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We studied 196 patients with suspicion of pulmonary embolism (PE), subsequently confirmed in 98 by positive pulmonary angiography and excluded in 98 by normal or near-normal perfusion lung scan. Patients had a clinical questionnaire for history, and, soon after. a radiograph, blood gas analysis, and an ECG. Clinical and instrumental signs were matched in patients with confirmed and unconfirmed PE to find those more frequent in embolic patients and, thus, more characteristic of PE. The following were: previous PE, immobilization and thrombophlebitis (p < 0.05); dyspnea and cough (p < 0.05); enlarged descending pulmonary artery (DPA), enlarged right heart, pulmonary infarction, Westermark sign (p < 0.001), and elevated diaphragm (p < 0.05); hypoxemia. No ECG sign was more frequent in PE. Thereafter, all variables were processed separately with a logistic multiple regression analysis and those significantly associated to PE were tested in a final logistic model that was able to predict the actual result of angiography or scintigraphy; accordingly, previous PE, immobilization, thrombophlebitis, enlarged DPA, pulmonary infarction, Westermark sign, hypoxemia were significantly associated with a high risk of PE (from 2.8 to 15 times greater than in patients without these signs). Therefore, we may conclude that clinical assessment and noninvasive tests may help to detect patients at higher risk for PE where heparin coverage should be started while waiting for conclusive diagnostic procedures.

We studied 84 consecutive patients referred with the suspicion of pulmonary embolism (PE) to investigate the influence of clinical and hematological profiles on the diagnosis and severity of this disease and recovery. Diagnosis of PE was confirmed in 48 out of 84 patients by perfusion scintigraphy and/or pulmonary arteriography. Severity of PE and entity of recovery were investigated by measuring standard PaO2 on blood gas analysis and the number of unperfused lung segments ULS on perfusion scintigraphy. Most common clinical predisposing conditions were more frequent, though not significantly so, in embolic patients and a very low prevalence of PE was appreciable in patients without clear predisposing conditions. Among coagulation factors, only thrombin-antithrombin (TAT) complexes were twice as high in embolic as in nonembolic patients (14.0 +/- 13.6 vs. 7.0 +/- 4.2 ng/ml; p0.02), while there was no statistically significant difference between embolic and nonembolic patients for activated partial thromboplastin time, prothrombin time, antithrombin III, protein C, fibrinogen, plasminogen, alpha 2-plasmin inhibitor, and plasminogen activator inhibitor-1. Sensitivity and specificity of TAT complexes in diagnosis of PE were 95.8% and 30.5%, respectively. Therefore, normal values of TAT complexes may help exclude the diagnosis of PE, while abnormal values allow to reinforce the clinical suspicion of PE. No relation was found between coagulation parameters and the severity of PE. The follow-up of 48 patients with confirmed PE was favorable on the average; however, neither the presence of predisposing conditions nor abnormal coagulation parameters allow to predict the degree of functional and scintigraphic improvement during follow-up.

The past and present clinical history of 13 patients with hemodynamic and angiographic diagnosis of chronic thromboembolic pulmonary hypertension (CTPH) was reviewed in order to investigate the reasons for failure of resolution of acute pulmonary embolism (PE) and findings useful for diagnosis of CTPH. All patients had chest radiograph, ECG, arterial blood gas analysis and pulmonary perfusion scintigraphy performed. Clinical assessment demonstrated that no patient had diagnosis and treatment of the several retrospectively identified episodes of PE (from 1 to 8); the lack of diagnosis was due to underestimation of symptoms and signs such as dyspnea (85%), pleuritic chest pain (31%) or phlebitis (46%) that were present months or years earlier. Alternative diagnoses erroneously made were dyspnea of unknown origin (5 cases), left heart failure (4 instances) and pneumonia (2 cases). Once CTPH has developed, chronic dyspnea (92%) and substernal chest pain (100%) are almost always present: chest radiograph and ECG show signs of chronic hypertension such as enlargement of hila (100%), right heart sections (77%), azygos vein (46%) and P pulmonale (67%), T inversion on right precordial leads (75%), S-T segment depression (75%), respectively. Perfusion scintigraphy shows severe perfusion impairment (55.7% of the total vascular bed) paralleled by severe hypoxia (standard PaO2 = 49 +/- 14.1 mm Hg). In conclusion, patients with PE who develop CTPH are not diagnosed and thus untreated because clinical symptoms and signs of acute PE have not been recognized. If CTPH develops, clinical assessment (including simple and noninvasive techniques such as chest radiograph, ECG and blood gas analysis) may show a quite characteristic pattern useful for diagnosis.

