Mechanics Of Breathing

Overview

Intrapleural pressure is usually subatmospheric, due to the balanced forces of chest wall expansion and elastic lung recoil acting in opposite directions. During inspiration, contraction of the diaphragm causes expansion of the thorax and a further decrease in intrapleural (and hence intra-alveolar) pressure. This provides the pressure gradient for air entry into the lungs. During very forceful breathing, intrapleural pressure becomes very negative during inspiration, and may become positive during expiration.

Forces at play during breathing

If the chest wall is pierced at autopsy (or during surgery, or sharp trauma for that matter), three related things happen:

These simple observations tell us a lot about the balance of forces in a normal thorax. Firstly, the lungs have sufficient recoil to collapse further than they already have at rest in the sealed thorax. Secondly, the chest wall can expand – and will do so if allowed – further than it is when the thorax is not opened to the atmosphere. In fact, the two opposing forces – chest expansion and lung recoil – are in balance. The opposing forces lead to a slightly negative pressure (of about 0.5 kPa) between the chest wall and the surface of the lung in the pleural cavity. When the thorax is no longer sealed the lung does what it is now free to do (collapse), as does the chest (expand) and the result is increased volume in the thorax.

When you expand a volume of gas its pressure is reduced. Now, intrapleural pressure (Pip) is usually slightly lower than barometric/atmospheric pressure (PB), so when the thorax is breached, we would expect some movement of air from outside to inside. This is a pneumothorax. With expansion of the chest and subsequent further reduction in Pip, even more air enters. Once Pip and PB are equal, no further movement of air occurs. Meanwhile, as the lung collapses, the pressure within the alveoli (Palv) increases (since the alveoli are compressed by the lung recoil) and air is pushed out of the lung, again until Palv is equal to PB

Figure 1: Left hand side: The lung is represented as a single ballon inside a sealed chamber connected to the atmosphere via a tube. The pressure in the pleural cavity (intrapleural pressure or Pip) is slightly below barometric (atmospheric) pressure (PB) because the lung and chest wall are pulling in opposite directions: the lung has recoil, and the chest has a tendency to expand to a slightly larger volume. These forces are balanced. When the thorax is opened to the atmosphere, Pip increases further, as the chest expands. Simultaneously, as the lung is allowed to recoil more than usual, the volume of the lung shrinks, increasing Palv. Air then leaves the lung until pressures are balanced. This is a dynamic process which the right hand panel attempts to summarise, but you’ll need to picture the changes over time in your mind.

The pleural cavity

The outer surface of the lung and the inner surface of the chest wall are lined with smooth pleural membranes. Between them, the pleural cavity is filled with a small volume of pleural fluid. We tend to draw this cavity quite large in schematic diagrams to make it easy to see (as above), but it is, in fact, quite small, comprising only a few millilitres. With the lung recoil and chest wall expansion forces acting in different directions, the pleural fluid acts in much the same way as water between two sheets of glass that are difficult, if not impossible to pull apart. Because the diaphragm and intercostal muscles can overcome lung recoil fairly easily, when they contract to expand chest volume, the lung is brought along for the ride and expands. Expiration is generally a passive process: the diaphragm and intercostal muscles relax and lung recoil is sufficient to bring lung volume back to baseline. How does this process move air into and out of the lungs though?

Pressures during the breathing cycle

Figure 2: Changes in pressures with the pleura (Pip) and alveoli (Palv) during inspiration in our simple balloon lung model. Before inspiration, Palv is equal to PB and there is no movement of air into the lungs. During inspiration, the volume of the thorax expands, as does the lung. This reduces Pip (the magnitude of this drop depends on the depth of breathing), and consequently Palv, generating a driving force for airflow into the lung.

Figure 3: At the end of inspiration the increased lung volume is held in place by the inspiratory muscles of respiration. Once these muscles relax, lung recoil drives lung volume down, increasing Pip and Palv in the process and producing the pressure gradient for air to leave the lungs.

FRC and other lung volumes

Consider the diagram below (Figure 4) which illustrates the changes in volume in someone’s lungs during different patterns of breathing. Initially, during quiet breathing, tidal volume (V_T) is low and at the end of each breath when the muscles of breathing are completely relaxed lung recoil and the recoil of the chest wall are balanced. The volume remaining in the lung at this point is the Functional Residual Capacity (FRC). This isn’t a fixed volume, as it is influenced by posture, ageing, disease and drugs. Apart from the dead space in the conducting airways (usually about 150 ml), FRC represents the volume of air in the alveoli contributing to gas exchange. During quiet breathing FRC is a much larger volume (ca. 2100 ml) than V_T (ca. 490 ml), so breathing isn’t really a process of emptying and filling the alveoli, but rather topping up a large volume of FRC with a bit (about 500 ml during quiet breathing) of fresher air.

Figure 4: Static lung volumes. Initially this person is breathing quietly with a low tidal volume (V_T). During a lung function test, a patient is asked to breathe in as deeply as they can to reach their inspiratory reserve volume (IRV) and then exhale forcefully to reach their expiratory reserve volume (ERV). The volume that remains in the lung at ERV - which can’t be blown out without collapsing the lungs - is the residual volume (RV). The sum of RV and ERV is the functional residual capacity (FRC), which is altered by factors that can change either volume. Vital capacity (VC) is the range from ERV to IRV, while total lung capacity (TLC) is the sum of VC and RV.

Let’s consider a few ways in which FRC can be altered, both acutely and chronically:

Obesity: Having more tissue bulk around the chest works against its mechanical recoil, so lung recoil will dominate and hence FRC will be reduced. For this reason, obese patients are often chronically hypoventilated.

Anaesthesia: Classically, FRC is defined as the volume in the lungs when lung recoil and chest expansion are balanced. However, it has become clear that when someone is anaesthetised, FRC falls significantly. This is thought to be due to a certain degree of muscle tone in the musculature of the chest and diaphragm that is present when conscious, but lost during anaesthesia.

Pregnancy: At full term, the abdominal contents are pushed up against the diaphragm reducing the FRC. Think about what would happen if you anaesthetised a patient for an emergency Caesarian section. They’re FRC is already reduced and anaesthesia will reduce this further (see above). There’s a risk in this situation that such a patient would have such a limitation of their FRC that their O₂ saturation would fall and they would require supplemental O₂.

Emphysema: Lung compliance is increased in emphysema and this is associated with reduced lung recoil. As a result, the recoil of the chest wall tends to dominate and FRC increases. This is part of the reason why COPD patients often have expanded chests. (The other reason is hyperinflation due to dynamic compression of airways).

Posture: When standing, your abdominal organs are drawn down by gravity, away from the diaphragm. However, when lying down this effect is markedly reduced and FRC falls accordingly, as the diaphragm is pushed into the thoracic cavity.