Journal articles: 'Pulmonary hyperinflation'

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McCarren, Bredge. "Dynamic pulmonary hyperinflation." Australian Journal of Physiotherapy 38, no. 3 (1992): 175–79. http://dx.doi.org/10.1016/s0004-9514(14)60560-2.

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Richter, M., R. Voswinkel, H. Tiede, W. Seeger, R. Schulz, H. Ghofrani, and F. Reichenberger. "Dynamische Hyperinflation bei der pulmonal arteriellen Hypertonie: „Hyperinflator“ und „Non-Hyperinflator“." Pneumologie 67, no. 05 (May 15, 2013): 280–87. http://dx.doi.org/10.1055/s-0033-1343148.

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Gibson, G. J. "Pulmonary hyperinflation a clinical overview." European Respiratory Journal 9, no. 12 (December 1, 1996): 2640–49. http://dx.doi.org/10.1183/09031936.96.09122640.

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Lotvall, J. O., R. J. Lemen, K. P. Hui, P. J. Barnes, and K. F. Chung. "Airflow obstruction after substance P aerosol: contribution of airway and pulmonary edema." Journal of Applied Physiology 69, no. 4 (October 1, 1990): 1473–78. http://dx.doi.org/10.1152/jappl.1990.69.4.1473.

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We have studied the effects of aerosolized substance P (SP) in guinea pigs with reference to lung resistance and dynamic compliance changes and their recovery after hyperinflation. In addition, we have examined the concomitant formation of airway microvascular leakage and lung edema. Increasing breaths of SP (1.5 mg/ml, 1.1 mM), methacholine (0.15 mg/ml, 0.76 mM), or 0.9% saline were administered to tracheostomized and mechanically ventilated guinea pigs. Lung resistance (RL) increased dose dependently with a maximum effect of 963 +/- 85% of baseline values (mean +/- SE) after SP (60 breaths) and 1,388 +/- 357% after methacholine (60 breaths). After repeated hyperinflations, methacholine-treated animals returned to baseline, but after SP, mean RL was still raised (292 +/- 37%; P less than 0.005). Airway microvascular leakage, measured by extravasation of Evans Blue dye, occurred in the brain bronchi and intrapulmonary airways after SP but not after methacholine. There was a significant correlation between RL after hyperinflation and Evans Blue dye extravasation in intrapulmonary airways (distal: r = 0.89, P less than 0.005; proximal: r = 0.85, P less than 0.01). Examination of frozen sections for peribronchial and perivascular cuffs of edema and for alveolar flooding showed significant degrees of pulmonary edema for animals treated with SP compared with those treated with methacholine or saline. We conclude that the inability of hyperinflation to fully reverse changes in RL after SP may be due to the formation of both airway and pulmonary edema, which may also contribute to the deterioration in RL.

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Calvin, J. E., R. W. Baer, and S. A. Glantz. "Pulmonary injury depresses cardiac systolic function through Starling mechanism." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 4 (October 1, 1986): H722—H733. http://dx.doi.org/10.1152/ajpheart.1986.251.4.h722.

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To determine whether pulmonary microvascular injury or lung hyperinflation changes left ventricular (LV) performance and whether ventricular interaction plays a role in mediating such changes, we studied seven open-chest, closed-pericardium, anesthetized dogs before and after right ventricular (RV) injections of 150- to 200-micron glass beads. Because people with pulmonary disease are often treated with positive end-expiratory pressure, we also hyperinflated the lungs before and after creating the pulmonary microvascular injury. Measurements of LV and RV pressures and dimensions were taken at end expiration during the basal state, during lung hyperinflation, and after microvascular injury at RV end-diastolic pressures of 5, 10, and 15 mmHg produced by volume loading. Acute volume loading produced upward shifts in the LV diastolic pressure-size curve both before and after microvascular injury. Neither microvascular injury nor lung hyperinflation substantially affected the LV diastolic pressure-size relationship. LV end-diastolic size determined LV stroke work with no consistent independent influence of microvascular injury or lung hyperinflation. Neither microvascular injury nor lung hyperinflation depressed systolic performance beyond that associated with changes in end-diastolic heart size.

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Bruyneel, Marie, and Vincent Ninane. "Extrathoracic hyperinflation." Thorax 73, no. 1 (September 2, 2017): 96. http://dx.doi.org/10.1136/thoraxjnl-2017-210804.

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Smith, Benjamin M., Steven M. Kawut, David A. Bluemke, Robert C. Basner, Antoinette S. Gomes, Eric Hoffman, Ravi Kalhan, et al. "Pulmonary Hyperinflation and Left Ventricular Mass." Circulation 127, no. 14 (April 9, 2013): 1503–11. http://dx.doi.org/10.1161/circulationaha.113.001653.

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Rossi, A., A. Ganassini, G. Polese, and V. Grassi. "Pulmonary hyperinflation and ventilator-dependent patients." European Respiratory Journal 10, no. 7 (July 1, 1997): 1663–74. http://dx.doi.org/10.1183/09031936.97.10071663.

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van Dijk, Marlies, Karin Klooster, Jorine E. Hartman, Nick H. T. ten Hacken, and Dirk-Jan Slebos. "Change in Dynamic Hyperinflation After Bronchoscopic Lung Volume Reduction in Patients with Emphysema." Lung 198, no. 5 (July 24, 2020): 795–801. http://dx.doi.org/10.1007/s00408-020-00382-x.

