Maldistribution Of Ventilation Research Articles

The Effect of Chronic Altitude Exposure on COPD Outcomes in the SPIROMICS Cohort.

Individuals with COPD have airflow obstruction and maldistribution of ventilation. For those living at high altitude, any gas exchange abnormality is compounded by reduced partial pressures of inspired oxygen. Does residence at higher-altitude exposure affect COPD outcomes, including lung function, imaging characteristics, symptoms, health status, functional exercise capacity, exacerbations, or mortality? From the SPIROMICS cohort, we identified individuals with COPD living below 1,000 ft (305 m) elevation (n= 1,367) versus above 4,000 ft (1,219 m) elevation (n= 288). Multivariable regression models were used to evaluate associations of exposure to high altitude with COPD-related outcomes. Living at higher altitude was associated with reduced functional exercise capacity as defined by 6MWD (-32.3 m, (-55.7 to -28.6)). There were no differences in patient-reported outcomes as defined by symptoms (CAT, mMRC), or health status (SGRQ). Higher altitude was not associated with a different rate of FEV1 decline. Higher altitude was associated with lower odds of severe exacerbations (IRR 0.65, (0.46 to 0.90)). There were no differences in small airway disease, air trapping, or emphysema. In longitudinal analyses, higher altitude was associated with increased mortality (HR 1.25, (1.0 to 1.55)); however, this association was no longer significant when accounting for air pollution. Chronic altitude exposure is associated with reduced functional exercise capacity in individuals with COPD, but this did not translate into differences in symptoms or health status. Additionally, chronic high-altitude exposure did not affect progression of disease as defined by longitudinal changes in spirometry.

A Model of the Maldistribution of Ventilation and Perfusion, in the Lungs of Heart Failure Patients

A Model of the Maldistribution of Ventilation and Perfusion, in the Lungs of Heart Failure Patients

Association between clinical, serological, functional and radiological findings and ventilatory distribution heterogeneity in patients with rheumatoid arthritis.

In rheumatoid arthritis (RA), the involvement of the pulmonary interstitium can lead to structural changes in the small airways and alveoli, leading to reduced airflow and maldistribution of ventilation. The single-breath nitrogen washout (SBN2W) test is a measure of the ventilatory distribution heterogeneity and evaluates the small airways. This study aimed to find out which clinical, serological, functional and radiological findings are useful to identify RA patients with pathological values of the phase III slope (SIII) measured by the SBN2W test. This was a cross-sectional study in which RA patients were assessed using the Health Assessment Questionnaire-Disability Index (HAQ-DI) and the Clinical Disease Activity Index (CDAI) and underwent serological analysis of autoantibodies and inflammatory markers. In addition, they underwent pulmonary function tests (including the SBN2W test) and chest computed tomography (CT). Of the 60 RA patients evaluated, 39 (65%) had an SIII >120% of the predicted value. There were significant correlations between SIII and age (r = 0.56, p<0.0001), HAQ-DI (r = 0.34, p = 0.008), forced vital capacity (FVC, r = -0.67, p<0.0001), total lung capacity (r = -0.46, p = 0.0002), residual volume/total lung capacity (TLC) (r = 0.44, p = 0.0004), and diffusing capacity of the lungs for carbon monoxide (r = -0.45, p = 0.0003). On CT scans, the subgroup with moderate/severe disease had a significantly higher SIII than the normal/minimal/mild subgroup (662 (267-970) vs. 152 (88-283)% predicted, p = 0.0004). In the final multiple regression model, FVC, extent of moderate/severe involvement and age were associated with SIII, explaining 59% of its variability. In patients with RA, FVC, extent of lung involvement and age, all of which are easily obtained variables in clinical practice, identify poorly distributed ventilation. In addition, the presence of respiratory symptoms and deteriorated physical function are closely related to the distribution of ventilation in these patients.

Small airway dysfunction in chronic hypersensitivity pneumonitis.

