The definition of expiratory flow limitation implies that in this condition a further increase in transpulmonary pressure will cause no further increase in expiratory flow . Therefore, direct assessment of expiratory flow limitation requires de- termination of isovolume relationships between flow and transpulmonary pressure. In the 1950s, F RY et al.  were the first to develop such curves. The explanation of an isovolumic pressure flow curve lies in understanding its construction. Flow, volume and oesophageal pressure (P oes ) are measured simultaneously during the performance of repeated expiratory vital capacity efforts by a subject seated in a volume body plethysmograph, in which gas compression artefact is corrected. The subject is instructed to exhale with varying amounts of effort that are reflected by changes in P oes . From a series of such efforts ( , 30) it is possible to plot flow against P oes at any given lung volume . The flow reaches a plateau at a low positive pleural pressure and once maximum flow for that volume is reached it remains constant, despite increasing P oes by making expiratory efforts of increasing intensity.
Tidal expiratory flow limitation (EFL) occurs when an increase in transpulmonary pressure causes no increase in resting expiratory flow. This phenomenon is common in patients with severe COPD and is a major determinant of dynamic hyperinflation and exercise limitation [1,2]. Dellacà et al. indicated that the differences between in- spiratory and expiratory phases of respiratory system reactance ( Δ Xrs) measured by the forced oscillation technique (FOT) allowed the detection of EFL . It is supposed that Xrs normally reflects the elastic and inertial properties of the respiratory system but, with flow limi- tation, oscillatory signals cannot pass through the choke points and reach the alveoli. During EFL, respiratory sys- tem resistance (Rrs) and Xrs will reflect the mechanical
CFB: Cumulative fluid balance; CFO: Cumulative fluid overload; CKD: Chronic kidney disease; CI: Confidence interval; COPD: Chronic obstructive pulmonary disease; Cst,rs: Static compliance of the respiratory system; Δ P: Driving pressure; Δ Rrs: Additional resistance of the respiratory system; EFL: Expiratory flow limitation; EPP: Equal pressure point; KDIGO: Kidney Disease Improving Global Outcomes; IBW: Ideal body weight; ICU: Intensive care unit; MRC: Modified Medical Research Council; NYHA: New York Heart Association classification; OR: Odds ratio; OSAS: Obstructive sleep apnoea syndrome; PEEP: Positive end-expiratory pressure; PEEPappl: Positive end-expiratory pres- sure applied at the ventilator; PEEPi: Intrinsic positive end-expiratory-pressure; P/F: Arterial partial oxygen pressure to fraction of inspired oxygen ratio; Ppeak: Peak inspiratory pressure; Pplat: Plateau pressure; RR: Respiratory rate; Rrs,max: Total resistance of the respiratory system; Rrs,min: Flow resistance of the respiratory system; SAPS: Simplified Acute Physiology Score;
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Background: Lung dysfunction commonly occurs after cardiopulmonary bypass (CPB). Randomized evidence suggests that the presence of expiratory flow limitation (EFL) in major abdominal surgery is associated with postoperative pulmonary complications. Appropriate lung recruitment and a correctly set positive end-expiratory pressure (PEEP) level may prevent EFL. According to the available data in the literature, an adequate ventilation strategy during cardiac surgery is not provided. The aim of this study is to assess whether a mechanical ventilation strategy based on optimal lung recruitment with a best PEEP before and after CPB and with a continuous positive airway pressure (CPAP) during CPB would reduce the incidence of respiratory complications after cardiac surgery.
ventilation became mechanically inefficient. P max values of the patients were lower than those of normal subjects. Evidence of expiratory flow augmentation during exercise was noted in two subjects. Since 10 subjects achieved maximal expiratory flow predicted from flow-volume curves when heart rate was not maximal, we conclude that exercise capacity in most subjects was clearly limited by the deranged ventilatory apparatus. Elevations in mean intrathoracic pressure during exercise also may interfere with venous return and impose an additional limitation.
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This study has some limitations. The small sample size has already been mentioned. It is possible in this uncon- trolled observational study that unrecognized confounding factors other than EFL could have also contributed to the significant association between EFL and hospital length of stay. The lack of lung-volume measurements as a marker of hyperinflation over the course of the admission limited our ability to interpret the relationship between flow limitation, Rrs, and Borg scores. However, accurate measurement of lung volumes is difficult in these patients with significant dyspnea and tachypnea. The current study did not include measures of airway or systemic inflammation to examine possible mechanisms underlying changes in EFL index values, reactance, and symptoms during recovery. Repeat- ing this study with more detailed markers would therefore be worthwhile.