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Abstract Background and Purpose In patients with severe emphysema, dynamic hyperinflation is superimposed on top of already existing static hyperinflation. Static hyperinflation reduces significantly after bronchoscopic lung volume reduction (BLVR). In this study, we investigated the effect of BLVR compared to standard of care (SoC) on dynamic hyperinflation. Methods Dynamic hyperinflation was induced by a manually paced tachypnea test (MPT) and was defined by change in inspiratory capacity (IC) measured before and after MPT. Static and dynamic hyperinflation measurements were performed both at baseline and 6 months after BLVR with endobronchial valves or coils (treatment group) or SoC (control group). Results Eighteen patients underwent BLVR (78% female, 57 (43–67) years, FEV1 25(18–37) %predicted, residual volume 231 (182–376) %predicted). Thirteen patients received SoC (100% female, 59 (44–74) years, FEV1 25 (19–37) %predicted, residual volume 225 (152–279) %predicted. The 6 months median change in dynamic hyperinflation in the treatment group was: + 225 ml (range − 113 to + 803) (p < 0.01) vs 0 ml (− 1067 to + 500) in the control group (p = 0.422). An increase in dynamic hyperinflation was significantly associated with a decrease in residual volume (r = − 0.439, p < 0.01). Conclusion Bronchoscopic lung volume reduction increases the ability for dynamic hyperinflation in patients with severe emphysema. We propose this is a consequence of improved static hyperinflation.

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van der Meer, Akke-Nynke, Kim de Jong, Aranka Hoekstra-Kuik, Elisabeth H. Bel, and Anneke ten Brinke. "Dynamic hyperinflation impairs daily life activity in asthma." European Respiratory Journal 53, no. 4 (January 24, 2019): 1801500. http://dx.doi.org/10.1183/13993003.01500-2018.

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IntroductionDynamic hyperinflation has been documented in asthma, yet its impact on overall health and daily life activities is unclear. We assessed the prevalence of dynamic hyperinflation in moderate to severe asthma and its relationship with the scores of a set of specific and general respiratory health questionnaires.Methods77 nonsmoking asthma patients (Global Initiative for Asthma steps 4–5) were recruited consecutively and completed five questionnaires: Asthma Control Questionnaire, Clinical COPD (chronic obstructive pulmonary disease) Questionnaire, St George's Respiratory Questionnaire, London Chest Activity of Daily Living scale (LCADL) and Shortness of Breath with Daily Activities (SOBDA). Dynamic hyperinflation was defined as ≥10% reduction in inspiratory capacity induced by standardised metronome-paced tachypnoea. Associations between level of dynamic hyperinflation and questionnaire scores were assessed and adjusted for asthma severity.Results81% (95% CI 71.7–89.4%) of patients showed dynamic hyperinflation. Higher levels of dynamic hyperinflation were related to poorer scores on all questionnaires (r=0.228–0.385, p<0.05). After adjustment for asthma severity, dynamic hyperinflation remained associated with poorer scores on LCADL (p=0.027) and SOBDA (p=0.031).ConclusionDynamic hyperinflation is associated with poorer overall health and impaired daily life activities, independent of asthma severity. Because of its major impact on everyday life activities, dynamic hyperinflation is an important target for treatment in asthma.

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Lee, V. V., N. Yu Timofeeva, V. S. Zadionchenko, T. V. Adasheva, and N. V. Vysotskaya. "RECENT ASPECTS OF CARDIAC REMODELING IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE." Rational Pharmacotherapy in Cardiology 14, no. 3 (July 5, 2018): 379–86. http://dx.doi.org/10.20996/1819-6446-2018-14-3-379-386.

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The paper aimed to present evidence of the effect of some pathophysiological features of chronic obstructive pulmonary disease (COPD) on cardiac remodeling in patients free of overt cardiovascular diseases, traditional cardiovascular risk factors and pulmonary hypertension. Contrary to traditional beliefs that cardiac abnormalities in COPD have been mainly associated with the right ventricle, several recent studies have shown an independent effect of pulmonary hyperinflation and emphysema on left ventricular (LV) diastolic filling and LV hypertrophy. Pulmonary hyperinflation and emphysema cause intrathoracic hypovolemia, low preload, small end-diastolic dimension and mechanical compression of LV chamber which could worsen end-diastolic stiffness. Interestingly, that the presence of LV hypertrophy in COPD patients is important but currently poorly understood area of investigation. Pulmonary hyperinflation, increased arterial stiffness and sympathetic activation may be associated with LV hypertrophy. Two-dimensional ultrasound speckle tracking studies have shown the presence of sub-clinical LV systolic dysfunction in patients even with moderate COPD and free of overt cardiovascular diseases. Sarcopenia related to the inflammatory-catabolic state in COPD and hypoxia could play an important role regarding LV systolic dysfunction. Recent data reported the effects of long-acting bronchodilators on reducing lung hyperinflation (inducing lung deflation). Further studies are required to evaluate the effects of pharmacological lung deflation therapy on cardiac volume and function.

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van der Meer, Akke-Nynke, Kim de Jong, Aranka Hoekstra-Kuik, Elisabeth H. Bel, and Anneke ten Brinke. "Targeting dynamic hyperinflation in moderate-to-severe asthma: a randomised controlled trial." ERJ Open Research 7, no. 3 (June 3, 2021): 00738–2020. http://dx.doi.org/10.1183/23120541.00738-2020.

