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Books on the topic 'Cardiovascular and autonomic response'

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Published: 4 June 2021
Last updated: 10 February 2022

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1

Gabriel, Edmo Atique, and Sthefano Atique Gabriel, eds. Inflammatory Response in Cardiovascular Surgery. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4429-8.

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2

Turner, J. Rick, Andrew Sherwood, and Kathleen C. Light, eds. Individual Differences in Cardiovascular Response to Stress. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4899-0697-7.

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3

Turner, J. Rick, Andrew Sherwood, and Kathleen C. Light. Individual differences in cardiovascular response to stress. Boston, MA: Springer, 1992.

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4

Javorka, Michal. Cardiovascular signals in diabetes mellitus: A new tool to detect autonomic neuropathy. Hauppauge, N.Y: Nova Science, 2009.

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5

How motivation affects cardiovascular response: Mechanisms and applications. Washington, DC: American Psychological Association, 2011.

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6

Urquhart, Nathan Alexander. The cardiovascular response to acute, repeated orthostatic stress. Ottawa: National Library of Canada, 2003.

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7

Cardiovascular reactivity and stress: Patterns of physiological response. New York: Plenum Press, 1994.

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8

Wright, Rex A., and Guido H. E. Gendolla, eds. How motivation affects cardiovascular response: Mechanisms and applications. Washington: American Psychological Association, 2012. http://dx.doi.org/10.1037/13090-000.

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9

The autonomic nervous system in health and disease. New York: M. Dekker, 2001.

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10

Matrichnoe teplovidenie v fiziologii: Issledovanie sosudistykh reakt︠s︡iĭ, perspirat︠s︡iĭ i termoreguli︠a︡t︠s︡ii u cheloveka = FPA-based infrared thermography in physiology : investigation of vascular response, perspiration, and thermoregulation in humans. Novosibirsk: Izdatelʹstvo Sibirskogo otdelenii︠a︡ Rossiĭskoĭ akademii nauk, 2004.

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11

The language of the heart: The body's response to human dialogue. New York: Basic Books, 1985.

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12

1935-, Fletcher Gerald F., ed. Cardiovascular response to exercise. Mt. Kisco, NY: Futura Pub. Co., 1994.

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13

Arena, Ross, Dejana Popovic, Marco Guazzi, Amy McNeil, and Michael Sagner. Cardiovascular response to exercise. Edited by Guido Grassi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0026.

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The body’s response to an exertional stimulus, if performed adequately to meet the imposed demand, is an orchestrated response predominantly among the cardiovascular, pulmonary, and skeletal systems. These physiological systems work together to ensure that up-titrated energy and force production demands are met. The magnitude of the exertional stimulus these systems are able to respond to, when an individual is in a true state of physiological health, is influenced by multiple factors including age, sex, biomechanics, genomics, and exercise training history. When one or more of these systems suffers from dysfunction, as is the case when an individual is at risk for (i.e. unhealthy lifestyle history) or diagnosed with a chronic disease, the response to a physical stimulus ultimately fails and exertional capacity is limited. There is a clear and well-established clinical relevance to the cardiovascular response to an exertional stimulus, commonly assessed through a graded aerobic exercise test on a treadmill or cycle ergometer. In fact, aerobic capacity has been referred to a key vital sign. We are also gaining an appreciation of how communication and presentation of information between health professionals and individuals receiving care significantly impacts comprehension and adherence to a plan of care. This chapter addresses these areas, beginning with a brief granular description of exertional cardiovascular physiology, transitioning to practical clinical implications of this information for health professionals, and ending with how the individuals seeking healthcare receive, process, and comprehend this information with the ultimate goal being real-world application and improved health outcomes.
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14

Inflammatory Response In Cardiovascular Surgery. Springer, 2012.

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15

Barthelmes, Jens, and Isabella Sudano. Cardiovascular response to mental stress. Edited by Guido Grassi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0027.

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Mental stress, intrinsically subjective, lacks clear operationalization by any universally accepted gauge in routine clinical practice. There is not even an accepted single conceptualization of mental stress as opposed to the classic risk factors measured by, for example, resting blood pressure or low-density lipoprotein cholesterol among others. Yet, the link between psychosocial stress and cardiovascular events is a century-old intuition substantiated by many studies. Likely, mental stress affects cardiovascular health over the whole course of at-risk-stage up to cardiovascular events. This chapter discusses the major pathophysiologic effects of mental stress on cardiovascular pathogenesis.
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16

Novak, Peter. Autonomic Testing. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190889227.001.0001.

