Relevant bibliographies by topics / Pulmonary hyperinflation

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Pulmonary hyperinflation'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "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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Dissertations / Theses on the topic "Pulmonary hyperinflation"

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Moore, Alastair. "Physiological approaches to hyperinflation in chronic obstructive pulmonary disease." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505304.

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Chronic Obstructive Pulmonary Disease (COPD) is one of the leading causes of mortality and morbidity worldwide. The purpose of this thesis was to explore the role of hyperinflation in COPD by investigating its effect on mortality, and then having established that hyperinflation is a predictor of mortality in COPD, to then explore how it has an effect on the mechanics of the diaphragm at a sub-cellular level.
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Gazzana, Marcelo Basso. "Investigação da hiperinsuflação pulmonar dinâmica durante o exercício e sua relação com a força dos músculos inspiratórios em pacientes com hipertensão arterial pulmonar." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/119416.

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Introdução: A redução da capacidade inspiratória (CI) induzida pelo exercício observada em alguns pacientes com hipertensão arterial pulmonar (HAP) poderia potencialmente ser influenciada por disfunção muscular respiratória. Objetivos: Investigar se há alguma relação entre CI e força muscular respiratória antes e após o exercício máximo e estudar o papel da pressão muscular respiratória e da CI na dispneia e na capacidade de exercício em pacientes com HAP. Métodos: 27 pacientes com HAP e 12 controles saudáveis pareados foram comparados. Todos os participantes foram submetidos a teste de exercício cardiopulmonar (TECP) com determinação seriada da CI. As pressões inspiratória e expiratória máximas (PImáx e PEmáx, respectivamente) foram medidas antes, no pico e após o exercício. Resultados: Os pacientes tiveram menor volume expiratório forçado no primeiro segundo (VEF1), capacidade vital forçada (CVF) (com relação VEF1/CVF semelhante) e capacidade aeróbia máxima e maior dispneia no exercício. A PImáx e a PEmáx foram significativamente menores nos pacientes com HAP que nos controles. Entretanto, a variação pós exercício em relação ao repouso não foi significativamente diferente nos dois grupos. Os pacientes apresentaram redução significativa da CI do repouso ao pico do exercício em comparação aos controles. 17/27 pacientes (63%) apresentaram redução da CI durante o exercício. Considerando-se apenas os pacientes, não houve associação entre CI e PImáx ou PEmáx (pré, pós exercício ou mudança do repouso). Comparando-se os pacientes com e sem redução da CI, não houve diferença na proporção de pacientes que apresentaram redução da PImáx (41 vs 44%) ou da PEmáx (76 vs 89%) após o exercício. Da mesma forma, nenhuma diferença na PImáx ou PEmáx foi observada no exercício comparando estes subgrupos. Conclusões: Em resumo, a força muscular respiratória foi significativamente menor em pacientes com HAP em comparação com controles e uma proporção significativa de pacientes com HAP apresentaram redução da CI durante o exercício. No entanto, não foram observadas associações entre CI e alterações de força muscular respiratória com o exercício, sugerindo que ocorra verdadeira hiperinsuflação dinâmica. Além disso, o único parâmetro relacionado com a dispneia induzida pelo exercício foi a CI no repouso e com capacidade aeróbia no pico foi a magnitude da redução da PEmáx após o exercício.
Rationale: The exercise induced inspiratory capacity (IC) reduction observed in some patients with pulmonary arterial hypertension (PAH) could potentially be influenced by respiratory muscle dysfunction. Aims: To investigate if there is any relationship between IC and respiratory muscle strength before and after maximal exercise and to study the contribution of respiratory muscle pressure and IC in exercise dyspnea and capacity in PAH patients. Methods: 27 patients with PAH and 12 healthy matched controls were compared. All participants underwent cardiopulmonary exercise test (CPET) with serial IC measurements. Inspiratory and expiratory maximal mouth pressure (PImax and PEmax, respectively) were measured before and at peak/post exercise. Results: Patients had lower forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) (with similar FEV1/FVC ratio) and peak aerobic capacity and higher exercise dyspnea. PImax and PEmax were significantly lower in PAH patients compared to controls. However, post exercise variations from rest were not significant different in either group. Patients presented significant rest-to-peak reduction in IC compared to controls. 17/27 patients (63%) exhibited IC reduction during exercise. Considering only patients, there was no association between IC and PImax or PEmax (pre, post exercise or change from rest). Comparing patients with and without IC reduction, there was no difference in the proportion of patients presenting inspiratory (41 vs 44%) or expiratory (76 vs 89%) pressure reduction after exercise, respectively. In the same way, no difference in both inspiratory and expiratory respiratory pressure change with exercise was observed comparing these subgroups. Conclusions: In summary, respiratory muscle strength was significantly lower in PAH patients compared to controls and a significant proportion of PAH presented IC reduction during exercise. Nonetheless, no associations between IC and respiratory muscle strength changes with exercise were observed, suggesting a true dynamic lung hyperinflation. Additionally, the only parameter associated with exercise induced dyspnea was resting IC and with peak aerobic capacity was the magnitude of PEmax reduction after exercise.
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Robillard, Julie. "Lung hyperinflation does not impair central and peripheral blood flow adaptation to rhythmic knee extension exercise in chronic obstructive pulmonary disease (COPD)." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32277.

