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One of the main characteristics of patients with COPD is the inability to expire air, resulting...

One of the main characteristics of patients with COPD is the inability to expire air, resulting in air trapping. This combines with loss of elastic recoil in the alveoli contributes to the development of the _____________ of the chest.

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The loss of the elastic recoil, especially in the case of emphysema, the fact that the COPD patient breaths in “a higher level” which means that the functional tests show a functional residual capacity (FRC) which exceeds the predicted one, in order to maintain the airways open and the air trapping during premature closure are all aspects of lung hyperinflation

In normal subjects, lung volume at end expiration approximates the relaxation volume of the respiratory system. However, in patients with airflow obstruction, the end-expiratory lung volume may exceed the predicted FRC. Indeed, lung emptying is slowed, and expiration is interrupted by the next inspiratory effort, before the patient has reached the static equilibrium volume .This is termed dynamic hyperinflation and is affected by VT, expiratory time, resistance, and compliance. It is also called intrinsic positive end-expiratory pressure (auto-PEEP) and was firstly described by Bergman in 1972 and Johnson et al. in 1975 and represents the positive intrapulmonary pressure at the end of expiration . The presence of auto-PEEP means that the inspiratory muscles must firstly overcome the combined inward recoil of the lung and the chest wall before inspiratory flow can be initiated. Thus, auto-PEEP acts essentially as an inspiratory threshold load and has been measured to be as much as 6–9 cmH2O during quiet breathing at rest in clinically stable but hyperinflated COPD patients

During severe airflow obstruction episodes, increased expiratory efforts simply raise alveolar pressure without improving expiratory airflow. When tidal volume (VT) is increased or the expiratory time is short because of a high respiratory rate, the lung cannot deflate to its usual resting equilibrium between breaths. This raise in alveolar pressure and lung volume results in several events which affect the dynamic status of the lung. Breathing takes place near the total lung capacity.Tidal breathing during an exacerbation in a patient with COPD may be shifted upwards close to the total lung capacity as a consequence of dynamic hyperinflation

Hyperinflation has detrimental effects on the function of diaphragm that increase the work of breathing. First of all, the diaphragm is displaced into a flattened position which results in the decrease of the zone of apposition between the diaphragm and the abdominal wall. Secondly, the muscle fibers of the flattened diaphragm are shorter and are less capable of generating inspiratory pressures that will overwhelm the transpulmonary pressure . The positive pressure within the hyperinflated lung raises the mean intrathoracic pressure and causes the inspiratory muscles to operate at a higher than resting lung volume. The sarcomere length of the diaphragm in COPD patients is shorter and indirectly proportional to the TLC and the RV. This adjustment improves the capability of the diaphragm to generate force in “higher lung volumes.” The ideal length of inspiratory muscles during relaxation is considered to be near the level of residual volume (RV). In COPD patients, however, because of hyperinflation, the length of the muscle fibers is even shorter. Furthermore, an increase in the relative proportion of the type I fibers which are slow twitch and fatigue resistantand an increase in mitochondrial concentration and efficiency of the electron transport chain which improves oxidative capacity are other structural adaptations to chronic intrinsic mechanical loading. As a result, the developing force produced by the muscles is even more reduced on the expense of a considerable mechanical disadvantage which further impairs respiratory muscle function rendering this way the diaphragm

The ventilatory muscles partially adapt to chronic hyperinflation to preserve their force generating capacity during resting breathing. During COPD exacerbations, these adaptations can become overwhelmed The already burdened inspiratory muscles become subject to increased elastic loading, which means that they require a greater effort for a given change of volume. Acute dynamic hyperinflation further shortens the inspiratory muscles, particularly the diaphragm, and causes functional muscle weakness Exposure to oxidative stress and local activation of proteases may also result in diaphragmatic injury during periods of increased inspiratory loading and result in inspiratory muscle dysfunction .The net effect of this increased loading and functional weakness of the inspiratory muscles is that the effort required for tidal inspiration represents a relatively high fraction of the maximal possible effort that the patient can develop at that lung volume.


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