Breathlessness in Patients with Chronic Airflow Limitation: Dynamic Lung Hyperinflation in CAL
Effort is generally expressed in physiologic terms as a function of the ratio of esophageal pressure (Pes) to the maximal pressure-generating capacity (Pimax). This ratio correlates strongly with breathlessness. In exercising patients with CAL, resistive loading and particularly acute increases in elastic/threshold loading result in greater tidal excursions of inspiratory pressure required to maintain ventilation in pace with metabolic demand. Moreover, maximal power output is reduced by acute DH. Thus, the inspiratory muscles are forced to operate at a high fraction of their maximal force-generating capacity and perceived inspiratory effort is greatly increased. While heightened inspiratory muscle contractile effort undoubtedly contributes to breathlessness in CAL, awareness of disproportionate or unsatisfied inspiratory effort, ie, “cannot get enough air in,” is almost uniformly reported by breathless patients (personal communication). This latter qualitatively discrete sensation may have its physiologic origins in neuroventilatory dissociation (NVD) of the respiratory pump.
The concept of NVD implies that, in addition to motor output, sensory feedback from peripheral respiratory mechanoreceptors contributes importantly to respiratory sensation. Thus, during resting spontaneous breathing in normal healthy subjects, there is more or less harmonious neuroventilatory coupling so that the level of inspiratory muscle activity is commensurate with perceived effort (motor output) and unpleasant sensation is not experienced (Fig 2). In normal subjects, this close coupling of motor output with the anticipated ventilatory consequence is preserved during exercise. While perceived breathing effort may increase, normal subjects do not report inspiratory difficulty per se. By contrast, in exercising patients with CAL, the relationship between effort (motor output) and the anticipated ventilatory consequence (instantaneous change in respired volume) is seriously disrupted, ie, NVD, as a result of impeded inspiratory muscle action and weakness due to DH (Fig 2). Under these conditions, the patient experiences marked inspiratory difficulty. The psychophysical basis of NVD likely resides in the complex central processing of integrated sensory information relating to (1) the level of central motor command output and (2) instantaneous feedback from an abundance of respiratory mechanoreceptors that provide precise proprioceptive information. Afferent information from peripheral receptors signal instantaneous changes in respired flow (airway mechanoreceptors) and volume (stretch receptors), muscle tension (Golgi tendon organs), muscle displacement (spindles), and chest wall displacement (joint receptors).
Figure 2. Schematic. For a given breath in normal subjects there is a harmonious relationship between effort (Pes/Pimax) and instantaneous ventilatory output—“neuroventilatory coupling”. In CAL, because of intrinsic mechanical loading and functional muscle weakness, this relationship is disrupted (“neuroventilatory dissociation”) and greater levels of inspiratory difficulty or breathlessness are experienced. ITL =inspiratory threshold load.
Category: Respiratory Symptoms
Tags: breathlessness, chronic airflow limitation, copd, dynamic compression, dynamic hyperinflation, exercise