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1
František, Kolář, ed. Cardiac ischemia: From injury to protection. Boston: Kluwer Academic Publishers, 1999.
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2
Ostadal, Bohuslav. Cardiac ischemia: From injury to protection. Boston: Kluwer Academic Publishers, 1999.
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3
Ošt’ádal, Bohuslav, and František Kolář. Cardiac Ischemia: From Injury to Protection. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4757-3025-8.
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4
American College of Emergency Physicians and American Academy of Orthopaedic Surgeons, eds. First aid, CPR, and AED essentials. 6th ed. Burlington, MA: Jones & Bartlett Learning, 2013.
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5
Initiative, Acute Dialysis Quality, Conference on Biomarkers in AKI (10th : 2011 : Dublin, Ireland), and Conference on CRS (11th : 2012 : Venice, Italy), eds. ADQI consensus on AKI biomarkers and cardiorenal syndromes. Basel: Karger, 2013.
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6
Volpe, Joseph, Richard Jonas, and Jane Newburger. Brain Injury and Pediatric Cardiac Surgery. Taylor & Francis Group, 2019.
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7
Volpe, Joseph, Richard Jonas, and Jane Newburger. Brain Injury and Pediatric Cardiac Surgery. Taylor & Francis Group, 2019.
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8
Volpe, Joseph, Richard Jonas, and Jane Newburger. Brain Injury and Pediatric Cardiac Surgery. Taylor & Francis Group, 2019.
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9
Volpe, Joseph, Richard Jonas, and Jane Newburger. Brain Injury and Pediatric Cardiac Surgery. Taylor & Francis Group, 2019.
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10
Friedhelm, Beyersdorf, ed. Ischemia-reperfusion injury in cardiac surgery. Georgetown, Tx: Landes Bioscience, 2000.
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11
Jonas, Richard A., Jane W. Newburger, Joseph J. Volpe, and John W. Kirklin. Brain Injury and Pediatric Cardiac Surgery. CRC Press, 2019. http://dx.doi.org/10.1201/9780367813864.
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12
A, Jonas Richard, Newburger Jane W, and Volpe Joseph J, eds. Brain injury and pediatric cardiac surgery. Boston: Butterworth Heinemann, 1996.
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13
McLean, Anthony S., and Stephen J. Huang. Cardiac injury biomarkers in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0301.
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To be clinically relevant, a good cardiac biomarker should have four main characteristics. It should be organ-, disease- and stage-specific to be useful in diagnosis. Its release should be timely and its half-life should be long enough to make measurement possible and meaningful. Its serum or blood concentration should be proportional to disease severity; hence, can be used as a monitoring tool. Finally, their concentrations have implications on long-term outcomes. To date, only a handful of cardiac biomarkers have clinical relevance in the intensive care setting—cardiac troponins (as a marker of cardiac injury) and B-type natriuretic peptide (as a marker of cardiac stress) being probably the most useful. However, cautious interpretations of these biomarkers are needed in intensive care patients as several confounding factors can affect their concentrations.
14
Rivera-Lara, Lucia, and Romergryko G. Geocadin. Neurobiology of Brain Injury after Cardiac Arrest. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0189.
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The publication of two sentinel, multicenter, randomized controlled trials in The New England Journal of Medicine in 2002 provided evidence for the beneficial use of therapeutic hypothermia (TTH) to 32° to 34°C in resuscitated patients after cardiac arrest with a shockable rhythm. The number needed to treat to provide a favorable neurological outcome was 6, and TTH is a recommended treatment in the American Heart Association (AHA) Resuscitation Guidelines. This chapter describes the biological basis of disorders of arousal and awareness after cardiac arrest, the mechanisms of ischemic cell death, and the biological bases of the some therapeutic interventions.
15
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.
16
Michel, Piper Hans, and Preusse C. J, eds. Ischemia-reperfusion in cardiac surgery. Dordrecht: Kluwer Academic Publishers, 1993.
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17
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.
18
Gevaert, Sofie A., Eric Hoste, and John A. Kellum. Acute kidney injury. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0068.
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Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term ‘acute renal failure’ and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.