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BackgroundDynamic hyperinflation is highly prevalent in moderate-to-severe asthma, which may significantly impede activities of daily life. We hypothesised that dynamic hyperinflation in asthma is due to inflammation of large and small airways and can be reduced by systemic anti-inflammatory treatment. Therefore, we investigated the effect of systemic glucocorticoids on dynamic hyperinflation in moderate-to-severe asthma patients and explored the relationships between inflammatory markers and changes in dynamic hyperinflation.MethodsIn this randomised placebo-controlled trial we included 32 asthma patients on inhaled glucocorticoid therapy showing dynamic hyperinflation, defined by a ≥10% reduction in inspiratory capacity measured by standardised metronome-paced tachypnea test. Patients received either triamcinolone (80 mg) or placebo intramuscularly. Before and 2 weeks after treatment, patients completed respiratory health questionnaires, had blood eosinophils and exhaled nitric oxide levels measured, and underwent lung function and dynamic hyperinflation testing.ResultsAfter adjustment for potential confounders, dynamic hyperinflation was significantly reduced by 28.1% in the triamcinolone group and increased by 9.4% in the placebo group (p=0.027). In the triamcinolone-treated patients, the reduction in dynamic hyperinflation was greater in patients with higher blood eosinophils at baseline (r=−0.592, p=0.020) and tended to be associated with a reduction in blood eosinophils (r=0.412, p=0.127) and exhaled nitric oxide (r=0.442, p=0.099).ConclusionsThis exploratory study suggests that dynamic hyperinflation in asthma can be reduced by systemic anti-inflammatory treatment, particularly in patients with elevated blood eosinophils. This supports the hypothesis that dynamic hyperinflation in asthma is due to airway inflammation and should be considered an important target for treatment.

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Cekerevac, Ivan, Zorica Lazic, Ljiljana Novkovic, Marina Petrovic, Vojislav Cupurdija, Gordana Kitanovic, Zoran Todorovic, and Olgica Gajovic. "Exercise tolerance and dyspnea in patients with chronic obstructive pulmonary disease." Vojnosanitetski pregled 67, no. 1 (2010): 36–41. http://dx.doi.org/10.2298/vsp1001036c.

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Background/Aim. Peripheral muscle weakness and nutritional disorders, firstly loss of body weight, are common findings in patients with chronic obstructive pulmonary disease (COPD). The aim of this study was to analyse the impact of pulmonary function parameters, nutritional status and state of peripheral skeletal muscles on exercise tolerance and development of dyspnea in COPD patients. Methods. Thirty COPD patients in stable state of disease were analyzed. Standard pulmonary function tests, including spirometry, body pletysmography, and measurements of diffusion capacity were performed. The 6-minute walking distance test (6MWD) was done in order to assess exercise tolerance. Level of dyspnea was measured with Borg scale. In all patients midthigh muscle cross-sectional area (MTCSA) was measured by computerized tomography scan. Nutritional status of patients was estimated according to body mass index (BMI). Results. Statistically significant correlations were found between parameters of pulmonary function and exercise tolerance. Level of airflow limitation and lung hyperinflation had significant impact on development of dyspnea at rest and especially after exercise. Significant positive correlation was found between MTCSA and exercise tolerance. Patients with more severe airflow limitation, lung hyperinflation and reduced diffusion capacity had significantly lower MTCSA. Conclusion. Exercise tolerance in COPD patients depends on severity of bronchoobstruction, lung hyperinflation and MTCSA. Severity of bronchoobstruction and lung hyperinflation have significant impact on dyspnea level.

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van Dijk, Marlies, Jorine E. Hartman, Sonja W. S. Augustijn, Nick H. T. ten Hacken, Karin Klooster, and Dirk-Jan Slebos. "Comparison of Multiple Diagnostic Tests to Measure Dynamic Hyperinflation in Patients with Severe Emphysema Treated with Endobronchial Coils." Lung 199, no. 2 (March 9, 2021): 195–98. http://dx.doi.org/10.1007/s00408-021-00430-0.

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Abstract Purpose For this study, we aimed to compare dynamic hyperinflation measured by cardiopulmonary exercise testing (CPET), a six-minute walking test (6-MWT), and a manually paced tachypnea test (MPT) in patients with severe emphysema who were treated with endobronchial coils. Additionally, we investigated whether dynamic hyperinflation changed after treatment with endobronchial coils. Methods Dynamic hyperinflation was measured with CPET, 6-MWT, and an MPT in 29 patients before and after coil treatment. Results There was no significant change in dynamic hyperinflation after treatment with coils. Comparison of CPET and MPT showed a strong association (rho 0.660, p < 0.001) and a moderate agreement (BA-plot, 202 ml difference in favor of MPT). There was only a moderate association of the 6-MWT with CPET (rho 0.361, p 0.024). Conclusion MPT can be a suitable alternative to CPET to measure dynamic hyperinflation in severe emphysema but may overestimate dynamic hyperinflation possibly due to a higher breathing frequency.

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Gould, D. Allen, and Mara M. Baun. "The Role of the Pulmonary Afferent Receptors in Producing Hemodynamic Changes during Hyperinflation and Endotracheal Suctioning in an Oleic Acid–Injured Animal Model of Acute Respiratory Failure." Biological Research For Nursing 1, no. 3 (January 2000): 179–89. http://dx.doi.org/10.1177/109980040000100303.

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The purpose of this study was to examine the role of the pulmonary afferent receptors in producing hemodynamic changes during hyperinflation and endotracheal suctioning (ETS) in an oleic acid–injured animal model of acute respiratory failure. Previous investigations of hyperinflation as a method to prevent hypoxia-induced sequelae of ETS have demonstrated unrecognized hemodynamic consequences. In this within-subject, repeated-measures study, instrumented, oleic acid–injured dogs had continuous measurements of heart rate (HR), mean aortic blood pressure (MAP), left ventricular pressure (Plv), pulmonary artery pressure (Ppa), right ventricular afterload (Ppa(tm)), right atrial pressure (Pra), and right ventricular filling pressure (Pra(tm)) during hyperinflation and ETS when the vagi were intact and after the pulmonary branches of the vagus nerves had been severed. After severing the vagi, MAP and Plv were decreased and HR and Ppa were increased. With the vagi severed, there was less variation in MAP and Ppa but increased variation in HR. These findings suggest that vagally mediated reflexes from the lungs produce some, but not all, of the hemodynamic effects associated with hyperinflation and ETS. Continued research is necessary to discover a method of hyperoxygenation and suctioning that does not produce potentially harmful hemodynamic effects.