Although it is accepted that thoracic structures are enlarged in supine chest radiographs, it is not known whether the lying posture may also influence the radiographic detection of abnormalities, such as those suggestive for pulmonary embolism (PE). For this purpose, we performed planar chest radiographs both in the seated and supine positions, keeping the target-to-film distance at 2 m, in 20 patients with acute PE. Chest radiograph was then repeated 1 month later in either position with the radiological conditions unchanged to investigate the effect of posture on the detection of resolution of signs. The detection of signs due to modifications of preexisting thoracic structures (elevation of the diaphragm and enlargement of the heart, right descending pulmonary artery and azygos vein) in acute PE was different between films taken in the supine and seated positions: both hemidiaphragms were more elevated (p less than 0.001), heart and central vessels were wider (p less than 0.05 or less) when patients were supine. On the contrary, the detection of signs of new occurrences ('sausage'-like appearance of the descending pulmonary artery, linear atelectasis, densities compatible with pulmonary infarction, pleural effusion and focal hyperlucency) was not influenced by the patient's position. During recovery, both kinds of abnormalities were reduced concomitantly in seated and supine radiographs. In conclusion, in acute PE, chest radiographs should be obtained in the seated position since the supine posture may overestimate signs due to modifications of preexisting thoracic structures even though it does not influence the detection of signs of new occurrences. On the contrary, films taken in either position are useful to follow the evolution of PE, provided the film is obtained in the same position and with the same technique as in the acute phase.

The anamnesis is believed to be poor in identifying patients with pulmonary embolism (PE), but the method of data collection may be critical for inference on this issue. We compared the prevalences of history findings recorded after a free verbal interview (VI) by the referring physicians with those recorded after completion of a standardized questionnaire (SQ) by the admitting physicians in a group of 177 consecutive patients referred to our Emergency Unit with the suspicion of PE (subsequently confirmed in 97). VI data were incomplete in 18 patients. In the remaining 159 patients, prevalences of symptoms and predisposing factors were higher after SQ than after VI. Accordingly, 8 items (obesity, prolonged immobilization, surgery, varicose leg veins, deep venous thrombosis, pleuritic chest pain, and sudden-onset dyspnea) were significantly more prevalent in patients with confirmed PE after SQ, compared to only 2 items (prolonged immobilization and pleuritic chest pain) after VI. When we tested for the agreement between the two methods of data collection, kappa values ranged from high values (for surgery and hemoptysis) to very low values (for prolonged immobilization and recurrent phlebitis). These results show that the use of an SQ could improve the accuracy of collecting clinical data in patients with suspected PE, as they are also consistent in separating patients with PE from those with unconfirmed suspicion of PE. Moreover, it allows the clinician to be alert towards findings which could be missed when not carefully searched for and which may be useful to raise or strengthen the suspicion of this disease.

