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Nicotine replacement therapy (NRT) is an effective treatment for smokers who want to quit, however, the rates of successful quitting can be improved even more. In this context, nicotine dependence (assessed via the Fagerström Tolerance Questionnaire, FTQ), psychological distress (measured via the Symptom Rating Test, SRT), and personality traits (evaluated via the Adult Eysenck Personality Inventory, AEPI) were evaluated as possible predictors of smoking cessation.A total of 297 cigarette smokers were followed for one year as part of a NRT double-blind, parallel group, randomized trial. Baseline nicotine dependence (weeks 12 and 26: p0.05), AEPI neuroticism (weeks 12 and 52: p0.05), and AEPI psychoticism (weeks 12 and 52: p0.05) scores significantly influenced the outcome of smoking cessation during one-year of follow-up. An increase in psychological distress during follow-up was associated with a lower probability of quitting smoking (p=0.000).Nicotine dependence, neuroticism, psychoticism and, over time, psychological distress were the main factors influencing the long-term outcome (i.e., up to 12 months) of smoking cessation under NRT.

Background Estimating COPD occurrence is perceived by the scientific community as a matter of increasing interest because of the worldwide diffusion of the disease. We aimed to estimate COPD prevalence by using administrative databases from a city in central Italy for 2002–2006, improving both the sensitivity and the reliability of the estimate. Methods Multiple sources were used, integrating the hospital discharge register (HDR), clinical charts, spirometry and the cause-specific mortality register (CMR) in a longitudinal algorithm, to reduce underestimation of COPD prevalence. Prevalence was also estimated on the basis of COPD cases confirmed through spirometry, to correct misclassification. Estimating such prevalence relied on using coefficients of validation, derived as the positive predictive value (PPV) for being an actual COPD case from clinical and spirometric data at the Institute of Clinical Physiology of the National Research Council. Results We found that sensitivity of COPD prevalence increased by 37%. The highest estimate (4.43 per 100 residents) was observed in the 5-year period, using a 3-year longitudinal approach and combined data from three sources. We found that 17% of COPD cases were misclassified. The above estimate of COPD prevalence decreased (3.66 per 100 residents) when coefficients of validation were applied. The PPV was 80% for the HDR, 82% for clinical diagnoses and 91% for the CMR. Conclusions Adjusting the COPD prevalence for both underestimation and misclassification of the cases makes administrative data more reliable for epidemiological purposes.

Summary Background In Italy, infections with carbapenem-resistant Klebsiella pneumoniae (CRKP) have increased markedly since 2009, creating unprecedented problems in healthcare settings and limiting treatment options for infected patients. Aim To assess the attributable mortality due to CRKP in ten Italian hospitals and to describe the clinical characteristics of patients with an invasive CRKP and carbapenem-susceptible K. pneumoniae (CSKP) infection. Methods We conducted a matched cohort study, and calculated crude and attributable mortality for CRKP. The attributable mortality was calculated by subtracting the crude mortality rate of the patients with CSKP from the crude mortality rate of the patients with CRKP. We also described the clinical characteristics of CRKP and CSKP patients and analysed the determinants of mortality by using conditional Poisson regression. Findings The study included 98 patients, 49 with CRKP and 49 with CSKP. CRKP patients had undergone more invasive procedures and also tended to have more serious conditions, measured by higher Simplified Acute Physiology Score II. The attributable mortality of CRKP at 30 days was 41%. CRKP patients were three times more likely to die within 30 days [matched incidence rate ratio (mIRR): 3.0; 95% confidence interval (CI): 1.5–6.1]. Adjusting for potential confounders, the risk remained the same (adjusted mIRR: 3.0; 95% CI: 1.3–7.1). Conclusion CRKP infection had a marked effect on patient mortality, even after adjusting for other patient characteristics. To control the spread of CRKP we recommend prioritization of control measures in hospitals where CRKP is found.