19
Gevaert, Sofie A., Eric Hoste, and John A. Kellum. Acute kidney injury. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0068_update_001.
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Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term ‘acute renal failure’ and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.
20
Brain Injury and Cardiac Arrest, An Issue of Neurologic Clinics. Saunders, 2006.
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21
1945-, Hori M., Maruyama Yukio 1941-, and Reneman R. S, eds. Cardiac adaptation and failure. [Tokyo: Springer, 1994.
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22
Hori, Masatsugu, Robert S. Reneman, and Yukio Maruyama. Cardiac Adaptation and Failure. Springer, 2013.
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23
(Editor), Bohuslav Ost'ádal, and Frantisek Kolár (Editor), eds. Cardiac Ischemia: - From Injury to Protection (Basic Science for the Cardiologist). Springer, 1999.
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24
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.
25
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.
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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.
26
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.
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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.
27
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.
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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.
28
Brown, Jeremiah R., and Chirag R. Parikh. Cardiovascular surgery and acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0245.
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Over the last decade, cardiac surgery-associated acute kidney injury (AKI) has been recognized as a frequent adverse event following cardiac surgery. In this clinical context and others, AKI has been strongly associated with increased morbidity, mortality, and length of hospitalization. These adverse events that accompany AKI have been shown to be directly proportional to the magnitude of the peak rise in serum creatinine and the duration of AKI making AKI a costly complication and a target for prevention in hospitalized patients around the world. This chapter discusses the subsequent healthcare costs, utilization, mortality, and morbidity that follow subtle changes in serum creatinine known as AKI in the perioperative setting of cardiac surgery.
29
Lucien, Jamie George. The necrotic and apoptotic injury of cardiac xenotransplants caused by human serum. 2001.
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30
Pepper, John. Cardioprotection During Cardiac Surgery. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0007.
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• Overall early mortality for cardiac surgery is low at 2–3% but in high risk patients it can be high as 10–15%• The demography of cardiac surgical patients is changing to older and sicker patients• Myocardial ischaemia-reperfusion injury and the systemic inflammatory response are closely related• Several pharmacological agents that have been demon-strated to confer cardioprotection in the experimental setting have been applied to the clinical setting of cardiac surgery. However, the transfer of these findings from the bench to the bedside has been largely disappointing• Potential cardioprotective strategies include pharma-cological agents such as adenosine, and mechanical interventional strategies such as acute normovolaemic haemodilution and remote ischaemic preconditioning.
31
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.
32
Lameire, Norbert. Prevention of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0226_update_001.
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This chapter summarizes the pharmacological interventions that can be used in the prevention of acute kidney injury (AKI). These following interventions are discussed: the use and selection of vasopressors; the administration of loop diuretics and mannitol; vasodilating drugs including dopamine, atrial natriuretic peptide, nesiritide, fenoldopam, and adenosine antagonists. The role of N-acetylcysteine in the prevention of contrast-induced AKI and cardiac surgery is discussed. The chapter concludes with a summary of the potential role of insulin-like growth factor and erythropoietin in the prevention of AKI.
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Lameire, Norbert. Prevention of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0224_update_001.
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The prevention of acute kidney injury (AKI) should start with an assessment of the risk to develop AKI, by identification of co-morbidities, use of potentially nephrotoxic medications, and early recognition of acute reversible risk factors associated with AKI. This chapter discusses first the most relevant general risk factors for AKI and describes the recent introduction of several surveillance systems. In addition, some specific risk factors play a role in the pathogenesis of post-cardiac surgery AKI. Finally risks associated with commonly used drugs such as non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, statins, and warfarin are considered.
34
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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Nolan, Jerry P., and Michael J. A. Parr. Management after resuscitation from cardiac arrest. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0066.
