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Books on the topic 'Cardiac arrest'

Author: Grafiati

Published: 4 June 2021

Last updated: 31 July 2024

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1

Paradis, Norman A., Henry R. Halperin, Karl B. Kern, Volker Wenzel, and Douglas A. Chamberlain, eds. Cardiac Arrest. Cambridge: Cambridge University Press, 2007. http://dx.doi.org/10.1017/cbo9780511544828.

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2

Way, John H. Cardiac arrest. New York: Charter Books, 1988.

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3

Laymon, Richard. Cardiac arrest. Wisbech: Learning Development Aids, 1989.

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4

Lundbye, Justin B., ed. Therapeutic Hypothermia After Cardiac Arrest. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2951-6.

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5

Antonio, Bayés de Luna, ed. Sudden cardiac death. Dordrecht: Kluwer Academic Publishers, 1991.

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6

O, Cummins Richard, and Ho Mary T, eds. Code blue: Cardiac arrest and resuscitation. Philadelphia: Saunders, 1987.

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7

Gardiner, J. Cardiac arrest: What do you do? Cheltenham: Thornes, 1986.

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8

A, Paradis Norman, Halperin Henry R, and Nowak Richard M, eds. Cardiac arrest: Science and practice of resuscitation medicine. Baltimore: Williams & Wilkins, 1996.

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9

McCoy, Margaret A., and Andrea M. Schultz, eds. Exploring Strategies to Improve Cardiac Arrest Survival. Washington, D.C.: National Academies Press, 2017. http://dx.doi.org/10.17226/23695.

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10

Aibiki, Mayuki, and Susumu Yamashita, eds. A Perspective on Post-Cardiac Arrest Syndrome. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1099-7.

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11

Ramiro, Albarran-Sotelo, and American Heart Association, eds. Textbook of advanced cardiac life support. 2nd ed. Dallas: The Association, 1987.

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12

J, Roberts Arthur, and Boston University Medical Center, eds. Myocardial protection in cardiac surgery. New York: Dekker, 1987.

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13

Hackel, Donald B. Sudden death: Cardiac and other causes. Durham, N.C: Carolina Academic Press, 1993.

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14

Mohammad, Shenasa, Borggrefe Martin, and Breithardt Günter, eds. Cardiac mapping. Mount Kisco, NY: Futura Pub. Co., 1993.

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15

M, Owen Patricia, ed. Sudden cardiac death: Theory and practice. Gaithersburg, Md: Aspen Publishers, 1991.

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16

Chu-Jeng, Chiu Ray, ed. Cardioplegia: Current concepts and controversies. Austin, Tex: R.G. Landes, 1993.

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17

McNally, Bryan. Out-of-hospital cardiac arrest surveillance: Cardiac Arrest Registry to Enhance Survival (CARES), United States, October 1, 2005-December 31, 2010. Atlanta, GA: U.S. Dept. of Health and Human Services, Centers for Disease Control and Prevention, 2011.

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18

Waien, Sohail Akbar. Outcomes of cardiac arrest patients in Metropolitan Toronto. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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19

B, Kostis John, and Sanders Michael 1943-, eds. The Prevention of sudden cardiac death. New York: Liss, 1990.

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20

Aronson, Miriam. Maʻatsar lev. T.A. [z.o. Tel Aviv]: Y. Golan, 1993.

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21

Aronson, Miriam. Maʻatsar lev. T.A. [z.o. Tel Aviv]: Y. Golan, 1993.

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22

Chong, Ji Y., and Michael P. Lerario. Cardiac Arrest. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190495541.003.0028.

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Hypoxic–ischemic brain injury is common following cardiopulmonary arrest and is associated with high rates of mortality and morbidity. Therapeutic hypothermia has been helpful in increasing survival and functional outcomes in these patients. The neurological examination, neuroimaging studies, and ancillary serological and neurophysiological testing can be helpful in prognostication post-arrest.

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23

Laymon, Richard. Cardiac Arrest. Bt Bound, 1999.

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24

Cardiac Arrest. W.B. Saunders Company, 2011.

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25

Heaney, Wayne. Cardiac Arrest. Independently Published, 2017.