Single cell gel electrophoresis (SCGE), or comet assay, appears to be a promising tool to estimate DNA damage at the single cell level and it provides information on the presence of damage among individual cells. A follow-up study of 90 smokers who ceased smoking was undertaken to determine the possible decrease of DNA damage in their leukocytes. Before beginning the trial, volunteers smoked on average 26.1 +/- 8.4 cigarettes/day. Comet length did not correlate with the number of cigarettes/day or with the condensate tar content. At the end of the study, 28 volunteers had abandoned the trial, 40 volunteers relapsed into smoking at different times, but with a reduced number of cigarettes/day, whereas 22 fully succeeded in smoking cessation. Throughout the 5 sampling times, a great variability of comet length at individual level was found. However, after 1 year of follow-up, comet length means were found to be significantly shorter (p0.0001) in those volunteers who completely quit smoking compared to those who relapsed into smoking (27.2 +/- 1.6 vs. 31.9 +/- 5.1 microns, respectively), irrespective of the amount of cigarettes previously smoked. No effect of age or sex was found. Six months later, these results were confirmed by a further study carried out on a reduced sample of volunteers. The present data strongly suggest that, in spite of the great variability observed, 1 year of smoking cessation is associated with a significant reduction of DNA damage in circulating leukocytes.

Breath-hold divers may experience haemoptysis during diving. Central pooling of blood as well as compression of pulmonary gas content can damage the integrity of the blood-gas barrier, resulting in alveolar hemorrhage. The single-breath carbon monoxide test (DL,CO) was used to investigate the blood-gas barrier following diving. The study population consisted of 30 divers recruited from a training course. DL,CO levels were measured before diving and at 2, 10 and 25 min after the last of a series of four dives to depths of 10, 15, 20 and 30 m. When compared to pre-diving values, DL,CO values increased significantly at 2 min following diving in all subjects except one. Thereafter values progressively decreased toward baseline at 10 and 25 min in all subjects but one, while in four divers DL,CO values decreased below baseline. The early but transient increase in DL,CO levels shortly after diving supports the persistence of capillary pooling of red blood cells following emersion. Persistence at 25 min of high DL,CO values in one subject could be attributed by lung CT to extravasation of blood into the alveoli. Early or late DL,CO values10% below baseline values suggest the presence of pulmonary edema. The relatively high prevalence of DL,CO alterations found suggests caution on the safety of breath-hold diving activities.

The aim of this retrospective analysis was to assess the extent of smoking reduction in smokers who were compliant to a smoking cessation trial with nicotine patch, and failed to completely quit smoking. Out of 297 smokers in total, 237 participants received active treatment (60 received placebo). Eighty treated subjects attended all the scheduled visits and were classified as either abstainers (nonsmokers), regular smokers or occasional smokers. Compared to the remaining 157 participants, these 80 subjects had significantly lower mean baseline daily cigarette consumption (24 versus 30; p0.001), expired carbon monoxide levels (25 versus 33 ppm; p0.001), plasma nicotine and cotinine levels, and Fagerström Tolerance Questionnaire score (5.7 versus 7.0; p0.001). All subjects received active treatment for up to 18 weeks (full dose for 12 weeks plus tapering dose for 6 weeks), with follow-up visits scheduled up to 1 yr. A statistically significant reduction in cigarette consumption (versus baseline) was observed among both the occasional (-99%) and regular (-77%) smokers between week 1 and week 52 (p0.001). Concomitant smoking and patch use was well tolerated since adverse events were infrequent, mild and transient. Thus, in addition to those subjects who successfully quit smoking, a further group of subjects who attended all the follow-up visits during the smoking cessation trial significantly reduced their mean daily cigarette consumption.