Lung biopsies from patients with hypersensitivity pneumonitis (HP) have demonstrated small airway (SA) involvement, but there is no information concerning SA function in HP, and it is unknown whether pharmacological treatment could modify its function. SA function in patients with chronic HP using ultrasonic pneumography (UPG) and impulse oscillometry (IOS) was explored. We also compared initial results with those obtained after 4 weeks of standardized treatment with azathioprine and prednisone. The study group consisted of adults with recent diagnoses of HP. All patients completed UPG, IOS, spirometry, body plethysmography, single-breath carbon monoxide diffusing capacity (DLCO ) and the 6-min walk test (6MWT). The fraction of exhaled nitric oxide (FENO ) was obtained to assess eosinophilic airway inflammation. Measurements were taken at diagnosis and after 4 weeks of treatment. A total of 20 consecutive patients (16 women) with chronic HP participated in the study. Median age was 50 years (interquartile range (IQR): 42-54). At diagnosis, the UPG phase 3 slope was abnormally high, consistent with maldistribution of ventilation. For IOS, all patients had low reactance at 5 Hz (X5) and elevated reactance area (AX) reflecting low compliance, and only eight (40%) patients had elevated R5 (resistance at 5 Hz (total)) and R5-20 (resistance at 5 Hz-resistance at 20 Hz (peripheral)) attributed to SA resistance. In contrast, FENO parameters were within normal limits. After treatment, forced vital capacity (FVC), the 6-min walk distance and the distribution of ventilation showed significant improvement, although DLCO did not. Patients with chronic HP have SA abnormalities that are partially revealed by the UPG and IOS tests. Lung volumes, but not gas exchange, improved after treatment with azathioprine and prednisone.

Resting Physiological Correlates of Reduced Exercise Capacity in Smokers with Mild Airway Obstruction

ABSTRACTSmokers with minor spirometric abnormalities can experience persistent activity-related dyspnea and exercise intolerance. Additional resting tests can expose heterogeneous physiological abnormalities, but their relevance and association with clinical outcomes remain uncertain. Subjects included sixty-two smokers (≥20 pack-years), with cough and/or dyspnea and minor airway obstruction [forced expiratory volume in one-second (FEV1) ≥80% predicted and >5th percentile lower limit of normal (LLN) (i.e., z-score >−1.64) using the 2012-Global Lung Function Initiative equations]. They underwent spirometry, plethysmography, oscillometry, single-breath nitrogen washout, and symptom-limited incremental cycle exercise tests. Thirty-two age-matched nonsmoking controls were also studied. Thirty-three (53%) of smokers had chronic obstructive pulmonary disease by LLN criteria. In smokers [n = 62; age 65 ± 11 years; smoking history 43 ± 19 pack-years; post-bronchodilator FEV1 z-score −0.60 ± 0.72 and FEV1/FVC z-score −1.56 ± 0.87 (mean ± SD)] versus controls, peak oxygen uptake (̇VO2) was 21 ± 7 vs. 32 ± 9 ml/kg/min, and dyspnea/̇VO2 slopes were elevated (both p < 0.0001). Smokers had evidence of peripheral airway dysfunction and maldistribution of ventilation when compared to controls. In smokers versus controls: lung diffusing capacity for carbon monoxide (DLCO) was 85 ± 22 vs. 105 ± 17% predicted, and residual volume (RV)/total lung capacity (TLC) was 36 ± 8 vs. 31 ± 6% (both p < 0.01). The strongest correlates of peak ̇VO2 were DLCO% predicted (r = 0.487, p < 0.0005) and RV/TLC% (r = −0.389, p = 0.002). DLCO% predicted was also the strongest correlate of dyspnea/̇VO2 slope (r = −0.352, p = 0.005). In smokers with mild airway obstruction, associations between resting tests of mechanics and pulmonary gas exchange and exercise performance parameters were weak, albeit consistent. Among these, DLCO showed the strongest association with important outcomes such as dyspnea and exercise intolerance measured during standardized incremental exercise tests.

Using the same cut-off for sulfur hexafluoride and nitrogen multiple-breath washout may not be appropriate.