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Alter, Peter, Jan Orszag, Christina Kellerer, Kathrin Kahnert, Tim Speicher, Henrik Watz, Robert Bals, Tobias Welte, Claus F. Vogelmeier, and Rudolf A. Jörres. "Prediction of air trapping or pulmonary hyperinflation by forced spirometry in COPD patients: results from COSYCONET." ERJ Open Research 6, no. 3 (July 2020): 00092–2020. http://dx.doi.org/10.1183/23120541.00092-2020.

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BackgroundAir trapping and lung hyperinflation are major determinants of prognosis and response to therapy in chronic obstructive pulmonary disease (COPD). They are often determined by body plethysmography, which has limited availability, and so the question arises as to what extent they can be estimated via spirometry.MethodsWe used data from visits 1–5 of the COPD cohort COSYCONET. Predictive parameters were derived from visit 1 data, while visit 2–5 data was used to assess reproducibility. Pooled data then yielded prediction models including sex, age, height, and body mass index as covariates. Hyperinflation was defined as ratio of residual volume (RV) to total lung capacity (TLC) above the upper limit of normal. (ClinicalTrials.gov identifier: NCT01245933).ResultsVisit 1 data from 1988 patients (Global Initiative for Chronic Obstructive Lung Disease grades 1–4, n=187, 847, 766, 188, respectively) were available for analysis (n=1231 males, 757 females; mean±sd age 65.1±8.4 years; forced expiratory volume in 1 s (FEV1) 53.1±18.4 % predicted (% pred); forced vital capacity (FVC) 78.8±18.8 % pred; RV/TLC 0.547±0.107). In total, 7157 datasets were analysed. Among measures of hyperinflation, RV/TLC showed the closest relationship to FEV1 % pred and FVC % pred, which were sufficient for prediction. Their relationship to RV/TLC could be depicted in nomograms. Even when neglecting covariates, hyperinflation was predicted by FEV1 % pred, FVC % pred or their combination with an area under the curve of 0.870, 0.864 and 0.889, respectively.ConclusionsThe degree of air trapping/hyperinflation in terms of RV/TLC can be estimated in a simple manner from forced spirometry, with an accuracy sufficient for inferring the presence of hyperinflation. This may be useful for clinical settings, where body plethysmography is not available.

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RUBIN, EBEN M., and HORST BAIER. "Unilateral pulmonary hyperinflation from mucus check-valve mechanism." Critical Care Medicine 14, no. 9 (September 1986): 828–29. http://dx.doi.org/10.1097/00003246-198609000-00015.

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Marchand, Eric, Jean-Paul d’Odemont, and Michael V. Dupont. "A Patient with GOLD Stage 3 COPD « cured » by One-Way Endobronchial Valves." Medicina 55, no. 3 (March 11, 2019): 65. http://dx.doi.org/10.3390/medicina55030065.

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Lung hyperinflation is a main determinant of dyspnoea in patients with chronic obstructive pulmonary disease (COPD). Surgical or bronchoscopic lung volume reduction are the most efficient therapeutic approaches for reducing hyperinflation in selected patients with emphysema. We here report the case of a 69-year old woman with COPD (GOLD stage 3-D) referred for lung volume reduction. She complained of persistent disabling dyspnoea despite appropriate therapy. Chest imaging showed marked emphysema heterogeneity as well as severe hyperinflation of the right lower lobe. She was deemed to be a good candidate for bronchoscopic treatment with one-way endobronchial valves. In the absence of interlobar collateral ventilation, 2 endobronchial valves were placed in the right lower lobe under general anaesthesia. The improvement observed 1 and 3 months after the procedure was such that the patient no longer met the pulmonary function criteria for COPD. The benefit persisted after 3 years.

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Hayden, Ann M., Mary V. Scarlett, and Kate Fox. "Relationship between Donor/Recipient Lung Size Mismatch and Functional Outcome in Single Lung Transplantation for COPD." Journal of Transplant Coordination 6, no. 3 (September 1996): 155–58. http://dx.doi.org/10.1177/090591999600600311.

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Single lung transplantation is an effective treatment for patients with severe chronic obstructive pulmonary disease. Pulmonary hyperinflation, which is seen in most patients with severe chronic obstructive pulmonary disease, makes the task of appropriately matching the donor and recipient difficult. It seems that the optimal matching strategy remains undefined. No correlation between donor/recipient size match (actual and predicted) and the degree of functional improvement after single lung transplantation was found. There were no significant differences noted when comparing the functional outcomes of right and left lung transplant recipients. It was concluded that the chronic hyperinflation associated with severe chronic obstructive pulmonary disease allows for the use of significantly larger donors. The use of expanded donor/recipient size match criteria in patients with severe chronic obstructive pulmonary disease may shorten the waiting period prior to single lung transplantation and provide better utilization of donor organs.

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Eichinger, M., S. Walterspacher, T. Scholz, K. Tetzlaff, K. Rocker, C.-M. Muth, M. Puderbach, H.-U. Kauczor, and S. Sorichter. "Lung hyperinflation: foe or friend?" European Respiratory Journal 32, no. 4 (May 14, 2008): 1113–16. http://dx.doi.org/10.1183/09031936.00118807.

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Van Meerhaeghe, A. "Flow limitation and dynamic hyperinflation." European Respiratory Journal 25, no. 4 (April 1, 2005): 772. http://dx.doi.org/10.1183/09031936.05.00009905.

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Brusasco, V., and J.-W. Fitting. "Lung hyperinflation in airway obstruction." European Respiratory Journal 9, no. 12 (December 1, 1996): 2440. http://dx.doi.org/10.1183/09031936.96.09122440.

