Final answer:
The primary mechanism of pulmonary hypertension due to chronic obstructive pulmonary disease (COPD) is related to the destruction of alveolar walls and loss of elasticity caused by long-term smoking. This leads to hyperinflation and increased resistance in the pulmonary arteries, straining the right ventricle and leading to high blood pressure within the lung vessels.
Step-by-step explanation:
The primary mechanism of the development of pulmonary hypertension (pHTN) due to chronic obstructive pulmonary disease (COPD) involves various pathophysiological changes. COPD is characterized by the destruction of alveolar walls and loss of their elasticity, which leads to a decrease in the surface area for gas exchange and trapping of air within the lungs. This condition is often caused by long-term smoking and exposure to air pollutants. The decrease in alveolar surface area and consequent air trapping result in increased lung volumes at the end of exhalation, also known as hyperinflation.
With the progression of COPD, the chronic obstruction of airflow increases resistance within the pulmonary arteries. This increased resistance puts a strain on the right ventricle of the heart, leading to pulmonary hypertension as the heart works harder to pump blood through the narrow, constricted vessels. The persistent high pressure in the pulmonary arteries eventually causes the remodeling of the vessel walls, which further exacerbates the condition. Treatments for COPD aim at reducing symptoms and improving quality of life as there is no cure except in severe cases where lung transplantation might be considered. Options include supplemental oxygen therapy and inhaled bronchodilators. However, pulmonary hypertension secondary to COPD remains a severe complication that significantly impacts a patient's prognosis.