Recent evidence suggests that results from multiple-breath washout (MBW) using nitrogen (N 2 ) as washout gas are different to those obtained by using sulfur hexafluoride (SF 6 ). Explanations were mainly related to different MBW equipment and gas properties. We aim to mention a new aspect, namely using the same cut-off in both techniques to determine lung clearance index (usually 2.5% of initial tracer concentration) irrespective of additional contribution of tissue-nitrogen in N 2 -MBW. In a simple model calculation we subtracted 1% tissue-N 2 from the N 2 -MBW in real washout traces from two children, one with cystic fibrosis (CF) and one healthy. This "SF 6 -washout simulation" decreased LCI differently in the children. In the healthy subject 1/40 th (2.5%) was achieved two breaths earlier compared to the original signal and changed LCI from 6.7 to 5.9 (12%), while in CF 1/40 th was achieved 19 breaths earlier leading to a LCI decrease from 13.7 to 10.0 (27%). It would have been required to wash out SF6 until 1/66 th (1.5%) to be comparable to N 2 washout at 1/40th (2.5%), or to stop N2-MBW already at 3.5% of the starting concentration to make both techniques comparable. We show that a basic physiological-mathematical difference between both techniques additionally accounts for different sensitivities and poor agreement between SF 6 - and N 2 -MBW. The best way of adjusting for the contribution of tissue-N 2 needs to be examined in future studies. Thus, despite increasing use in different disease groups, the books on MBW technology are obviously not closed yet.

Anesthetic concerns in patients with hyper-reactive airways

Hyperreactive airway disease occurs due to acute viral or bacterial infections in children, and due to chronic bronchitis, Asthma or Emphysema in adults. Smoking and exposure to allergens may worsen the disease. Anaesthesia in these patients is associated with higher incidence of perioperative bronchospasm, postoperative laryngospam, breath holding, and hypoxia due to maldistribution of Ventilation and Perfusion. Smoking and exposure to allergens may worsen the outcome. Severe bronchospasm is a life threatening emergency. Selective β2 agonists form the main drug of choice for bronchospasm. Corticosteroids should be given early to reduce inflammation and mucosal oedema. For anaesthesia, Propofol, Vecuronium or Rocuronium, Halothane or Sevoflurane and Fentanyl are drugs of choice. Histamine releasing drugs like morphine and atracurium should be avoided. If ventilator support is required, Non invasive Pressure Support ventilation should be used first. However, Intubation and mechanical ventilation may become necessary, which however, may be associated with difficult weaning.

Small-airways dysfunction associates with respiratory symptoms and clinical features of asthma: A systematic review

Traditionally, asthma has been considered a disease that predominantly involves the large airways. Today, this concept is being challenged, and increasing evidence has become available showing that abnormalities in the small airways also contribute to the clinical expression of asthma. The small airways can be affected by inflammation, remodeling, and changes in the surrounding tissue, all contributing to small-airways dysfunction. In this article we have performed a systematic review of the literature on the association between small-airways dysfunction and clinical signs and symptoms of asthma. This review shows that small-airways dysfunction associates with worse control of asthma, higher numbers of exacerbations, the presence of nocturnal asthma, more severe bronchial hyperresponsiveness, exercise-induced asthma, and the late-phase allergic response. Importantly, small-airways dysfunction can already be present in patients with mild asthma. Our review provides suggestive evidence that a better response of the small airways to inhaled steroids or montelukast associates with better asthma control. For this reason, an early recognition of small-airways dysfunction is important because it enables the physician to start timely treatment to target the small airways. It is important to develop simpler and more reliable tools (eg, questionnaires or bronchial provocation tests with small-particle stimuli) to assess the presence and extent of small-airways dysfunction in daily clinical practice.

Distinctive heat-shock response of bioleaching microorganismAcidithiobacillus ferrooxidansobserved using genome-wide microarray

Temperature plays an important role in the heap bioleaching. The maldistribution of ventilation in the heap leads to local hyperthermia, which does exert a tremendous stress on bioleaching microbes. In this study, the genome-wide expression profiles of Acidithiobacillus ferrooxidans at 40°C were detected using the microarray. The results showed that some classic proteases like Lon and small heat-shock proteins were not induced, and heat-inducible membrane proteins were suggested to be under the control of σ(E). Moreover, expression changes of energy metabolism are noteworthy, which is different from that in heterotrophic bacteria upon heat stress. The induced enzymes catalyzed the central carbon metabolism pathway that might mainly provide precursors of amino acids for protein synthesis. These results will deepen the understanding of the mechanisms of heat-shock response on autotrophic bacteria.

