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Mechanical abnormalities in COPD—the importance of dynamic hyperinflation

The hallmark of COPD is expiratory flow limitation which results from a combination of reduced lung recoil and airway tethering, as well as intrinsic airway narrowing [11]. However, while the most obvious mechanical defect is obstructive, in expiration, the most important mechanical consequence is a 'restrictive' ventilatory deficit in inspiration due to the effects of dynamic lung hyperinflation (DH) (Figs 5.1 and 5.2). One of the earliest descriptions of DH was provided by William Stokes, an Irish physician, in his treatise, Diseases of the Lung and Windpipe, published in 1837 [12]. Stokes recounted the following lucid clinical observations of a patient with emphysema: 'I shall describe a sign which promises to be of the greatest importance in diagnosis. By making the patient perform a number of forced inspirations rapidly, the repetition of the inspiratory efforts caused such an accumulation of air in the diseased portion of the lung as ultimately to nearly prevent its further expansion. The results of this experiment are readily explained by referring to the difficulty in expiration which occurs in this disease' [12].

DH occurs in flow-limited patients when ventilation increases, either voluntarily or reflexly (as for example during exercise) in response to increased levels of arterial carbon dioxide (Fig. 5.2). Thus, at higher levels of ventilation, tidal lung emptying becomes incomplete and lung volume fails to decline to its equilibrium point (i.e. functional residual capacity), causing dynamic end-

Fig. 5.3 Pressure-volume (P—V) curves of the respiratory system in (a) health and (b) COPD. Tidal loops at rest (enclosed area) and during exercise (open area) are constructed on each curve. In contrast to health, IC is reduced in COPD and tidal volume is positioned on the upper alinear extreme of the P—V relation where there is increased elastic loading.

Fig. 5.3 Pressure-volume (P—V) curves of the respiratory system in (a) health and (b) COPD. Tidal loops at rest (enclosed area) and during exercise (open area) are constructed on each curve. In contrast to health, IC is reduced in COPD and tidal volume is positioned on the upper alinear extreme of the P—V relation where there is increased elastic loading.

expiratory lung volume (EELVdyn) to progressively increase as a result of air trapping (Fig. 5.2) [11,13-15]. The extent of DH during exercise depends on:

1 The extent of expiratory flow limitation

2 The level of baseline lung hyperinflation

3 Ventilatory demand, and

4 The breathing pattern at any given ventilation.

The level and pattern of DH during exercise in COPD is highly variable: in a recent study, the average increase in EELVdyn during exercise in 105 patients with COPD was 0.37 ± 0.39L or 14 ± 15% of predicted [15].

Although DH serves to optimize tidal expiratory flow rates, it adversely affects dynamic ventilatory mechanics in three major ways: (i) it causes patients to breathe at a high lung volume where further volume expansion during exercise is seriously restricted (Fig. 5.2); (ii) it burdens inspiratory muscles with additional elastic loading; and (iii) it causes functional inspiratory muscle weakness. Theoretically, DH would also be expected to impair cardiovascular function during exercise but this question remains to be studied.

The inability to expand VT during exercise results in greater reliance on increasing breathing frequency to increase ventilation, but this tachypnoea results in further DH in a vicious cycle [11,15]. Tachypnoea also contributes to the reduced dynamic lung compliance which is known to have an exaggerated frequency dependence in COPD [11]. Because of DH, Vt encroaches more and more on the upper alinear extreme of the respiratory system's (combined lung and chest wall) pressure-volume relationship, where there is increased elastic loading of inspiratory muscles already overburdened with the work of overcoming increased airways resistance in COPD (Fig. 5.3) [11]. By

Fig. 5.4 Illustration of the rib cage and diaphragm in (a) health and (b) COPD. In COPD the diaphragm is shortened and functionally weakened because of hyperinflation and the combined recoil of the lung and chest wall at end-expiration is inwardly rather outwardly directed as in normals, creating an inspiratory threshold load (see text for details). (a)

Inspiratory threshold load

Decreased muscle strength

Inspiratory threshold load

Decreased muscle strength

contrast, VT remains within the linear portion of the pressure-volume (P-V) relationship in health, even at much higher levels of exercise (Fig. 5.3). Inspiratory threshold loading is another more recently recognized consequence of DH. In flow-limited patients with positive intrathoracic pressures at the end of expiration (the autoPEEP phenomenon) [11], the inspiratory muscles must first overcome the combined inward recoil of the lung and chest wall at end-expiration, before inspiratory flow is initiated (Fig. 5.4). This threshold load occurs throughout inspiration and the pressure required to overcome it can be substantial, particularly if DH is severe during higher levels of ventilation [9]. Lastly, DH alters the length-tension relationships of the inspiratory muscles, particularly the diaphragm (which becomes flattened), and compromises their ability to generate pressure (Fig. 5.4) [11]. Attendant tachypnoea during exercise, with increased velocity of inspiratory muscle shortening, results in further functional muscle weakness [11]. Moreover, DH may alter the pattern of ventilatory muscle recruitment to a more inefficient pattern with negative implications for muscle energetics and performance.

Due to the increased loading and functional inspiratory muscle weakness occasioned by DH, tidal inspiratory pressures represent a much higher fraction of their maximal force generating capacity than in health at similar work rates and ventilation (Fig. 5.5) [9]. Since, in exercising COPD patients, the ability to breathe enough air in is progressively curtailed despite mustering near maximal inspiratory efforts, the ratio of effort (tidal esophageal pressure swings relative to maximum) to tidal volume (Vt) is significantly higher than in health (Fig. 5.5) [9]. This may have important implications for respiratory sensation. It is reasonable to assume that some of the distinctive qualitative dimensions of dyspnoea in COPD, such as unsatisfied inspiration, may have their physiological basis in the marked disparity between inspiratory effort, which approaches the maximum, and the mechanical response of the system, which is greatly impaired because of breathing at high lung volumes and increased inspiratory airways resistance. The intensity of dyspnoea during exercise has been shown to correlate strongly with the extent of dynamic lung hyperinflation and with the

Fig. 5.5 Plots of (a) operational lung volumes, (b) inspiratory effort (esophageal pressure relative to maximal Pes/PImax) and the (c) ratio of effort to tidal volume (P /VT), and (d) Borg dyspnoea ratings, all expressed as a function of increasing ventilation during exercise. Compared with normals, in COPD inspiratory effort is greatly increased despite a reduced tidal volume response and this likely contributes to increased exertional dyspnoea. (Adapted from

Fig. 5.5 Plots of (a) operational lung volumes, (b) inspiratory effort (esophageal pressure relative to maximal Pes/PImax) and the (c) ratio of effort to tidal volume (P /VT), and (d) Borg dyspnoea ratings, all expressed as a function of increasing ventilation during exercise. Compared with normals, in COPD inspiratory effort is greatly increased despite a reduced tidal volume response and this likely contributes to increased exertional dyspnoea. (Adapted from

Fig. 5.6 Statistical correlations between Borg ratings of inspiratory difficulty, end-expiratory lung volume (reduced dynamic inspiratory capacity), and the ratio of inspiratory effort to tidal volume standardized for vital capacity (Pes/PImax:VT/% VC) at a standardized level of exercise in COPD patients [9].

Dyspnoea (Borg)

r=0.86

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