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In patients with chronic obstructive pulmonary disease (COPD), lung hyperinflation has been suggested to reduce cardiac output (Qc) and impede peripheral blood flow, thereby contributing to reduced peak oxygen utilization (VO2) and exercise intolerance observed in this population. However, investigations on peripheral blood flow responses to exercise in COPD are few and have provided divergent results. Moreover, evidence of hyperinflation-induced circulatory limitation is lacking in COPD. Therefore, this study aimed to clarify the impact of lung hyperinflation on central and peripheral perfusion, and the subsequent effects on oxygen delivery to exercising muscle during submaximal knee extension exercise. Results showed that despite the presence of clinically significant hyperinflation, COPD (n=9) presented with a normal Qc/VO2 relationship compared to controls (n=5). However, leg blood flow was significantly higher in COPD, which likely reflects a compensatory response for the lower arterial oxygen content or mean arterial blood pressure, thereby maintaining adequate oxygen delivery to exercising muscle. Thus, this study demonstrates that lung hyperinflation does not limit central or peripheral circulation during submaximal exercise in COPD.
Chez les patients atteints de maladie pulmonaire obstructive chronique (MPOC), il a été suggéré que l'hyperinflation pulmonaire pourrait causer une réduction du débit cardiaque (Qc) et nuire à la perfusion périphérique pour ainsi contribuer à la réduction de la consommation maximale d'oxygène (VO2) et à l'intolérance à l'exercice observées chez ces patients. Toutefois, peu d'études ont mesuré le débit sanguin fémoral chez les patients MPOC et elles rapportent des résultats hétérogènes. De plus, la démonstration que l'hyperinflation peut limiter la circulation est manquante chez les patients MPOC. Ainsi, l'objectif de cette étude était de clarifier l'impact de l'hyperinflation sur la circulation centrale et périphérique, et les effets conséquents sur l'apport en oxygène vers les muscles actifs pendant un exercice sous-maximal d'extension du genou. Les résultats ont démontré que malgré la présence d'hyperinflation cliniquement significative, les patients MPOC (n=9) présentaient une relation Qc/VO2 normale comparativement aux sujets contrôles (n=5). Toutefois, le débit sanguin fémoral était significativement plus élevé chez les MPOC, ce qui illustre probablement une réponse compensatoire afin de maintenir un apport en oxygène adéquat vers les muscles actifs malgré une concentration artérielle en oxygène réduite ou une pression artérielle diminuée. Ainsi, cette étude démontre que l'hyperinflation pulmonaire ne limite pas la circulation centrale ou périphérique pendant un exercice sous-maximal chez les patients MPOC.
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Bretonneau, Quentin. "Effet d'une pression expiratoire positive au repos et à l'exercice sur l'oxygénation des muscles intercostaux chez des sujets sains." Thesis, Poitiers, 2020. http://www.theses.fr/2020POIT2259.

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Chez les patients atteints de pathologies pulmonaires obstructives, le rétrécissement du calibre des bronches peut induire des perturbations fonctionnelles ventilatoires comme la limitation de débit expiratoire (LDE) et/ou l’hyperinflation pulmonaire (HP). Dans un tel contexte, l’équilibre métabolique pourrait être perturbé au sein du tissu musculaire intercostal, notamment à l’exercice, ce qui pourrait favoriser la survenue ou l’aggravation de la dyspnée.Pour simuler les perturbations ventilatoires que peuvent rencontrer les patients atteints de pathologies pulmonaires obstructives (e.g. résistance anormalement élevée des voies aériennes à l’expiration, LDE et HP), une pression expiratoire positive (PEP) de 20 cmH2O a été imposée au repos et à l’exercice chez des sujets sains. L’oxygénation des muscles intercostaux a été mesurée par spectroscopie dans le proche infrarouge au niveau du 7ème espace intercostal.Au repos, une diminution de la concentration en oxyhémoglobine ([O2Hb]) probablement liée à une baisse de la concentration en hémoglobine totale ([tHb], i.e. volume sanguin local) a été observée en réponse à la PEP (Étude 1). Toutefois, aucune diminution de l’indice de saturation tissulaire en oxygène (TSI) n’a été constatée (Études 1 à 3), y compris lorsque la PEP était à l’origine d’une HP (Étude 2). A l’exercice, une moindre augmentation de [O2Hb] et de [tHb] a été rapportée lorsque la PEP était imposée (vs. contrôle). Une diminution du TSI et de la capacité inspiratoire a aussi été observée entre le repos et l’exercice dans cette condition (Étude 3).D’après les résultats de nos études, lorsqu’une PEP de 20 cmH2O est imposée au repos chez de jeunes sujets sains, aucun déséquilibre métabolique ne semble se produire au niveau des muscles intercostaux. En revanche, lorsque cette PEP est imposée à l’exercice, une perturbation de l’équilibre métabolique semble avoir lieu. Cette dernière pourrait être en partie expliquée par des altérations hémodynamiques locales induites par l’HP. Toutefois, des études complémentaires sont nécessaires pour éclaircir cet aspect.Enfin, aucune relation entre la dyspnée et la condition métabolique des muscles intercostaux n’a été observée lors de nos études. En revanche, des corrélations entre l’inconfort respiratoire et les débits ventilatoires instantanés ont été mises en évidence au repos et à l’exercice lorsque la PEP était imposée (Études 1 et 3). Une relation entre la dyspnée et l’HP a aussi été observée au repos (Étude 2).Les travaux de recherche futurs auront pour objectif de vérifier, au repos et à l’exercice, si l’oxygénation des muscles intercostaux est influencée par l’HP chez des patients atteints de pathologies pulmonaires obstructives
In patients with obstructive pulmonary disease, airway narrowing can induce ventilatory disturbances such as expiratory flow limitation (EFL) and/or pulmonary hyperinflation (PH). In such a context, the metabolic balance could be disturbed within the intercostal muscle tissue, especially during exercise, which could promote the onset or worsening of dyspnea.To simulate ventilatory disturbances that may be encountered by patients with obstructive pulmonary diseases (e.g. abnormally high resistance of the airways to expiration, EFL and PH), a positive expiratory pressure (PEP) of 20 cmH2O was imposed at rest and during exercise in healthy subjects. Oxygenation of the intercostal muscles was measured by near-infrared spectroscopy at the 7th intercostal space.At rest, a decrease in oxyhemoglobin concentration ([O2Hb]) probably linked to a decrease in total hemoglobin concentration ([tHb], i.e. local blood volume) was observed in response to PEP (Study 1). However, no reduction in tissue oxygen saturation index (TSI) was reported (Studies 1 to 3), even in a context of PEP-induced PH (Study 2). During exercise, a lower increase in [O2Hb] and [tHb] was observed when PEP was imposed (vs. control). A decrease in TSI and inspiratory capacity was also reported between rest and exercise in this condition (Study 3).According to the results of our studies, when a PEP of 20 cmH2O is imposed at rest in young healthy subjects, no metabolic imbalance seems to occur in the intercostal muscles. However, when this PEP is imposed during exercise, a disturbance of the metabolic balance seems to happen. This could be partly explained by local hemodynamic alterations induced by PH. However, further studies are needed to clarify this aspect.Finally, no relationship between dyspnea and the metabolic condition of the intercostal muscles was observed during our studies. However, correlations between respiratory discomfort and instantaneous ventilatory flows were highlighted at rest and during exercise with PEP (Studies 1 and 3). A relationship between dyspnea and PH was also observed at rest (Study 2).Future research will aim to verify, at rest and during exercise, whether the oxygenation of the intercostal muscles is influenced by PH in patients with obstructive pulmonary pathologies
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Monteiro, Mariane Borba. "Efeitos da pressão expiratória positiva na hiperinsuflação dinâmica em pacientes portadores de doença pulmonar obstrutiva crônica submetidos ao exercício." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2008. http://hdl.handle.net/10183/17760.