The pathophysiology of reduced maximum expiratory flow in a canine model of pulmonary emphysema was studied, and the results interpreted in terms of the wave-speed theory of flow limitation. According to this theory, maximum expiratory flow is related both to the cross-sectional area and compliance at an airway site where a critical gas velocity is first reached ("choke-point") and to gas density. Pulmonary emphysema was produced by the repeated instillations of the enzyme papain into the airways of six dogs. In five control dogs, a saline solution was instilled. During forced vital capacity deflation, in an open-chest preparation, maximum expiratory flow, choke-point locations, and the response to breathing an 80:20 helium/oxygen gas mixture were determined at multiple lung volumes. To locate choke-points, a pressure measuring device was positioned in the airway to measure lateral and end-on intrabronchial pressures, from which the relevant wave-speed parameters were obtained. In general, the reduced maximum expiratory flow in emphysema can be explained by diminished lung elastic recoil pressure and by altered bronchial pressure-area behavior, which results in a more peripheral location of choke-points that have smaller cross-sectional areas than controls. With respect to the density dependence of maximum expiratory flow, this response did not differ from control values in four dogs with emphysema in which frictional pressure losses upstream from choke-points did not differ […]
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We have examined the interrelationships among transpulmonary pressure, flow, and volume during exhausting exercise in 10 normal adult males. Expiratory transpulmonary pressures during exercise were compared with flow-limiting pressures measured at rest by two techniques. In no case did pressures developed during exercise exceed to an
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parameter of sGrs was showed a high predictive value for OSAS diagnos, defined as the Apnea – Hypopnea Index (AHI) ≥ 15 . These results suggest that the caliber of both pharyngeal airway and intrathoracic airways in obese OSA patients are commonly prone to collapse on the exhale, due primarily to decrease in lung volumes. The cross-sectional area of pharyngeal airway as well as peri- pheral airways are well known to varies considerably with alterations in lung volume. The lumen size in those struc- tures are proved to a decrease when the end-expiratory lung volume (EELV) or FRC are artificially lowered, that either caused by negative expiratory pressure (NEP) or by positive extrathoracic pressure on exhalation, and mani- fests as expiratory flow limitation (EFL) in the both struc- tures as well as airflow resistance are markedly increased [12 – 14]. These phenomena appear to be more pronounced in obese OSAS patients while adopt on the supine position. It has been demonstrated in obese subjects with and with- out OSA that lung volume, in term of EELV or FRC, would be a further decrease when the supine position is take on from a seated. Such a lung volume decrease may facilitate pharyngeal airway and intrathoracic airways to collapse or even closure, due to loss effects of caudal traction tension on both structures, and contribute to resistance increase in the airways.
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In our study, the presence of COPD was shown to increase with age, as expected, but undiagnosed airflow limitation was also seen in patients as young as 40–49 years. There were statistically significant differences observed between patients with and without airflow limitation, for parameters including age, smoking pack-years, CAT score, chronic bronchitis, and body mass index. In patients with chronic bronchitic symptoms, 33.5% had airflow limitation, suggesting that this history may be a useful predictor of COPD amongst patients with CVD. This has also been demonstrated recently in another study, which showed that underdiagnosis of COPD was particularly a problem in younger men with chronic bronchitic symptoms – a phenotype which is not usually recognized as COPD in Japan 25 because the Japanese COPD
overlooked by the evaluation of MEFV curves based on absolute and relative values of volume and flow . In elderly healthy subjects, there is a steady increase in SR with the progression of expiration , and conse- quently the decrease in expiratory flow occurs mainly at lower lung volumes . The SR analysis used to detect difference in MEFV curves due to mild chronic obstruct- ive pulmonary disease has demonstrated that the late scooping observed in these subjects is indicative of the normative aging process . The interpretation of de- creased MEF 50 and MEF 25 should thus be made with
After reviewing the non-specific and immediate responses of the bronchus, welding exposures had acute and transient effects on the respiratory system . It seems evaluating lung functions during shift work and comparing with non-working days can be a good indicator of welding fume effects on respiratory systems. Among different approaches, we can mention serial peak expiratory flow changes as a confirmation of the relationship between asthma with patient’s occupation.
One possible limitation of the current investigation is related to the fact that our subjects’ demographics were different from the general US population. For example, in our dataset, 86% were White, 13% were African- American, while other ethnic or racial groups were poorly represented. Further, any specific working definition used for SAD will inevitably affect the perfor- mance of the new measurement, inducing ‘imprecision’. As shown in figure 2, there is great performance hetero- geneity for various predictive equations with respect to FEF 50 LLN . We found that even when the FEF 50 LLN ‘outliers’ were excluded from the set of predictive equations (eg, Forche and Miller equations), 5 33 34 the AEX stratification
Methods: We conducted a cross-sectional study analyzing prospectively collected data from the Ishinomaki COPD Network registry. All participants were diagnosed with COPD, confirmed by using spirometry, and were aged 40–90 years and former smokers. Patients with features of asthma including both variable respiratory symptoms and variable expiratory airflow limitation were identified and defined as having ACOS. Then, the inflammatory biomarkers such as frac- tional exhaled nitric oxide level, blood eosinophil count and percentage, total immunoglobulin E (IgE) level, and presence of antigen-specific IgE were evaluated.