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26

Laymon, Richard. Cardiac Arrest. Fearon Publishers, 1985.

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27

Hancock, Thelma. Cardiac Arrest. CreateSpace Independent Publishing Platform, 2017.

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28

Mathews, Lisa Q. Cardiac Arrest. Harlequin Enterprises ULC, 2015.

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29

MT-B. Cardiac Arrest. Independently Published, 2018.

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30

Cardiac arrest. Toronto, Canada: Doubleday Canada, 1985.

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31

Hospital, Centenary. Pediatric Cardiac Arrest. Hans Huber Pub, 1993.

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32

Cardiac Arrest (Charter). Diamond Books (NY), 1988.

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33

Swindell, Paul. Life after Cardiac Arrest: Writings from Sudden Cardiac Arrest UK. Independently Published, 2018.

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34

Jumean, Marwan F., and Mark S. Link. Post-cardiac arrest arrhythmias. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0065.

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Our understanding of arrhythmias following resuscitated cardiac arrest has evolved over the past two decades to entail complex pathophysiological processes including, in part, ischaemia and ischaemia-reperfusion injury. Electrical instability after the return of spontaneous circulation (ROSC) is common, ranging from atrial fibrillation to recurrent ventricular tachycardia and fibrillation. Electrical instability following out-of-hospital cardiac arrest is most commonly due to myocardial ischaemia and post-arrest myocardial dysfunction. However, electrolyte disturbances, elevated catecholamine levels, the frequent use of vasopressors and inotropes, and underlying structural heart disease or channelopathies also contribute in the acute setting. Limited data exists that specifically address the management of arrhythmias in the immediate post-arrest period. In addition to treating any potential reversible cause, the management in the haemodynamically-stable patient includes beta-blockers, class I (lignocaine and procainamide) and III anti-arrhythmic agents (amiodarone). Defibrillation is often needed for recurrent ventricular arrhythmias.

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35

Pitcher, Joseph H., and David B. Seder. Neuroprotection for Cardiac Arrest. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0009.

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This chapter reviews the pathophysiology of brain injury after resuscitation from cardiac arrest and describes a pragmatic approach to neuroprotection. Common mechanisms of brain injury in the postresuscitation milieu are discussed and strategies for optimizing physiological variables such as blood pressure, oxygen, ventilation, and blood glucose in order to minimize secondary injury are presented. Neuroprotective therapies, such as targeted temperature management and pharmacologic neuroprotective agents, are covered in detail. Finally, the use of raw and processed electroencephalography and other diagnostic tools are described for the purposes of determining severity of brain injury, triaging patients to different treatment pathways, and for prognostic value.

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36

Life after Cardiac Arrest Volume 2: Writings from Sudden Cardiac Arrest UK. Independently Published, 2020.

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37

Weiss, Raul, and Emile Daoud. Sudden Cardiac Death. Elsevier - Health Sciences Division, 2011.

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38

Capucci, Alessandro. Sudden Cardiac Death. Taylor & Francis Group, 2006.

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39

Morley, Peter Thomas. Pathophysiology and causes of cardiac arrest. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0061.

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Sudden cardiopulmonary arrest (CPA) is still the commonest cause of death globally. CPAs are usually categorized according to where they occur, with out-of-hospital arrests accounting for approximately 75% of CPA deaths and in-hospital the remaining 25%. The arrests are also sub-categorized according to the initial rhythm, with the best outcomes associated with shockable rhythms. Large registries have demonstrated a variable incidence of out-of-hospital CPAs in adults (50–150/100,000 person years), with a range of outcomes (3–16% survival to hospital discharge). The majority of CPAs in adults are due to cardiac causes, but teaching surrounding the management of cardiac arrests now includes an increased focus on the identification and correction of underlying causes, irrespective of the rhythm. While identifying an underlying cause is often challenging, this is probably one of reasons explaining the improved survival seen with in-hospital compared with the out-of-hospital CPA. The incidence of CPAs in children is highest in infants, and decreases with age. The majority of CPAs in children are due to respiratory causes. Cardiac causes in children and young adults include a variety of familial, genetic, and acquired conditions. The pathophysiology of cardiac arrests is also now better understood. A large number of biochemical pathways are activated as a result of the CPA. These result in the post-cardiac arrest syndrome, which affects many systems in the body, but in particular the brain, heart, and kidneys.

