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1
Bustin, Debra. Hemodynamic monitoring for critical care. Norwalk, Conn: Appleton-Century-Crofts, 1986.
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2
Interventional physiology rounds: Case studies in coronary pressure and flow for clinical practice. New York: Wiley-Liss, 1998.
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3
Demetriades, Demetrios, Leslie Kobayashi, and Lydia Lam. Cardiac complications in trauma. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0062.
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Post-traumatic cardiac complications may occur after penetrating or blunt injuries to the heart or may follow severe extracardiac injuries. The majority of victims with penetrating injuries to the heart die at the scene and do not reach hospital care. For those patients who reach hospital care, an immediate operation, sometimes in the emergency room, cardiac injury repair, and cardiopulmonary resuscitation provide the only possibility of survival. Many patients develop perioperative cardiac complications such as acute cardiac failure, cardiac arrhythmias, coronary air embolism, and myocardial infarction. Some survivors develop post-operative functional abnormalities or anatomical defects, which may not manifest during the early post-operative period. It is essential that all survivors undergo detailed early and late cardiac evaluations. Blunt cardiac trauma encompasses a wide spectrum of injuries that includes asymptomatic myocardial contusion, arrhythmias, or cardiogenic shock to full-thickness cardiac rupture and death. Clinical examination, electrocardiograms, troponin measurements, and echocardiography are the cornerstone of diagnosis and monitoring of these patients. Lastly, some serious extracardiac traumatic conditions, such as traumatic pneumonectomy and severe traumatic brain injury, may result in cardiac complications. This may include tachyarrhythmias, cardiogenic shock, electrocardiographic changes, troponin elevations, heart failure, and cardiac arrest.
4
Demetriades, Demetrios, Leslie Kobayashi, and Lydia Lam. Cardiac complications in trauma. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0062_update_001.
Full textAbstract:
Post-traumatic cardiac complications may occur after penetrating or blunt injuries to the heart or may follow severe extracardiac injuries. The majority of victims with penetrating injuries to the heart die at the scene and do not reach hospital care. For those patients who reach hospital care, an immediate operation, sometimes in the emergency room, cardiac injury repair, and cardiopulmonary resuscitation provide the only possibility of survival. Many patients develop perioperative cardiac complications such as acute cardiac failure, cardiac arrhythmias, coronary air embolism, and myocardial infarction. Some survivors develop post-operative functional abnormalities or anatomical defects, which may not manifest during the early post-operative period. It is essential that all survivors undergo detailed early and late cardiac evaluations. Blunt cardiac trauma encompasses a wide spectrum of injuries that includes asymptomatic myocardial contusion, arrhythmias, or cardiogenic shock to full-thickness cardiac rupture and death. Clinical examination, electrocardiograms, troponin measurements, and echocardiography are the cornerstone of diagnosis and monitoring of these patients. Lastly, some serious extracardiac traumatic conditions, such as traumatic pneumonectomy and severe traumatic brain injury, may result in cardiac complications. This may include tachyarrhythmias, cardiogenic shock, electrocardiographic changes, troponin elevations, heart failure, and cardiac arrest.
5
Lam, Lydia, Leslie Kobayashi, and Demetrios Demetriades. Cardiac complications in trauma. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0062_update_002.
Full textAbstract:
Post-traumatic cardiac complications may occur after penetrating or blunt injuries to the heart or may follow severe extracardiac injuries. The majority of victims with penetrating injuries to the heart die at the scene and do not reach hospital care. For those patients who reach hospital care, an immediate operation, sometimes in the emergency room, cardiac injury repair, and cardiopulmonary resuscitation provide the only possibility of survival. Many patients develop perioperative cardiac complications such as acute cardiac failure, cardiac arrhythmias, coronary air embolism, and myocardial infarction. Some survivors develop post-operative functional abnormalities or anatomical defects, which may not manifest during the early post-operative period. It is essential that all survivors undergo detailed early and late cardiac evaluations. Blunt cardiac trauma encompasses a wide spectrum of injuries that includes asymptomatic myocardial contusion, arrhythmias, or cardiogenic shock to full-thickness cardiac rupture and death. Clinical examination, electrocardiograms, troponin measurements, and echocardiography are the cornerstone of diagnosis and monitoring of these patients. Lastly, some serious extracardiac traumatic conditions, such as traumatic pneumonectomy and severe traumatic brain injury, may result in cardiac complications. This may include tachyarrhythmias, cardiogenic shock, electrocardiographic changes, troponin elevations, heart failure, and cardiac arrest.
