figure 2-9 Flow volume loops of an individual with chronic obstructive pulmonary disease (COPD), taken prior to tracheal stenosis and a bron-chodilator (A), with bronchodilator, where flow increases sufficiently to demonstrate a plateau due to concomitant tracheal stenosis (B), and progression of the tracheal stenosis, concealing much of the COPD (C). V= flow; VC = vital capacity.
Miller and Hyatt presented data suggesting that the ratio of the mid-expiratory flow rate (MEF50) to the mid-inspiratory flow rate (MIF50) would enhance the visual evaluation of the FVL.2 A normal ratio would be from 0.9 to 1.0. A fixed obstruction, with both loops limited, would remain at about 0.9, whereas a variable extrathoracic obstruction would be greater than 1.0, and a variable intrathoracic obstruction would be 0.2 or less. These values for variable obstruction relate mainly to severe disease.
The dorsal membrane of the trachea is invaginated to some degree in healthy individuals when exposed to high intraluminal pressures, such as may occur with a cough or during exercise. In some individuals with severe obstructive lung disease, this invagination as visualized at bronchoscopy may be so severe as to almost completely obliterate the lumen. The effect is to markedly limit the ability of individuals to clear secretions via coughing. This may be particularly important in patients with bronchitis extending to their distal airways. Herzog and colleagues investigated a group of these patients using a technique of intrabronchial pressure measurements, slowly withdrawing a catheter from distal to central airways and measuring simultaneous alveolar pressure and flow rate in a plethysmography2 They calculated the flow resistance over bronchial segments and found patients with collapse of the central airways, as well as those with collapse of both peripheral and central airways, when exposed to high intrapleural pressure. These findings were correlated with bronchoscopic inspection, under local anesthesia, of the posterior membrane being invaginated by high intrapleural pressure induced by coughing and hyperventilation. Herzog and colleagues described a typical appearance of a spirometric tracing, in which there is a sudden fall in the flow rate, known as the "check valve" phenomenon. In an individual with severe COPD, this can also be seen in an FVL as a sudden fall in expiratory flow, followed by a slow further decline in flow (Figure 2-10). The posterior membrane was stabilized by grafting fascia or plastic material. Herzog and colleagues showed a marked increase in FEVi in some cases, although not all. There was a general improvement in the partial pressure of oxygen (PO2) and a fall in the partial pressure of carbon dioxide (PCO2) where this was initially elevated. The authors were careful to point out that these results did not mean that the collapse of airways in COPD was solely in the central airways; the small airways were still the major site of collapse. However, the ability to clear secretions and limit the number of episodes of bronchitis and reactive airway constriction was probably the most important factor in the improvement. They noted that this process was of most assistance in individuals with a clinical syndrome of chronic bronchitis and severe attacks of coughing even up to the point of cough syncope. This is a concept that probably needs to be re-addressed. Certainly, the results in the small number of cases described appear to at least equal the effect of volume reduction surgery on the FEV1.
The effect of exercise in patients with tracheal stenosis has been sparsely studied. This is a difficult task because many patients with tracheal stenosis also have parenchymal disease, due to coexistent problems such as chronic obstructive lung disease, asthma, or bronchiectasis, which influences the results. Seven patients without diffuse lung disease were studied using mild exercise,7 since patients with tracheal stenosis are limited in their ability to exercise by dyspnea. In all patients, the PO2 decreased with exercise, with the mean being 11 mm Hg. In general, the magnitude of PO2 decrease correlated with the degree of obstruction. PCO2 only increased an average of 2 mm Hg. In the three subjects who had surgical correction, the PO2 rose by a mean of 9 mm Hg and the PCO2 fell slightly with exercise. The vital capacity was not changed by corrective surgery, but the FEV1, maximum breathing capacity, and peak expiratory flow rate all increased markedly.
figure 2-10 Flow volume loop showing a sudden dramatic decline in expiratory flow followed by a long plateau, normal inspiratory loop because of the effect of a negative inspiratory intrapleural pressure on the floppy airways. Flow is the vertical axis and volume is the horizontal axis. FEV, is the forced expiratory volume at first second. FVC is the forced vital capacity.
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