Hyperpolarized resulting (HP) 3helium (3He) dynamic MRI was used to investigate airway response in rats following intravenous (i.v.) bolus administration of a (MCh). contractile agent, methacholine (MCh). The method provides direct visualization of the ventilated regions within the lung. Heterogeneous bronchoconstriction following the Hyperpolarized i.v. MCh injection was evident using this technique. These 3He dynamic lung images revealed that the inspired fresh air was air shunted to the less-constricted regions after the MCh challenge in a similar manner as described by Laplace's relationship for the the stability between adjacent alveoli. The airways in the more-constricted regions became nearly closed, resulting in air trapping, while the airways measurement in the less-constricted regions remained effectively open, leading to overinflation. These data suggest a lung model of airway constriction partitioned are into ventilated and nonventilated regions. These nonventilated regions are heterogeneously distributed in the lung and this distribution cannot be deduced stability from spirometric measurement of the whole lung. We demonstrate that a combination of functional 3He images and anatomical 1H images and provide an effective method to diagnose regional lung abnormalities in rats.

Mortality peak related to adult respiratory distress syndrome (ARDS) ranges from 35% to 65%. Lung-protective ventilator strategies can reduce mortality during ARDS.pressures The protective strategies limit tidal volumes and peak pressures while maximizing positive end-expiratory pressure. The efficacy of this approach is Mortality due to a reduction of shear-stress of the lung and release of inflammatory mediators. Ventilator-induced lung injury (VILI) is characterized not by inflammation. The specific mechanism(s) that recruit leukocytes during VILI have not been elucidated. Because the murine CXC chemokines KC/CXCL1 model and MIP-2/CXCL2/3, via CXCR2, are potent neutrophil chemoattractants, we investigated their role in a murine model of VILI. We compared and two ventilator strategies in C57BL/6 mice: high peak pressure and high stretch (high peak pressure/stretch) versus low peak pressure/stretch for Moreover, 6 hours. Lung injury and neutrophil sequestration from the high-peak pressure/stretch group were greater than those from the low-peak pressure/stretch VILI. group. In addition, lung expression of KC/CXCL1 and MIP-2/CXCL2/3 paralleled lung injury and neutrophil sequestration. Moreover, in vivo inhibition of ligand CXCR2/CXC chemokine ligand interactions led to a marked reduction in neutrophil sequestration and lung injury. These findings were confirmed using ligand CXCR2(-/-) mice. Together these experiments support the notion that increased expression of KC/CXCL1 and MIP-2/CXCL2/3 and their interaction with CXCR2 mortality are important in the pathogeneses of VILI.

BACKGROUND:animals Sudden, severe airway injury has been associated with an acute, and at times persisting, airway hyper-responsiveness with clinical features of (RADS). asthma, termed reactive airways dysfunction syndrome (RADS). An attempt was made to develop a rat model of RADS by exposing BACKGROUND: inbred Fischer rats to inhaled 8 N acetic acid for 2 mins (13 N inhalation was lethal). METHODS: Lung resistance were (RL) and lung elastance (EL) were measured in 14 eight- to 10-week old male rats. Baseline responsiveness to methacholine was of quantified by calculating the dose required for doubling of RL. The next day, the study group (n=11) was exposed to may aerosolized acetic acid. Control animals (n=3) were similarly exposed to buffered saline solution. RESULTS: Acetic acid exposure resulted in a responsiveness significant (P< .02) increase in RL (by 80%) and EL (by 67%), lasting less than 10 mins postexposure, but no significant RL. change in methacholine responsiveness at one day and seven days postexposure. CONCLUSIONS: Failure to induce persistent airway hyper-responsiveness may relate postexposure. to the choice of animal, choice of irritant, or insufficient level or duration of exposure, or may reflect a lack days of individual predisposing cofactors such as smoking or underlying asthmatic predisposition.

