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Books on the topic 'Acute Respiratry Distress Syndrome'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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1

Tasaka, Sadatomo, ed. Acute Respiratory Distress Syndrome. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8371-8.

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2

Matalon, Sadis, and Jacob Lasha Sznajder, eds. Acute Respiratory Distress Syndrome. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4419-8634-4.

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3

Chiumello, Davide, ed. Acute Respiratory Distress Syndrome. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-41852-0.

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4

K, Choi Augustine M., ed. Acute respiratory distress syndrome. 2nd ed. New York: Informa Healthcare USA, 2009.

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5

P, Wiedemann Herbert, and Matthay Michael A, eds. Acute respiratory distress syndrome. Philadelphia: Saunders, 2000.

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6

A, Matthay Michael, ed. Acute respiratory distress syndrome. New York: M. Dekker, 2003.

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7

Acute respiratory distress syndrome. 2nd ed. New York: Informa Healthcare USA, 2010.

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8

1942-, Zapol Warren M., and Falke Konrad J, eds. Acute respiratory failure. New York: Dekker, 1985.

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9

Shein, Steven L., and Alexandre T. Rotta, eds. Pediatric Acute Respiratory Distress Syndrome. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-21840-9.

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10

W, Evans Timothy, and Haslett C, eds. ARDS: Acute respiratory distress in adults. London: Chapman & Hall Medical, 1996.

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11

A, Russell James, and Walley Keith R, eds. Acute respiratory distress syndrome: A comprehensive clinical approach. Cambridge, UK: Cambridge University Press, 1999.

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12

J, Marini John, and Evans Timothy W, eds. Acute lung injury. Berlin: Springer, 1998.

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13

Fraser, Debbie. Acute respiratory care of the neonate. 3rd ed. Petaluma, CA: NICU Ink Book Publishers, 2012.

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14

1959-, Askin Debbie Fraser, ed. Acute respiratory care of the neonate: A self-study course. 2nd ed. Petaluma, CA: NICU Ink Book Publishers, 1997.

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15

Ferguson, Niall Douglas. Development and testing of a modified clinical definition of the acute respiratory distress syndrome. Ottawa: National Library of Canada, 2002.

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16

Russell, James A., and Keith R. Walley, eds. Acute Respiratory Distress Syndrome. Cambridge University Press, 1999. http://dx.doi.org/10.1017/cbo9780511575112.

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17

Matthay, Michael A., ed. Acute Respiratory Distress Syndrome. CRC Press, 2003. http://dx.doi.org/10.3109/9780203912034.

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18

Elie, Marie C., and Donna Carden. Acute Respiratory Distress Syndrome. Morgan & Claypool Life Science Publishers, 2013.

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19

Choi, Augustine M. K., ed. Acute Respiratory Distress Syndrome. CRC Press, 2016. http://dx.doi.org/10.3109/9781420088410.

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20

Acute Respiratory Distress Syndrome. Springer My Copy UK, 1998.

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21

Choi, Augustine M. K. Acute Respiratory Distress Syndrome. Taylor & Francis Group, 2016.

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22

Acute Respiratory Distress Syndrome. New York: Marcel Dekker, Inc., 2003.

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23

Carden, Donna, and Marie Carmelle Elie. Acute Respiratory Distress Syndrome. Morgan & Claypool Life Science Publishers, 2013.

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24

Chiumello, Davide. Acute Respiratory Distress Syndrome. Springer, 2017.

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25

Choi, Augustine M. K. Acute Respiratory Distress Syndrome. Taylor & Francis Group, 2016.

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26

Matthay, Michael A. Acute Respiratory Distress Syndrome. Taylor & Francis Group, 2003.

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27

Chiumello, Davide. Acute Respiratory Distress Syndrome. Springer, 2018.

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28

Chiumello, Davide. Acute Respiratory Distress Syndrome. Springer, 2017.

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29

Kreit, John W. Acute Respiratory Distress Syndrome (ARDS). Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0012.

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Acute Respiratory Distress Syndrome reviews the definitions, causes, pathophysiology, and management of this relatively common, life-threatening disorder. This chapter describes how to ensure adequate tissue oxygen delivery while minimizing ventilator-induced lung injury and provides an in-depth review of how to determine the optimum level of positive end-expiratory pressure (PEEP). The first topic addressed is the precipitating factors and pathophysiology of acute respiratory distress syndrome. Next the chapter turns to mechanical ventilation, and covers the subjects of adequate oxygenation, ventilator-induced lung injury, ancillary therapies, ventilatory therapies, and high I:E ventilation. The topics addressed in the area of non-ventilatory therapies include: prone positioning of the patient, neuromuscular blockade, inhaled vasodilators, and extracorporeal membrane oxygenation (ECMO).
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30

Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0064.

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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
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31

Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0064_update_001.

