Hyperinflation and its management in COPD

Abstract

Chronic obstructive pulmonary disease (COPD) is characterized by poorly reversible airflow limitation. The pathological hallmarks of COPD are inflammation of the peripheral airways and destruction of lung parenchyma or emphysema. The functional consequences of these abnormalities are expiratory airflow limitation and dynamic hyperinflation, which then increase the elastic load of the respiratory system and decrease the performance of the respiratory muscles. These pathophysiologic features contribute significantly to the development of dyspnea, exercise intolerance and ventilatory failure. Several treatments may palliate flow limitation, including interventions that modify the respiratory pattern (deeper, slower) such as pursed lip breathing, exercise training, oxygen, and some drugs. Other therapies are aimed at its amelioration, such as bronchodilators, lung volume reduction surgery or breathing mixtures of helium and oxygen. Finally some interventions, such as inspiratory pressure support, alleviate the threshold load associated to flow limitation. The degree of flow limitation can be assessed by certain spirometry indexes, such as vital capacity and inspiratory capacity, or by other more complexes indexes such as residual volume/total lung capacity or functional residual capacity/total lung capacity. Two of the best methods to measure flow limitation are to superimpose a flow-volume loop of a tidal breath within a maximum flow-volume curve, or to use negative expiratory pressure technique. Likely this method is more accurate and can be used during spontaneous breathing. A definitive definition of dynamic hyperinflation is lacking in the literature, but serial measurements of inspiratory capacity during exercise will document the trend of end-expiratory lung volume and allow establishing relationships with other measurements such as dyspnea, respiratory pattern, exercise tolerance, and gas exchange.

Figures

Figure 1

Pressure volume relationship of the passive respiratory system. Lower and upper boundaries of the elastic recoil pressure–volume relationship of the respiratory system in healthy subjects (---), in patients with narrowed airways (—), and in patients with loss of lung elastic recoil (·····). The loops represent tidal breathing at rest (—) and during exercise (·····). Abbreviations: FRC, functional residual capacity; VC, vital capacity.

Figure 2

Effects of time and resistance on the change in expiratory volume. Rates of changes of volume after a similar given change of alveolar pressure in a subject with normal respiratory system resistance (—) and a resistance 3 times greater (---) such as in COPD, assuming a constant compliance. Note the marked effect of resistance on the volume change, particularly when the available time is shortened. Abbreviations: COPD, chronic obstructive pulmonary disease.

Figure 3

Iso-volume pressure-flow relationship. Schematic representation of the pressure-flow relationship in a healthy (normal) subject and a patient with COPD, showing the effect of the increased expiratory resistance upon the maximum expiratory flow and in both cases the independence of the maximum flow from the pleural pressure. Copyright © 1986. Modified with permission from Pride NB, Macklem PT. 1986. Lung mechanics in disease. In: Fishman AP (ed). Handbook of physiology, Section 3, Volume III, Part 2: The respiratory system. Bethesda MD: American Physiological Society, pp 659–92. Abbreviations: COPD, chronic obstructive pulmonary disease.

Figure 4

Maximum and tidal flow-volume curves in subjects with and without flow limitation. In this figure it can be seen an schematic representation of the spontaneous flow-volume curves generated at tidal volume at rest (inner dotted line ····) and peak exercise (dashed line ----) compared with the maximum flow volume curve in a subject without flow limitation able to reduce its end-expiratory lung volume (Panel A) and a flow-limited COPD patient with dynamic hyperinflation (Panel B). Abbreviations: COPD, chronic obstructive pulmonary disease; IC, inspiratory capacity.

Figure 5

Tidal volume encroachment by dynamic hyperinflation in COPD. In this figure the effects of respiratory rate and work rate on the end-inspiratory (EILV), end-expiratory lung volume (EELV), tidal volume (ie, EILV–EELV) and minute ventilation in subjects with severe COPD is displayed. While EILV increases with increasing respiratory rate from 20 to 30min−1 (lower left panel), so does EELV resulting in an almost constant (encroached) tidal volume. At respiratory rates higher than 30, though, EILV does not increase any more, however, EELV further increases resulting in a reduced tidal volume and even a drop in ventilation (left upper panel) at respiratory rates higher than 35min−1. In the right lower panel we can see how during progressive exercise tidal volume also decreases at high intensity due again to increase in EELV without parallel increase in EILV (Constructed with data from Puente-Maestu et al 2005). Abbreviation: COPD, chronic obstructive pulmonary disease; EELV, end-expiratory lung volume; EILV, end-inspiratory lung volume; TLC, total lung capacity.