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Wouters, E. F. M. "Nonpharmacological modulation of dynamic hyperinflation." European Respiratory Review 15, no. 100 (December 1, 2006): 90–96. http://dx.doi.org/10.1183/09059180.00010007.

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Solway, J., T. H. Rossing, A. F. Saari, and J. M. Drazen. "Expiratory flow limitation and dynamic pulmonary hyperinflation during high-frequency ventilation." Journal of Applied Physiology 60, no. 6 (June 1, 1986): 2071–78. http://dx.doi.org/10.1152/jappl.1986.60.6.2071.

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Dynamic hyperinflation of the lungs occurs during high-frequency oscillatory ventilation (HFOV) and has been attributed to asymmetry of inspiratory and expiratory impedances. To identify the nature of this asymmetry, we compared changes in lung volume (VL) observed during HFOV in ventilator-dependent patients with predictions of VL changes from electrical analogs of three potential modes of impedance asymmetry. In the patients, when a fixed oscillatory tidal volume was applied at a low mean airway opening pressure (Pao), which resulted in little increase in functional residual capacity, progressively greater dynamic hyperinflation was observed as HFOV frequency, (f) was increased. When mean Pao was raised so that resting VL increased, VL remained at this level during HFOV as f was increased until a critical f was reached; above this value, VL increased further with f in a fashion nearly parallel to that observed when low mean Pao was used. Three modes of asymmetric inspiratory and expiratory impedance were modeled as electrical circuits: 1) fixed asymmetric resistance [Rexp greater than Rinsp]; 2) variable asymmetric resistance [Rexp(VL) greater than Rinsp, with Rexp(VL) decreasing as VL increased]; and 3) equal Rinsp and Rexp, but with superimposed expiratory flow limitation, the latter simulated using a bipolar transistor as a descriptive model of this phenomenon. The fixed and the variable asymmetric resistance models displayed a progressive increase of mean VL with f at either low or high mean Pao. Only the expiratory flow limitation model displayed a dependence of dynamic hyperinflation on mean Pao and f similar to that observed in our patients. We conclude that expiratory flow limitation can account for dynamic pulmonary hyperinflation during HFOV.

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Cheyne, William S., Jinelle C. Gelinas, and Neil D. Eves. "Hemodynamic effects of incremental lung hyperinflation." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 3 (September 1, 2018): H474—H481. http://dx.doi.org/10.1152/ajpheart.00229.2018.

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Dynamic hyperinflation (DH) is common in chronic obstructive pulmonary disease and is associated with dyspnea and exercise intolerance. DH also has adverse cardiac effects, although the magnitude of DH and the mechanisms responsible for the hemodynamic impairment remain unclear. We hypothesized that incrementally increasing DH would systematically reduce left ventricular (LV) end-diastolic volume (LVEDV) and LV stroke volume (LVSV) because of direct ventricular interaction. Twenty-three healthy subjects (22 ± 2 yr) were exposed to varying degrees of expiratory loading to induce DH such that inspiratory capacity was decreased by 25%, 50%, 75%, and 100% (100% DH = inspiratory capacity of resting tidal volume plus inspiratory reserve volume ≈ 0.5 l). LV volumes, LV geometry, inferior vena cava collapsibility, and LV end-systolic wall stress were assessed by triplane echocardiography. 25% DH reduced LVEDV (−6 ± 5%) and LVSV (−9 ± 8%). 50% DH elicited a similar response in LVEDV (−6 ± 7%) and LVSV (−11 ± 10%) and was associated with significant septal flattening [31 ± 32% increase in the radius of septal curvature at end diastole (RSC-ED)]. 75% DH caused a larger reduction in LVEDV and LVSV (−9 ± 7% and −16 ± 10%, respectively) and RSC-ED (49 ± 70%). 100% DH caused the largest reduction in LVEDV and LVSV (−13 ± 9% and −18 ± 9%) and an increase in RSC-ED (56 ± 63%). Inferior vena cava collapsibility and LV afterload (LV end-systolic wall stress) were unchanged at all levels of DH. Modest DH (−0.6 ± 0.2 l inspiratory reserve volume) reduced LVSV because of reduced LVEDV, likely because of increased pulmonary vascular resistance. At higher levels of DH, direct ventricular interaction may be the primary cause of attenuated LVSV, as indicated by septal flattening because of a greater relative increase in right ventricular pressure and/or mediastinal constraint. NEW & NOTEWORTHY By systematically reducing inspiratory capacity during spontaneous breathing, we demonstrate that dynamic hyperinflation (DH) progressively reduces left ventricular (LV) end diastolic volume and LV stroke volume. Evidence of significant septal flattening suggests that direct ventricular interaction may be primarily responsible for the reduced LV stroke volume during DH. Hemodynamic impairment appears to occur at relatively lower levels of DH and may have important clinical implications for patients with chronic obstructive pulmonary disease.

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Niggemann, B., U. Klettke, Klaus Magdorf, and Ulrich Wahn. "Two cases of pulmonary tuberculosis presenting with unilateral pulmonary hyperinflation in infancy." European Journal of Pediatrics 154, no. 5 (April 1, 1995): 413–15. http://dx.doi.org/10.1007/s004310050317.

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Niggemann, Bodo, Uwe Klettke, Klaus Magdorf, and Ulrich Wahn. "Two cases of pulmonary tuberculosis presenting with unilateral pulmonary hyperinflation in infancy." European Journal of Pediatrics 154, no. 5 (May 1995): 413–15. http://dx.doi.org/10.1007/bf02072118.

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Powell, Randall W. "Vascular ring: Unusual cause of unilateral obstructive pulmonary hyperinflation." Journal of Pediatric Surgery 20, no. 2 (April 1985): 191. http://dx.doi.org/10.1016/s0022-3468(85)80314-6.