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Autonomic testing is an important addition to neurological evaluations. While there are many excellent textbooks on autonomic disorders, only a few texts focus on how to perform and interpret autonomic tests. This manual fills the gap, dealing mainly with the practical aspects of autonomic testing. In accord with the maxim that “a good picture is worth a thousand words,” signal drawings are heavily used throughout the text to explain and illuminate test results. This book has two parts. The first part describes in detail the Brigham protocol of autonomic tests, which includes cardiovascular tests (deep breathing, Valsalva maneuver, tilt tests), sudomotor assessment (quantitative sudomotor axonal reflex test and electrochemical skin conductance), and skin biopsies for assessment of epidermal and sweat gland small fibers. The cardiovascular tests use heart rate, blood pressure, respiratory parameters (respiratory rate and end tidal CO2), and cerebral blood flow velocity. All tests are graded with an updated quantitative scale for cardiovascular reflex tests and transcranial Doppler—the Quantitative Sudomotor Axon Reflex Test (QASAT)—and small fiber (epidermal sensory and sweat gland) densities from skin biopsies. The second part of the book describes 100 cases covering a variety of autonomic disorders. The cases are thematically grouped into orthostatic intolerance syndromes (neurally mediated syncope, orthostatic hypotension, postural tachycardia syndrome, inappropriate sinus tachycardia, orthostatic cerebral hypoperfusion syndrome, hypocapnic cerebral hypoperfusion, and pseudosyncope), dysautonomia in neurodegenerative disorders, small fiber neuropathies (idiopathic, secondary, inflammatory), and autonomic overactivity. The case descriptions are presented in a consistent format featuring pertinent clinical information, autonomic tests results, interpretation of testing, conclusions, and recommendations. This text is intended to be a guide for autonomic fellows, and for residents in neurology, general medicine, and other specialties, and for anyone who is interested in performing and interpreting autonomic tests.
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17

Neyrinck, Arne P., Patrick Ferdinande, Dirk Van Raemdonck, and Marc Van de Velde. Donor organ management. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0034.

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Organ transplantation is the standard treatment modality for end-stage organ disease in selected cases. Two types of potential organ donors can be identified: the brain-dead ‘heart-beating donors’, referred to as DBD (donation after brain death), and the warm ischaemic ‘non-heart-beating donors’, referred to as DCD (donation after circulatory death). Brain death induces several physiological changes in the DBD donor. An autonomic storm is characterized by massive catecholamine release, followed by autonomic depletion during a vasoplegic phase. This is associated with several hormonal changes (suppression of vasopressin, the hypothalamic-pituitary-adrenal axis, and the hypothalamic-pituitary-thyroid axis) and an inflammatory response. These physiological changes form the basis of organ donor management, including cardiovascular stabilization and hormonal therapy (including vasopressin and analogues, thyroid hormone, and cortisol). Donor management is the continuation of critical care, with a shift towards individual organ stabilization. An aggressive approach to maximize organ yield is recommended; however, many treatment strategies need further investigation in large randomized trials. DCD donors have now evolved as a valid alternative to increase the potential donor pool and challenge the clinician with new questions. Optimal donor comfort therapy and end-of-life care are important to minimize the agonal phase. A strict approach towards the determination of death, based on cardiorespiratory criteria, is prerequisite. Novel strategies have been developed, using ex situ organ perfusion as a tool, to evaluate and recondition donor organs. They might become more important in the future to further optimize organ quality.
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18

Rick, Turner J., Sherwood Andrew, and Light Kathleen C, eds. Individual differences in cardiovascular response to stress. New York: Plenum Press, 1992.

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19

Malik, Marek. Clinical Guide to Cardiac Autonomic Tests. M Malik, 2010.

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20

Marek, Malik, ed. Clinical guide to cardiac autonomic tests. Dordrecht: Kluwer Academic, 1998.

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21

Turner, J. Rick. Cardiovascular Reactivity and Stress: Patterns Of Physiological Response. Springer, 2013.

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22

Ramaekers, Dirk. Effects of Melanocortins and N-Terminal Proopiomelanocortin on Cardiovascular Function and Autonomic Dynamics. Leuven Univ Pr, 1999.

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23

Andrew, Armour J., and Ardell Jeffrey L, eds. Neurocardiology. New York: Oxford University Press, 1994.