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A hiperinsuflação dinâmica (HD) é considerada um importante contribuinte para a sensação de dispnéia e interrupção do esforço físico em pacientes portadores de doença pulmonar obstrutiva crônica (DPOC). Diversas estratégias são testadas para tentar amenizar a HD e, frequentemente, utiliza-se a capacidade inspiratória (CI) para avaliar esse efeito. Os objetivos deste estudo foram verificar a presença de HD através da pletismografia logo após a suspensão do exercício e avaliar os efeitos da pressão expiratória positiva em via aérea (EPAP) na HD em pacientes portadores de DPOC submetidos ao exercício. Foram incluídos portadores de DPOC moderada a muito grave, de ambos os sexos, considerados capazes de realizarem o teste de esforço. Todos os participantes submeteram-se à mensuração de fluxos expiratórios, volumes e capacidades pulmonares, além da análise de difusão dos gases através da pletismografia. Essas medidas foram feitas antes e após o uso do broncodilatador. A seguir utilizou-se um protocolo de exercício submáximo e nova prova de função pulmonar era realizada imediatamente após o esforço físico para avaliar a presença de hiperinsuflação, ainda sob efeito do broncodilatador. Os pacientes que apresentaram sinal de HD na pletismografia foram convidados a retornar após 48 horas para repetir o mesmo protocolo de estudo, porém com uso de máscara de EPAP durante o exercício. Os parâmetros de função pulmonar foram analisados e comparados nos diferentes momentos e entre os protocolos. A amostra foi composta inicialmente por 46 pacientes, com média de idade de 65±8,5 anos, sendo 32 (70%) do sexo masculino, 25 (54%) com doença em estágio IV. Do total, 17(37%) apresentaram HD na pletismografia realizada após o teste de exercício. Após o exercício, observou-se diferença significativa entre pacientes com e sem HD apenas nas variáveis: CI (p<0,0001), CI/CPT (p=0,001), CRF/CPT (p=0,002). O uso da EPAP durante o exercício aplicado em 17 pacientes com HD não alterou de maneira significativa a capacidade pulmonar total (CPT; p=0,64), a capacidade residual funcional (CRF; p=0,09) e o volume residual (VR; p=0,10) quando comparado aos valores obtidos após exercício sem EPAP. Entretanto na comparação da CI observou-se uma menor perda de CI (p=0,02) com o uso da máscara. Verificou-se diferença significativa na comparação da relação CI/CPT antes e após o exercício em cada protocolo, ambos apresentando uma queda do valor com o exercício. Na comparação entre protocolos observou-se diferença significativa (p=0,01), representado uma queda menor da relação CI/CPT no protocolo com EPAP. Também se observaram relações VR/CPT e CRF/CPT significativamente menores (p=0,03) após o exercício com EPAP em relação ao exercício isolado. Conclui-se que 37% dos 46 pacientes apresentaram HD, detectada através da redução da CI e da sua relação com a CPT, quando avaliados imediatamente após o teste de exercício através da pletismografia. O uso da EPAP através de máscara facial reduziu a HD em teste de exercício submáximo, observado através da redução significativa da queda da CI e da relação CI/CPT, e pela menor alteração das relações VR/CPT e CRF/CPT.
Dynamic hyperinflation (DH) contributes substantially to the sensation of dyspnea and the interruption of physical exercise in patients with chronic obstructive pulmonary disease (COPD). Several strategies have been tested to mitigate DH, and inspiratory capacity (IC) is often used to measure it. The purpose of this study was investigate the presence of DH immediately after exercise interruption using plethysmography and to evaluate the effects of expiratory positive airway pressure (EPAP) on DH of patients with COPD that underwent a exercise test. The study enrolled men and women with moderate to very severe COPD who were able to perform a exercise test. All participants underwent measurement of expiratory flows, volumes and lung capacities, and gas diffusion using plethysmography before and after the use of bronchodilators. A submaximal exercise test and repeated pulmonary function tests were conducted immediately after physical exercise to evaluate hyperinflation, still under the effect of the bronchodilator. The patients with DH according to plethysmography were invited to return 48 hours later to repeat the same protocol using an EPAP mask during exercise test. Pulmonary function parameters were analyzed and compared at the different time points and between the two tests. The sample consisted of 46 patients whose mean age was 65±8.5 years; 32 (70%) were men, and 25 (54%) had stage IV disease. Plethysmography performed after the exercise test revealed DH in 17 (37%) participants. After exercise, there was a significant difference between patients with and without DH only in IC (p<0.0001), IC/TLC (p=0.001), and FRC/TLC (p=0.002). The use of EPAP during exercise in 17 patients with DH did not significantly change total lung capacity (TLC; p=0.64), functional residual capacity (FRC; p=0.09), or residual volume (RV; p=0.10) when compared with the values obtained after exercise without EPAP. However, there was a lower loss of IC (p=0.02) in the EPAP mask group. There was a significant difference in IC/TLC before and after the exercise in each test, and both groups had a decrease in this value after exercise. The comparison between groups revealed a significant difference (p=0.01) and a smaller decrease in the IC/TLC ratio in the EPAP group. Moreover, significantly lower RV/TLC and FRC/TLC (p=0.03) were found after exercise with EPAP than after exercise alone. Of the 46 study patients, 37% developed DH, detected by a reduction in IC and in IC/TLC when evaluated immediately after exercise test using plethysmography. The use of EPAP delivered by face mask reduced DH in submaximal exercise tests, indicated by a significant reduction in IC and IC/TLC decreases and smaller changes in RV/TLC and FRC/TLC.
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Tonelotto, Bruno Francisco de Freitas. "Determinação da PEEP ideal e avaliação de atelectasia pulmonar com o uso da ultrassonografia durante intraoperatório de cirurgias eletivas." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5152/tde-27022019-151124/.

