Pneumonia II: Pathophysiology

Pneumonia follows a sequence of pathophysiological changes.

The process begins when pathogens enter the respiratory tract through various means, such as regular inhalation, aspiration of oropharyngeal flora, or bloodborne organisms trapped in the pulmonary capillary bed. Once these pathogens reach the alveoli, they invade the cells and multiply, triggering an immune response that leads to inflammation and exudate formation.

This accumulation of fluid and pus in the alveoli disrupts the normal gas exchange process, reducing the quantity of oxygen that reaches the bloodstream and causing symptoms like shortness of breath and hypoxia.

The white blood cells involved in this inflammatory process further increase capillary permeability, allowing more fluid to leak into the alveoli and leading to hypoventilation.

Common manifestations of pneumonia include a cough, which may be productive or not, fever, shaking chills, dyspnea, tachypnea, and pleuritic chest pain.

The sputum may be green, yellow, or rust-colored. Severe pneumonia may present with flushed cheeks and central cyanosis, while other nonspecific signs include headache, diaphoresis, anorexia, fatigue, and myalgia.