What is the mechanism by which pneumonia impairs gas exchange?

From the Guidelines

Pneumonia impairs gas exchange through inflammation and fluid accumulation in the alveoli, creating a physical barrier between the air in the alveoli and the surrounding capillaries, and altering blood flow through hypoxic pulmonary vasoconstriction, as described in the BTS guideline for oxygen use in adults in healthcare and emergency settings 1. The mechanism of impaired gas exchange in pneumonia involves several key factors, including:

• Inflammation and fluid accumulation in the alveoli, which creates a physical barrier between the air in the alveoli and the surrounding capillaries, preventing oxygen from efficiently crossing into the bloodstream and carbon dioxide from being removed.
• The inflammatory process causes the alveolar walls to thicken, further increasing the diffusion distance for gases.
• Blood flow may be redirected away from poorly ventilated areas of the lung through a process called hypoxic pulmonary vasoconstriction, creating ventilation-perfusion mismatches, as discussed in the BTS guideline 1.
• As the infection progresses, some alveoli may collapse completely (atelectasis), reducing the total surface area available for gas exchange. The combined effects of increased diffusion distance, fluid barriers, and reduced functional lung tissue lead to hypoxemia (low blood oxygen) and potentially hypercapnia (elevated carbon dioxide), manifesting as shortness of breath, increased respiratory rate, and in severe cases, respiratory failure. It is essential to note that the BTS guideline 1 provides the most recent and highest quality evidence on oxygen physiology and the mechanisms of impaired gas exchange in pneumonia, and its recommendations should be prioritized in clinical practice.

From the Research

Mechanism of Impaired Gas Exchange in Pneumonia

The mechanism by which pneumonia impairs gas exchange is complex and involves several factors. Some of the key factors include:

• Inflammatory exudate filling alveoli, causing a volume loss at functional residual capacity (FRC) and reducing total lung compliance 2
• Reduction in surfactant activity, further increasing the work of breathing 2
• Persistence of pulmonary artery blood flow to consolidated lung, resulting in an intrapulmonary shunt 2
• Intrapulmonary oxygen consumption by the lung during the acute phase and ventilation-perfusion mismatch later 2
• Relative failure of the hypoxic pulmonary vasoconstriction (HPV) mechanism during acute pneumonia, caused by endogenous vasodilator prostaglandins associated with the inflammatory process 2

Ventilation-Perfusion Mismatch

Ventilation-perfusion mismatch is a key factor in impaired gas exchange in pneumonia. This mismatch can result in:

• Shunt, where blood flows to consolidated lung and does not participate in gas exchange 3, 4
• Low V'A/Q' regions, where blood flow exceeds ventilation, resulting in hypoxemia 4
• High V'A/Q' regions, where ventilation exceeds blood flow, resulting in alveolar dead space and increased wasted ventilation 4

Gas Exchange Abnormalities

Gas exchange abnormalities in pneumonia can result in:

• Hypoxemia, due to shunt, low V'A/Q' regions, diffusion limitation, hypoventilation, and low inspired PO2 3, 4, 5
• Hypercapnia, due to alveolar hypoventilation and increased dead space 5, 6
• Increased work of breathing, due to reduced lung compliance and increased dead space 2, 5