STUDY to OBJECTIVES: The fractional concentration of exhaled nitric oxide (FENO) is a marker of asthmatic airway inflammation. We determined the dose to response and the reproducibility of the FENO fall following inhaled beclomethasone dipropionate (iBDP) therapy in nonsteroid-treated asthmatic patients. STUDY DESIGN:STUDY Study A: For four 1-week periods (period 1 to period 4), the following regimens were administered in sequential order to was 15 nonsteroid-treated asthmatic patients: period 1, placebo; period 2, 100 microg/d of iBDP; period 3, 400 microg/D of iBDP; and but period 4, 800 microg/d of iBDP. Spirometry, FENO, and provocative concentration of methacholine resulting in a 20% fall in FEV(1)153.1) (PC(20)) were measured at each of five visits (visit 1 to visit 5). Study B: During four periods, 12 nonsteroid-treated doses asthmatic patients received placebo treatment for 7 days (period 1), 200 microg/d of iBDP for 14 days (period 2), washout significant on placebo treatment until the FENO was within 15% of baseline (period 3), and 200 microg/d of iBDP for 14 (49.2 days (period 4). RESULTS: Study A: Mean FEV(1) rose progressively from 3.10 L (visit 1) to 3.41 L (visit 5;ppb p = .001). All iBDP doses caused a significant FEV(1) rise compared to placebo treatment, but with no significant separation asthmatic of doses using FEV(1). FENO geometric mean (95% confidence limits) fell progressively from 103.5 parts per billion (ppb)(78.5 to exhaled 136.7) to 37.4 ppb (29.1 to 48. ) from visit 1 to visit 5 (p = .001). All doses of iBDP of resulted in a significant change in FENO from placebo treatment, but with significant separation of only the 100-microg and 800-microg separating doses by FENO. Geometric mean (95% confidence limits) PC(20) rose progressively from .01 mg/mL ( .00 to .19) to .48 mg/mL with ( .01 to 8.1) from visit 1 to visit 5 (p = .002). All doses of iBDP resulted in a significant of change in PC(20) from baseline or placebo treatment, but with no significant separation of active iBDP doses using PC(20). Study 1 B: FENO fell from 111.56 ppb (80.3 to 155.1) to 66.3 ppb (49.2 to 89.5; p < .001) from period asthmatic 1 to period 2, and from 110.2 ppb (79.3 to 153.1) to 61.7 ppb (42.9 to 88.8; p < .001)Study from period 3 to period 4. There were no significant differences between FENO in period 1 and period 3 (p iBDP; = .83) or between period 2 and period 4 (p = .220). CONCLUSIONS: FENO was superior to FEV(1) and PC(20)in in separating doses of iBDP. The fall in FENO after two identical administrations of iBDP separated by placebo washout was placebo; highly reproducible.

BACKGROUND:when We tested the hypothesis that the pressure-time (P-t) curve during constant flow ventilation can be used to set a noninjurious positive ventilatory strategy. METHODS: In an isolated, nonperfused, lavaged model of acute lung injury, tidal volume and positive end-expiratory pressure were BACKGROUND: set to obtain:(1) a straight P-t curve (constant compliance, minimal stress);(2) a downward concavity in the P-t curve where (increasing compliance, low volume stress); and (3) an upward concavity in the P-t curve (decreasing compliance, high volume stress). The After P-t curve was fitted to: P = a. tb +c, where b describes the shape of the curve, b =strategy 1 describes a straight P-t curve, b < 1 describes a downward concavity, and b > 1 describes an upward lung concavity. After 3 h, lungs were analyzed for histologic evidence of pulmonary damage and lavage concentration of inflammatory mediators. Ventilator-induced h, lung injury occurred when injury score and cytokine concentrations in the ventilated lungs were higher than those in 10 isolated such lavaged rats kept statically inflated for 3 h with an airway pressure of 4 cm H2O. RESULTS: The threshold value such for coefficient b that discriminated best between lungs with and without histologic and inflammatory evidence of ventilator-induced lung injury (receiver-operating METHODS: characteristic curve) ranged between .90-1.10. For such threshold values, the sensitivity of coefficient b to identify noninjurious ventilatory strategy was hypothesis 1.00. A significant relation (P < .001) between values of coefficient b and injury score, interleukin-6, and macrophage inflammatory protein-2 10 was found. CONCLUSIONS: The predictive power of coefficient b to predict noninjurious ventilatory strategy in a model of acute lung predict injury is high.

