Obstructive airway diseases:
Obstructive airway diseases are characterized by diffuse obstruction of airflow within the lungs.
The most common obstructive airway diseases are emphysema, chronic bronchitis, and asthma. Collectively these are referred to as COPD
Obstructive airway diseases occur when positive pressure exerted during exhalation causes the small airways to pinch shut, trapping air in the alveoli. For this reason, these illnesses are often referred to as “air trapping” diseases.
These patients adapt their breathing to push gas out slowly at a lower pressure in order to reduce air trapping, and develop auto-PEEP. This manifests through pursed lip breathing, an increased inspiration/expiration ratio (normal would be 1:2, but they may be as high as 1:8), abdominal muscle use, and the presence of JVD (occurs due to increased intrathoracic pressure exerted on the vena cava, causing backflow into the jugular veins).
Emphysema:
Emphysema occurs when there is a breakdown of the connective tissue structures of the terminal airways, leading to collapse of the alveolar septa, and the merging of alveoli into blebs or bullae, which remain hyperinflated. Some individuals have a congenital enzyme deficiency of alpha-1 anti-trypsin, which allows for this breakdown to occur, but the most common cause worldwide is cigarette smoking.
The result is hyperinflation of the alveoli, and difficulty moving air out of the lungs. This means hypoventilation and the development of hypercarbia. These patients adapt to an abnormally high PaCO2, and often compensate by producing a higher than normal erythrocyte count. They frequently rely on pursed lip breathing in order to maintain oxygenation. For this reason they are called “pink puffers”. The energy expended to maintain adequate respiratory status often leads to muscle wasting and thin stature.
Chronic bronchitis:
CB occurs as a result of the development of an abnormal number of goblet cells in the lungs. These cells produce excessive mucous that obstructs the terminal airways, leading to air trapping, and frequent infections.
Like their emphysemic counterparts, these individuals are unable to move trapped air out of the lungs efficiently.
Due to hypoxia, many of these patients develop peripheral cyanosis, and a significantly decreased exercise capacity. The result in this case is that may of these patients are sedentary, overweight, and have a chronic productive cough. Hence the term “blue bloater”
Heart failure in the progression of COPD:
Damage to the pulmonary vasculature is a natural occurrence in the structural remodelling that occurs during COPD. The result is impaired pulmonary circulation, increased resistance, and an increase in the afterload that the right ventricle has to pump against. The right ventricle has a lower percentage of muscle tissue than the left and relies primarily on preload (Starling's Law) to overcome pulmonary pressures during the cardiac cycle. In COPD, the increased afterload causes dilation and hypertrophy in the right ventricle, and ultimately right sided heart failure. This manifests with backflow of blood into systemic circulation, and associated symptoms of pedal edema, JVD, and in severe cases ascites and liver distension. It also causes the septal wall between the left and right ventricles to bulge into the left ventricle. This diminishes the volume of blood that can fill the left side of the heart during diastole; creating left heart failure with a preseved ejection fraction. This will not likely present initially as typical left heart failure, due to the preservation of ejection fraction, however the left ventricle will begin to fail over time due to the tachycardia required to maintain MAP. Eventually the left ventricle itself will enter heart failure and pulmonary edema is a natural result.
This is why many COPD patients have comorbid CHF. One disease naturally leads to the next.
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