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Systemic ischaemia during cardiac arrest and the reperfusion response after return of spontaneous circulation (ROSC) cause the post-cardiac arrest syndrome (PCAS). The severity and duration of this syndrome is determined by the cause and duration of cardiac arrest, quality of resuscitation, and interventions after ROSC. Four key clinical components are recognized—post-cardiac arrest brain injury, myocardial dysfunction, other organ ischaemia/reperfusion (e.g. liver, kidney), and potential persistence of the precipitating pathology causing the cardiac arrest. The interventions applied after ROSC impact significantly on the quality of survival. All components of the PCAS need to be addressed if outcome is to be optimized; treatment should start immediately after ROSC. An ‘ABCDE’ (Airway, Breathing, Circulation, Disability, Exposure) systems approach is used to identify and treat physiological abnormalities and organ injury. All survivors of out-of-hospital cardiac arrest should be considered for urgent coronary angiography unless the cause of cardiac arrest is clearly non-cardiac or continued treatment is considered futile. Targeted temperature management (mild hypothermia and avoidance of hyperthermia) should be considered for those patients who remain comatose after ROSC. If targeted temperature management has been used, early prognostication on outcome is unreliable and should be delayed until 3 days after return to normothermia; it should not rely on just one modality.
36
Cruz, Dinna N., Anna Giuliani, and Claudio Ronco. Acute kidney injury in heart failure. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0248.
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Acute kidney injury (AKI) occurring during heart failure (HF) has been labelled cardiorenal syndrome (CRS) type 1. CRS is defined as a group of ‘disorders of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other’. This consensus definition was proposed by the Acute Dialysis Quality Initiative, with the aim to standardize those disorders where cardiac and renal diseases coexist. Five subtypes have been proposed, according to which organ is affected first (cardiac vs renal) and whether the dysfunction is acute or chronic. Another subtype which includes systemic conditions leading to both heart and kidney dysfunction is also described.The term ‘worsening renal function’ has been regularly used to describe the acute and/or subacute changes that occur in the kidneys following HF. However, the AKI classification according to the current consensus definition better represents the entire spectrum of AKI in the setting of HF.The pathophysiology of heart–kidney interaction is complex and still poorly understood. Factors beyond the classic haemodynamic mechanisms appear to be involved: neurohormonal activation, venous congestion, and inflammation have all been implicated.Diuretics are still a cornerstone in the management of HF. Intravenous administration by bolus or continuous infusion appears to be equally efficacious. Biomarkers and bioelectrical impedance analysis can be helpful in estimating the real volume overload and may be useful to predict and avoid AKI. The role of ultrafiltration remains controversial, and it is currently recommended only for diuretic-resistant patients as it has not been associated with better outcomes. The occurrence of AKI during HF is associated with substantially greater short- and long-term mortality.
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Wise, Matt, and Paul Frost. ICU treatment of acute kidney injury. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0151.
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Traditionally, the etiology of acute kidney injury (AKI) is considered in terms of prerenal, renal, and obstructive causes. However, this categorization is less useful in the ICU, where the etiology of AKI is usually multifactorial and often occurs in the context of multi-organ failure. Hypotension, nephrotoxic drugs, and severe sepsis or septic shock are the most important identifiable factors. Less frequently encountered causes include pancreatitis, abdominal compartment syndrome, and rhabdomyolysis. Primary intrinsic renal disease such as glomerulonephritis is extremely uncommon. A previous history of cirrhosis, cardiac failure, or haematological malignancy, and age >65 years, are important risk factors. This chapter covers symptoms, complications, diagnosis, investigations, prognosis, and treatment of renal failure in the ITU.
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Fichtner, Alexander, and Franz Schaefer. Acute kidney injury in children. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0239.