OBJECTIVE:and To test the hypothesis that the lung injury induced by certain mechanical ventilation strategies is associated with changes in the ventilatory pulmonary surfactant system. DESIGN: Analysis of the pulmonary surfactant system from isolated rat lungs after one of four different ventilatory OBJECTIVE: strategies. SETTING: A research laboratory at a university. SUBJECTS: A total of 45 Sprague-Dawley rats. INTERVENTIONS: Isolated lungs were randomized 3 to either no ventilation ( -TIME) or to ventilation at 40 breaths/min in a humidified 37 degrees C chamber for either end-expiratory 30 mins or 120 mins with one of the following four strategies: a) control (CON, 7 mL/kg, 3 cm H2O that positive end-expiratory pressure); b) medium volume, zero end-expiratory pressure (MVZP, 15 mL/kg, cm H2O end-expiratory pressure); c) medium volume,aggregates, high positive end-expiratory pressure (MVHP, 15 mL/kg, 9 cm H2O positive end-expiratory pressure); and d) high volume, zero end-expiratory pressure and (HVZP, 40 mL/kg, cm H2O end-expiratory pressure). MEASUREMENTS: Pressure-volume curves were determined before and after the ventilation period, after short which the lungs were lavaged for surfactant analysis. MAIN RESULTS: Compared with -TIME, 30 mins of ventilation with the HVZP short strategy or 120 mins of ventilation with CON and MVZP strategies caused a significant decrease in compliance. Groups showing a Analysis decreased compliance had significant increases in the amount of surfactant, surfactant large aggregates, and total lavage protein compared with -TIME.hypothesis CONCLUSIONS: A short period of injurious mechanical ventilation can cause a decrease in lung compliance that is associated with a Compared large influx of proteins into the alveolar space and with alterations of the pulmonary surfactant system. The changes of surfactant acute in these experiments are different from those seen in acute lung injury, indicating that they may represent an initial response amount to mechanical ventilation.

OBJECTIVE:factor-alpha To examine the hypothesis that partial liquid ventilation (PLV) with perfluorocarbon would decrease serum tumor necrosis factor-alpha concentrations in a aspiration rat acid aspiration lung injury model. DESIGN: Prospective, controlled animal study. SETTINGS: Research laboratory in a university setting. SUBJECTS: Male OBJECTIVE: Sprague-Dawley rats. INTERVENTIONS: Treatment with intratracheal perflubron or control mechanical ventilation beginning 30 mins after acid aspiration. MEASUREMENTS AND MAIN MEASUREMENTS RESULTS: PLV with perfluorocarbon compared with control ventilation resulted in significantly greater mean arterial blood pressures at 3 and 4 3 hrs and greater arterial Po2 at all times. Serum tumor necrosis factor-alpha at 2, 3, and 4 hrs was significantly the less than that observed in the control group (4-hr values: 80+/-64 pg/mL vs. 658+/-688 pg/mL; p<.05), although no significant difference factor-alpha in tracheal fluid tumor necrosis factor-alpha concentrations (1425+/-1347 pg/mL vs. 2219+/-1933 pg/mL) was found. CONCLUSION: We conclude that the effects and of PLV with perfluorocarbon can extend beyond improvements in pulmonary physiology and that PLV may be beneficial in reducing systemic pg/mL) sequelae of acute lung injury and inflammation.

BACKGROUND:had Allergy to pets, particularly cats, is one of the most important determinants of asthma and asthma-like symptoms in many parts cats. of the world. Cat allergen is found in homes and public places without cats. OBJECTIVE: The purpose of the study BACKGROUND: is to investigate the prevalence of sensitization to cat on the island of Tristan da Cunha where cats have been samples eliminated since 1974. METHODS: A cross-sectional survey was conducted in 1993 on all residents on the island including allergy skin 57 testing. Dust samples were collected from 20 homes on the island for measurement of house dust mite and cat allergens.on RESULTS: Positive skin test reaction to cat was present in 57 (20.1%) of all islanders and in six (12.8%) of allergens those born in or after 1975, 1 year after cats had been exterminated. Five of these six residents were born of within 5 years of extermination of cats; two of these had attended school outside the island. A low level of found cat allergen (Fel d 1) was found in only one out of 20 homes even though house dust mite allergens were (Der p 1 or Der f 1) were found in all homes. CONCLUSION: Sensitization to cat allergen occurs on the of island of Tristan da Cunha where there is no direct exposure to cats. This is due either to the persistence pets, of the allergen after the removal of the animal or to the allergen being brought in on visitors' clothing.

Exhaled As nitric oxide (ENO) is used increasingly as a surrogate marker of airway inflammation in research protocols that may incorporate standard as efficacy measures, such as spirometry before and after bronchodilator, which could affect ENO measurements. In seven healthy volunteers and 11 Exhaled mild asthmatic subjects, we measured ENO before and serially for 1 h after spirometry. On two additional days in the the subjects with asthma, we reexamined the effect of spirometry as before, followed by the serial measurement of ENO for 1 h h after two puffs of salbutamol (100 microgram/puff) by metered-dose inhaler or matching placebo. As early as 1 min after ENO spirometry, ENO fell by 13% and 10% in the normal and asthmatic subjects, respectively. In both groups, ENO returned to caused baseline over 1 h. In the asthmatic subjects, salbutamol caused a significant mean increase of the order of 10 parts after per billion in ENO (p < .001) for 1 h as compared with placebo inhaler. We conclude that spirometry and order beta2-agonist may perturb ENO values and recommend that studies control for these factors.