Physiological consequences of early-life insult

The most commonly observed severe lung injuries in early life are the respiratory distress syndrome in premature infants and the acute respiratory distress syndrome in children. Both diseases are characterised by alveolar instability, fluid filled airspace and some degree of airway obstruction. In the acute phase, collapsed alveoli can be reopened with positive end-expiratory pressure and lung recruitment. New insight into the physiology of lung recruitment suggests that the shape of the pressure-volume curve is defined by the change in rate of alveolar opening and closing. Reduced lung volumes and severe ventilation maldistribution are found in the acute phase but may persist during childhood. Any severe lung injury in this early phase of life can cause significant structural and functional damage to the developing lung. Follow-up studies of children with chronic lung disease have shown that the functional abnormalities will improve but may still be present in later childhood.

Closing Capacity and Gas Exchange in Chronic Heart Failure

Although it is commonly assumed that pulmonary congestion and edema in patients with chronic heart failure (CHF) promotes peripheral airway closure, closing capacity (CC) has not been measured in CHF patients. To measure CC and the presence or absence of airway closure and expiratory flow limitation (FL) during resting breathing in CHF patients. In 20 CHF patients and 20 control subjects, we assessed CC, FL, spirometry, blood gas levels, control of breathing, breathing pattern, and dyspnea. The patients exhibited a mild restrictive pattern, but the CC was not significantly different from that in control subjects. Nevertheless, airway closure during tidal breathing (ie, CC greater than functional residual capacity [FRC]) was present in most patients but was absent in all control subjects. As a result of the maldistribution of ventilation and the concurrent impairment of gas exchange, the mean (+/- SD) alveolar-arterial oxygen pressure difference increased significantly in CHF patients (4.3 +/- 1.2 vs 2.7 +/- 0.5 kPa, respectively; p < 0.001) and correlated with systolic pulmonary artery pressure (r = 0.49; p < 0.03). Tidal FL is absent in CHF patients. Mouth occlusion pressure 100 ms after onset of inspiratory effort (P0.1) as a percentage of maximal inspiratory pressure (Pimax) together with ventilation were increased in CHF patients (p < 0.01 and p < 0.005, respectively). The increase in ventilation was due entirely to increased respiratory frequency (fR) with a concurrent decrease in Paco2. Chronic dyspnea (scored with the Medical Research Council [MRC] scale) correlated (r2= 0.61; p < 0.001) with fR and P0.1/Pimax. In CHF patients at rest, CC is not increased, but, as a result of decreased FRC, airway closure during tidal breathing is present, promoting the maldistribution of ventilation, ventilation-perfusion mismatch, and impaired gas exchange. The ventilation is increased as result of increased fR, and Pimax is decreased with a concurrent increase in P0.1, implying that there is a proportionately greater inspiratory effort per breath (P0.1/Pimax). These, together with the increased fR, are the only significant contributors to increases in the MRC dyspnea score.

Multimodality measurements of small airways disease

Small airways disease has long been recognised as being physiologically important in obstructive lung diseases, particularly in chronic obstructive pulmonary disease (COPD) 1. The study of Cosio et al. 2, in which the severity of small airway inflammation and remodelling in smokers correlated with airway closure and ventilation maldistribution, as measured by single breath washout tests, is a landmark one because it linked small airways tests with pathology. Furthermore, these parameters of small airway function were more sensitive than spirometry for the presence of small airways disease. Results of more recent studies, in which small airway function was measured by the newer multiple breath nitrogen washout, showed that small airway function becomes abnormal after only 10 pack-yrs smoking, whereas spirometry becomes abnormal after 20 pack-yrs 3. In asthma, however, the function of the small airways has been studied much less, perhaps due to the paucity of resected lung specimens on which correlations can be made between measurements of small airway function and pathology. The disease-related changes to the structural components of the airways in asthma involve both small and large airways 4. These pathological changes, often referred to as remodelling, lead to thickening of the walls of the small airways. This is a feature that seems particularly characteristic of asthma as opposed to COPD 5. There is now an increasing body of evidence suggesting that small airways disease in asthma has important clinical consequences, to which the study by Zeidler et al. 6, in this issue of the European Respiratory Journal , makes an important contribution. In the study by Zeidler et al. 6, high-resolution computed tomography (HRCT) …