In order to evaluate the pattern of airway response to a specific bronchial provocative test (sBPT) with an extract of Phleum pratensis standardized in biological units (BU), we studied 27 patients with seasonal asthma due to grass pollen by means of allergologic evaluations, methacholine inhalation test and sBPT, outside the pollen season in all patients and, in 10 of them, also during the pollen season. We used a DeVilbiss 646 nebulizer with a dosimeter, giving increasing doses (0.01–2.5 BU) of the allergen solution and we monitored FEV1 to assess early (EAR) and late (LAR) airway responses. Outside the pollen season sBPT elicited an isolated EAR in 16 and a dual asthmatic response (DAR) in 11 patients. We observed no significant difference between EAR and DAR patients as regards the provocative dose causing a 15% fall in FEV, (PD15FEV1) methacholine, EAR (expressed by PD15FEV1, allergen) or allergologic data. There was a significant relationship between PD15FEV1 allergen and PD15FEV1 methacholine (r = 0.43, p 15FEV1 allergen; r = 0.95, p 1 during LAR. Ten patients repeated all tests during the grass pollen season. PD15FEV1 methacholine and baseline FEV1 decreased significantly during the pollen season, but PD15FEV1 allergen did not change significantly during the season. Although 6 patients with a DAR outside the pollen season showed an isolated EAR during the season, the mean percent fall in FEV1 during EAR and LAR was not different between seasons

Accessible online at: www.karger.com/res Pulmonary embolism (PE) is a common disease that may be fatal if untreated, while it may show a favorable course when promptly recognized and treated. Although clinicians have searched for objective tests to confirm or rule out the diagnosis, PE remains a challenging diagnostic problem since it is detected only at autopsy in about two thirds of cases, even in most recent published series. In recent years, several diagnostic strategies have been introduced in clinical practice. In outpatients, the sequential use of D-dimer measurement, lower limb venous compression ultrasonography, clinical evaluation of the likelihood of PE and a correct interpretation of lung scan results make it possible to correctly treat more than 90% of patients with suspected PE and to safely not treat more than 99% [1]. In both outand inpatients, the evaluation of clinical likelihood combined with a simple, practical reading of perfusion lung scintigraphy helps to restrict the need for angiography to a minority of patients [2]. Nevertheless, the demand for a single test that might accurately and noninvasively allow diagnosis of PE has remained high, more than for other diseases; lately, the hope of such a test seems finally to have become reality with the helical CT scan. Indeed, after the skeptical conclusion of Rathbun et al. [3] in their systematic review reported in 2000, evidence has been published that in patients with suspected PE, helical CT scan may be used efficaciously and safely as the primary test to detect and rule out PE [4]. A valid contribution to the exclusion of PE by helical CT scan is also given by Friera et al. [5] in their paper published in this issue of Respiration. In a prospective study including more than 200 patients, the authors give an elegant demonstration of the utility of a negative CT scan (when used as the only imaging method) in excluding clinically suspected PE. In their report, patients with clinically suspected PE, not otherwise anticoagulated and followed for a 3-month period of time, did not show venous thromboembolic events during the entire follow-up. Though the aforementioned studies have raised widespread enthusiasm, we believe that the old issue concerning the entire diagnostic process and the following management of PE still remains far from having a definitive solution, and it deserves further consideration. Firstly, the strategy for diagnosis varies among different centers according to the availability of one or more techniques that may integrate with each other. For instance, strong evidence has existed for a long time that perfusion lung scan, when normal, reliably excludes the diagnosis of PE without the necessity of further tests. Perfusion lung scan is objective, has a low cost and is easily repeatable, while helical CT is perhaps not cost-effective as a single test. Thanks to the same characteristics, perfusion lung scan may be used to control the efficacy of therapy after an adequate lapse of time, usually before hospital discharge. Is it cost-effective to perform such a control by helical CT? Is it feasible to use an instrument designed for emergencies for routine controls? As a matter of fact, it