Twenty healthy, asymptomatic long-term cigarette smokers (8 males, 12 females; mean age: 43 +/- 9 years) were selected at random from a larger series receiving nicotine replacement therapy (NRT) for 12 weeks to study the effects of NRT on plasma markers of oxidative stress. Plasma aliquots, obtained at baseline (T0) and after 12 weeks (T12) of NRT, were used to measure malondialdeyde (MDA) and total Trolox-equivalent antioxidant capacity (TEAC). In subjects who completely quit smoking ('quitters', n = 10), MDA was higher at T0 (1.08 mumol/l, interquartile range 0.85-1.16) than at T12 (0.71 mumol/l, range 0.32-0.92; p < 0.01), and TEAC was lower at T0 (1.20 mM, range 1.11-1.31) than at T12 (1.43 mM, range 1.31-1.49; p < 0.05). In subjects who had only reduced the number of cigarettes smoked per day ('reducers', n = 10), differences between the T0 and T12 levels of MDA (0.81 [0.75-0.96] vs. 0.76 [0.58-0.84] mumol/l) and TEAC (1.28 [1.05-1.50] vs. 1.25 [1.09-1.42] mM) were not significant. At T0, MDA and cotinine levels correlated in reducers (r = 0.79, p < 0.05) and, though not significantly, in quitters (r = 0.50, p = 0.12). At T12 this relationship between MDA and cotinine was still present in the reducers (r = 0.70, p < 0.05), while the scatter of points in quitters was completely dispersed (r = (0.09). These results show that smoking cessation but not smoking reduction is associated with decreased markers of oxidative stress in the plasma of active cigarette smokers.

Studies on gas exchange in pulmonary embolism are not numerous. A few of them have been performed in experimental animals [4]. The methods employed comprise the determination of gas exchange parameters [14], including the physiologic dead space [1], and the multiple inert gas elimination technique [2,8,10].

The aim of this study was to evaluate whether ozone exposure induces a similar airway inflammatory response in subjects with different degrees of asthma severity. Two groups of asthmatic subjects were studied: seven with intermittent mild asthma not requiring regular treatment (group A); and seven with persistent mild asthma requiring regular treatment with inhaled corticosteroids and long-acting beta2-agonists (group B). All subjects were exposed, in a randomized cross-over design, to air or O3 (0.26 parts per million (ppm) for 2 h with intermittent exercise); subjects in group B withdrew from regular treatment 72 h before each exposure. Before the exposure, and 1 and 2 h after the beginning of the exposure they performed a pulmonary function test, and a questionnaire was completed to obtain a total symptom score (TSS). Six hours after the end of the exposure, hypertonic saline (HS) sputum induction was conducted. Sputum cell percentages, eosinophil cationic protein (ECP) and interleukin (IL)-8 concentrations in the sputum supernatant were measured. TSS significantly increased and forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) significantly decreased after O3 exposure in comparison with air exposure in group A, whereas no changes were observed in group B except for a significant decrement of FEV1 2 h after the beginning of O3 exposure. Sputum neutrophil percentage was significantly higher after O3 exposure than after air exposure in both groups (Group A: 70.2% (28-87) versus 26.6% (8.6-73.2); Group B: 62.1% (25-82.4) versus 27.9% (14.4-54)). IL-8 was higher in sputum supernatant collected 6 h after O3 exposure than after air, only in group A. No change due to O3 has been found in sputum eosinophil percentage and ECP concentration in both groups. In conclusion, the degree of airway response to a short-term exposure to ozone is different in subjects with asthma of different severity. The available data do not allow elucidation of whether this difference depends on the severity of the disease or on the regular anti-inflammatory treatment.

Trends in mortality rates for respiratory disorders were investigated in Italy from 1979 to 1990, using data from the Italian Central Statistical Institute (ISTAT). Mortality from lung cancer increased in all age groups, except for those aged 45-64 yrs after 1985. Respiratory diseases showed a consistent reduction; in particular, mortality from emphysema decreased slowly, and mortality from chronic bronchitis showed a significant reduction in all age groups. However, mortality from asthma increased markedly in all age groups up to 1985, and then levelled off and slightly decreased, although remaining at a higher level than in the 1970s. In 1990, data stratified for age group and gender indicated a higher mortality rate in males, that tended to be age-dependent, with the highest rate ratio male/female in those aged 65-74 yrs. Overall, these data indicate a trend to increased mortality from lung cancer and asthma in Italy in the 1980s.

