Mechanical correlates of dyspnea in bronchial asthma

Abstract

We hypothesized that dyspnea and its descriptors, that is, chest tightness, inspiratory effort, unrewarded inspiration, and expiratory difficulty in asthma reflect different mechanisms of airflow obstruction and their perception varies with the severity of bronchoconstriction. Eighty‐three asthmatics were studied before and after inhalation of methacholine doses decreasing the 1‐sec forced expiratory volume by ~15% (mild bronchoconstriction) and ~25% (moderate bronchoconstriction). Symptoms were examined as a function of changes in lung mechanics. Dyspnea increased with the severity of obstruction, mostly because of inspiratory effort and chest tightness. At mild bronchoconstriction, multivariate analysis showed that dyspnea was related to the increase in inspiratory resistance at 5 Hz (R5) (r2 = 0.10, P = 0.004), chest tightness to the decrease in maximal flow at 40% of control forced vital capacity, and the increase in R5 at full lung inflation (r2 = 0.15, P = 0.006), inspiratory effort to the temporal variability in R5‐19 (r2 = 0.13, P = 0.003), and unrewarded inspiration to the recovery of R5 after deep breath (r2 = 0.07, P = 0.01). At moderate bronchoconstriction, multivariate analysis showed that dyspnea and inspiratory effort were related to the increase in temporal variability in inspiratory reactance at 5 Hz (X5) (r2 = 0.12, P = 0.04 and r2 = 0.18, P < 0.001, respectively), and unrewarded inspiration to the decrease in X5 at maximum lung inflation (r2 = 0.07, P = 0.04). We conclude that symptom perception is partly explained by indexes of airway narrowing and loss of bronchodilatation with deep breath at low levels of bronchoconstriction, but by markers of ventilation heterogeneity and lung volume recruitment when bronchoconstriction becomes more severe.

Asthma and Lung Mechanics

“…Loss of lung recoil, whether anatomic or functional, may predispose to sudden, acute worsening or even near fatal asthma [79]. Recently, Antonelli and colleagues examined the mechanical correlates of dyspnea in asthma by carefully comparing symptoms to alterations in lung mechanics measured by the FOT in response to methacholine [7]. Low levels of bronchoconstriction caused dyspnea that were associated with dyspnea related to airway narrowing and loss of bronchodilation after DI, perhaps due to more central airway narrowing, whereas higher levels of bronchoconstriction were associated with dyspnea related to ventilation heterogeneity and loss of lung volume from airway closure, perhaps due to more peripheral airway narrowing [7].…”

“…Recently, Antonelli and colleagues examined the mechanical correlates of dyspnea in asthma by carefully comparing symptoms to alterations in lung mechanics measured by the FOT in response to methacholine [7]. Low levels of bronchoconstriction caused dyspnea that were associated with dyspnea related to airway narrowing and loss of bronchodilation after DI, perhaps due to more central airway narrowing, whereas higher levels of bronchoconstriction were associated with dyspnea related to ventilation heterogeneity and loss of lung volume from airway closure, perhaps due to more peripheral airway narrowing [7]. Thus, it is clearly apparent that the symptoms and clinical manifestations of asthma extend well beyond the simple effects of airway narrowing and resulting increase in airway resistance (Figure 17).…”

TNF and IL‐1β exposure increases airway narrowing but does not alter the bronchodilatory response to deep inspiration in airway segments

“…The perception of dyspnoea in subjects with asthma correlates with an attenuated response to DI, 27 the mechanism of which is unknown. The present study determined how pro-inflammatory cytokines alters the bronchodilatory response to DI in bronchial segments.…”