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Alm, Ann-Sophie, Annika Ingvarsson, and Xiangdong Wang. "Significance of lung hyperinflation in chronic obstructive pulmonary disease." Journal of Organ Dysfunction 3, no. 1 (January 2007): 44–54. http://dx.doi.org/10.1080/17471060600845190.

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Agusti, A., and J. B. Soriano. "Dynamic hyperinflation and pulmonary inflammation: a potentially relevant relationship?" European Respiratory Review 15, no. 100 (December 1, 2006): 68–71. http://dx.doi.org/10.1183/09059180.00010003.

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Kondo, Tetsuri, Toshimori Tanigaki, Chizuko Tsuji, Hiroshi Ishii, Gen Tazaki, and Yuusuke Kondo. "Aerosolized methacholine-induced bronchoconstriction and pulmonary hyperinflation in rats." Journal of Physiological Sciences 59, no. 5 (June 9, 2009): 341–45. http://dx.doi.org/10.1007/s12576-009-0040-z.

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Calverley, P. M. A. "Dynamic Hyperinflation: Is It Worth Measuring?" Proceedings of the American Thoracic Society 3, no. 3 (May 1, 2006): 239–44. http://dx.doi.org/10.1513/pats.200508-084sf.

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Garner, Justin L., and Pallav L. Shah. "Lung Volume Reduction in Pulmonary Emphysema." Seminars in Respiratory and Critical Care Medicine 41, no. 06 (May 20, 2020): 874–85. http://dx.doi.org/10.1055/s-0040-1702192.

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AbstractSevere emphysema with hyperinflation presents a therapeutic challenge. Inhaled medication has limited efficacy in individuals with mechanical constraints to the respiratory pump and impaired gas exchange. Lung volume reduction surgery (LVRS) reestablishes some semblance of normal physiology, resecting grossly expanded severely diseased tissue to restore the function of compromised relatively healthy lung, and has been shown to significantly improve exercise capacity, quality of life, and survival, especially in individuals with upper-lobe predominant emphysema and low-baseline exercise capacity, albeit with higher early morbidity and mortality. Bronchoscopic lung volume reduction achieved by deflating nonfunctioning parts of the lung is promoted as a less invasive and safer approach. Endobronchial valve implantation has demonstrated comparable outcomes to LVRS in selected individuals and has recently received approvals by the National Institute of Clinical Excellence in the United Kingdom and the Food and Drug Administration in the United States of America. Endobronchial coils are proving a viable treatment option in severe hyperinflation in the presence of collateral ventilation in selected cases of homogeneous disease. Modalities including vapor and sealant are delivered using a segmental strategy preserving healthier tissue within the same target lobe-efficacy and safety-data are, however, limited. This article will review the data supporting these novel technologies.

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Aisanov, Z. R., A. G. Chuchalin, and E. N. Kalmanova. "Chronic obstructive pulmonary disease and cardiovascular comorbidity." Kardiologiia 59, no. 8S (September 16, 2019): 24–36. http://dx.doi.org/10.18087/cardio.2572.

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In recent years, a greater understanding of the heterogeneity and complexity of chronic obstructive pulmonary disease (COPD) has come from the point of view of an integrated clinical assessment of severity, pathophysiology, and the relationship with other pathologies. A typical COPD patient suffers on average 4 or more concomitant diseases and every day about a third of patients take from 5 to 10 different drugs. The mechanisms of the interaction of COPD and cardiovascular disease (CVD) include the effects of systemic inflammation, hyperinflation (hyperinflation) of the lungs and bronchial obstruction. The risk of developing CVD in patients with COPD is on average 2–3 times higher than in people of a comparable age in the general population, even taking into account the risk of smoking. The prevalence of coronary heart disease, heart failure, and rhythm disturbances among COPD patients is significantly higher than in the general population. The article discusses in detail the safety of prescribing various groups of drugs for the treatment of CVD in patients with COPD. Achieving success in understanding and managing patients with COPD and CVD is possible using an integrated multidisciplinary approach.

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Windisch, Wolfram, and Carl Criée. "COPD – Stellenwert der Lungenfunktionsanalyse in Diagnostik und Therapie." DMW - Deutsche Medizinische Wochenschrift 143, no. 08 (April 2018): 593–96. http://dx.doi.org/10.1055/s-0043-123846.

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AbstractPulmonary function testing is essential for diagnosis and treatment-guidance of chronic obstructive pulmonary disease (COPD). Airway obstruction as assessed by spirometry should follow the reference-values provided by the Global Lung Initiative (GLI) of the European Respiratory Society (ERS). In addition, lung function testing should also include the assessment of lung hyperinflation and pulmonary emphysema by full-body plethysmography and determination of diffusion capacity. This is important since both, lung hyperinflation and pulmonary emphysema, can present without existing airway obstruction. Even though this formally excludes the diagnosis of COPD, these entities still belong to this disease complex. However, strictly speaking, pharmaceutical treatment is valid only for those patients with co-existing airway obstruction according to Global Lung Initiative for Chronic Obstructive Lung Disease (GOLD) criteria – since the absence of airway obstruction serves as exclusion criterion in nearly all randomized controlled trials. Nevertheless, progressive symptoms still require detailed pulmonary function testing for the guidance of non-pharmaceutical treatment – such as endoscopic or surgical lung volume reduction, long-term oxygen therapy, long-term non-invasive ventilation, and lung transplantation.

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Singh, Bhajan, Peter R. Eastwood, and Kevin E. Finucane. "Volume displaced by diaphragm motion in emphysema." Journal of Applied Physiology 91, no. 5 (November 1, 2001): 1913–23. http://dx.doi.org/10.1152/jappl.2001.91.5.1913.