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24

de Geus, Eco, Rene van Lien, Melanie Neijts, and Gonneke Willemsen. Genetics of Autonomic Nervous System Activity. Edited by Turhan Canli. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.010.

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Large individual differences in the activity of the autonomic nervous system (ANS) play a key role in risk for cardiovascular disease. This chapter presents an overview of the measurement strategies that can be used to study ANS activity in samples that are sufficiently large to allow genetic analyses. Heart rate variability, in particular, respiratory sinus arrhythmia (RSA) is identified as the measure of choice to index parasympathetic activity, whereas preejection period (PEP) is the measure of choice to index sympathetic activity. Twin studies have demonstrated significant genetic contributions to resting levels of both RSA (heritability estimates range from 25 to 71 percent) and PEP (heritability estimates range from 48 to 74 percent) and the genetic variance in these traits seems to further increase under conditions of psychological stress. Identifying the genetic variants that influence parasympathetic and sympathetic activity may increase our understanding of the role of the ANS in cardiovascular disease.
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25

Reliability of cardiovascular and metabolic response to hydraulic resistive exercise. 1985.

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26

Reliability of cardiovascular and metabolic response to hydraulic resistive exercise. 1985.

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27

A, Obrist Paul, ed. Cardiovascular psychophysiology: Current issues in response mechanisms, biofeedback and methodology. New Brunswick: AldineTransaction, 2008.

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28

Cardiovascular Psychophysiology: Current Issues in Response Mechanisms, Biofeedback and Methodology. Aldine Transaction, 2007.

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29

Obrist, Paul A., Jasper Brener, A. H. Black, and Leo V. DiCara. Cardiovascular Psychophysiology: Current Issues in Response Mechanisms, Biofeedback and Methodology. Taylor & Francis Group, 2017.

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30

Reliability of cardiovascular and metabolic response to hydraulic resistive exercise. 1985.

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31

Normal And Abnormal Circadian Characteristics in Autonomic Cardiac Control: New Opportunities for Cardiac Risk Prevention. Nova Science Publishers, 2006.

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32

Covassin, Naima, and Virend K. Somers. The cardiovascular system during sleep. Edited by Guido Grassi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0028.

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The majority of molecular, physiological, and behavioural processes undergo substantial variations across a 24 h period. The health implications of such fluctuations, whether they are expressions of an intrinsic circadian rhythmicity or are secondary to changes in physical activity, posture, and/or sleep, are increasingly recognized. Similar to other biological functions, the cardiovascular system exhibits a prominent day–night profile, with profound haemodynamic, autonomic, and hormonal oscillations occurring during the sleep period. These time-dependent and sleep stage-dependent patterns of function have important clinical significance. The cardiovascular downregulation achieved throughout the night while asleep may be restorative and protective against adverse events, while the morning physiological activation coincident with awakening facilitates resumption of daytime activities. Nevertheless, rather than beneficial, these activity configurations may be pathogenic in individuals with a vulnerable substrate and may favour onset and progression of cardiovascular diseases. Cardiovascular complications may also arise as a consequence of abnormal day–night periodicity and disturbed sleep quantity and quality. Hence, consideration of the diurnal pattern of cardiovascular activity is critical in the clinical setting.
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33

Breedon, Todd H. Guidelines for the response to exercise in patients receiving cardiovascular medications. 1988.

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34

M, Evans Joyce, and United States. National Aeronautics and Space Administration., eds. Validation of spectral analysis as a noninvasive tool to assess autonomic regulation of cardiovascular function: Final report. Lexington, KY: Center for Biomedical Engineering, Wenner-Gren Research Laboratory, University of Kentucky, 1996.

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35

Rowland, Thomas W. Cardiovascular function. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0011.

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The circulatory response to increased metabolic demands of endurance exercise is best explained by a model in which volume of circulatory flow is governed by alterations in peripheral vascular resistance. These dynamics of the cardiovascular response to an acute bout of progressive endurance exercise are similar in children and adults, and, when adjusted for body size, true cardiovascular fitness (ability to generate cardiac output) is no different in healthy, untrained pre- and postpubertal individuals. As in adults, the capacity to eject stroke volume at maximal exercise differentiates levels of physiological fitness (maximal oxygen uptake) between individual children. Stroke volume at exhaustive exercise, in turn, appears to be governed by factors which influence left ventricular diastolic size rather than those which dictate myocardial systolic and diastolic function.
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36

Peter, Koepchen Hans, Huopaniemi T, and International Union of Physiological Sciences. Congress, eds. Cardiorespiratory and motor coordination. Berlin: Springer-Verlag, 1991.