Breathing Patterns During Vaso-occlusive Crisis of Sickle Cell Disease

To determine the effect of sickle cell pain and its treatment on patients' breathing patterns, and to compare the effect of thoracic cage pain to pain at other sites. Prospective, observational study. Sickle Cell Center Day Hospital. Twenty-five patients with sickle cell disease admitted to the Sickle Cell Center Day Hospital for treatment of vaso-occlusive crisis (VOC) [10 patients with chest (thoracic cage) pain]. Breathing patterns were measured by respiratory inductive plethysmography. Tidal breathing data, including respiratory rate, tidal volume (VT), minute ventilation, and the rib cage contribution to VT, were collected at baseline and then following treatment with opioid analgesia. The patients with chest pain had smaller V(Ts) at baseline than those with pain at other sites (355 +/- 37 mL vs 508 +/- 141 mL, p = 0.003), and higher respiratory rates (23.2 +/- 8.2 breaths/min vs 17.6 breaths/min, p = 0.03). These differences became insignificant following opioid treatment. Six patients had respiratory alternans (four patients in the chest pain group, and two patients with pain at other sites). All cases of respiratory alternans resolved following opioid administration. Patients with VOC and chest pain have more shallow, rapid breathing than patients with pain elsewhere. Analgesia reduces these differences. As pain-associated shallow breathing and maldistribution of ventilation may contribute to the pathogenesis of acute chest syndrome, these results support the need for adequate pain relief and monitoring of ventilatory patterns during the treatment of VOC.

Rat model of lung fibrosis: comparison of functional, biochemical, and histopathological changes 4 months after single irradiation of the right hemithorax

This study investigated changes in lung function, hydroxyproline (OH-pro) content of lung tissue and histopathology in anesthetized, spontaneously breathing rats after a single, selective irradiation of the right hemithorax with a single dose of 20 Gy. The objective of this animal model was to examine as to whether non-invasive lung function measurements (LFM) could be used to analyze the magnitude of the irradiation-related pneumonitis and its long-term sequel occurring in the right lung in the presence of a normal left lung. Four months after irradiation, the OH-pro content in the irradiated right lung was determined and compared with the non-irradiated contralateral left lung, as well as lungs from non-irradiated sham controls. LFM revealed significantly depressed flow-volume curves and reduced quasistatic compliance, suggesting a marked diminution of elastic recoil of the lung. Total lung capacity (TLC) was significantly decreased, while the residual volume (RV) and functional residual capacity (FRC) remained almost unchanged. One of the most predominant dysfunction of the lung was a severe maldistribution of ventilation shown by the single-breath N 2-wash-out test. Single-breath carbon monoxide diffusing capacity (Dlco) was significantly decreased. The content of OH-pro, a marker of increased collagen, was significantly increased in the irradiated right lung but was indistinguishable from sham controls in the non-irradiated left lung. Histopathological examinations provided evidence of both inflammatory and fibrotic lesions in the irradiated lobes, including bronchiolo-alveolar hyperplasia. No changes were observed in the non-irradiated left lung. In summary, effects observed in the irradiated right lung were largely consistent with effects described in other animal models of human interstitial pulmonary fibrosis. Non-invasive LFM were considered to be particularly sensitive to study the overall extent of changes, however, the interpretation of findings appears to be complicated by the lobar heterogeneity of tissue- and flow-related functional end points.

N-acetylcysteine prevents cigarette smoke induced small airways alterations in rats.

This study investigated the effect of cigarette smoke exposure and the potential protection N-acetylcysteine (NAC) in rat lungs. Forty-eight rats were exposed to cigarette smoke (CS) for 10 weeks, without (CS group) or with (CS+NAC group) oral intake of NAC 200 mg x rat(-1) x day(-1), or to fresh air (Control). All rat lungs were assessed in terms of lung function, ventilation distribution (nitrogen, helium and sulphur hexafluoride phase III slopes), and morphometry (airway wall thickening of small, medium and large bronchi). The small bronchi, defined as the airways with an internal perimeter <1,000 microm showed significantly thicker airway walls in the CS than in the Control group. By contrast, no airway wall thickening was observed in the CS+NAC group with respect to Control. Except for decreased lung volumes and compliance in CS and CS+NAC groups, which were entirely attributable to smaller body weight gain, lung function was indistinguishable from Control. Phase III slopes were significantly increased only in the CS group. In conclusion, smoke-induced alterations in the rat lungs were reflected in wall thickening of the small bronchi and increased ventilation maldistribution. These smoke-induced morphometric and ventilation distribution alterations were prevented by N-acetylcysteine.