6
Lam, Lydia, Leslie Kobayashi, and Demetrios Demetriades. Cardiac complications in trauma. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0062_update_003.
Full textAbstract:
Post-traumatic cardiac complications may occur after penetrating or blunt injuries to the heart or may follow severe extracardiac injuries. The majority of victims with penetrating injuries to the heart die at the scene and do not reach hospital care. For those patients who reach hospital care, an immediate operation, sometimes in the emergency room, cardiac injury repair, and cardiopulmonary resuscitation provide the only possibility of survival. Many patients develop perioperative cardiac complications such as acute cardiac failure, cardiac arrhythmias, coronary air embolism, and myocardial infarction. Some survivors develop post-operative functional abnormalities or anatomical defects, which may not manifest during the early post-operative period. It is essential that all survivors undergo detailed early and late cardiac evaluations. Blunt cardiac trauma encompasses a wide spectrum of injuries that includes asymptomatic myocardial contusion, arrhythmias, or cardiogenic shock to full-thickness cardiac rupture and death. Clinical examination, electrocardiograms, troponin measurements, and echocardiography are the cornerstone of diagnosis and monitoring of these patients. Lastly, some serious extracardiac traumatic conditions, such as traumatic pneumonectomy and severe traumatic brain injury, may result in cardiac complications. This may include tachyarrhythmias, cardiogenic shock, electrocardiographic changes, troponin elevations, heart failure, and cardiac arrest.
7
Vincent, Jean-Louis. Ethical issues in cardiac arrest and acute cardiac care: a European perspective. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0013.
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The respiratory system is key to the management of patients with respiratory, as well as haemodynamic, compromise and should be monitored. The ventilator is more than just a machine that delivers gas; it is a true respiratory system monitoring device, allowing the measurement of airway pressures and intrinsic positive end-expiratory pressure and the plotting of pressure/volume curves. For effective and reliable monitoring, it is necessary to keep in mind the physiology, such as the alveolar gas equation, heart-lung interactions, the equation of movement, etc. Monitoring the respiratory system enables adaptation of not only respiratory management, but also haemodynamic management.
8
Vincent, Jean-Louis. Ethical issues in cardiac arrest and acute cardiac care: a European perspective. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0013_update_001.
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The respiratory system is key to the management of patients with respiratory, as well as haemodynamic, compromise and should be monitored. The ventilator is more than just a machine that delivers gas; it is a true respiratory system monitoring device, allowing the measurement of airway pressures and intrinsic positive end-expiratory pressure and the plotting of pressure/volume curves. For effective and reliable monitoring, it is necessary to keep in mind the physiology, such as the alveolar gas equation, heart-lung interactions, the equation of movement, etc. Monitoring the respiratory system enables adaptation of not only respiratory management, but also haemodynamic management.
9
A, Amini Amir, and Prince Jerry L, eds. Measurement of cardiac deformations from MRI: Physical and mathematical models. Dordrecht: Kluwer Academic Publishers, 2001.
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10
Sainz, Jorge G., and Bradley P. Fuhrman. Basic Pediatric Hemodynamic Monitoring. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0005.