Among biomarkers of tobacco smoke (TS)-induced genotoxic damage, benzo[a]pyrene diolepoxide-DNA adducts (BPDE-DNA) are extensively studied. Adducted DNA becomes antigenic and antibodies anti-BPDE-DNA (BPDE-DNA-Abs) may be found in serum of exposed subjects. Little is known about the persistence of BPDE-DNA, and no study has been performed to evaluate the persistence of BPDE-DNA-Abs after cessation of exposure. Fifty heavy smokers, enrolled in a smoking cessation program with nicotine patch substitution therapy, were evaluated for the presence of BPDE-DNA-Abs before (w0) and 1, 3, 6 and 12 weeks (w1–12) after the start of the program. Nicotine or placebo patches were randomly assigned to the subjects. BPDE-DNA-Abs were determined in serum by non-competitive ELISA. After the start of the cessation program, 28 subjects quit smoking (group Q) and the other 22 reduced by about 75% the number of cigarettes smoked per day (group R). At the start of the program (w0) 8% of subjects were positive. At w1 the prevalence of positivity had increased both in subjects who quit smoking (Q: 21%) and in subjects who had reduced the number of cigarettes per day (R: 27%). Positivity remained stable up to w12 (21%) for group Q, whereas it increased to 41% in group R. Serum BPDE-DNA-Abs can be detected in smokers, and their persistence for months after smoking cessation suggests their usefulness for relatively long-term surveys. The low percentage of positivity in actual heavy smokers and the increase in antibody positivity with smoking cessation or reduction must be taken into account when interpretating serum BPDE-DNA-Ab measurement in exposed individuals. Int. J. Cancer, 70:145–149, 1997. © 1997 Wiley-Liss, Inc.

Nicotine replacement by transdermal patches is more effective than placebo in smoking cessation, but has a low success rate after one year (9-18%). We tested whether this was attributed to insufficient nicotine replacement. We conducted a randomized trial to investigate the effect on outcome of different doses of transdermal nicotine replacement after stratification according to baseline plasma cotinine values. Two hundred and ninety seven adult smokers were enrolled. Those with baseline cotinine < or = 250 ng.ml-1 (low cotinine) were randomly assigned to placebo (LC-P) or to 15 mg 16 h nicotine patches (LC-15), and those with baseline cotinine > 250 ng.mL-1 (high cotinine) were randomly assigned to 15 mg (HC-15) or 25 mg (HC-25) 16 h nicotine patches. Plasma nicotine and cotinine values, expired carbon monoxide and withdrawal symptoms were measured at scheduled intervals during treatment. Smokers in the LC-15 group had a significantly higher success rate than placebo (28 vs 9%). Smokers with high baseline cotinine had lower success rates, and a high dose of nicotine did not increase success rate (HC-25 9% vs HC-15 11%). Subjects in the HC-15 group had the lowest percentage of nicotine replacement and a higher prevalence of withdrawal symptoms than the HC-25 group. Replacement was similar in groups LC-15 and HC-25, but the success rate was significantly lower in HC-25 group, despite similar levels of withdrawal symptoms. We conclude that a higher success rate was obtained after one year in smokers with low baseline plasma cotinine values. Determination of plasma cotinine values may be, thus, helpful in identifying smokers who could benefit from transdermal nicotine replacement.

In the investigation of dyspnoea and severe hypoxaemia the clinical relevance of multiple diagnostic techniques was studied. The patient was sequentially studied utilizing several techniques. The degree of lung impairment by spirometry, diffusing capacity for carbon monoxide, haemodynamics, pulmonary gas exchange, ventilation-perfusion relationships assessed by the multiple inert gases elimination techniques, ventilation and perfusion lung scans, gallium 67 scintigraphy, bronchoalveolar lavage and high resolution computerized tomography, twice over a period of 12 months during recovery under treatment. A marked impairment of pulmonary gas exchange was first explained by diffusion impairment and ventilation-perfusion mismatch. The multiple inert gas elimination technique allowed determination of the cause of hypoxaemia by ventilation-perfusion inequality. A pathological correlate of the ventilation-perfusion inequality was the appearance of honeycomb lungs detected by high resolution computed tomograph and active alveolitis by bronchoalveolar lavage. All results were consistent with a diagnosis of fibrosing alveolitis. The patient was evaluated again during treatment. Some functional improvement occurred despite persistence of the same pathological findings. In conclusion, this study demonstrates the value of information derived from different tests. Physiological correlations complemented by pathological observations expand understanding of the pathogenesis of disease. These procedures contribute to understanding mechanisms responsible for functional impairment.