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To examine the effect of hyperinflation on the volume displaced by diaphragm motion (ΔVdi), we compared nine subjects with emphysema and severe hyperinflation [residual volume (RV)/total lung capacity (TLC) 0.65 ± 0.08; mean ± SD] with 10 healthy controls. Posteroanterior and lateral chest X rays at RV, functional residual capacity, one-half inspiratory capacity, and TLC were used to measure the length of diaphragm apposed to ribcage (Lap), cross-sectional area of the pulmonary ribcage, ΔVdi, and volume beneath the lung-apposed dome of the diaphragm. Emphysema subjects, relative to controls, had increased Lap at comparable lung volumes (4.3 vs. 1.0 cm near predicted TLC, 95% confidence interval 3.4–5.2 vs. 0–2.1), pulmonary rib cage cross-sectional area (emphysema/controls 1.22 ± 0.03, P < 0.001 at functional residual capacity), and ΔVdi/ΔLap (0.25 vs. 0.14 liters/cm, P < 0.05). During a vital capacity inspiration, relative to controls, ΔVdi was normal in five (1.94 ± 0.51 liters) and decreased in four (0.51 ± 0.40 liters) emphysema subjects, and volume beneath the dome did not increase in emphysema (0 ± 0.36 vs. 0.82 ± 0.80 liters, P < 0.05). We conclude that ΔVdi can be normal in emphysema because 1) hyperinflation is shared between ribcage and diaphragm, preserving Lap, and 2) the diaphragm remains flat during inspiration.

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Chuang, Ming-Lung, and I.-Feng Lin. "Investigating the relationships among lung function variables in chronic obstructive pulmonary disease in men." PeerJ 7 (October 1, 2019): e7829. http://dx.doi.org/10.7717/peerj.7829.

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Background In patients with chronic obstructive pulmonary disease (COPD), the independent contributions of individual lung function variables to outcomes may be lower when they are modelled together if they are collinear. In addition, lung volume measurements may not be necessary after spirometry data have been obtained. However, these hypotheses depend on whether forced vital capacity (FVC) can predict total lung capacity (TLC). Moreover, the definitions of hyperinflation and air trapping according to lung function variables overlap and need be clarified. Therefore, the aim of this study was to evaluate the relationships among various lung function parameters to elucidate these issues. Methods Demographic data and 26 parameters of full lung function were measured in 94 men with COPD and analyzed using factor and correlation analyses. Results Factor analysis revealed five latent factors. Inspiratory capacity (IC)/TLC and residual volume (RV)/TLC were most strongly correlated with all other lung volumes. IC/TLC, RV/TLC, and functional residual capacity (FRC)/TLC were collinear and were potential markers of air trapping, whereas TLC%, FRC%, and RV% were collinear and were potential markers of hyperinflation. RV/TLC >0.4 (or IC/TLC <0.4) was comparable with the ratio of forced expiratory volume in one second (FEV1) and FVC <0.7. FVC% and FEV1% were poorly correlated with TLC%. The correlation study showed that TLC%, RV/TLC, and FEV1% could be used to represent individual latent factors for hyperinflation, air trapping, inspiration, expiration, and obstruction. Combined with diffusion capacity%, these four factors could be used to represent comprehensive lung function. Conclusions This study identified collinear relationships among individual lung function variables and thus selecting variables with close relationships for correlation studies should be performed with caution. This study also differentiated variables for air trapping and lung hyperinflation. Lung volume measurements are still required even when spirometry data are available. Four out of 26 lung function variables from individual latent factors could be used to concisely represent lung function.

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Tweed, W. A., W. T. Phua, K. Y. Chong, E. Lim, and T. L. Lee. "Tidal Volume, Lung Hyperinflation and Arterial Oxygenation during General Anaesthesia." Anaesthesia and Intensive Care 21, no. 6 (December 1993): 806–10. http://dx.doi.org/10.1177/0310057x9302100610.

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Impaired pulmonary oxygen (O2) exchange is common during general anaesthesia but there is no clinical unanimity as to methods of prevention or treatment. We studied 14 patients at risk for pulmonary dysfunction because of increased age, obesity, cigarette smoking, or chronic lung disease. Pulmonary O2 exchange was measured during four conditions of ventilation: awake spontaneous, conventional tidal volume (CVT, 7 ml.kg-1) or high tidal volume (HVT, 12 ml.kg-1) controlled ventilation, and five min after manual hyperinflation (H1) of the lungs. The F1O2 was controlled at 0.5, and FETCO2 was kept constant by adding dead space during HVT. Eight patients were ventilated with N2O/O2 and six with air/O2. Arterial blood gases were used to calculate the (A-a)DO2. In seven patients (A-a)DO2 worsened after induction of anaesthesia, while in seven there was no change or an improvement. Manual HI significantly reduced (A-a)DO2, but changing tidal volume (VT) had no effect. Using a multivariate model to predict O2 exchange, obesity and type of surgery were significantly associated with worsening, while level of VT and inspiratory gas (N2O or N2) were not significant predictors. Thus patient and surgical factors were more important determinants of pulmonary gas exchange during anaesthesia than were tidal volume or inspiratory gas. Manual HI is a simple and effective manoeuvre to improve gas exchange.

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Kyhl, Kasper, Ivan Drvis, Otto Barak, Tanja Mijacika, Thomas Engstrøm, Niels H. Secher, Zeljko Dujic, Ante Buca, and Per Lav Madsen. "Organ perfusion during voluntary pulmonary hyperinflation; a magnetic resonance imaging study." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 3 (February 1, 2016): H444—H451. http://dx.doi.org/10.1152/ajpheart.00739.2015.