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Physiological monitoring using a variety of technological advances supplements, but does not replace, our ability to distinguish normal from abnormal physiology traditionally gleaned from physical examination. Pulse oximetry uses the wavelengths of saturated and unsaturated hemoglobin to estimate arterial oxygenation noninvasively. Similar technology included on vascular catheters provides estimation of central or mixed venous oxygenation and helps assess the adequacy of oxygen delivered to tissues. End-tidal carbon dioxide measurements contribute to the assessment of ventilation. Systemic arterial blood pressure and central venous pressure measurements help evaluate cardiac performance, including the impact of ventilatory support. Intra-abdominal pressure may increase as a result of intraluminal air or fluid, abnormal fluid collections within the peritoneal cavity, or abnormal masses. Increased pressure may impede venous return to the heart and compromise intra-abdominal organ perfusion. Pressure measurement guides related management decisions.
11
Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0036.
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Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among troponin-negative subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
12
Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0036_update_001.
Full textAbstract:
Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among normal-troponin subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
13
Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0036_update_002.
Full textAbstract:
Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among normal-troponin subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
14
Prout, Jeremy, Tanya Jones, and Daniel Martin. Cardiovascular system. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199609956.003.0001.
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This chapter covers the assessment and investigation of perioperative cardiac risk, the principles of perioperative haemodynamic monitoring and physiological changes in cardiac comorbidity with their relevance to anaesthetic management. Perioperative cardiovascular risk includes assessment of cardiac risk factors, functional capacity and evidence-based guidelines for preassessment. Cardiovascular investigations such as cardiopulmonary exercise testing and scoring systems for cardiac risk are included. Management of the cardiac patient for non-cardiac surgery is detailed. Invasive monitoring with arterial, central venous and pulmonary artery catheters is described. Cardiac output measurement systems including dilution techniques, pulse contour analysis and Doppler are compared. The physiological changes, management and implications for anaesthesia of common cardiac comorbidity including ischaemic heart disease, heart failure, valvular heart disease, pacemakers and pulmonary hypertension are described.
15
(Foreword), A. Grenvik, Michael A. DeVita (Editor), Kenneth Hillman (Editor), and Rinaldo Bellomo (Editor), eds. Medical Emergency Teams: Implementation and Outcome Measurement. Springer, 2005.
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16
Brazier, John, Julie Ratcliffe, Joshua A. Salomon, and Aki Tsuchiya. Using ordinal response data to estimate cardinal values for health states. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198725923.003.0006.
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There exists a strong methodological foundation for estimating cardinal values from ordinal information, originating in psychology but commonly applied in areas as diverse as consumer marketing, political science, transportation research, and environmental economics. Over recent years there has been a steady rise in the use of these approaches to estimate health state values. Potential advantages claimed for ordinal data collection approaches include relative ease of comprehension and administration, and greater reliability corresponding to reduced measurement error. Another advantage of some types of ordinal data collection methods is that the preferences or judgements they elicit are not contaminated by risk aversion (as in the standard gamble), or by time preference (as in the time trade-off).
17
Normal And Abnormal Circadian Characteristics in Autonomic Cardiac Control: New Opportunities for Cardiac Risk Prevention. Nova Science Publishers, 2006.
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18
Sidhu, Kulraj S., Mfonobong Essiet, and Maxime Cannesson. Cardiac and vascular physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0001.
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This chapter discusses key components of cardiovascular physiology applicable to clinical practice in the field of anaesthesiology. From theory development to ground-breaking innovations, the history of cardiac and vascular anatomy, as well as physiology, is presented. Utilizing knowledge of structure and function, parameters created have allowed adequate patient clinical assessment and guided interventions. A review of concepts reveals the impact of multiple physiological variables on a patient’s haemodynamic state and the need for more accurate and efficient measurements. In particular, it is noted that a more reliable index of ventricular contractility is the end-systolic elastance rather than the ejection fraction. Constant direct preload assessment has not yet been achieved but continues to be determined through surrogate variables, and continuous cardiac output monitoring for oxygen delivery, although advancing, has limitations. Considering the effect of compound factors perioperatively, especially heart failure, modifies the goals and interventions of anaesthetists to achieve improved outcomes. Therefore, medical management prior to surgery and complete assessment through history, physical examination, and diagnostic tests are a priority. This chapter also details the expectations following volume expansion to augment haemodynamics during surgery, the concept of functional haemodynamic monitoring, and limitations to the parameters applied in assessing fluid responsiveness. Challenging the accuracy of conventional indices to predict volume status led to the use of goal-directed therapy, reducing morbidity and minimizing length of hospital stay. The mainstay of this chapter is to reinforce the relevance of advances in haemodynamic monitoring and homeostasis optimization by anaesthetists during surgery, using fundamental concepts of cardiovascular physiology.
