Emphysema
aEmphysema
Emphysema is a long-term lung disease that results in the destruction of the alveolar walls. Many individuals have both bronchitis, which involves a long term couch with mucus, and emphysema. This condition is often referred to Chronic Obstructive Pulmonary Disease or COPD. People with this disease do not get enough oxygen and suffer buildup of carbon dioxide in their blood. In normal breathing, air is drawn in through the bronchi and into the alveoli, which are tiny sacs surrounded by capillaries. Alveoli absorb oxygen and then transfer it into the blood. When toxins such as cigarette smoke, are breathed into the lungs, the harmful particles become trapped in the alveoli, causing localized inflammatory response. Chemicals released during the inflammatory response can eventually cause the alveolar septum to disintegrate. This condition, known as septal rupture, leads to significant deformations of the lung architecture that have important functional consequences. The key mechanical event consequent to septal rupture is that the resulting cavity is larger than the sum of the two alveolar spaces, because of the lacking mechanical support of the broken septa the lung elastic recoil further enlarges this new space, necessarily at the expenses of the surrounding healthy parenchyma. As an immediate consequence of septal rupture, the elastic lung recoil resets healthy parenchyma expansion at a lower level, in proportion to the amount of septal disruption. The large cavities left by the septal rupture are known as bullae. These deformations result in a large decrease of alveoli surface area used for gas exchange, as well as decreased ventilation of the surrounding healthy parenchyma. This results in a decreased Transfer Factor of the Lung for Carbon Monoxide or TLCO. To accommodate the decreased surface area, thoracic cage expansion and diaphragm contraction take place. Expiration, which depends on lung elastic recoil, increasingly depends on the thoracic
Emphysema is a long-term lung disease that results in the destruction of the alveolar walls. Many individuals have both bronchitis, which involves a long term couch with mucus, and emphysema. This condition is often referred to Chronic Obstructive Pulmonary Disease or COPD. People with this disease do not get enough oxygen and suffer buildup of carbon dioxide in their blood. In normal breathing, air is drawn in through the bronchi and into the alveoli, which are tiny sacs surrounded by capillaries. Alveoli absorb oxygen and then transfer it into the blood. When toxins such as cigarette smoke, are breathed into the lungs, the harmful particles become trapped in the alveoli, causing localized inflammatory response. Chemicals released during the inflammatory response can eventually cause the alveolar septum to disintegrate. This condition, known as septal rupture, leads to significant deformations of the lung architecture that have important functional consequences. The key mechanical event consequent to septal rupture is that the resulting cavity is larger than the sum of the two alveolar spaces, because of the lacking mechanical support of the broken septa the lung elastic recoil further enlarges this new space, necessarily at the expenses of the surrounding healthy parenchyma. As an immediate consequence of septal rupture, the elastic lung recoil resets healthy parenchyma expansion at a lower level, in proportion to the amount of septal disruption. The large cavities left by the septal rupture are known as bullae. These deformations result in a large decrease of alveoli surface area used for gas exchange, as well as decreased ventilation of the surrounding healthy parenchyma. This results in a decreased Transfer Factor of the Lung for Carbon Monoxide or TLCO. To accommodate the decreased surface area, thoracic cage expansion and diaphragm contraction take place. Expiration, which depends on lung elastic recoil, increasingly depends on the thoracic