Chronic Obstructive Pulmonary Disease (COPD)

Emphysema is the most common COPD and it is frequently classified with chronic bronchitis because patients with one disease commonly have the other. Emphysema is generally caused by many separate injuries that occur over a long time. Smoking is the most common cause of emphysema but it can also be caused by a genetic condition characterized by a deficiency in alpha1-antitrypsin.
Alpha1-antitrypsin is a plasma protein produced by the liver that inhibits the action of proteolytic enzymes such as trypsin. The alpha1-antitrypsin deficiency will also lead to a deficiency in the protease of elastase and collagenase. The end result is the destruction of lung tissue.

Yeah for the Alveoli
Alveoli/acinus are the structures involved with pulmonary gas exchange. The alveoli have a large and extensive capillary network. Gas exchange occurs as the blood and gas meet divided by the semi-permeable alveoli membrane allowing carbon dioxide and oxygen exchange. The principle behind COPDs is that oxygen and carbon dioxide exchange is impaired resulting in hypoxemia as well as hypercapnia.

Pathophysiology - Emphysema
Emphysema is characterized by alveolar destruction. As the elastin and fiber network of the alveoli are broken down the alveoli enlarge and many of the alveoli walls are destroyed. This results in the formation of larger than normal air pools which greatly reduces surface area, thus decreasing the area available for gas exchange.
1. Inflammation of the bronchial mucosa
2. Excessive mucous production
3. Loss of elastic recoil of the airways
4. Collapse of bronchioles and redistribution of air to the functional alveoli

Complicating matters…
The alveolar walls break down reducing the pulmonary capillary bed. Pulmonary blood flow is increased and the right ventricle is forced to maintain a higher blood pressure in the pulmonary artery (as the blood leaving the heart from the right ventricle is deoxygenated blood going to the lungs via the pulmonary artery). A serious complication results from the high demands placed on the right ventricle: right sided heart failure or cor pulmonale.
Although sputum in emphysema is scant, as this disease often occurs simultaneously with chronic bronchitis people with emphysema may have excessive secretions. The problem with secretions is that individuals with emphysema are often unable to generate a cough forceful enough to expel the secretions and infection results.

Clinical Manifestations
Typically patients with emphysema will have a very distinct “barrel chest.” This is due to the problem with the lungs being in constant state of hyperexpansion. The normal negative pressure required for inspiration and the positive pressure required for expiration is lost as the lungs are in a constant state of inflation. Therefore, expiration becomes an active task, increasing the work of breathing. The “barrel chest” is directly related to the ribs as they become fixed in the inspiratory position combined with the loss of elastic recoil of the lungs. Dorsal kyphosis, prominent anterior chest and elevated ribs will contribute to this appearance.
As the work of breathing is increased dramatically, simple tasks become strenuous and require significant amounts of energy. Increased energy and oxygen demands combined with the decreased surface area available for gas exchange leads to decreased activity tolerance.
Hyperventilation and adequate tissue perfusion (in early stages emphysema) causes the “pink puffer” appearance also characteristic of emphysema patients.
The chronic hypoxemia can cause release of erythropoietin resulting in polycythemia. The polycythemia will increase blood viscosity which further impedes tissue oxygenation. Increased blood viscosity is not good, as it causes pooling and stagnation which have their own side effects.

Common treatments- Caution
Obviously patients with decreased oxygen saturation will require some form of oxygen (generally via nasal prongs at 2L/min). Oxygen therapy in any patient with COPD can be very dangerous. People who are in constant state of hypercapnia (PaCO2 >45mmHG) will develop a tolerance to the chronic increase in carbon dioxide concentrations. Under normal circumstances the body’s respiratory center (the medulla oblongata) is stimulated by increased carbon dioxide concentrations rather than low oxygen saturation. The body will adapt to the chronically high carbon dioxide concentrations by developing the hypoxic drive where the stimulation to breathe is by low oxygen concentrations rather than high carbon dioxide concentrations. This is the rationale behind never increasing a patient’s oxygen flow to greater than 3L/min unless it has been predetermined that doing so is safe. Death has resulted from respiratory depression. Normally orders will come up to maintain the oxygen saturation at >92% via 2-3L/min NP.