20
McNeill, John H. Measurement of Cardiac Function Approaches, Techniques, and Troubleshooting (Crc Press Methods in the Life Sciences. Methods in Pharmacology). Informa Healthcare, 1996.
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21
Magder, Sheldon. Central venous pressure monitoring in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0132.
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Central venous pressure (CVP) is at the crucial intersection of the force returning blood to the heart and the force produced by cardiac function, which drives the blood back to the systemic circulation. The normal range of CVP is small so that before using it one must ensure proper measurement, specifically the reference level. A useful approach to hypotension is to first determine if arterial pressure is low because of a decrease in vascular resistance or a decrease in cardiac output. This is done by either measuring cardiac output or making a clinical assessment blood flow. If the cardiac output is decreased, next determine whether this is because of a cardiac pump problem or a return problem. It is at this stage that the CVP is most helpful for these options can be separated by considering the actual CVP or even better, how it changed with the change in cardiac output. A high CVP is indicative of a primary pump problem, and a low CVP and return problem. Understanding the factors that determine CVP magnitude, mechanisms that produce the components of the CVP wave form and changes in CVP with respiratory efforts can also provide useful clinical information. In many patients, CVP can be estimated on physical exam.
24
Adam, Sheila, Sue Osborne, and John Welch. Cardiovascular problems. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199696260.003.0005.
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The cardiovascular chapter discusses the physiology, assessment, and treatment of cardiovascular disorders in the critically ill patient. It gives an in-depth explanation of non-invasive and invasive monitoring procedures (such as ECG, pulse oximetry, oesophageal Doppler, and pulmonary artery catheterization). It includes the measurement of oxygen delivery and consumption, and explains diagnostic techniques such as echocardiography. The chapter includes the management and optimization of goal-directed therapies for specific conditions including coronary heart disease (such as myocardial infarction and angina), shock, valvular heart disease, and heart failure. Interventional treatment and specific drug therapy are discussed, including percutaneous coronary intervention, cardiac pacing, and electrical conversion.
27
Cardinale, Daniela, and Carlo Maria Cipolla. Anthracycline-related cardiotoxicity: epidemiology, surveillance, prophylaxis, management, and prognosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0290.
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Anthracycline-induced cardiotoxicity is of considerable concern, as it may compromise the clinical effectiveness of treatment, affecting both quality of life and overall survival in cancer patients, independently of the oncological prognosis. It is probable that anthracycline-induced cardiotoxicity is a unique and continuous phenomenon starting with myocardial cell injury, followed by progressive left ventricular ejection fraction (LVEF) decline that, if disregarded and not treated progressively leads to overt heart failure. The main strategy for minimizing anthracycline-induced cardiotoxicity is early detection of high-risk patients and prompt prophylactic treatment. According to the current standard for monitoring cardiac function, cardiotoxicity is usually detected only when a functional impairment has already occurred, precluding any chance of its prevention. At present, anthracycline-induced cardiotoxicity can be detected at a preclinical phase, very much before the occurrence of heart failure symptoms, and before the LVEF drops by measurement of cardiospecific biochemical markers or by Doppler myocardial and deformation imaging. The role of troponins in identifying subclinical cardiotoxicity and treatment with angiotensin-converting enzyme inhibitors, in order to prevent LVEF reduction is an effective strategy that has emerged in the last 15 years. If cardiac dysfunction has already occurred, partial or complete LVEF recovery may still be achieved if cardiac dysfunction is detected early after the end of chemotherapy and heart failure treatment is promptly initiated.