Breathlessness has been defined as “a subjective experience of breathing discomfort that consistent of qualitatively distinct sensations that vary in intensity”. It is a complex phenomenon, which is influenced by both neurophysiological and psychological factors. Breathlessness impacts upon individuals’ capacity to undertake physical activity. This can limit exercise capacity and, in severe cases, restrict the ability to mobilise, undertake daily activities and independently self-care, thereby deleteriously impacting upon health-related quality of life.

The sensation of breathlessness arises as a consequence of respiratory muscle motor activity through proprioceptive pathways. Inspiratory muscle activity increases in health during exercise, and in disease states where there is imbalance in the loads and capacity of the respiratory muscle pump. This imbalance leads to increased neural respiratory drive in the medulla. Conscious awareness of this ventilatory drive is perceived as breathlessness. It has been proposed that breathlessness intensity increases when there is mismatch between sensory afferents and efferent neural respiratory drive.

Disease states leading to load-capacity-drive imbalance can broadly be considered under the classifications of obstructive airways disease, neuromuscular and chest wall disease and obesity. In obstructive lung disease, most commonly chronic obstructive lung disease (COPD), airway inflammation, bronchospasm and sputum impose resistive loads, loss of alveolar fibroelasticity leads to elastic loading, and expiratory flow limitation with consequent intrinsic positive end expiratory pressure (PEEP_i) imposes a threshold load. Capacity of the respiratory muscle pump is reduced in COPD due to hyperinflation, which impairs force generating capacity. In neuromuscular and chest wall disease, respiratory muscle weakness reduces pump capacity, and upper airway obstruction, secretions and stiff lungs. In obese subjects, upper airways obstructive imposes resistive loading, reduced lung compliance contributes to elastic loading and threshold loading arises through early airway closure leading to PEEP_i. Capacity may be impaired through reduced functional residual capacity and ventilation:perfusion mismatch.

It is not possible to directly quantify central ventilatory drive, therefore surrogate indices are utilised. Inspiratory muscle activity increases in response to increased neural respiratory drive, and thus represents a measurable and potentially clinically valuable objective physiological marker of neural respiratory drive. Electromyography (EMG) has been implemented using invasive and non-invasive techniques amongst healthy subjects and in patients with load-capacity imbalance. This talk will provide an overview of these approaches and clinical applications of respiratory muscle EMG.