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Introdução: A atelectasia intraoperatória ocorre imediatamente após a indução anestésica e pode ser detectada por ultrassom pulmonar (LUS). No entanto, até o momento o LUS não é utilizado para avaliar a hiperdistensão pulmonar. Neste estudo, descreveu-se um método para detectar hiperdistensão pulmonar usando LUS. A tomografia de impedância elétrica (TIE) foi a referência para comparação dos métodos. Métodos: Dezoito (18) pacientes, com 63 ± 6 anos de idade, com pulmões normais, submetidos à cirurgia abdominal inferior. O TIE foi calibrado, realizada a indução anestésica, intubação e ventilação mecânica. Para reverter a atelectasia posterior, realizou-se uma manobra de recrutamento alveolar com o uso de pressão expiratória final positiva (PEEP) 20 cmH20 e pressão aérea do platô 40 cmH2O durante 120 segundos. A titulação PEEP foi então obtida com valores descendentes: 20, 18, 16, 14,12,10, 8, 6 e 4 cmH2O. Os dados de ultrassom e TIE foram coletados em cada nível PEEP e interpretados por dois observadores independentes. O número de linhas H foi contado usando um filtro especial. O teste de correlação de Spearman e a curva ROC foram utilizados para comparar os dados do LUS e TIE. Resultados: O número de linhas H aumentou linearmente com PEEP: de 3 em PEEP 4 cmH2O a 10 em PEEP 20 cmH2O. Cinco linhas H foram o limiar para a detecção de hiperdistensão pulmonar, definida como hiperdistensão na TIE >= 24,5%. A área sob a curva ROC foi 0,947 (IC 95% 0.901-0.976). Conclusão: O LUS intraoperatório detectou hiperdistensão pulmonar em valores descendentes de PEEP. A presença de cinco ou mais linhas H podem ser consideradas como indicando hiperdistensão pulmonar
Purpose: Intraoperative atelectasis occurs immediately after anaesthetic induction and can be detected by lung ultrasound (LUS). However, LUS is considered as unable to assess pulmonary hyperinflation. In this study, we propose a method to detect pulmonary hyperinflation using LUS. Electrical impedance tomography (EIT) was the reference method. Methods: We included 18 patients, 63 ± 6-year old, with normal lungs, undergoing lower abdominal surgery. The following protocol was used: EIT was calibrated, followed by anaesthetic induction, intubation and mechanical ventilation. To reverse posterior atelectasis, a recruitment maneuver - positive end-expiratory pressure (PEEP) 20 cmH20 and plateau airway pressure 40 cmH2O during 120 sec was performed. PEEP titration was then obtained during a descending trial: 20, 18, 16, 14,12,10, 8, 6 and 4 cmH2O. Ultrasound and EIT data were collected at each PEEP level and analyzed by two independent observers. The number of H lines was counted using a special filter. Spearman correlation test and ROC curve were used to compare LUS and EIT data. Results: The number of H lines increased linearly with PEEP: from 3 at PEEP 4 cmH2O to 10 at PEEP 20 cmH2O. Five H lines was the threshold for detecting pulmonary hyperinflation, defined as a mean decrease in maximum EIT compliance >= 24,5 %. The area under the ROC curve was 0.947 (CI 95% 0.901-0.976). Conclusion: Intraoperative transthoracic LUS can detect pulmonary hyperinflation during a PEEP descending trial. Five or more H lines can be considered as indicating pulmonary hyperinflation in normally aerated lung regions
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Sabapathy, Surendran, and n/a. "Acute and Chronic Adaptations To Intermittent and Continuous Exercise in Chronic Obstructive Pulmonary Disease Patients." Griffith University. School of Physiotherapy and Exercise Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070115.170236.