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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
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32

Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.

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The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.
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33

Choi, Augustine M. K. Acute Respiratory Distress Syndrome, Second Edition. Taylor & Francis Group, 2017.

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34

(Editor), Timothy Evans, and Christopher Haslett (Editor), eds. ARDS: Acute Respiratory Distress in Adults. A Hodder Arnold Publication, 1996.

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35

Summers, Charlotte, and Geoffrey Bellingan. Therapeutic strategy in acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0109.

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Acute respiratory distress syndrome (ARDS) is a pathological syndrome characterized by arterial hypoxaemia and bilateral pulmonary infiltrates. Until recently, the diagnosis of ARDS was made in accordance with the American–European Consensus Conference criteria established in 1994, although an updated ‘Berlin’ definition was produced in 2012. It is important to remember that ARDS is not a single disease, but rather a constellation of conditions with similar pathophysiology, and thus there may not be one unifying clinical treatment. The mainstay of ARDS management is the identification and treatment of the predisposing condition, surveillance for the presence of intercurrent infection, and supportive care, including lung-protective ventilation, and even prone ventilation in more severe cases. Fluid restriction, after patients are appropriately resuscitated, is probably of benefit. Despite many clinical trials, there are currently no licensed pharmacological therapies for ARDS, however a number of novel agents are under development.
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36

Acute Respiratory Distress Syndrome: A Comprehensive Clinical Approach. Cambridge University Press, 1999.

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37

Russell, James A., and Keith R. Walley. Acute Respiratory Distress Syndrome: A Comprehensive Clinical Approach. Cambridge University Press, 2010.

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38

Russell, James A., and Keith R. Walley. Acute Respiratory Distress Syndrome: A Comprehensive Clinical Approach. University of Cambridge ESOL Examinations, 2012.

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39

Russell, James A., and Keith R. Walley. Acute Respiratory Distress Syndrome: A Comprehensive Clinical Approach. Cambridge University Press, 2012.

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40

Evans, Timothy W., and J. J. Marini. Acute Lung Injury. Springer London, Limited, 2012.

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41

Dangayach, Neha S., Charles L. Francoeur, Stephan A. Mayer, and Tarek Sharshar. Neuroprotection in Sepsis and Acute Respiratory Distress Syndrome. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0013.

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Diffuse cerebral dysfunction in sepsis and acute respiratory distress syndrome (ARDS) patients is highly prevalent. Delirium and alterations in level of consciousness in septic patients are symptoms that constitute sepsis-associated encephalopathy (SAE), which is distinct from hypoxic encephalopathy. SAE is associated with substantial mortality and long-term cognitive impairment. The underlying pathophysiology of SAE is complex and poorly understood. The pathophysiology of SAE includes neuroinflammation, microglial activation, microcirculatory failure, autoregulation impairment, blood–brain barrier disruption, apoptosis, and development of microinfarcts and microhemorrhages. Apart from standard resuscitation techniques targeted at maintaining adequate cerebral perfusion and oxygenation, specific neuroprotective interventions are not currently available. Given the vast unmet need for improving functional outcome among survivors of SAE, it is a priority for the critical care community to better define, understand, and prevent this common and devastating form of neurological injury.
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42

Shein, Steven L., and Alexandre T. Rotta. Pediatric Acute Respiratory Distress Syndrome: A Clinical Guide. Springer International Publishing AG, 2020.

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43

Shein, Steven L., and Alexandre T. Rotta. Pediatric Acute Respiratory Distress Syndrome: A Clinical Guide. Springer, 2019.

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44

1934-, Kazemi Homayoun, Hyman Albert L, Kadowitz Philip J. 1941-, and American Heart Association. Cardiopulmonary Council., eds. Acute lung injury: Pathogenesis of adult respiratory distress syndrome. Littleton, Mass: PSG Pub. Co., 1986.

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45

Matalon, Sadis. Acute Respiratory Distress Syndrome: Cellular And Molecular Mechanisms And Clinical Management. Springer, 2012.

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46

Severe Acute Respiratory Syndrome: From Benchtop to Bedside. World Scientific Publishing Company, 2004.

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47

Matthay, Michael, and Kathleen Dori Liu. Acute Respiratory Distress Syndrome, an Issue of Critical Care Clinics. Elsevier, 2021.

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48

Fey, Twila. Coloring Book - You Will Get Better - Acute Respiratory Distress Syndrome. Independently Published, 2021.

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49

Acute respiratory distress syndrome: Cellular and molecular mechanisms and clinical management. New York: Plenum Press, 1998.

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50

(Editor), Sadis Matalon, and Jacob Iasha Sznajder (Editor), eds. Acute Respiratory Distress Syndrome: Cellular and Molecular Mechanisms and Clinical Management. Springer, 1998.

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