises 1 or 2 cm. above it. The intercostal membranes and muscles are kept tense by the constant elevation of the ribs due to the muscular tension.

Fig. 216.   Upper end of the thorax, at the level of the first rib.

Fig. 216. - Upper end of the thorax, at the level of the first rib.