Volume L from Total Lung Capacity

figure 2-4 Flow volume loops obtained from breathing through progressively smaller orifices. The solid line is the unobstructed loop. C = control. Reproduced with permission from Miller RD and Hyatt RE.2

figure 2-5 Inspiratory and expiratory flows obtained through progressively narrower external tubes. FEVi = forced expiratory volume; FIV1 = forced inspiratory volume; MMF = maximum mid-expiratory flow; MVV = maximum voluntary ventilation; PEF = peak expiratory volume; PIF = peak inspiratory volume. Reproduced with permission from Miller RD and Hyatt RE.2

figure 2-5 Inspiratory and expiratory flows obtained through progressively narrower external tubes. FEVi = forced expiratory volume; FIV1 = forced inspiratory volume; MMF = maximum mid-expiratory flow; MVV = maximum voluntary ventilation; PEF = peak expiratory volume; PIF = peak inspiratory volume. Reproduced with permission from Miller RD and Hyatt RE.2

The most common cause of fixed stenosis is postintubation stenosis. The lesion is circumferential and usually related to mucosal and cartilage damage at the site of the cuff. Other causes are neoplasms, goiters, and stenosis of both main bronchi. Flow volume loops performed though a tracheostomy tube also show the same pattern. Gamsu and colleagues (Figure 2-6) derived a graphic representation of flow related to driving pressure through a series of fixed tubes of varying diameters.3 From this, and assuming a driving pressure of 100 cm H2O, the diameter of a stenotic segment may be estimated by measuring the MIF50 and MEF50. The method is reasonably accurate, within about a 1.5-mm tracheal diameter for rigid lesions, but it is less accurate when individuals have emphysema or marked malacic segments.

Variable Upper Airway Obstruction

The term variable obstruction describes the situation where intraluminal and extraluminal pressures affect the anatomy of the lesion. This may occur because the involved area is malacic, or because the lesion, although firm, is not circumferential, and normal tracheal wall movement, usually the posterior membrane, alters the shape of the lumen. The alteration may also be postural, as in the case of a hemangioma.

Diameter

Images Normal Diameter Trachea

Driving Pressure (cm H20)

figure 2-6 Graphic representation of airway diameter and flow (forced expiratory flow50 or forced inspiratory flow50) with airway pressure between 50 and 150 cm H2O, derived from progressively increasing external resistances in a normal subject. Reproduced with permission from Gamsu G et al.3

In variable extrathoracic obstruction (see Figures 2-1D, 2-7), the negative intraluminal pressure relative to the atmospheric pressure produced during inspiration causes narrowing of, for example, a malacic segment, resulting in limited inspiratory flow.4 During exhalation, a positive intraluminal pressure is generated, which results in maintenance or expansion of the diameter of the airway and a normal expiratory flow rate. Thus, a plateau is observed on the inspiratory loop alone, and the MEF50/MIF50 is greater than 1. Vocal cord paralysis, usually bilateral but also unilateral, is one of the most common causes of this pattern.5 The features are also seen in individuals with severe burns and vocal cord dysfunction.

Variable intrathoracic obstructions (see Figures 2-1C, 2-8), such as tracheomalacia, demonstrate a reduction in the peak flow rate and a flattening of the expiratory loop, in response to the high positive intrapleural and, therefore, extraluminal pressures generated.4 The inspiratory loop is normal, responding to negative inspiratory pressures. The MEF50/MIF50 is low and the FEVi less than the forced inspiratory volume in first second (FIV1). The major causes are malacic segments or noncircumferential tumors.

Upper Airway Obstruction and Chronic Obstructive Pulmonary Disease

Tracheal abnormalities frequently develop in the presence of chronic obstructive pulmonary disease (COPD). This may be due to injuries, such as cicatrization at the site of an endotracheal cuff producing fixed stenosis, tracheomalacia at the site of an endotracheal cuff leading to a variable intrathoracic stenosis, or variable extrathoracic stenosis due to vocal cord dysfunction or malacia at the site of a tracheostomy. The differentiation between the effect of COPD and tracheal injury is important because (a) recognition can lead to repair and (b) it is important to understand the relative contribution of the stenosis and COPD to symptoms such as dyspnea. For example, the presence of a minor degree of radiographically and bron-choscopically recognizable stenosis may have little significance in the presence of very severe COPD, where the flow limitation is mainly in the distal airways, hence the stenosis does not provide any further impediment to flow nor to expectoration of secretions.

Extrathoracic Airway Obstruction

figure 2-7 Inspiration and expiration influencing variable extrathoracic obstruction. Patm is the atmospheric pressure; Ptt is the intratracheal pressure. Reproduced with permission from Kryger M et al.4

Variable Intrathoracic Obstruction

figure 2-8 Inspiration and expiration influencing variable intrathoracic obstruction. Ppl is the intrapleural pressure; Pu is the intratracheal pressure. Reproduced with permission from Kryger M et al.4

Fixed tracheal stenosis, variable intrathoracic stenosis, and COPD all reduce the peak flow rate. However, the tracheal lesions produce a plateau, whereas a sharp peak is still seen in COPD, together with concave expiratory flow patterns. The length of the plateau and the reduction of peak flow by the plateau, as described earlier, are approximately proportional to the severity of the stenosis. As exhalation proceeds, the site of flow limitation moves peripherally until the collapsing small airways inhibit flow. At that point, the concave pattern of COPD will become the visible feature (Figure 2-9). Thus, the ratio of plateau to concavity gives an approximation of the relative significance of the lesions. If no plateau is visible, the stenosis is not contributing to flow limitation, nor is it likely to contribute to dyspnea. However, the reverse is not necessarily true; that is, where stenosis is contributing to flow limitation, release of stenosis may not relieve dyspnea much, since other factors such as hyperinflation related to the residual COPD or the presence of cor pulmonale may be very important in the mechanism of dyspnea. However, improvement in the ability to cough up secretions may have a significant effect. Thus, COPD may conceal stenosis, and stenosis may cause one to underestimate the severity of COPD. In addition, the presence of signs or symptoms also depends on the relationship between the flow required for a specific activity and the degree of obstruction. Geffin and colleagues demonstrated that, at rest, stridor was only heard when the airway was reduced to a 5 mm stenosis.6 However, with exercise, a less severe stenosis may also cause stridor.7

Another useful technique is the superimposition of the tidal volume loop on the FVL, with tidal volume expressed both at rest and during hyperventilation. The point of contact of the tidal volume with inspiratory or expiratory plateaus or with the concavity of COPD provides very useful information about the limiting factors and the contribution of the plateau to limiting flow and to the symptoms. Accurate positioning of the tidal volume on the axis can however be difficult.

Helium-oxygen inhalation, which reduces the density of the gas, has also been used to differentiate COPD from upper airway obstruction (UAO).8 Since flow in the upper airway is density dependent, helium-oxygen inhalation can increase expiratory flow in the UAO, but not in COPD when laminar flow is much less dependent on density.9 Nitrogen washout using 100% oxygen is normal in UAO, but abnormal in COPD10,11; however, this is mainly useful when pure forms of these processes are present, whereupon an FVL should suffice.

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