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The primary aim of this thesis was to develop a better understanding of the physiology and perceptual responses associated with the performance of continuous (CE) and intermittent exercise (IE) in patients with moderate chronic obstructive pulmonary disease (COPD). A secondary aim was to examine factors that could potentially limit exercise tolerance in COPD patients, particularly in relation to the dynamics of the cardiovascular system and muscle metabolism. The results of the four studies conducted to achieve these aims are presented in this thesis. In Study 1, the physiological, metabolic and perceptual responses to an acute bout of IE and CE were examined in 10 individuals with moderate COPD. Each subject completed an incremental exercise test to exhaustion on a cycle ergometer. Subjects then performed IE (1 min exercise: 1 min rest ratio) and CE tests at 70% of peak power in random order on separate days. Gas exchange, heart rate, plasma lactate concentration, ratings of breathlessness, inspiratory capacity and the total amount of work completed were measured during each exercise test. Subjects were able to complete a significantly greater amount of work during IE (71 ± 32 kJ) compared with CE (31 ± 24 kJ). Intermittent exercise was associated with significantly lower values for oxygen uptake, expired ventilation and plasma lactate concentration when compared with CE. Subjects also reported a significantly lower rating of breathlessness during IE compared to CE. The degree of dynamic lung hyperinflation (change in end-expiratory lung volume) was lower during IE (0.23 ± 0.07 L) than during CE (0.52 ± 0.13 L). The results suggest that IE may be superior to CE as a mode of training for patients with COPD. The greater amount of total work performed and the lower measured physiological responses attained with intermittent exercise could potentially allow greater training adaptations to be achieved in individuals with more limited lung function. The purpose of Study 2 was to compare the adaptations to 8 wk of supervised intermittent and continuous cycle ergometry training, performed at the same relative intensity and matched for total work completed, in patients with COPD. Nineteen subjects with moderate COPD were stratified according to age, gender, and pulmonary function, and then randomly assigned to either an IE (1 min exercise: 1 min rest ratio) or CE training group. Subjects trained 3 d per week for 8 wk and completed 30 min of exercise. Initial training intensity, i.e., the power output applied during the CE bouts and during the exercise interval of the IE bouts, was determined as 50% of the peak power output achieved during incremental exercise and was increased by 5% each week after 2 wk of training. The total amount of work performed was not significantly different (P=0.74) between the CE (750 ± 90 kJ) and IE (707 ± 92 kJ) groups. The subjects who performed IE (N=9) experienced significantly lower levels of perceived breathlessness and lower limb fatigue during the exercise-training bouts than the group who performed CE (N=10). However, exercise capacity (peak oxygen uptake) and exercise tolerance (peak power output and 6-min walk distance) improved to a similar extent in both training groups. During submaximal constant-load exercise, the improved (faster) phase II oxygen uptake kinetic response with training was independent of exercise mode. Furthermore, training-induced reductions in submaximal exercise heart rate, carbon dioxide output, expired ventilation and blood lactate concentrations were not different between the two training modes. Exercise training also resulted in an equivalent reduction for both training modes in the degree of dynamic hyperinflation observed during incremental exercise. Thus, when total work performed and relative intensity were the same for both training modes, 8 wk of CE or IE training resulted in similar functional improvements and physiological adaptations in patients with moderate COPD. Study 3 examined the relationship between exercise capacity (peak oxygen uptake) and lower limb vasodilatory capacity in 9 patients with moderate COPD and 9 healthy age-matched control subjects. While peak oxygen uptake was significantly lower in the COPD patients (15.8 ± 3.5 mL·min-1·kg-1) compared to the control subjects (25.2 ± 3.5 mL·kg-1·min-1), there were no significant differences between groups in peak calf blood flow or peak calf conductance measured 7 s post-ischemia. Peak oxygen uptake was significantly correlated with peak calf blood flow and peak conductance in the control group, whereas there was no significant relationship found between these variables in the COPD group. However, the rate of decay in blood flow following ischemia was significantly slower (p less than 0.05) for the COPD group (-0.036 ± 0.005 mL·100 mL-1·min-1·s-1) when compared to the control group (-0.048 ± 0.015 mL·100 mL-1·min-1·s-1). The results of this study suggest that the lower peak exercise capacity in patients with moderate COPD is not related to a loss in leg vasodilatory capacity. Study 4 examined the dynamics of oxygen uptake kinetics during high-intensity constant-load cycling performed at 70% of the peak power attained during an incremental exercise test in 7 patients with moderate COPD and 7 healthy age-matched controls. The time constant of the primary component (phase II) of oxygen uptake was significantly slower in the COPD patients (82 ± 8 s) when compared to healthy control subjects (44 ± 4 s). Moreover, the oxygen cost per unit increment in power output for the primary component and the overall response were significantly higher in patients with COPD than in healthy control subjects. A slow component was observed in 5 of the 7 patients with COPD (49 ± 11 mL·min-1), whereas all of the control subjects demonstrated a slow component of oxygen uptake (213 ± 35 mL·min-1). The slow component comprised a significantly greater proportion of the total oxygen uptake response in the healthy control group (18 ± 2%) than in the COPD group (10 ± 2%). In the COPD patients, the slow component amplitude was significantly correlated with the decrease in inspiratory capacity (r = -0.88, P less than 0.05; N=5), indicating that the magnitude of the slow component was larger in individuals who experienced a greater degree of dynamic hyperinflation. This study demonstrated that most patients with moderate COPD are able to exercise at intensities high enough to elicit a slow component of oxygen uptake during constant-load exercise. The significant correlation observed between the slow component amplitude and the degree of dynamic hyperinflation suggests that the work of breathing may contribute to the slow component in patients with COPD.
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Singh, Bhajan. "The function of the human diaphragm as a volume pump and measurement of its efficiency." University of Western Australia. School of Biomedical and Chemical Sciences, 2004. http://theses.library.uwa.edu.au/adt-WU2004.0029.