ObjectivesAlthough Nicotine replacement therapy (NRT) is an effective treatment for smokers who want to quit, the rates of smoking cessation can be still improved. In an effort to increase these proportions, factors that may influence the occurrence of relapse have been increasingly studied (e.g. pharmacotherapy, socio-demographic characteristics) and there has been a growing interest in psychological and psychiatric clinical factors.MethodsNicotine dependence (assessed via the Fagerström Tolerance Questionnaire, FTQ), psychological distress (measured via the Symptom Rating Test, SRT), and personality traits (evaluated via the Adult Eysenck Personality Inventory, AEPI) were evaluated as possible predictors of smoking cessation in a sample of 297 cigarette smokers followed for one year as part of a NRT double-blind, parallel group, randomized trial.ResultsBaseline nicotine dependence (weeks 12 and 26: p < 0.05), AEPI neuroticism (weeks 12 and 52: p < 0.05), and AEPI psychoticism (weeks 12 and 52: p < 0.05) scores significantly influenced the outcome of smoking cessation during one - year of follow-up. An increase in psychological distress during follow-up was associated with a lower probability of quitting smoking (p = 0.000).ConclusionsNicotine dependence, neuroticism, psychoticism and, over time, psychological distress were the main factors influencing the long-term outcome (i.e., up to 12 months) of smoking cessation under NRT. Thus, psychological distress and personality characteristics should be evaluated in smokers who apply for assistance in smoking cessation with the aim to have a complete assessment and propose tailor-made interventions.

Perfusion lung scintigrams, pulmonary gas exchange data, and chest roentgenograms were obtained in 33 patients during acute embolism and over the following six months in order to assess their clinical usefulness in monitoring the effect of therapy. To this purpose, the measurement of pulmonary gas exchange and the presence of chest x-ray findings were compared with perfusion lung scintigraphic abnormalities both at diagnosis and after 7, 30, and 180 days during treatment. More than 50 percent of the pulmonary arterial tree was obstructed at diagnosis, and a large part of perfusion recovery was complete within the first month. All of the gas exchange parameters were abnormal at diagnosis, and the rate of their improvement was related to that of perfusion recovery. Interestingly, PaO2st (ie, PaO2 corrected for hyperventilation) and VE tended to return to normal during the first month as a consequence of the progressive recovery of perfusion, whereas oxygen and carbon dioxide gradients and physiologic dead space showed the persistence of some abnormalities six months after diagnosis. Significant correlations were observed between the number of ULSs evaluated on the perfusion lung scintigram (and considered an index of the severity of pulmonary embolization) and all of the gas exchange parameters at diagnosis (correlation coefficients averaged from 0.41 to 0.73) and after 7 and 30 days. The enlargement of the right descending pulmonary artery and particularly the "sausage" sign and the Westermark sign were significantly associated with a higher degree of gas exchange impairment and with a more severe embolization. In conclusion, this study demonstrates that perfusion lung scintigraphy has a primary role in monitoring the recovery of patients with pulmonary embolism under treatment. Moreover, the chest roentgenogram may help in this purpose. A second major result is that the simple measurement of some gas exchange parameters may allow the assessment of functional recovery of these patients, thus giving additional information about the effect of therapy.

