Bronchial Pressure Measurements in Emphysema and Bronchitis*

Abstract

Koblet and Wyss were the first to use bronchial pressure measurements to locate the airway obstruction in emphysema and asthma (1). Their results showed that in emphysema expiratory obstruction occurred in large airways whereas in asthma it was in small airways. It had already been established, in particular by Dayman (2), that emphysema was characterized by a marked increase in airway resistance during forced expiration, due to airway compression, and that this increase limited expiratory flow. Subsequently Hyatt, Schilder, and Fry (3) and Fry and Hyatt (4) showed that the inability of the patient with emphysema to breathe was directly attributable to expiratory airway compression and that maximal expiratory flow bore a unique relationship to lung volume. Out of these investigations grew the concept of the "flow-limiting segment," which was regarded as the airway or airways which were the first to narrow enough to limit flow. Thus, Koblet and Wyss's work took on added importance because it suggested that the flow limitation in emphysema was due to narrowing of large bronchi. Our laboratory has confirmed and extended their results by measuring bronchial pressures during cinebronchography (5). It was found that in emphysema the expiratory obstruction as demonstrated by the pressure measurements coincided with collapse of the lobar bronchi visualized cinebronchographically. Furthermore, this collapse * Submitted for publication October 9, 1964; accepted February 11, 1965. This appeared to be the result of an increase in bronchial compliance.These investigations suggested that the collapsing lobar bronchi were flow limiting in emphysema. This was not proven, as the possibility remained that flow was initially limited in smaller airways and that subsequent to this event the lobar bronchi collapsed obstructing flow. The crucial role played by the small airways would thus be masked, and the lobar bronchi would spuriously appear as the flow-limiting segments. The present study was designed to investigate this problem further. MethodsSubjects. Nine patients were studied. The only criterion for inclusion in the study was chronic airway obstruction with a reduction in forced expiratory volume in the first three-quarters of a second (FEVo.75) that was unresponsive to therapy. Thus, all patients with episodic asthma were excluded. Included were six patients who, on the basis of clinical findings and lung function tests, were thought to have emphysema and three patients who were thought to have chronic airway obstruction due to bronchitis without emphysema. The criteria for making this distinction have been previously described (5, 6). The three function tests used in the differentiation are the diffusing capacity, maximal negative static transpulmonary pressure, and over-all lung compliance. For the present purposes it was arbitrarily decided that nor -TABLE I

Relative contributions of large and small airways to flow limitation in normal subjects before and after atropine and isoproterenol.

“…Bouhuys and van de Woestijne (4) could find no changes in Pst(l) and concluded that isoproterenol made large airways more compliant and therefore increased their dynamic compressibility. Green and Mead (13), studying the volume and time-dependent behavior of airway smooth muscle tone, concluded that a deep inspiration produced bronchodilation and suggested that, since isoproterenol abolished this time-dependence of Vmax, the reappearance of airway tone 70 and 25% of vital capacity during forced expiration (15). Therefore upstream segments contain both small peripheral and larger, more central airways, and Vmax is highly density dependent in such subjects (16).…”

Expiratory flow limitation and the response to breathing a helium-oxygen gas mixture in a canine model of pulmonary emphysema.

“…Further, at least at CP, as determined by the estimated Reynold's numbers at these sites, turbulent flow was present. Although Dosman suggested that in patients with small airways obstruction, EPP would move into airways where cross-sectional area was large and flow laminar, Macklem et al (8) showed that in patients with emphysema or bronchitis airflow limitation still occurred at lobar bronchi. Accordingly, the findings in the present experiment with respect to loci of flow limitation were similar to those previously reported by Macklem et al Interestingly, Dosman et al suggested that when the only mechanical change in the lung was a decrease in Pel, A Vmax would not decrease.…”

“…In previous studies, the pathophysiology of reduced Vmax in PE has been examined in terms of theories of flow limitation, which are based on conceptual analyses. These included "equal pressure point" theory or theories based on the concept of a flow-limiting segment (6)(7)(8)(9). However, recent evidence suggests that in healthy lungs Vmax may be explained in terms ofwave-speed theory (10, 1 1).…”

Bronchial Hyperreactivity in the Peripheral Airways.

“…Macklem et al (1965) measured the intrabronchial pressure of segmental bronchi using a catheter, and found that the iespiratory obstruction in emphysema and bronchitis lies somewhere in the small airways between the segmental bronchi and the alveoli. However, the catheter itself disturbed the airflow of the located segment.…”