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Pulmonary hyperinflation is used by competitive breath-hold divers and is accomplished by glossopharyngeal insufflation (GPI), which is known to compress the heart and pulmonary vessels, increasing sympathetic activity and lowering cardiac output (CO) without known consequence for organ perfusion. Myocardial, pulmonary, skeletal muscle, kidney, and liver perfusion were evaluated by magnetic resonance imaging in 10 elite breath-hold divers at rest and during moderate GPI. Cardiac chamber volumes, stroke volume, and thus CO were determined from cardiac short-axis cine images. Organ volumes were assessed from gradient echo sequences, and organ perfusion was evaluated from first-pass images after gadolinium injection. During GPI, lung volume increased by 5.2 ± 1.5 liters (mean ± SD; P < 0.001), while spleen and liver volume decreased by 46 ± 39 and 210 ± 160 ml, respectively ( P < 0.05), and inferior caval vein diameter by 4 ± 3 mm ( P < 0.05). Heart rate tended to increase (67 ± 10 to 86 ± 20 beats/min; P = 0.052) as right and left ventricular volumes were reduced ( P < 0.05). Stroke volume (107 ± 21 to 53 ± 15 ml) and CO (7.2 ± 1.6 to 4.2 ± 0.8 l/min) decreased as assessed after 1 min of GPI ( P < 0.01). Left ventricular myocardial perfusion maximum upslope and its perfusion index decreased by 1.52 ± 0.15 s−1 ( P < 0.001) and 0.02 ± 0.01 s−1 ( P < 0.05), respectively, without transmural differences. Pulmonary tissue, spleen, kidney, and pectoral-muscle perfusion also decreased ( P < 0.05), and yet liver perfusion was maintained. Thus, during pulmonary hyperinflation by GPI, CO and organ perfusion, including the myocardium, as well as perfusion of skeletal muscles, are reduced, and yet perfusion of the liver is maintained. Liver perfusion seems to be prioritized when CO decreases during GPI.

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Greenough, A., J. Pool, J. G. Gleeson, and J. F. Price. "Effect of budesonide on pulmonary hyperinflation in young asthmatic children." Thorax 43, no. 11 (November 1, 1988): 937–38. http://dx.doi.org/10.1136/thx.43.11.937.

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O'DONNELL, DENIS E, SUSAN M REVILL, and KATHERINE A WEBB. "Dynamic Hyperinflation and Exercise Intolerance in Chronic Obstructive Pulmonary Disease." American Journal of Respiratory and Critical Care Medicine 164, no. 5 (September 2001): 770–77. http://dx.doi.org/10.1164/ajrccm.164.5.2012122.

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Richter, Manuel J., Robert Voswinckel, Henning Tiede, Richard Schulz, Christian Tanislav, Andreas Feustel, Rory E. Morty, Hossein A. Ghofrani, Werner Seeger, and Frank Reichenberger. "Dynamic hyperinflation during exercise in patients with precapillary pulmonary hypertension." Respiratory Medicine 106, no. 2 (February 2012): 308–13. http://dx.doi.org/10.1016/j.rmed.2011.10.018.

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Riou, Yvon, Laurent Storme, Francis Leclerc, Thameur Rakza, Veronique Neve, and Pierre Lequien. "Determination of Pulmonary Hyperinflation (PH) in Mechanically Ventilated Neonates 226." Pediatric Research 43 (April 1998): 41. http://dx.doi.org/10.1203/00006450-199804001-00247.

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Hammer, Gregory B. "Differential lung ventilation in infants and children with pulmonary hyperinflation." Pediatric Anesthesia 13, no. 5 (June 2003): 373–74. http://dx.doi.org/10.1046/j.1460-9592.2003.01086.x.

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O'Donnell, D. E. "Hyperinflation, Dyspnea, and Exercise Intolerance in Chronic Obstructive Pulmonary Disease." Proceedings of the American Thoracic Society 3, no. 2 (April 1, 2006): 180–84. http://dx.doi.org/10.1513/pats.200508-093do.

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BATINIC, TONCI, WOLFGANG UTZ, TONI BRESKOVIC, JENS JORDAN, JEANETTE SCHULZ-MENGER, STIPAN JANKOVIC, ZELJKO DUJIC, and JENS TANK. "Cardiac Magnetic Resonance Imaging during Pulmonary Hyperinflation in Apnea Divers." Medicine & Science in Sports & Exercise 43, no. 11 (November 2011): 2095–101. http://dx.doi.org/10.1249/mss.0b013e31821ff294.

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Dominguez, R., R. A. Weisgrau, and M. Santamaria. "Pulmonary hyperinflation and emphysema in infants with the Marfan syndrome." Pediatric Radiology 17, no. 5 (July 1987): 365–69. http://dx.doi.org/10.1007/bf02396609.

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Vassilakopoulos, Theodoros, Dimitrios Toumpanakis, and Jordi Mancebo. "What’s new about pulmonary hyperinflation in mechanically ventilated critical patients." Intensive Care Medicine 46, no. 12 (May 29, 2020): 2381–84. http://dx.doi.org/10.1007/s00134-020-06105-3.

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Johnson, Margaret M., E. Wesley Ely, Caroline Chiles, David L. Bowton, Rita I. Friemanas, Robert H. Choplin, and Edward F. Haponik. "Radiographic Assessment of Hyperinflation." Chest 113, no. 6 (June 1998): 1698–704. http://dx.doi.org/10.1378/chest.113.6.1698.

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Marshall, I. Hertz, S. Bonser Robert, W. Jamieson Stuart, Joseph Tashjian, and A. Halvorsen Robert. "Reversible Hyperinflation in Emphysema." Chest 96, no. 2 (August 1989): 421–22. http://dx.doi.org/10.1378/chest.96.2.421.

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Journal articles on the topic 'Pulmonary hyperinflation'

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