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[Truncated abstract] The function of the diaphragm as a volume pump has not been adequately evaluated because there are no accurate methods to measure the volume displaced by diaphragm motion (ΔVdi). As a consequence, the work done, power output and efficiency of the diaphragm have not been measured. Efficiency of the diaphragm could be measured by relating the power output of the diaphragm to its neural activation. The aims of this thesis were to (a) develop a new biplanar radiographic method to measure ΔVdi and use this to evaluate the effect of costophrenic fibrosis and emphysema on ΔVdi, (b) develop a new fluoroscopic method to enable breath-by-breath measurements of ΔVdi, (c) evaluate a method for quantifying neural activation of the diaphragm, and (d) combine measurements of transdiaphragmatic pressure, ΔVdi, inspiratory duration and neural activation of the diaphragm to quantify the neuromechanical efficiency of the diaphragm
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Laveneziana, Pierantonio. "Dynamic lung hyperinflation as the common pathway for exercise-induced dyspnoea in cardio-respiratory diseases." Phd thesis, Université Pierre et Marie Curie - Paris VI, 2012. http://tel.archives-ouvertes.fr/tel-00831616.

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Les patients atteints de BPCO de stade I, d'ICC et d'HTAP peuvent présenter une diminution des débits aériens à bas volume pulmonaire. Il s'agit d'un déterminant majeur de la distension thoracique dynamique, particulièrement délétère, et facteur important de la dyspnée d'exercice. Nos travaux montrent sans ambiguïté une forte association entre la distension thoracique dynamique (limitant l'augmentation du volume courant) et la dyspnée à l'effort chez ces patients. Le corollaire de ces constatations est que des interventions thérapeutiques qui réduisent la distension thoracique devraient diminuer la dyspnée d'effort et améliorer la tolérance à l'exercice, et ce y compris dans des situations cliniques où les anomalies de la mécanique respiratoire ne sont a priori pas le primum movens de la maladie. Et en effet, la réduction de la dyspnée d'effort est bien corrélée avec la réduction du volume pulmonaire induite directement par des interventions pharmacologiques ou indirectement par des interventions non-pharmacologiques. De plus, du point de vue thérapeutique, la mise en évidence dans la troisième étude d'une propension à la distension thoracique induite par l'exercice chez certains patients atteints d'HTAP qui présentent une nette diminution des débits aériens à bas volume pulmonaire peut elle fournir une base théorique à l'adjonction de bronchodilatateurs aux traitements à visée hémodynamique. En conclusion, cette thèse contribue à une meilleure connaissance de la physiopathologie de la dyspnée d'exercice dans le contexte de la BPCO à un stade précoce, de l'ICC et de l'HTAP, en mettant en évidence le rôle d'un mécanisme pathogénétique qui n'avait pas été décrit auparavant.
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Silva, Aline Grandi da. "Efeitos da perda de peso na hiperinsuflação pulmonar dinâmica em asmáticos obesos." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-27092018-122111/.

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Introdução: Adultos obesos com asma apresentam maior ocorrencia e intensidade de hiperinsuflação dinâmica (HD) e limitação do fluxo expiratório (LFE) em comparação aos asmáticos não obesos e a perda de peso parece melhorar a mecânica respiratória durante o exercício. Contudo, desconhece-se, até o momento, estudos que tenham avaliado o efeito da perda de peso na HD em asmáticos obesos. Objetivo: Avaliar o efeito de um programa de perda de peso na hiperinsuflação pulmonar dinâmica em asmáticos obesos. Métodos: Trata-se de um estudo secundário a um ensaio clinico randomizado no qual 42 pacientes com asma moderada ou grave foram previamente submetidos a um programa de perda de peso (dieta e psicologia associados ou não ao treinamento físico, 2vezes/semana, 60 minutos/sessão durante 3 meses). Posteriormente, foram divididos em 2 grupos de acordo com a % da perda de peso: (grupo >= 5%, n=19) e (grupo < 5%, n=23). Antes e após as intervenções, foram avaliados a HD e a LFE (exercício com carga constante) assim como os fatores de saúde relacionados a qualidade de vida (FSRQV), o controle da asma, a força e endurance muscular de quadríceps, a composição corporal e a função pulmonar. A comparação entre os dados categóricos foi realizada pelo teste qui-quadrado e entre os dados numéricos pela ANOVA de dois fatores com medidas repetidas. A associação entre a perda de peso e a melhora da HD foi analisada pelo teste de Correlação de Pearson. O nível de significância estatística foi ajustado para 5% (p <= 0,05). Resultados: O grupo >= 5% apresentou redução clinicamente significante da HD em relação ao grupo < 5% pós intervenção (-9,1 ± 14,5% vs. -12,5 ± 13,5%, respectivamente), que foi acompanhado por um retardo significante no tempo de inicio da HD e LFE. Além disso, o grupo >= 5% obteve melhora clinicamente significativa nos FSRQV e no controle da asma. Também foi observado uma correlação entre a redução da circunferência da cintura e o aumento da CI (r = -0,45, p = 0,05) no grupo >= 5%. Não foi encontrada diferença nos volumes pulmonares avaliados. Conclusão: A perda de peso moderada ( >= 5% do peso corporal), principalmente na presença da diminuição da circunferência da cintura, melhora a HD em adultos obesos com asma. Além disso, o grupo que perdeu mais peso também retardou o tempo de início da HD e da LFE durante a progressão do exercício, apresentando melhora nos FSRQV e controle clínico da asma
Rationale: Obese adults with asthma develop dynamic hyperinflation (DH) and expiratory flow limitation (EFL) more likely than no obese asthmatics and weight loss seems to improve the breathing mechanic during exercise. However, studies to evaluate the effect of weight loss on DH in obese asthmatics are unknown. Objective: To evaluate the effect of a weight loss program on dynamic pulmonary hyperinflation in obese asthmatics. Methods: This was a secondary study of a randomized clinical trial in which 42 subjects with moderate or severe asthma previously participated in a weight loss program (diet and psychology associated or not with physical training, 2x/ week, 60 min/ session for 3 months). Posteriorly, they were divided into 2 groups according to %weight loss: (group >= 5%, n = 19) and (group < 5%, n = 23). Before and after the intervention, DH and EFL (constant load exercise), health-related quality of life (HRQoL), asthma control, quadriceps muscle strength and endurance, body composition and lung function were assessed. The comparison between the categorical data was performed using the chi-square test and between the numerical data by two-way ANOVA with repeated measures. The association between weight loss and DH improvement was analyzed by the Pearson\'s correlation test. The level of statistical significance was adjusted to 5% (p <= 0.05). Results: Group >= 5% presented a clinically significant reduction of DH compared to group < 5% post intervention (-9.1±14.5% vs. - 12.5±13.5%, respectively), that was following by a significant delay at the onset time for both DH and EFL. Besides, group >= 5% obtained clinically significant improvement in the HRQoL and asthma control. Furthermore, was observed a correlation between reduction waist circumference and increased IC (r=-0.45, p=0.05) in the group >= 5%. No difference was found in the lung volumes evaluated. Conclusion: A moderate weight loss ( >= 5% body weight) mainly with the decrease in waist circumference can improved DH in obese adults with asthma. In addition the greater weight loss group also delayed the onset time of DH and EFL during the progression of the exercise and presented an improvement in the asthma clinical control and in the HRQoL
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Books on the topic "Pulmonary hyperinflation"