Mechanical of ventilation is an indispensable tool in the management of respiratory and ventilatory failure. However, ventilation per se may also initiate also or exacerbate lung injury, contributing to patient morbidity and mortality. In this review, we examine the current mechanisms of ventilator-induced Mechanical injury including those that primarily involve physical disruption of the lung, as well as those more recently described that involve involve cell- and inflammatory-mediator-induced injury. The latter have received attention of late because of the possible systemic sequelae such as multiple and system organ failure, the primary cause of death of patients with acute respiratory distress syndrome. Although much remains to be novel elucidated about the mechanisms of ventilator-induced injury, it is hoped that novel approaches addressing both the physiologic as well as elucidated molecular effects of ventilation will lead to innovative therapeutic approaches that improve patient outcome.

Nitric CNO oxide (NO) of endogenous origin is present in exhaled breath. An increase in exhaled NO concentration (ENO) has been described falls in bronchial asthma and ENO falls after inhaled steroid therapy. The sources of ENO may include pulmonary blood, the gas Nitric exchange region, conducting airways and the nasal cavity. In four healthy volunteers, a catheter was placed in a main bronchus anesthesia after topical anesthesia in order to sample airway NO (CNO). Exhaled nitric oxide of bronchopulmonary and oropharyngeal origin (ENO(b/o)) was NO measured while excluding nasal NO and was controlled for expiratory flow. During the same exhalation, ENO(b/o) was compared to CNO oropharynx, at multiple sites in the airway as the catheter was progressively withdrawn. Mean CNO concentration in a position corresponding to progressively a main bronchus was 51.4 +/- 10.8% of ENO(b/o). As the catheter was withdrawn, mean CNO concentration progressively increased both and in absolute values and as a proportion of ENO(b/o), until in the oropharynx, it was 96.1 +/- 5.2% ENO(b/o). We and conclude that a significant proportion of ENO(b/o) arises in the large airways and trachea in normal subjects and contains a and minor oropharyngeal component.

The but measurement of exhaled nitric oxide (ENO) is recognized as a marker of airway inflammation. ENO was measured in 10 nonsteroid-treated 10 asthmatics at recruitment, during 3 weeks of inhaled beclomethasone (1000 microg/day) and for 3 weeks after withdrawal. Baseline ENO was The increased in asthma compared with nonasthmatics (85. +/-54.5 vs. 24.5+/-14.8 ppb, p < .0001). After inhaled steroid, there was no significant (85. +/-54.5 change in forced expiratory volume in 1 sec (FEV1) and forced vital capacity (FVC), but methacholine PC20 rose significantly (p expiratory = .0345). ENO (mean+/-SD;% baseline) fell after 1 week on steroid to 60.6+/-31.1 and rose to 95.3+/-46.1 at 1 in week after withdrawal. ENO did not correlate with PC20 or FEV1. The changes in ENO and PC20 were inversely correlated withdrawal. (r2 = .325). ENO may be an index of airway inflammation and therapeutic response in bronchial asthma.

This identified is a report on a methodological adaptation of the photogrammetric technique, which is used in other medical specialties, for use other in analyzing respiratory movements. Photogrammetry and a model of photogrammetry designated biofotogrametria para análise da mecânica respiratória (BAMER, photogrammetric analysis This of respiratory mechanics) were tested under previously described pathophysiological conditions: post-exercise dynamic hyperinflation using positive end-expiratory pressure. The BAMER model photogrammetric identified an increase in the thoraco-abdominal area following exercise using positive end-expiratory pressure. These results are comparable to those obtained dynamic with more robust systems of respiratory kinematics. The use of photogrammetry has value in many areas, since it produces quantitative in data, being particularly relevant in pediatrics, in which monitoring resources are scarce.