REPEATED PULMONARY FUNCTION MEASUREMENTS IN RATS AFTER INTRATRACHEAL INSTILLATION OF A POLYAMINE TEXTILE PIGMENT COMPONENT

The pulmonary response of Wistar rats to a cumulative dose of 1 mg/kg body weight of a polymeric alpha,omega-diamine was examined using the intratracheal route of administration. Instillation of the test substance was on days 0 and 7 followed by a 3-month postobservation period. Static and dynamic pulmonary function tests, including arterial blood gas determinations, were performed during wk 5, 9, and 13. At all time points, significantly depressed flow-volume curves, reduced quasistatic compliance, and reduced vital capacity were observed. These were associated with increases of residual volume and functional residual capacity in the presence of unremarkable changes of total lung capacity (TLC). One of the most predominant dysfunctions of the lung was a severe maldistribution of ventilation, indicated by the single-breath nitrogen washout test. The carbon monoxide diffusing capacity (DL(CO)), in turn, was only mildly decreased, and differences between treatment and control groups did not reach statistical significance. Assessment of arterial blood gases demonstrated a statistically significantly increased venous admixture with subsequent slight hypoxemia. In summary, the predominant dysfunction appeared to be consistent with an obstructive rather than restrictive lung disease. The functional changes observed may account for the effect on arterial blood gases, suggesting a mismatch of the ventilation-perfusion relationship. Either measurement appear to demonstrate a relative stable dysfunction during the 3-mo postinstillation observation period. Collectively, this study supports the view held that polymeric alpha, omega-diamines appear to be potent pneumotoxicants.

Theoretical Study of Inspiratory Flow Waveforms during Mechanical Ventilation on Pulmonary Blood Flow and Gas Exchange

A lumped two-compartment mathematical model of respiratory mechanics incorporating gas exchange and pulmonary circulation is utilized to analyze the effects of square, descending and ascending inspiratory flow waveforms during mechanical ventilation. The effects on alveolar volume variation, alveolar pressure, airway pressure, gas exchange rate, and expired gas species concentration are evaluated. Advantages in ventilation employing a certain inspiratory flow profile are offset by corresponding reduction in perfusion rates, leading to marginal effects on net gas exchange rates. The descending profile provides better CO2 exchange, whereas the ascending profile is more advantageous for O2 exchange. Regional disparities in airway/lung properties create maldistribution of ventilation and a concomitant inequality in regional alveolar gas composition and gas exchange rates. When minute ventilation is maintained constant, for identical time constant disparities, inequalities in compliance yield pronounced effects on net gas exchange rates at low frequencies, whereas the adverse effects of inequalities in resistance are more pronounced at higher frequencies. Reduction in expiratory air flow (via increased airway resistance) reduces the magnitude of upstroke slope of capnogram and oxigram time courses without significantly affecting end-tidal expired gas compositions, whereas alterations in mechanical factors that result in increased gas exchanges rates yield increases in CO2 and decreases in O2 end-tidal composition values. The model provides a template for assessing the dynamics of cardiopulmonary interactions during mechanical ventilation by combining concurrent descriptions of ventilation, capillary perfusion, and gas exchange.

Evidence of acinar airway involvement in asthma.