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Grassino, A., C. Rampulla, N. Ambrosino, and C. Fracchia, eds. Chronic Pulmonary Hyperinflation. London: Springer London, 1991. http://dx.doi.org/10.1007/978-1-4471-3782-5.

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Workshop on "Chronic Pulmonary Hyperinflation" (1988 Montescano, Italy). Chronic pulmonary hyperinflation. London: Springer-Verlag, 1989.

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Grassino, A. Chronic Pulmonary Hyperinflation. Springer, 2013.

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Grassino, A., C. Rampulla, and R. Corsico. Chronic Pulmonary Hyperinflation. Springer, 2014.

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Chronic pulmonary hyperinflation (Current topics in rehabilitation). Bi & Gi, 1991.

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Grassino, A., C. Rampulla, and N. Ambrosino. Chronic Pulmonary Hyperinflation (Current Topics in Rehabilitation). Springer, 1991.

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(Foreword), R. Corsico, A. Grassino (Editor), C. Rampulla (Editor), N. Ambrosino (Editor), and C. Fracchia (Editor), eds. Chronic Pulmonary Hyperinflation (Current Topics in Rehabilitation). Springer-Verlag Berlin and Heidelberg GmbH & Co. K, 1991.

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Extended pulmonary preservation: The role of prostaglandin pretreatment and donor hyperinflation. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1992.

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Kreit, John W. Dynamic Hyperinflation and Intrinsic Positive End-Expiratory Pressure. Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0010.

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Dynamic hyperinflation and intrinsic PEEP almost always occur in patients with severe obstructive lung disease, in whom slowing of expiratory flow prevents complete exhalation. Occasionally, patients without airflow obstruction develop dynamic hyperinflation when expiratory time, is excessively shortened by a rapid respiratory rate, a long set inspiratory time (TI), or both. Dynamic Hyperinflation and Intrinsic Positive End-Expiratory Pressure describes the causes of dynamic hyperinflation and the mechanisms of its adverse effects, including reduced cardiac output and blood pressure, pulmonary barotrauma, and ineffective ventilator triggering. The chapter also describes how to screen for and measure intrinsic PEEP, and how to reduce or eliminate its adverse effects.
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Lucangelo, Umberto, and Massimo Ferluga. Pulmonary mechanical dysfunction in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0084.

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In intensive care units practitioners are confronted every day with mechanically-ventilated patients and should be able to sort out from all the data available from modern ventilators to tailored patient ventilatory strategy. Real-time visualization of pressure, flow and tidal volume provide valuable information on the respiratory system, to optimize ventilatory support and avoiding complications associated with mechanical ventilation. Early determination of patient–ventilator asynchrony, air-trapping, and variation in respiratory parameters is important during mechanical ventilation. A correct evaluation of data becomes mandatory to avoid a prolonged need for ventilatory support. During dynamic hyperinflation the lungs do not have time to reach the functional residual capacity at the end of expiration, increasing the work of breathing and promoting patient-ventilator asynchrony. Expiratory capnogram provides qualitative information on the waveform patterns associated with mechanical ventilation and quantitative estimation of expired CO2. The concept of dead space accounts for those lung areas that are ventilated but not perfused. Calculations derived from volumetric capnography are useful indicators of pulmonary embolism. Moreover, alveolar dead space is increased in acute lung injury and its value decreased in case of positive end-expiratory pressure (PEEP)-induced recruitment, whereas PEEP-induced overdistension tends to increment alveolar dead space.
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Book chapters on the topic "Pulmonary hyperinflation"

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Dreyfuss, D., and G. Saumon. "Acute Pulmonary Hyperinflation and Pulmonary Edema." In Current Topics in Rehabilitation, 41–46. London: Springer London, 1991. http://dx.doi.org/10.1007/978-1-4471-3782-5_6.

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Poggi, R., L. Dal Vecchio, M. Bernasconi, R. Brandolese, and A. Rossi. "Pharmacological Management of Pulmonary Hyperinflation." In Current Topics in Rehabilitation, 127–34. London: Springer London, 1991. http://dx.doi.org/10.1007/978-1-4471-3782-5_16.

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Collet, P. W., and L. A. Engel. "Efficientcy of breathing during hyperinflation." In Respiratory Muscles in Chronic Obstructive Pulmonary Disease, 89–93. London: Springer London, 1988. http://dx.doi.org/10.1007/978-1-4471-3850-1_9.

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Emery, C. "Effects of Lung Hyperinflation on Pulmonary Circulation." In Current Topics in Rehabilitation, 57–65. London: Springer London, 1991. http://dx.doi.org/10.1007/978-1-4471-3782-5_8.