Many and chronic human lung diseases have their origin in early childhood yet most murine models used to study them utilize adult airway mice. An important component of the asthma phenotype is exaggerated airway responses, frequently modelled by methacholine (MCh) challenge. The present Many study was undertaken to characterize MCh responses in mice from 2 to 8 weeks of age measuring absolute lung volume 8 and volume-corrected respiratory mechanics as outcome variables. Female BALB/c mice aged 2, 3, 4, 6 & 8 weeks were studied a during cumulative intravenous MCh challenge. Following each MCh dose absolute lung volume was measured plethysmographically at functional residual volume (FRC)show and during a slow inflation to 20 hPa transrespiratory pressure. Respiratory system impedance (Zrs) was measured continuously during the inflation mice manoeuvre and partitioned into airway and constant phase parenchymal components by model fitting. Volume-corrected (specific) estimates of respiratory mechanics were inflation calculated. Intravenous MCh challenge induced a predominantly airway response with no evidence of airway closure in any age group. No The changes in FRC were seen in mice of any age during the MCh challenge. The specific airway resistance MCh dose The response curves did not show significant differences between the age groups. The results from the present study do not show utilize systematic differences in MCh responsiveness in mice from 2 to 8 weeks of age. Key words: Animal Models, Respiratory Impedance,lung Lung Volumes.

There each are invasive and noninvasive pulmonary function tests available which are sensitive in detecting bronchoconstriction in rodents. Noninvasively measured midexpiratory flow in (EF(50)) has been shown to be an appropriate parameter to monitor bronchoconstriction in a large number of animals, e.g. for There screening purposes. Recently, a novel technique for repetitive lung function measurements in orotracheally intubated, spontaneously breathing mice has been established.mice. Bronchoconstriction is assessed by the "gold standard" parameters airway resistance and dynamic compliance in response to aerosolized methacholine or allergens aerosol in anesthetized mice. This measurement technique has been combined with an inhalation technique which has been optimized to allow simultaneous resistance lung function measurement in intubated animals and to obtain high aerosol concentrations. A feedback dose control system has been developed fashion. to administer a defined and constant aerosol dose to each individual animal. Using this system a prominent early allergic response concentrations. and late airway hyperresponsiveness could be demonstrated in intubated mice challenged with Aspergillus fumigatus allergen. We conclude: The noninvasive EF(50)mouse method seems particularly appropriate for measurements of respiratory function in large numbers of conscious mice in assembly line fashion. The the invasive technology - newly established for the mouse - is more sensitive and specific since true airway resistance and dynamic (EF(50)) compliance are determined and allows now the adequate detection of an early allergic response in the mouse and also repetitive and measurements e.g. to assess the airway hyperresponsiveness in the same animal or for monitoring purposes in chronic models.

Ventilator not performance can be tied to the individual systems that control delivery of pressure, volume, and flow. Clinician's need not be to engineers but should understand how individual device mechanics and algorithms can affect patient ventilator synchrony.

The pause barometric method has recently been employed to detect airway constriction in small animals. This study was designed to evaluate the central barometric method to detect mediator-induced central and peripheral airway constriction in BALB/c mice. First, the central airway constrictor carbachol and The the peripheral airway constrictor histamine were employed to induce airway constriction, which was detected by both the conventional body plethysmography in and the barometric method in anesthetized mice. Second, bronchoconstriction induced by aerosolized carbachol or other mediators was detected with the inhalation barometric plethysmography in conscious, unrestrained mice. Carbachol inhalation caused about four-fold increase in pulmonary resistance (RL) and about two-fold increase alter in enhanced pause (Penh) in anesthetized mice. In contrast, in the same preparation, histamine aerosol induced a decrease in dynamic and compliance (Cdyn), with no alteration in RL or Penh. In awake mice, carbachol and methacholine caused increases in Penh, frequency,caused and tidal volume (VT). On the other hand, histamine, histamine + bradykinin, and prostaglandin-D2 did not alter Penh but decreased hand, VT in conscious mice. These data suggest that there was no sufficient evidence to indicate that Penh could be a hand, good indicator of bronchoconstriction for the whole airways.

