Bronchial obstruction is associated with a progressive increase in lung volume. Expiration time is prolonged and inspiration begins before the exhalation of inspired gas is complete. A number of factors are responsible for the impairment of expiration flow rate. During expiration, there is a persistent contraction of inspiratory muscles promoting an outward motion of the thoracic cage, thus opposing expiration. There is a decreased lung recoil elastic force, the mechanism of which is not clearly understood. Moreover, resistance to flow is increased due to airway obstruction, sometimes associated with closure of the glottic aperture. This explains the use of expiratory muscles, as expiration is no longer passive. Bronchial obstruction is not uniform throughout the lungs; airways are completely closed, partially occluded, occasionally with check valve phenomena, or completely open. The ensuing prolonged expiration time in some areas leads to air gas trapping and progressive dilatation of the alveoli. This results in progressive hyperinflation.
In addition, there is an increased ventilatory drive associated with enhanced respiratory muscle activity and secondary to stimulation of pulmonary receptors of the vagus nerve. The resulting tachypnea interferes with a necessarily prolonged expiration and enhances further hyperinflation. However, an increase in lung volume is an advantage for the patient as it helps to keep open narrowed airways which would otherwise close at normal lung volumes. This is achieved by the radial traction exerted on the bronchial wall in this situation. With severe obstruction, there is an increase in total lung capacity (up to 100 per cent over control values), residual volume, and functional residual capacity (up to several-fold). Concomitantly, tidal volume and vital capacity decrease. All indices of expiratory flow rate are markedly reduced, as evidenced by the two more useful pulmonary function tests available at the bedside: the forced expiratory volume in 1 s (FEV 1) or the peak expiratory flow rate (PEFR).
Changes occur not only in lung volumes but also in airway pressure. Lung deflation is not completely achieved when the next inspiration begins. At the end of expiration, airway pressure does not return to zero or atmospheric pressure, but remains elevated, i.e. a positive end-expiratory pressure (PEEP), known as intrinsic PEEP or auto-PEEP, progressively develops.
With the development of hyperinflation, auto-PEEP, and higher airways resistance, initiation of inspiratory flow requires greater force. Normal inspiration is achieved by inspiratory muscle work generating intrapleural pressures from -3 to -6 cmH2O. During asthma, profound negative intrapleural pressures are necessary to obtain normal tidal volume. Expiration requires active muscle contraction. This results in increased work of breathing, with increased CO 2 production and O2 consumption. Furthermore, increased minute ventilation, which is wasted in many areas with impaired ventilation-perfusion ratio, is stimulated. Dyspnea is a usual finding, and patients may be able to evaluate the degree of bronchial obstruction better than physicians. However, perception of breathlessness is reduced in some patient categories, particularly after severe attacks or in older asthmatics.
The diaphragm is flattened or even everted in the abdominal cavity. During inspiration, this leads to a paradoxical inward movement of the base of the thoracic cage associated with a tracheal tug concomitant with contractions of the sternocleidomastoid and intercostal muscles. The flattened and elongated diaphragm loses its efficacy. Muscle fatigue can develop, with the appearance of alternating abdominothoracic respiration, abdominal paradox, and a progressive decrease in respiratory rate.
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