We investigated acinar airway involvement in 20 patients with stable asthma, using the phase III slope analysis of the multiple breath N2 washout previously applied in a group of patients with COPD (Am. J. Respir. Crit. Care Med. 1998;157:1573-1577). This technique quantifies severity of conductive and acinar components of ventilation maldistribution separately, through indices S(cond) and S(acin), which increase when respective ventilation inhomogeneities increase. We also investigated the effect of salbutamol inhalation on S(cond) and S(acin) in patients with asthma and compared it with that obtained in patients with COPD. Baseline measurements in the patients with asthma show that (1) acinar ventilation inhomogeneity was indeed abnormal in patients with asthma (S(acin) = 0.195 +/- 0.026 L-1) despite the normal diffusing capacity in this group; S(acin) values were intermediate between those obtained in unaffected individuals and patients with COPD, and that (2) conductive ventilation inhomogeneity was abnormal in the patients with asthma (S(cond) = 0.076 +/- 0.006 L-1) but similar to that obtained in the patients with COPD. Measurements after salbutamol inhalations showed significant changes in S(cond) and S(acin) only in the patients with asthma (p < 0.001). This study primarily demonstrated significant, but partially reversible, acinar airway impairment in patients with asthma, as compared with the more severe baseline acinar airway impairment in patients with COPD, which was not reversible after salbutamol inhalation.

INTRAOPERATIVE MULTI-BREATH NITROGEN WASHOUT ANALYSIS TO PREDICT PULMONARY FUNCTION AFTER LUNG VOLUME REDUCTION SURGERY

S139 INTRODUCTION: Lung volume reduction surgery (LVRS) may restore impaired lung function in patients with severe emphysema. We reported that LVRS improved the distribution of ventilation in the lung immediately [1]. The purpose of this study was: (1) compare intraoperative multi-breath nitrogen washout curve (N2 curve) obtained immediately pre-lung reduction (pre-LR) with immediate post-lung reduction (post-LR) values; (2) compare preoperative pulmonary function tests with one month postoperative values and; (3) investigate the hypothesis that improvement in intraoperative N2 washout curve can predict significant postoperative increase in forced expiratory volume in one second (FEV1). METHODS: With IRB approval and informed consent, nine patients undergoing bilateral VRS for severe emphysema were studied under general anesthesia. All patients were given fentanyl, propofol and vecuronium with epidural analgesia. A left-sided double lumen endobronchial tube was placed. An artificial ventilator (PB7200, Puritan-Bennet Co., KS, USA) was used. Two lung ventilation consisted of a tidal volumes of 8 ml/kg and respiratory rate of 15 breaths/min.N2 concentration was analyzed continuously by a respiratory mass spectrometer system (AMIS 2000SP, Innovision A/S, Denmark). The gas leaving the ventilator via the exhalation port was routed through a mixing chamber to the system. When the N2 signal was stable the ventilator was switched to 100% O2, and the N2 curve was obtained. The measurements were made before sternotomy (pre-LR) and after sternal closure with chest tubes to water seal (post-LR). Lung function tests were performed one day before surgery (pre-op) and one month after surgery (post-op). RESULTS: The pre-LR fall of N2 concentration after 100% O2 inhalation was obviously delayed by maldistribution of ventilation in all patients. In five of them (group A), the post-LR N2 concentration approximated a simple exponential curve, and FEV1 significantly increased from 834 +/- 170 ml to 1300 +/- 290 ml after surgery. Four of nine patients (group B) did not show remarkable change in N2 curve. In group B, pre-op and post-op FEV1 were 697 +/- 254 ml and 850 +/- 360 ml, respectively. Three subjects in group B showed little change in FEV1 less than 90 ml. CONCLUSION: Group A patients demonstrated remarkable increases in clinical improvement one month after LVRS. Improvement in intraoperative multi-breath N2 washout analysis can predict significant postoperative improvement in FEV1.

Airway obstruction in interstitial lung disease.

There is no question that most interstitial lung diseases result in structural alteration of the small airways as well as the alveoli. These structural changes of the airways produce airflow abnormalities that, depending on their extent and severity, are reflected in a variety of tests of pulmonary function. However, in most situations, obstructive lung disease rarely dominates the clinical picture. Airflow limitation may be the predominant defect in patients with Wegener's granulomatosis, lymphangioleiomyomatosis, and chronic eosinophilic pneumonia. Concomitant risk factors such as cigarette smoking or dust inhalation may contribute to airway obstruction. Sporadic cases of interstitial lung disease progressing to overt airflow obstruction have been reported. The clinical significance of airway narrowing in interstitial lung disease is a maldistribution of ventilation that causes abnormalities on gas exchange, thereby increasing the work of breathing and possibly the sensation of dyspnea.