We evaluated changes of maximum expiratory flow-volume (MEFV) curves and of partial expiratory flow-volume (PEFV) curves caused by bronchoconstrictor drugs and dust, and compared these to the reverse changes induced by a bronchodilator drug in previously bronchoconstricted subjects. Measurements of maximum flow at constant lung inflation (i.e. liters thoracic gas volume) showed larger changes, both after constriction and after dilation, than measurements of peak expiratory flow rate, 1 sec forced expiratory volume and the slope of the effort-independent portion of MEFV curves. Changes of flow rates on PEFV curves (made after inspiration to mid-vital capacity) were usually larger than those of flow rates on MEFV curves (made after inspiration to total lung capacity). The decreased
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Background: Asthma is a condition that effects the air ways, characterised by bronchoconstriction and inflammation. Salbutamol, is a bronchodilator medicine that relaxes the muscles of airways leading to the lung and improves the amount of air flow to and from the lungs. The aim of this study is to compare and assess the efficacy of oral and inhalational salbutamol on the lung function. Methodology: A prospective, observational study was conducted at District Head Quaters Hospital, Khammam. A total of 110 patients were included in the study as per inclusion criteria. Subjects were classified into two groups, one group of patients (n=54) were given oral Salbutamol- (Asthalin - 2 mg) and the other group (n=56) with Levosalbutamol (Levolin-100mcg/ 2 puffs) metered dose inhaler. PEFR was measured before and after administration of drug. Highest value obtained after three attempts is recorded. Resuts and Discussion: Subjects were classified based on gender as 39% males and 60.9% females. Based on severity as mild (42), and moderate (68). Mean increase in PEFR after 15 minutes of Salbutamol inhalation was found to be 12.96% with SD - 7.63 and after 30 minutes of oral therapy to be 9.68% with SD – 8.38. Conclusion: Increase in post PEFR values has been achieved with both inhalational and oral therapy. However the mean increase in lung function has been greatly achieved with inhalational therapy. The study thus concludes that the inhalational therapy was most effective than oral therapy in improving PEFR.
respiratory velocities.” He suggested that a simple, whistle – like instrument might be developed and might become a standard clinical tool. (Wright 1959; Hardon (1942) measured peak flow rate on expiration by arenoid manometer connected across a simple orifice but its resistence was high, only recording by maximum deflection by judging it by eye. The instrument, called a “pneumometer” incorporates an aneroid manometer fitted with a device for recording the maximum flow rate. Rates up to about 700 L/min can be recorded. Silverman, Whittenberger, Lilly (1950), has used improved forms of Pneumatochograph themselves had very low resistance but were complicated and not easily portable. A much simpler and portable instrument, called ‘ puff meter’ for measuring the peak flow rate were designed. Wright BM and McKerrow described the peak flow meter (Wright 1978). The standard Wrights peak flow meter ranges from 50 – 1000 L/min and weight 900gm. Subsequently more portable, lower- cost version (Mini- Wright peak flow meter) other designs and copies have being available. (Airmed, Clement Clarke International Ltd).Now brands of electronic peak flow meters are also available.
Results: Of the 751 subjects, 484(64.4%) were boys and 267(35.5%) were girls. The overall mean age was 12.96±2.8 years. The mean lung volume for forced vital capacity was 2.21±0.75, forced expiratory volume in 1 second 2.08±0.73, ratio between the two 92.9±4.7, peak expiratory flow 231.3 ± 70.5 and forced expiratory flow between 25% and 75% expired volume was , , , 2.68±1.2. These lung volumes directly increased with age from children to adolescents (p<0.05). All variables showed a significant difference between boys and girls (p<0.05).
FeNO level was measured according to the American Tho- racic Society/European Respiratory Society recommendations using an NO analyzer (NIOX MINO Analyzer; Aerocrine AB, Solna, Sweden). Patients were instructed to inhale NO-free air to total lung capacity and immediately exhale fully into the device at a flow rate of 50 mL/s for 10 seconds. 10
The later in expiration that the flow is measured, the more the measurement reflects the resistance of the very small airways . A significant decrease in tidal expiratory flows at the remaining 10% of tidal volume in the present study may suggest narrowing of the small airways after albuterol admin- istration. The ratio 25/PT will be influenced by the values of TEF25 as well as PTEF. In the present study, PTEF signifi- cantly increased and TEF25 decreased (although not statisti- cally significant) after albuterol administration. Both these changes have lead to significant decrease in the ratio of 25/PT. Increased effort during exhalation can theoretically lead to an increase in PTEF and, by dynamic compression of smaller airways, to a decrease in TEF25; this leads to a decrease in 25/PT. The resistance of small airways is believed to have a greater effect on flow at lower lung volumes . Although tidal volumes remained constant in the present study, we do not know whether the expiratory flows at the remaining 10% of tidal volume were measured at identical lung volumes before and after aerosol treatment. The lack of improvement of tidal flow indices of airflow obstruction in the present study may be because of a true absence of bronchodilation in these patients, or because these indices are not sensitive enough to detect bronchodila- tion if one existed. As the index t PTEF /t E reflects the neuromus-