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Cibella, F., P. Pipitone, C. Macaluso, V. Bellia, and G. Bonsignore. "Alveolar Gas Mixing in Chronic Pulmonary Hyperinflation." In Current Topics in Rehabilitation, 33–39. London: Springer London, 1991. http://dx.doi.org/10.1007/978-1-4471-3782-5_5.

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Saetta, M., L. M. Fabbri, A. Papi, and A. Ciaccia. "Pathology and Biochemical Basis of Chronic Pulmonary Hyperinflation." In Current Topics in Rehabilitation, 11–18. London: Springer London, 1991. http://dx.doi.org/10.1007/978-1-4471-3782-5_2.

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Laveneziana, Pierantonio, Katherine A. Webb, and Denis E. O’Donnell. "Static and Dynamic Hyperinflation in Chronic Obstructive Pulmonary Disease." In Mechanics of Breathing, 73–97. Milano: Springer Milan, 2014. http://dx.doi.org/10.1007/978-88-470-5647-3_7.

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Torchio, R., C. Gulotta, G. Sera, D. Boaro, A. Tosadori, and C. Banaudi. "Is Pulmonary Hyperinflation a Feature in Advancing Interstitial Lung Disease?" In Current Topics in Rehabilitation, 47–53. London: Springer London, 1991. http://dx.doi.org/10.1007/978-1-4471-3782-5_7.

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Maskey-Warzechowska, M., M. Mierzejewski, K. Gorska, R. Golowicz, L. Jesien, and R. Krenke. "Effects of Osteopathic Manual Therapy on Hyperinflation in Patients with Chronic Obstructive Pulmonary Disease: A Randomized Cross-Over Study." In Advances in Experimental Medicine and Biology, 17–25. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/5584_2019_418.

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M. Jelic, Tomislav. "Emphysema." In Update in Respiratory Diseases. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.83273.

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Emphysema (Greek word meaning to inflate/to blow) is an increase in the size of airspace distal to the terminal bronchiolus, that is, hyperinflation of the alveoli due to the destruction of the gas-exchanging structures: alveolar walls, alveolar ducts, and respiratory bronchioles with coalescence of airspaces into the abnormal, much larger airspaces. The main consequences are the reduction of alveolar surface for gas exchange and the chronic obstructive pulmonary disease due to the destruction and disappearance of respiratory bronchioles with decreased total small airway diameter sum. Both decreased alveolar surface for gas exchange and chronic obstructive pulmonary disease lead to difficulty in breathing with dyspnea varying from mild to very severe. Two main pathohistologic types of emphysema are centriacinar and panacinar. Centriacinar emphysema involves the central portion of the acinus, and inflation mainly involves respiratory bronchioles and adjacent alveoli, and not all alveoli inside the acinus are involved. Panacinar (panlobular) emphysema is characterized by uniform enlargement and destruction of alveoli throughout the entire acinus. The panacinar emphysema is rare and its most common cause is hereditary alpha-1 antitrypsin deficiency. The centriacinar emphysema is the most frequent emphysema. It is mainly caused by smoking but also by coal dust exposure and advanced age.
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Conference papers on the topic "Pulmonary hyperinflation"

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Pereira, Ana Carolina Alves Caporali, Rafaella Fagundes Xavier, Cristino Carneiro Oliveira, Aline Costa Lopes, Cibele Cristine Berto Marques da Silva, Ross Clark, Rafael Stelmach, Linda Denehy, and Celso Ricardo Fernandes de Carvalho. "Pulmonary hyperinflation and postural balance in COPD patients." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa1349.

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Chapman, D. G., C. Arnott, R. Puranik, G. Prael, K. Patel, K. O. Tonga, S. Milne, et al. "Elastic Chest Compression Reduced Hyperinflation in People with Chronic Obstructive Pulmonary Disease." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6430.

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van Geffen, Wouter H., and Huib Kerstjens. "Static and dynamic hyperinflation during severe acute exacerbations of chronic obstructive pulmonary disease." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2228.

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Stone, Ian S., Steffen E. Petersen, and Neil Barnes. "The Influence Of Hyperinflation On Arterial Stiffness In Stable Chronic Obstructive Pulmonary Disease." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3982.

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Gomes, Evelim, Carla Feitoza, and Dirceu Costa. "Acute effects of Positive Expiratory Pressure on pulmonary dynamic hyperinflation in patients with COPD." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2202.

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Chapman, D., K. Jetmalani, C. Thamrin, C. S. Farah, R. R. Grunstein, M. Comas-Soberats, P. M. Young, C. L. Phillips, and G. King. "Reduced Sleep Quality Correlates with Worse Hyperinflation in Patients with Chronic Obstructive Pulmonary Disease." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3872.

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Ferreira dos Santos, Vanessa Maria, Rita Boaventura, Leonor Meira, Paula Martins, Luís Gaspar, Paulo Viana, Emília Araújo, and Isabel Gomes. "Influence of critical hyperinflation in exercise capacity improvement after pulmonary rehabilitation in severely obstructed patients." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa1562.

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Ansarin, Khalil, Payam Salehirad, and Mohammadamin Rezazadehsaatlou. "Effect of tiotropium compared to salmetrol on dynamic hyperinflation in patients with chronic obstructive pulmonary disease." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa4053.

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Górska, Katarzyna, Marta Maskey-Warzechowska, Michał Mierzejewski, and Rafał Krenke. "Immediate effect of osteopathic manual therapy on hyperinflation in patients with severe chronic obstructive pulmonary disease." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3685.

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Minville, C., F. Maltais, and D. Saey. "Dynamic Hyperinflation in Patients with Chronic Obstructive Pulmonary Disease: Comparison of Incremental and Constant Load Cycle Exercise Tests." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1553.

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You might also be interested in the extended bibliographies on the topic 'Pulmonary hyperinflation' for particular source types:
Journal articles
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