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)

Alveolar to arterial differences (AaD) may be computed from representative alveolar gas pressures (PA). These are particularly difficult to obtain in patients with chronic airways obstruction (CAO) and severe inhomogeneity of the ventilation/perfusion (VA/Q) ratio. In 25 such patients, using a computerized mass spectrometer, representative values of alveolar gas were obtained: 1. as end-tidal concentrations (ET); 2. using the alveolar air equation with PACO2 derived from Bohr's equation (BE); 3. putting PACO2 = PACO2 into the alveolar air equation to compute ideal O2 alveolar pressure (ID); 4. applying Rahn's definition of "mean" alveolar gas (RD), i.e. taking within each jth breath, the alveolar pressures corresponding to the moment when the instantaneous gas exchange ratio R(t)j equals the overall exchange ratio for that breath Rj. During quiet breathing, the point where R(t)j equals Rj occurred at 71% of tidal volume (VT). Alveolar pressures by BE and RD resulted in similar values (115.5 +/- 6.9 and 115.5 +/- 6.6 mmHg for O2 and 30.3 +/- 5.7 and 30.8 +/- 5.7 mmHg for CO2, respectively), but they were significantly different from those by ET and ID (106.2 +/- 9.5 and 95.6 +/- 13.5 mmHg for O2 and 36.3 +/- 7.7 and 48.2 +/- 11.2 mmHg for CO2, respectively). These findings may be explained considering that PA(BE) and PA(RD) represent both high and low VA/Q units, whereas PA(ET) and PA(ID) represent mainly low VA/Q units. AaDCO2 by RD and BE appeared proportional to the severity of CAO as estimated from VT. Automated techniques make it possible to substitute end-tidal determinations with more accurate estimates either by measuring anatomical dead-space and using Bohr's equation or by applying Rahn's definition.

Lung function studies were performed in 23 patients with the syndrome of essential mixed cryoglobulinemia. Signs of exposure to hepatitis B virus were present in nine (HBV+) and absent in 14 (HBV−). Pulmonary symptoms were generally absent or moderate except in three patients who presented with either asthma, hemoptysis or pleurisy together with the other manifestations of the disease. On the contrary, tests indicative of small airways disease, such as forced end-expiratory flow (FEF 0.75-0.85VC ) and maximal expiratory flow at low lung volume (Vmax 0.75VC ) were markedly altered (61.9 per cent and 40.4 per cent of the expected values, respectively). Other lung function tests, such as residual volume (RV), airway resistance (Raw), FEF 0.25-0.75VC , maximal expiratory flow at 50 per cent vital capacity (VC)(Vmax 0.50VC ) showed smaller deviations from normal, whereas vital capacity (VC), total lung capacity (TLC), forced expiratory volume in 1 second (FEV 1 ), FEV 1 :VC, RV:TLC and intrathoracic gas volume (ITGV) were within the normal limits. Nine of 14 of the HBV− patients showed impairment of gas exchange, measured as alveoloarterial oxygen gradient D(A-a)O 2 , which, on the contrary, was always within normal limits in the nine HBV+ patients. The difference between the two groups was significant (28.4 mm Hg and 18.6 mm Hg, respectively, p

The authors have evaluated the trend of the forced expiratory flows at low lung volumes and of the diffusing capacity for CO in a group of chemical workers of a dye factory, exposed to mineral dusts, organic pigments and solvents. Prevalences of chronic bronchitis and dyspnea, as evaluated by CNR questionnaire, were 15 and 32%. FEF25-75, MEF50 and MEF75 showed statistically significant differences with reference values. The reduction of KCO% was almost completely accounted for by smoking habit. During exercise, DLCOSS2 did not reach the expected values. 71% of the subjects with a diagnosis of COLD had worked more than 15 years in the dye factory. These results suggest a negative effect of the working environment, together with cigarette smoking, on lung function of subjects with a medium-long-term exposure.

Single breath nitrogen test (SBN) provides a considerable amount of information about different indices of lung function:1 closing volume (CV), slope of alveolar plateau (ΔN2%lt), total lung capacity (TLC) and derived indexes (functional residual capacity and residual volume). CV and ΔN2%lt are considered suitable to detect early stages of airways obstruction. Thus they have been proposed for epidemiological studies.