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40

Luna, Antonio Bayés de. Sudden Cardiac Death. Springer, 2011.

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41

Aguilar, J. Cosin, F. Navarro Lopez, and Antonio Bayés de Luna. Sudden Cardiac Death. Springer London, Limited, 2012.

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42

PILBERY. Standby Cpd: Traumatic Cardiac Arrest. Class Publishing, 2016.

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43

Elmer, Jonathan, and Abhishek Freyer. In-Hospital Cardiac Arrest (DRAFT). Edited by Raghavan Murugan and Joseph M. Darby. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190612474.003.0004.

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In-hospital cardiac arrest (IHCA) is a major public health problem. Despite its prevalence, there remains a paucity of high-level evidence to guide patient management during and after resuscitation from IHCA and most guidelines are extrapolated from studies of out-of-hospital cardiac arrest. This chapter reviews the cornerstones of IHCA management: early recognition, provision of high quality compressions, and early defibrillation of shockable rhythms. It also summarizes key actions in early post-resuscitation care, including multiple system organ support to prevent rearrest and restore hemodynamic stability and prevention of secondary brain injury. Finally, brief attention is given to adjuncts to traditional IHCA resuscitation including thrombolysis, corticosteroids, and extracorporeal circulatory support.

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44

Adam, Sheila, Sue Osborne, and John Welch. Cardiac arrest and cardiopulmonary resuscitation. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199696260.003.0006.

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Critically ill patients are at high risk of cardiac arrest, and the critical care nurse needs to recognize early signs of deterioration, understand what can be done to prevent arrest, and understand the different functions of cardiac arrest team members. This chapter outlines the pathophysiology associated with cardiac arrest, reviews the management of arrest, the practicalities of the techniques and drugs used in cardiopulmonary resuscitation, and the care of the patient and family following both successful and unsuccessful resuscitation.

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45

Lundbye, Justin B. Therapeutic Hypothermia After Cardiac Arrest. Springer, 2012.

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46

DUNCAN. Traumatic Cardiac Arrest ? Hott Press. Class Publishing, 2020.

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47

Sutton, Martin St John, Josep Brugada, Jeroen Bax, Mariell Jessup, and Martin Schalij. Cardiac Resynchronization Therapy. Taylor & Francis Group, 2007.

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48

Sutton, Martin St John, Josep Brugada, Jeroen Bax, Mariell Jessup, and Martin Schalij. Cardiac Resynchronization Therapy. Taylor & Francis Group, 2019.

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49

Sutton, Martin St John, Josep Brugada, Jeroen Bax, Mariell Jessup, and Martin Schalij. Cardiac Resynchronization Therapy. Taylor & Francis Group, 2007.

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50

Perkins, Gavin D. Cardiac massage and blood flow management during cardiac arrest. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0062.

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When cardiac arrest occurs, blood flow to the vital organs diminishes rapidly. Chest compressions are an essential element of cardiopulmonary resuscitation (CPR), yet they achieve, at best, one-third of the normal cardiac output. The speed of initiating CPR, as well as its quality is critical to patient outcomes. Optimal chest characteristics of compressions are defined as pushing hard (depth > 5 cm) and fast (compression rate 100–120/min). Pressure should be released fully between sequential chest compressions and interruptions in chest compressions should be minimized. Even short interruptions in CPR around the time of attempted defibrillation can be harmful. CPR feedback and prompt devices can be used to monitor the quality of CPR. Studies have shown these devices can improve the quality of CPR, but do not improve overall survival. Mechanical chest compression devices may be usefully deployed when it is difficult or unsafe to perform manual CPR, but there is no evidence that the routine deployment of these devices improves outcome. Vasoactive drugs improve coronary perfusion pressure and increase the chances of return of spontaneous circulation. However, there is no definitive evidence that they improve long-term survival. Recent data have raised the possibility that adrenaline may worsen long-term outcomes.

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