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From the question bank Respiratory System

A patient with obstructive lung disease performs forced expiratory manoeuvres with increasing effort. In the later part of expiration, airflow at a given lung volume does not increase despite the greater effort, and an abnormally large volume of air remains in the lungs after maximal expiration. Which mechanism best explains these findings?

A Alveolar expansion during forced expiration compresses the small airways from outside and limits airflow
B Laminar flow becomes turbulent in the trachea, which is the main site of airflow resistance
C Higher expiratory effort produces turbulent airflow in the small airways, and this turbulence limits further airflow
D Dynamic narrowing of small airways during forced expiration increases resistance and limits airflow ✓
E Progressive fatigue of the expiratory muscles during forced expiration reduces the pressure generated and limits airflow

The answer is D: Dynamic narrowing of small airways during forced expiration increases resistance and limits airflow

Explanation

Why D is correct

See What is Ventilation?. Option D is correct. In forced expiration the respiratory muscles raise the pressure in the chest (pleural pressure) so high that it can exceed the pressure inside the small airways. These airways have no cartilage in their walls, so they are squeezed narrow. This is called dynamic compression. At the point where the two pressures are equal (the equal-pressure point), compression begins. After this, the harder the patient blows, the more the airways are squeezed, so flow does not increase. This is why the maximum expiratory flow at lower lung volumes is effort independent, and it is the physical basis for the characteristic scooped-out shape of the expiratory flow-volume loop (a graph of airflow against lung volume). In obstructive disease the weakened airways collapse earlier, trapping air behind them, so more air remains in the lungs at the end of expiration: the residual volume rises. A clinical pearl is that pursed-lip breathing moves the equal-pressure point towards the mouth, which relieves breathlessness. A simple memory aid: squeeze a soft tube harder and it just closes harder.

Dynamic compression: in forced expiration, pleural pressure exceeds the pressure inside the small airways, which have no cartilage and so narrow
Effort independence: beyond the equal-pressure point, blowing harder does not increase flow
Obstructive disease: weakened airways collapse earlier, trapping air and raising the residual volume

Why the other options are incorrect

A. Alveolar expansion during forced expiration compresses the small airways from outside and limits airflow: Alveoli do not expand during expiration; they shrink as the lungs deflate. The compression that limits airflow comes from high pleural pressure around the airways, not from expanding alveoli.
B. Laminar flow becomes turbulent in the trachea, which is the main site of airflow resistance: Turbulence adds to resistance, but the trachea is not the main site of resistance in the lungs, and it does not explain a flow limit that appears only with forced expiration. The problem arises in the smaller airways lacking cartilage.
C. Higher expiratory effort produces turbulent airflow in the small airways, and this turbulence limits further airflow: Flow in the small airways is laminar because their total cross-sectional area is large, so turbulence there is not the limiting factor. The plateau is caused by dynamic compression of these airways, not by turbulent flow.
E. Progressive fatigue of the expiratory muscles during forced expiration reduces the pressure generated and limits airflow: Muscle fatigue would reduce the force of contraction, but the plateau in flow occurs even when maximal effort is maintained, so it is not caused by tired muscles. The flow limit is effort independent and set by airway compression.

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