We studied 120 volunteers, 20 to 49 year old, equally divided into sex and smoking habit groups to assess the ability of lung function tests to discriminate smokers from non smokers. The subjects performed routine spirometry including helium dilution, body plethysmography, single breath nitrogen test and forced expiratory manoeuvre. Admission criteria were: 1) normal chest x-ray, 2) absence of cardiorespiratory diseases, 3) absence of repiratory symptoms and exposures (by a questionnaire), 4) normal routine spirometry, and 5) FEV1/VC% > 70. The F-value was calculated for the difference between means in smokers and non-smokers, adjusted for age and height by covariance analysis on transformed variables. Results showed that CV, CV/VC%, N2%1, FEF75-85 and Vmax75 had the highest ability to discriminate smokers and non smokers both in males and females. Other tests, such as plethysmography and helium dilution, were not sensitive. A ranking approach, with the determination of percentage of misclassification for each test using a statistical method, confirmed this trend for both sexes. Assumptions of Gaussian distribution, use of equations based on other population, and use of arbitrary criteria of abnormality were thus avoided.

The mechanisms by which the disturbances of gas exchange develop in human pulmonary embolism are unknown. We investigated whether the inequality of ventilation-perfusion ratio is associated with the abnormalities of pulmonary gas exchange as evaluated by two different computerized techniques. We measured the alveolar to arterial gradients of oxygen and carbon dioxide by means of a computer based system with a mass spectrometer and the ventilation-perfusion distributions by the multiple inert gas technique in 5 patients with acute pulmonary embolism. In these subjects there was a marked ventilation-perfusion inhomogeneity, as detected from inert gases and this finding was in agreement with the impairment of the alveolar to arterial gradients and of their derived indexes. Consideration on the responsible mechanisms for the disturbances of gas exchange are also reported. In conclusion these two computerized techniques provide a useful assessment of the ventilation-perfusion relationships in order to explain the disturbances of gas exchange in critically ill patients.

The determination of alveolar-arterial differences of O2 and CO2 allows assessment of the overall efficiency of gas exchange.

A computer program to measure breath by breath alveolar pressure (PA) and alveolar to arterial difference (AaD) for O2 and CO2, by a mass-spectrometer has been implemented. The program allows the determination of alveolar gas by different methods: 1. Bohr's equation (BE); 2. ideal alveolar air equation for O2 (IDO2); 3. end-tidal (ET); 4. by the Rahn's definition of 'mean alveolar gas', i.e., alveolar pressures are defined when instantaneous respiratory exchange ratio (IRQ) equals mean respiratory exchange ratio (MRQ). This automated technique has been used in 16 patients with chronic obstructive lung disease (COLD) and 15 patients with pulmonary embolism (APE). In both groups of patients it was always possible to find in each breath the point where IRQ = MRQ and therefore to measure AaD by RD. IDO2 was significantly lower than PAO2 by the other methods. Also ET values of O2 and CO2 were significantly different from RD and BE in both groups of patients, however the difference was consistently higher in COLD patients. The different shape of the expirograms (steeper expirograms in COLD) is responsible for this different result. RD and BE AaD characterize gas exchange more precisely than ET, because the contribution of high VA/Q units is also evaluated. This is particularly important in COLD patients. Consideration on dead space measurements are also reported both for COLD and APE patients. In conclusion this automated technique provides the assessment of gas exchange for the use in clinical respiratory physiology and for the monitoring of gas-exchange in critically ill patients.

Patterns of radioaerosol deposition in patients with COPD may be interpreted on the basis of derangements in convective ventilation. Thus, in patients with asthma, central deposition is consistently associated with increased airway resistance, in the absence of acute attack, indicating that in this condition major airways are usually the site of bronchial constriction. In patients with chronic bronchitis, inhomogeneous and spotty deposition patterns are strongly associated with indexes of uneven and wasted ventilation and may be explained on the basis of destruction or obstruction of peripheral airways. Spotty deposition is ascribed to very uneven convective ventilation reduced to a limited number of air streams, as opposed to the normal situation of a very high number of air streams giving rise to the uniform pattern of radioaerosol deposition. Patients with emphysema show less distinctive patterns of deposition and may resemble those of the patients with asthma and chronic bronchitis. Nevertheless, the deposition features are very useful to better characterize the patient even in the emphysematous group. From the practical point of view, the features of aerosol deposition provide useful information for evaluation and treatment of the patient with COPD. They may also prove useful to better define and characterize the different disease entities grouped as COPD.

