In diseases that cause airway obstruction, for example, asthma and chronic obstructive pulmonary disease (COPD), in an attempt to obviate the degree of airway ­narrowing, patients tend to breathe at a higher lung volume; closer to total lung capacity (TLC) than usual (Fig.2.1). In this way lung tissue is stretched and the airways that are embedded within it experience a greater retractile force and are, to some extent, widened. In that sense the strategy works. This, of course, is not a deliberate or even conscious change; patients are unaware that they are breathing at a higher lung volume. There are a number of other consequences to this adaptation which can give rise to specific symptoms. As can be seen, breathing at a higher lung volume implies that the inspiratory capacity is diminished. Therefore, if a patient attempts to take a deep breath in, they will find they reach their limit (TLC) sooner than expected. Unaware that their inspiratory maneuver began at a high lung volume and unaware that they are already at TLC, this limitation to further inspiration will be perceived as an “inability to get a full breath in.”

In healthy subjects at the end of a normal tidal expiration, the intrinsic tendency for the lungs to contract is just counterbalanced by the natural tendency for the chest wall to “spring outward.” No muscular effort (no work) is required to hold this “neutral” position. Breathing close to this lung volume is therefore quite effort efficient, like gently stretching and releasing a spring that has no baseline tension. As lung volume increases, lung tissue is stretched, and like the spring it tends to resist ­further stretch. In fact, unlike the perfect spring of Hooke’s law, the greater the stretch, the greater the force that is required to further expand the lung. When, as in airway obstruction, tidal breathing occurs at a higher lung volume, the muscular effort needed simply to move the chest wall (the work of breathing) is hugely increased. Like attempting to stretch and relax a spring that is already under considerable tension. For a normal degree of ventilation, much greater effort is needed. This ­“mismatch” contributes to the sensation of breathlessness and is another price paid for airway dilatation achieved by hyperinflation.

To gain some appreciation yourself of how important a factor this is in the perception of breathlessness try it! From a normal lung volume, take a breath in, about half way to full capacity. Then spend just a minute trying to breathe normally, at this hyper-inflated position. A minute will seem like a long time. Remember, those with airway obstruction are breathing at this high lung volume all the time.

The link between hypoxia and breathlessness is weak. To the lay person, the reason we breathe is to take in oxygen. Whilst this is of course an important imperative, the first priority of the respiratory system is to maintain a normal pH. It is not possible to survive for long with a pH outside of the normal range. Control is achieved by adjustments in pCO₂(pH and pCO₂are intimately linked). So, if for example a metabolic alkalosis were to arise (e.g., after vomiting), to correct the high pH, ­ventilation would be reduced and CO₂would accumulate. By reducing ventilation however pO₂would also fall. Fortunately (within limits) this has no detrimental effect. The level of oxygenation we normally maintain (pO₂11–14 kPa) is far above what is required to sustain life, even in the long term. A modest fall in oxygenation would not normally be perceived by the individual as breathlessness and it would not, per se, drive up ventilation. Only at a much lower level (pO₂around 8 kPa) does the center in the brain stem responsible for protecting us from hypoxia wake up and start to take action.

The first stage after an assessment of the underlying cause of dyspnea will be to offer disease-modifying treatment in an attempt to reverse the process. Mostly this will be drug treatment, but, particularly in cancer-related dyspnea, radiotherapy or physical interventions may also be employed. These will be discussed in the lung cancer or mesothelioma chapters.

Purely symptomatic strategies for breathlessness management include:

Of the drugs that have been tried for the symptomatic relief of breathlessness, only benzodiazepines and opioids are widely used. Other drugs such as nebulized ­furosemide and antidepressants are unproven.