Some science behind the scenes
In pulmonary emphysema the lungs are in a state of over-distention, with enlargement and fusion of air sacs and reduction in the number of alveoli due to atrophy of inter-alveolar septa.
This results in a reduction in the total respiratory surface. There is also reduction in pulmonary elastic tissue. The lungs, when removed from the thorax, do not collapse normally, but remain in an over-distended state. In addition, there is thickening of the alveolar and capillary walls and a general increase in interstitial tissue.
Capillaries may become occluded.
As a result of dorsal kyphosis and a more horizontal position of the ribs, the antero-posterior diameter of the bony thorax increases, producing a barrel-shape chest. The position of the chest eventually becomes one of almost full inspiration. The level of the diaphragm is much lower than normal and its excursion may be limited. Indeed, it may become fixed and not move at all or, worse still, it may exhibit paradoxical movement. Respiration therefore becomes mainly costal.
As a result of these changes, expiration no longer remains a passive movement, but requires forcible contractions of the expiratory muscles. The residual air is greatly increased and may be two or three times normal. The tidal air is normal or slightly reduced, but the vital capacity is lowered by as much as 20 to 60 per cent. When the patient is asked to inspire deeply he is unable to expel all the air during the next expiration, even though expiration is forced. A series of expirations must occur before the chest returns to its original size. Visual proof of this fact is provided when a patient, following maximal inspiratory effort, is unable to blow out a candle. The total lung volume remains normal or may be increased.
The primary biochemical changes associated with severe pulmonary emphysema are essentially those of carbon dioxide retention and anoxemia. These abnormalities are the direct result of impaired gaseous exchange.