MECHANICS OF BREATHING AND PEEP

What is the closing volume?

• The closing volume (CV) is the point at which dynamic compression of the airways begins.

• The CV increases with age, smoking, lung disease, and body position (supine>erect).

If lungs were perfect or uninfluenced by gravity, all of the airways would be dynamically compressed at residual volume, but, in reality, this is not the case. We know that the lungsthemselves as macroscopic organs are influenced by gravity: they hang down in the pleural cavity and the surrounding pleural pressure is more negative in non dependent zones (in the upright position the apex) than in the dependent zones (the bases). This pressure is transmitted across to the alveoli, so that, at end expiration (FRC), alveoli in dependent zones are less inflated than those in non-dependent zones.

If you look at the respective alveoli's position on the pressure volume curve (see figure 1 above), you will note that the alveoli at the apex sit near full inflation (on the flat part of the curve) and that those at the bases are on the steep part of the curve: they thus get a high minute ventilation. This is appropriate as these zones also are better perfused. However, these alveoli are also vulnerable: as they have the lowest resting volume, they also have the lowest resting pressure and by inference the lowest gradient to the mouth: and are the first airways to be compressed during active expiration. This is important because, during active emptying of the lungs, these airways close off long before residual volume is reached: the point at which this begins to occur is known as the closing volume (the closing volume plus the residual volume is the closing capacity). As one ages and one loses ones lung elasticity, the closing volume moves upwards deep into the expiratory reserve volume, such that, by one’s mid 40s, airway closure occurs, while supine, at the end of a normal tidal volume, and by one’s mid 60s, closure occurs while erect (i.e. at FRC).

Why is this important?

Smokers, elderly patients, and patients with chronic lung disease will experience airway closure within tidal breathing, and this is recognized by the presence of a hyperinflated chest. This is extremely important, because anything that adversely affects airway girth (bronchospasm, edema, inspissated mucus, foreign objects), or lung compliance (lung volume – interstitial edema or fibrosis), will increase the closing volume or reduce the FRC.

In order for airways to be involved in alveolar ventilation, they need to be patent. Obstruction of passages at any point in the breathing cycle may lead to venous admixture. So to involve closed airways in alveolar ventilation, they need to be reopened. The problem is that the pressure-volume curve has now shifted into positive territory. For dependent airways to open, the local intrapleural pressure must first go below atmospheric, and the gradient must be great enough to overcome the resistance to airway opening. In other words, a large amount of pressure must be generated to move a very small amount of air: the pressure volume curve is very flat and the work of breathing very high. This is analogous to starting a race 10 meters behind the start line – just getting to the beginning can be exhausting. Key message: airway closure above residual volume increases the work of breathing.

In pathological conditions, or where tidal volumes are low or where the patient does not sigh or yawn, airways may remain collapsed throughout the respiratory cycle: this lead to a situation whereby lung units may be ventilated but not perfused (low V/Q) – shunt and venous admixture.

If cyclical gas flow stops, true airway collapse (atelectasis) will ensue: the contents of the alveoli will gradually be reabsorbed (this is enhanced by the use of high FiO2 – absorption atelectasis).

In effect: any condition that causes 1. A reduction in lung volumes, FRC, chest wall compliance or, 2. An increase in closing volume, will cause a reduction in physiological oxygenation reserve, airway collapse and atelectasis. The item that most commonly does this is the endotracheal tube, which, by increasing the resistance to both inspiration and expiration, reduces FRC and increases closing capacity.

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