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37

Santillo, Mariarosaria, and Pasquale Pagliaro, eds. Redox and Nitrosative Signaling in Cardiovascular System: from Physiological Response to Disease. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-726-7.

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38

Pstras, Leszek, and Jacek Waniewski. Mathematical Modelling of Haemodialysis: Cardiovascular Response, Body Fluid Shifts, and Solute Kinetics. Springer, 2019.

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39

Elwell, Thomas Richard. Specificity of cardiovascular response to free-weight resistance exercise in weight lifters and runners. 1985.

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40

Kernicki, Jeanette Geraldine. THE ADAPTIVE RESPONSE OF CARDIOVASCULAR - PULMONARY PATIENTS TO NURSING MEASURES AS REFLECTED BY MIXED VENOUS OXYGEN SATURATION MEASUREMENTS. 1987.

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41

Pecaric, Martin R. Factors influencing the cardiovascular response to +Gz: Implications on the design of life support systems for acceleration protection. 1999.

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42

Vincent, Alex. Effects of workload, processing level, and arousal on memory performance, subjective rating, and cardiovascular response: a psychophysiological analysis. 1993.

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43

The effects of aerobic exercise on cardiovascular reactivity and baroreflex response in women with parental history of hypertension. 1993.

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44

Colbert, Bruce J., and Barbara J. Mason. Integrated Cardiopulmonary Pharmacology. Prentice Hall, 2001.

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45

Colbert, Bruce J., and Barbara J. Mason. Integrated Cardiopulmonary Pharmacology. Prentice Hall, 2001.

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46

Helge, Refsum, Sulg Ilmar A. 1919-, and Rasmussen Knut, eds. Heart & brain, brain & heart. Berlin: Springer-Verlag, 1989.

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47

Terence, Bennett, and Gardiner Sheila M, eds. Nervous control of blood vessels. [Chur, Switzerland]: Harwood Academic Publishers, 1996.

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48

Barthélémy, Romain, Etienne Gayat, and Alexandre Mebazaa. Pathophysiology and clinical assessment of the cardiovascular system (including pulmonary artery catheter). Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0014.

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Haemodynamic instability in acute cardiac care may be related to various mechanisms, including hypovolaemia and heart and/or vascular dysfunction. Although acute heart failure patients are often admitted for dyspnoea, many mechanisms can be involved, including left ventricular diastolic and/or systolic dysfunction and/or right ventricular dysfunction. Many epidemiological studies show that clinical signs at admission, morbidity, and mortality differ between the main scenarios of acute heart failure: left ventricular diastolic dysfunction, left ventricular systolic dysfunction, right ventricular dysfunction, and cardiogenic shock. Although echocardiography often helps to assess the mechanism of cardiac dysfunction, it cannot be considered as a monitoring tool. In some cases (in particular, in cases of refractory shock secondary to both vascular and heart dysfunction or in cases of refractory haemodynamic instability associated with severe hypoxaemia), pulmonary artery catheter can help to assess and monitor cardiovascular status and to evaluate response to treatments. Last, macro- and microvascular dysfunctions are also important determinants of haemodynamic instability.
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49

(Editor), J. Andrew Armour, and Jeffrey L. Ardell (Editor), eds. Basic and Clinical Neurocardiology. Oxford University Press, USA, 2004.

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50

Lipman, Jeffrey, and Robert J. Boots. Diagnosis, assessment, and management of tetanus, rabies, and botulism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0245.

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Tetanus, rabies and botulism are all infections characterized by the production of a neurotoxin, and generally do not give rise to a systemic inflammatory response. Typically tetanus result from the infection of wounds by the ubiquitious soil-borne bacteria Clostridium tetanii, botulism is most commonly due to toxin produced in food contaminated with Clostridium botulinum. Rabies usually results from an animal bite infected with the rabies virus of the Lyssavirus group. Neurological involvement by all three infections is characterized by paralysis and autonomic instability with tetanus also being associated with muscular rigidity. Importantly, the autonomic dysfunction of tetanus can be severe and may necessitate prolonged treatment in an intensive care unit (ICU). Active immunization can prevent or minimize the symptoms of tetanus and rabies, while passive immunization may slow symptom progression in botulism. Intensive care support is often required to manage respiratory failure and autonomic dysfunction. Rabies is typically fatal in the absence of prior immunization.
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