Detection of expiratory flow limitation by manual compression of the abdominal wall.

We have assessed a new method, manual compression of the abdominal wall (MCA) during expiration, in the detection of expiratory flow limitation. Twelve stable patients with chronic obstructive pulmonary disease (COPD) and five normal subjects were studied during spontaneous breathing in the supine and seated posture. MCA was performed during expiration with one hand at the umbilical level and we measured flow, volume, pleural (Ppl) and gastric (Pga) pressures and abdominal anteroposterior (AP) diameter at the umbilical level with magnetometers. No increase in expiratory flow during MCA relative to the preceding breath despite associated increases in pressures was considered as indicating expiratory flow limitation. In seven additional patients with increased upper airway collapsibility (obstructive sleep apnea syndrome [OSAS]), MCA was compared with negative expiratory pressure (NEP). In normal seated subjects, MCA was associated with a decrease in abdominal AP dimension (mean +/- SD: -27 +/- 6%), an increase in Pga (14.7 +/- 7.4 cm H(2)O) and Ppl (6.2 +/- 2.2 cm H(2)O), and an increase in expiratory flow. MCA caused similar changes in abdominal AP dimension and pressures in seated patients with COPD but six of them (50%), including four patients with FEV(1) less than 1 L, had no increase in expiratory flow. In the supine posture, MCA always increased expiratory flow in normal subjects but four additional patients with COPD showed evidence of flow limitation. MCA invariably increased expiratory flow in patients with OSAS whereas the NEP method suggested flow limitation in some cases. We conclude that MCA is a very simple method that allows detection of flow limitation in different positions.

Oleic acid-induced lung injury: thin-section CT evaluation in dogs.

PURPOSE: To validate lung attenuation measurements for quantifying extravascular lung water in oleic acid-induced pulmonary edema, compare subjective assessment with attenuation measurements, and compare this permeability-type pulmonary edema with hydrostatic-type pulmonary edema. MATERIALS AND METHODS: Thin-section computed tomography (CT) and pulmonary hemodynamic examinations were performed sequentially in six dogs before and after intravenous administration of 0.08 mg of oleic acid per kilogram of body weight. Extravascular lung water and pulmonary capillary pressure were measured. Results were compared with those reported in a canine model of hydrostatic edema. RESULTS: Oleic acid induced a progressive increase in extravascular lung water without a change in capillary pressure, which indicated pure permeability-type edema. Ground-glass opacification was detected as soon as extravascular lung water increased. Lung attenuation was highly correlated to extravascular lung water (r = 0.76, P<.001), as in hydrostatic edema, but was characterized by an almost absent gravitational gradient. CONCLUSION: Thin-section CT is sensitive for early detection and quantification of oleic acid-induced pulmonary edema in a canine model. Different from early canine hydrostatic edema, which is characterized by a gravitational gradient, early oleic acid-induced pulmonary edema in a supine dog is characterized by nearly homogeneous distribution, except for ventral sparing.

Partitioning of pulmonary vascular resistance in primary pulmonary hypertension.

OBJECTIVES: This study sought to determine the site of increased pulmonary vascular resistance (PVR) in primary pulmonary hypertension by standard bedside hemodynamic evaluation. BACKGROUND: The measurement of pulmonary vascular pressures at several levels of flow (Q) allows the discrimination between active and passive, flow-dependent changes in mean pulmonary artery pressure (Ppa), and may detect the presence of an increased pulmonary vascular closing pressure. The determination of a capillary pressure (Pc') from the analysis of a Ppa decay curve after balloon occlusion allows the partitioning of PVR in an arterial and a (capillary + venous) segment. These approaches have not been reported in primary pulmonary hypertension. METHODS: Ppa and Pc' were measured at baseline and after an increase in Q induced either by exercise or by an infusion of dobutamine, at a dosage up to 8 microg/kg body weight per min, in 11 patients with primary pulmonary hypertension. Reversibility of pulmonary hypertension was assessed by the inhalation of 20 ppm nitric oxide (NO), and, in 6 patients, by an infusion of prostacyclin. RESULTS: At baseline, Ppa was 52+/-3 mm Hg (mean value+/-SE), Q 2.2+/-0.2 liters/min per m2, and Pc' 29+/-3 mm Hg. Dobutamine did not affect Pc' and allowed the calculation of an averaged extrapolated pressure intercept of Ppa/Q plots of 34 mm Hg. Inhaled NO had no effect. Prostacyclin decreased Pc' and PVR. Exercise increased Pc' to 40+/-3 mm Hg but did not affect PVR. CONCLUSIONS: ns. These findings are compatible with a major increase of resistance and reactivity at the periphery of the pulmonary arterial tree.