Fig. 5:  Factors related to dyspnea and COPD are quite numerous.  Often the patient believes that a low oxygen level is the major reason why he or she is short of breath, and they are quite disturbed when the physician demonstrates that their oxygen saturation is normal.  The patient will say, “Well doctor, I’m still very short of breath,” and the physician must reassure them that their shortness of breath is due to other factors.  Certainly the increased resistive work of breathing, breathing through narrowed airways, is prominent as a cause of dyspnea in COPD.  Also the increased elastic work of breathing from static and dynamic hyperinflation is also important.  The reader can appreciate how important this is by taking a full breath and then trying to breathe near total lung capacity.  The effect is distressing because you are trying to stretch already hyperinflated lungs, and they do not want to stretch that much more; that increased elastic work of breathing is perceived as difficult breathing, or dyspnea. 

Bronchospasm, which will increase the resistive work of breathing and also indirectly increase the elastic work of breathing, is important.  Bronchospasm also produces the other quality of dyspnea, chest tightness.  Increased dead-space work in breathing is often under-recognized in COPD, as evidenced by an increased dead-space::tidal volume ratio, which requires more ventilation per unit of work and could conceivably be associated with dyspnea. 

Certainly hypoxemia leading to chemoreceptor activation is important, but it is probably causing dyspnea in the minority of COPD patients, especially those with emphysema and without hypoxemia.  Cardiovascular and pulmonary vascular abnormalities may exist in patients with pulmonary hypertension, who have dyspnea even though they may not have hypoxemia or increased resistive or elastic work of breathing. 

An early lactate threshold from loss or decrease in oxidative enzymes in leg muscles is an important cause of dyspnea.  The lactate introduced into the system from exercise has to be buffered through the ventilatory system; this translates as increased dyspnea and is an important factor explaining why pulmonary rehabilitation works in reducing dyspnea.  Anxiety and fear associated with dyspnea-producing activities modulate the intensity and affect associated with this disturbing symptom, and even improper pacing during exercise can aggravate dyspnea. 

These are some of the many other factors that physicians must deal with in a day-to-day clinical setting.