Lung involvement in essential mixed cryoglobulinemia (EMC) has been recently described. In order to assess whether patients with EMC experience an accelerated deterioration of lung function, nineteen patients (17 females, 2 males; 49.6 +/- 6.6 years) underwent a short-term follow-up of lung function, chest X-ray and serologic investigations. Reduction of forced expiratory flows and presence of roentgenologic signs of interstitial involvement were confirmed in the baseline evaluation. In addition, a decrease of diffusing capacity was shown. After a mean interval of 15 months, no significant change in lung function was found, with the exception of decrease in maximal expiratory flow at 50% of forced vital capacity, total lung capacity, functional residual capacity, coefficient of transfer of CO. A slight decrease of hemolitic complement (CH50) and of complement fraction (C3) was also observed. This study suggests that patients with EMC tend to have an involvement of pulmonary interstitial space, possibly related to immune complex deposition, but they do not show a severe decline of lung function. Periodical assessment of lung function and chest X-ray is, however, worthwhile.

Functional images of pulmonary ventilation during tidal breathing can be obtained with a gamma camera by adding a continuous flow of radioactive krypton-81m (half-life = 13 sec) to the inspired air. The procedure is readily repeatable and provides ventilation images.81mKr ventilation scans were obtained in six asthmatic patients in various phases of the disease. During acute exacerbations, while chest x-rays showed only large-volume lungs, ventilation scans were grossly abnormal, showing large, segmental, or even lobar areas of reduced ventilation as well as an increase in size of the lung images. Similar alterations, although less pronounced, were shown in patients with mild-to-moderate shortness of breath and wheezing. Bronchodilators immediately improved the ventilation defects and reduced lung size. There was further improvement and eventual restoration of normal patterns following prolonged hospital treatment.

The determination of alveolar to arterial differences (AaD) is a simple and available method to determine the overall efficiency of gas exchange. AaD are strongly related to the measurement of alveolar gas, and the different methods commonly used to measure alveolar gas concentrations are not able to give an estimate of the “mean alveolar gas”.

Mechanisms of hypoxemia and hypocapnia in pulmonary embolism (PE) are incompletely understood. We studied 10 patients at diagnosis (D) and five of these again after 10 to 14 d of heparin treatment (T). Patients had right heart catheterization, assessment of ventilation-perfusion ratio (VA/Q) distribution by inert gas, radioisotopic perfusion and ventilation scans, and angiography. At D, two-thirds of the pulmonary circulation was obstructed, patients were hypoxemic (PaO2 = 63.0 +/- 11.7 mm Hg) and hypocapnic (PaCO2 = 30.0 +/- 4.1 mm Hg), mixed venous oxygen pressure (PvO2) was reduced (30.9 +/- 3.9 mm Hg), minute ventilation (VE) markedly increased (14.1 +/- 5.1 L/min), and cardiac output measured by applying the Fick principle to arteriovenous oxygen content difference (QT) slightly low (4.7 +/- 1.7 L/min). Hypoxemia was mainly explained by VA/Q inequality, reduced PvO2 also contributed. Hypocapnia was the result of hyperventilation. VA/Q inequality was characterized by shift of VA and Q distribution mean to regions with higher VA/Q ratio through a fraction of blood flow (19.0 +/- 24.3% of cardiac output) went to lung units with low VA/Q ratio. Log SDQ and log SDvA were increased. Shunt, diffusion limitation, or true alveolar dead space occurred in occasional patients but were generally insignificant. Regional ventilation and perfusion maps indicated that in the unperfused lung segments, ventilation was reduced. Furthermore, they disclosed overperfused lung segments. At T, hypoxemia and hypocapnia improved considerably. However, temporal imbalances in recovery between regional ventilation and perfusion occurred with the former normalizing sooner. However, perfusion recovered sooner than ventilation in some regions.

[This corrects the article DOI: 10.1371/journal.pone.0149302.].