Accessible online at: www.karger.com/res ‘Flow limitation’ is an expression classically used to indicate that there is a reduction in the maximal expiratory flows that may be attained during the forced vital capacity (FVC) maneuver. It is measured from the ratio FEV1/VC, which dates back to Tiffeneau, where FEV1 is the forced expiratory volume in the first second and VC is the slow expiratory vital capacity. As such it is proposed in the ERS consensus statement [1] as a relatively sensitive index of chronic obstructive respiratory disease (COPD). As a matter of fact, measurement of expiratory flow limitation should be based on the isovolume relationships between flow and transpulmonary pressure, but this procedure is time-consuming and invasive [2]. To overcome these drawbacks, Hyatt [3] proposed that expiratory flow limitation should be evaluated by comparing tidal volume with FVC curves. Since this approach may lead to erroneous conclusions [4], a new definition of airflow limitation has been recently proposed to better assess changes in the mechanical properties of airways and lung parenchyma [4, 5]. This new definition is based on a simple and noninvasive approach, namely, the negative expiratory pressure (NEP) technique, which does not require performance of FVC maneuvers on the part of the subject. It entails applying a negative pressure at the mouth during tidal expiration and comparing the ensuing flow-volume curve with that of the previous control expiration. It can be applied in different body positions, both at rest and during muscular exercise [6]. It has been observed that the NEP technique provides a rapid and reliable method to detect expiratory flow limitation at rest and during exercise in COPD patients [6]. Schroeder et al. [7, this issue of Respiration] have chosen to assess flow limitation and breathing reserve at rest and during exercise in patients with congestive heart failure (CHF) by comparing FVC loops (MFVL) with subsequently obtained tidal flow-volume loops (FVL). Similarly to Koulouris et al. [6] in COPD patients, they report a significant increase of flow limitation during exercise in CHF patients, whereas the increase in expiratory flow volume reserve (EFVR) and in end inspiratory lung volume (EILV) is not significant. They conclude that, unlike normal subjects, CHF patients cannot utilize their full respiratory capacity during exercise secondary to expiratory flow limitation and an inability to increase EILV and EFVR. It remains to be ascertained whether these interesting conclusions on expiratory flow limitation and breathing strategy are affected by the mentioned shortcomings inherent in comparisons between tidal volume and FVC curves obtained from measurements of expired gas volume. In particular, the reported results on expiratory airflow limitation (i.e., inability to further increase flow

The determination of the prevailing site of bronchial constriction in asthma is of noteworthy interest as regards knowledge of the pathophysiological mechanisms of this disease, and of practical importance because the intrapulmonary distribution of inhaled drugs depends chiefly on airway caliber. To visualize the alteration of convective ventilation caused by the alterations of airway caliber, we developed a technique based on inhalation of a monodispersed aerosol of human albumin minimicrospheres (mean aerodynamic diameter 0.75 micron, geometric SD 1.19) labeled with 99mTc(Hamm). Intrapulmonary HAMM deposition is revealed externally by means of a gamma camera in 4 projections, soon after inhalation and 4 h later, when the mucociliary activity has removed the fraction of HAMM deposited in larger airways. In normal subjects, about 16% of the inhaled HAMM deposited in airways, mostly (90% of total deposited fraction) by sedimentation in airways peripheral to the 16th generation. We obtained 58 determinations of the HAMM deposition pattern in 38 patients (17 males and 21 females, mean age 35.2 +/- 16.8 years) with symptomatic or asymptomatic asthma, none under acute attack. At the same time we obtained the determination of bronchoconstriction degree by measuring the forced expiratory volume in 1 s (FEV1) and the airway resistance (Raw) by plethysmographic technique. In 10 asymptomatic patients with normal bronchoconstriction indexes, we revealed the pattern of HAMM deposition before and after a reduction of about 30% in FEV1 in induced by bronchial challenge with carbachol.(ABSTRACT TRUNCATED AT 250 WORDS)

In order to assess the variability of forced expiratory flows, 15 male players (age 16-19 years, height 182-201 cm) of the Italian National Junior Volley team were studied twice with the pneumotachygraph of the computerized Hewlett-Packard Pulmonary System. The first time (April), but not the second (July), all the subjects were physically trained. Each subject performed at least three acceptable forced vital capacity (FVC) maneuvers, following the standard of the American Thoracic Society, with the exception of the criterion for determining the FVC end point. Mean values of forced mid- and end-expiratory flows were significantly higher in April than in July. Inter- and intrasubject coefficients of variation were lower for FVC and forced expiratory volume in 1 s (FEV1) than for the flows. However, the within-subject variability of expiratory flows is lower in our athletes than in the subjects described by other authors. Our findings indicate the importance of forced expiratory flows in detecting even minor intra-subject variations related to physical training and suggest that flow in the terminal portion of the FVC curve may be at least moderately dependent upon effort.