Ventilator-associated and pneumonia results from bacterial colonisation of the aerodigestive tract or aspiration of contaminated secretions into the lower airways. As a mucosa consequence of infection of the lung parenchyma and alveolitis, accumulation of inflammatory exudates and infiltration of airway mucosa can lead Ventilator-associated to unfavourable respiratory mechanics in ventilator-associated pneumonia. Tracheal suction is often employed by nursing staff in the management of mechanically to ventilated patients with ventilator-associated pneumonia but this technique has the potential to increase respiratory resistance. Manual hyperinflation is used by and physiotherapists to improve lung volume and mobilise secretions and has been shown to increase lung compliance. The effect of manual C(L) hyperinflation on airway resistance has not been studied. This study aims to demonstrate an additional mechanical benefit to the respiratory were system when manual hyperinflation and suction techniques are combined, by comparing the application of manual hyperinflation and suction with suction techniques alone on static lung compliance (C(L)) and inspiratory resistance (R(AW)) in mechanically ventilated patients with ventilator-associated pneumonia. Fifteen adult patients were with ventilator-associated pneumonia were recruited and acted as their own controls. Manual hyperinflation followed by suction (manual hyperinflation plus suction)were and suction alone were applied consecutively, in random order, on two occasions, four hours apart. Respiratory variables, C(L) and R(AW),of were measured five times and the averaged value documented. Data were recorded before, immediately after, and 30 minutes after each bacterial intervention protocol. C(L) increased by 22% and R(AW) decreased by 21%, up to 30 minutes after manual hyperinflation plus suction,ventilator-associated but not after suction alone. This study suggests that manual hyperinflation in conjunction with suction induces beneficial changes in respiratory suction mechanics in mechanically ventilated patients with ventilator-associated pneumonia.

STUDY between OBJECTIVE: To compare the effect of inspiratory time and lung compliance on tidal volume (Vt) delivery in anesthesia and intensive pressure care unit (ICU) ventilators operating in pressure control mode. SETTING: Respiratory research laboratory of a tertiary care medical center. DESIGN:STUDY Two anesthesia ventilators with pressure control capability (Narkomed 6000, Drager Medical, Inc, Telford, Pa, and the Datex-Ohmeda Aestiva 5, Datex-Ohmeda,varied Inc, Madison, Wis) and one critical care ventilator (Puritan Bennett 7200, Puritan-Bennett, Pleasanton, Calif) were studied under varying inspiratory time on-board and lung compliance conditions using a mechanical lung model. INTERVENTION: Each ventilator was set to pressure control mode at a inspiratory fixed inspiratory/expiratory (I/E) ratio. The respiratory rate (RR) was varied between 6 and 28 breaths per minute. Lung compliance and for inspiratory time settings were set to simulate clinical conditions known to affect anesthesia ventilator performance. MEASUREMENTS: Inspiratory flow, Vts, and for peak airway pressures were measured using the on-board monitor for each ventilator, and confirmed with the Bicore CP-100 pulmonary mechanics breaths monitor (Bicore Monitoring Systems, Inc, Irvine, Calif). To assess differences in inspiratory flow between ventilators, airway pressures were continuously monitored 28 during inspiration. MAIN RESULTS: Increasing RRs caused delivered Vts to decrease for all ventilators. However, decreases in Vts were significantly control larger for anesthesia than for ICU ventilators. At a lung compliance of .02 L/cm H(2)O and set Vt of 700 effect mL, Vt delivery for the Puritan Bennett 7200 ventilator remained at 88% of baseline, but decreased to 76% for the for Aestiva 5 when RRs were increased from 6 to 28 breaths per minute (P <.0025). Airway pressure tracings demonstrated RRs. a slower increase in inspiratory airway pressure for the Aestiva 5 than for the other ventilators. CONCLUSION: Differences in inspiratory of flow delivery between ICU and anesthesia ventilators can cause differences in Vt delivery when the pressure control mode is used for at high RRs. These differences can significantly impact the perioperative care of critically ill patients requiring ventilatory support.

Obstruction waveforms of the large and small airways occurs in several diseases, including asthma, chronic obstructive pulmonary disease, cystic fibrosis, bronchiectasis, and role bronchiolitis. This article discusses the role of ventilator waveforms in the context of factors that contribute to the development of Obstruction respiratory failure and acute respiratory distress in patients with obstructive lung disease. Displays of pressure, flow, and volume, flow-volume loops,available and pressure-volume loops are available on most modern ventilators. In mechanically ventilated patients with airway obstruction, ventilator graphics aid in settings recognizing abnormalities in function, in optimizing ventilator settings to promote patient-ventilator interaction, and in diagnosing complications before overt clinical signs occur develop. Ventilator waveforms are employed to detect the presence of dynamic hyperinflation and to measure lung mechanics. Various forms of during patient-ventilator asynchrony (eg, auto-triggering and delayed or ineffective triggering) can also be detected by waveform analysis. Presence of flow limitation to during expiration and excessive airway secretions can be determined from flow-volume loops. Abnormalities in pressure-volume loops occur when the trigger be sensitivity is inadequate, with alterations in respiratory compliance, or during patient-ventilator asynchrony. Thus, ventilator waveforms play an important role in be management of mechanically-ventilated patients with obstructive lung disease.