Figures
- FIGURE 1.
Increased load and/or reduced capacity of the respiratory muscles leads to an increased level of neural respiratory drive to the respiratory muscles. Conscious awareness of the level of neural respiratory drive is important to the perception of breathlessness [16].
- FIGURE 2.
The relationship between triggers, pathological changes, disease characteristics, symptoms and quality of life (QoL) in chronic obstructive pulmonary disease (COPD). Inhaled environmental noxious stimuli, particularly cigarette smoke, trigger a cycle of pulmonary parenchymal and airway damage, mucociliary dysfunction and airway and systemic inflammation. This cycle is also driven by exacerbations. Breathlessness is one of the cardinal symptoms of COPD and has a negative impact on QoL, in particular by reducing patients’ exercise tolerance and ability to carry out daily activities.
- FIGURE 3.
The impact of disordered ventilatory mechanics on breathlessness in chronic obstructive pulmonary disease (COPD). Static and dynamic hyperinflation leads to respiratory muscle shortening and altered chest wall geometry, leading to functional respiratory muscle weakness in COPD. This, in combination with mechanical abnormalities that increase the load on the respiratory muscles, increases load–capacity imbalance and neural respiratory drive, and contributes to breathlessness. Although these abnormalities may be present at rest, they are exacerbated when minute ventilation (V′E) increases during activity. PEEP: positive end-expiratory pressure.
- FIGURE 4.
Disordered ventilatory mechanics progressively uncouple increased neural respiratory drive from generation of respiratory muscle tension, intrathoracic pressure and ventilation in chronic obstructive pulmonary disease (COPD). This phenomenon is often referred to as “neuromechanical dissociation”. PEEPi: intrinsic positive end-expiratory pressure; V′E: minute ventilation.
- FIGURE 5.
A physiological model of breathlessness in chronic obstructive pulmonary disease. The model links the pathological processes triggered by inhaled noxious particles (1) to physiological factors leading to respiratory muscle load–capacity imbalance and efferent–afferent mismatch (2). This drives the perception of breathlessness (3) and results in exercise intolerance and reduced quality of life (4). In line with patients’ descriptions of their experience of breathlessness, there is evidence that intensity (sensory) and emotional (affective) components of breathlessness are processed separately in the brain. Lower limb activity, upper limb activity and postural changes required to carry out daily activities increase load–capacity imbalance, neural respiratory drive, efferent–afferent mismatch and breathlessness. Activities that interrupt the automatic rhythm of respiration, e.g. eating and talking, reduce ventilation transiently and may cause breathlessness through resultant increases in efferent–afferent mismatch. NRD: neural respiratory drive; PEEPi: intrinsic positive end-expiratory pressure; V′E: minute ventilation; PO2: oxygen tension; PCO2: carbon dioxide tension.
- FIGURE 6.
The physiological model can also be used to explain the mechanisms by which interventions impact on breathlessness. The final common physiological step is improved efferent–afferent mismatch through reductions in neuromechanical dissociation. Psychological support aims to impact on breathlessness distal to the physiological mechanisms. There is currently insufficient evidence to support the routine use of psychological interventions, such as counselling and support programmes and psychotherapy, alone to palliate breathlessness in routine clinical practice [129]. NRD: neural respiratory drive; PEEPi: intrinsic positive end-expiratory pressure; V′E: minute ventilation; PO2: oxygen tension; PCO2: carbon dioxide tension.