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In the past few decades, the overall incidence of acute kidney injury (AKI) in paediatric patients has increased and the aetiological spectrum has shifted from infection-related and intrinsic renal causes towards secondary forms of AKI related to exposure to nephrotoxic drugs and complex surgical, oncological, and intensive care manoeuvres. In addition, neonatal kidney impairment and haemolytic uraemic syndrome continue to be important specific paediatric causes of AKI raising unique challenges regarding prevention, diagnosis, and treatment. The search for new biomarkers is a current focus of research in paediatric as in adult AKI research.Pharmacological intervention studies to prevent or attenuate AKI have provided positive evidence only for the prophylactic use of theophylline in severely depressed neonates, whereas dopamine and loop diuretics did not demonstrate any efficacy. Preliminary findings support a dose-dependent renoprotective action of fenoldopam in infants undergoing cardiac surgery.Critical issues in the management of AKI in children include fluid handling, maintenance of adequate nutrition, and the choice of renal replacement therapy modality. Observational studies have suggested an adverse impact of fluid overload and late start of renal replacement therapy, and a randomized clinical trial revealed detrimental effects of aggressive fluid bolus therapy in volume-depleted children.Technological advances have made it possible to apply continuous replacement therapies in children of all ages, including preterm neonates, using appropriately sized catheters, filters, tubing, and flow settings adapted to paediatric needs. However, the majority of children with AKI worldwide are still treated with peritoneal dialysis, and comparative studies demonstrating superiority of extracorporeal techniques over peritoneal dialysis are lacking.The outcomes of paediatric AKI are comparable to adult patients. In critically ill children, mortality risk increases with each stage of AKI; mortality rates typically range between 15% and 30% for all AKI stages and 30% to 60% in children requiring renal replacement therapy. Chronic kidney disease develops in approximately 10% of children surviving AKI.
39
Nolan, Jerry P. Cardiopulmonary resuscitation and the post-cardiac arrest syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0006.
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Cardiac arrest is the most extreme of medical emergencies. If the victim is to have any chance of high-quality neurological recovery, cardiac arrest must be diagnosed quickly, followed by summoning for help as basic life support (chest compressions and ventilations) is started. In most cases, the initial rhythm will be shockable, but this will have often deteriorated to a non-shockable rhythm by the time a monitor and/or defibrillator is applied. While basic life support will sustain some oxygen delivery to the heart and brain and will help to slow the rate of deterioration in these vital organs, it is important to achieve restoration of a spontaneous circulation as soon as possible (by defibrillation if the rhythm is shockable). Once return of spontaneous circulation is achieved, the quality of post-cardiac arrest management will influence the patient’s final neurological outcome. These interventions aim to restore myocardial function and minimize neurological injury.
40
Nolan, Jerry P. Cardiopulmonary resuscitation and the post-cardiac arrest syndrome. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0006_update_001.
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Cardiac arrest is the most extreme of medical emergencies. If the victim is to have any chance of high-quality neurological recovery, cardiac arrest must be diagnosed quickly, followed by summoning for help as basic life support (chest compressions and ventilations) is started. In most cases, the initial rhythm will be shockable, but this will have often deteriorated to a non-shockable rhythm by the time a monitor and/or defibrillator is applied. While basic life support will sustain some oxygen delivery to the heart and brain and will help to slow the rate of deterioration in these vital organs, it is important to achieve restoration of a spontaneous circulation as soon as possible (by defibrillation if the rhythm is shockable). Once return of spontaneous circulation is achieved, the quality of post-cardiac arrest management will influence the patient’s final neurological outcome. These interventions aim to restore myocardial function and minimize neurological injury.
41
Golper, Thomas A., Andrew A. Udy, and Jeffrey Lipman. Drug dosing in acute kidney injury. Edited by William G. Bennett. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0364.
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Drug dosing in acute kidney injury (AKI) is one of the broadest topics in human medicine. It requires an understanding of markedly altered and constantly changing physiology under many disease situations, the use of the drugs to treat those variety of diseases, and the concept of drug removal during blood cleansing therapies. Early in AKI kidney function may be supraphysiologic, while later in the course there may be no kidney function. As function deteriorates other metabolic pathways are altered in unpredictable ways. Furthermore, the underlying disorders that lead to AKI alter metabolic pathways. Heart failure is accompanied by vasoconstriction in the muscle, skin and splanchnic beds, while brain and cardiac blood flow proportionally increase. Third spacing occurs and lungs can become congested. As either kidney or liver function deteriorates, there may be increased or decreased drug sensitivity at the receptor level. Acidosis accompanies several failing organs. Protein synthesis is qualitatively and quantitatively altered. Sepsis affects tissue permeability. All these abnormalities influence drug pharmacokinetics and dynamics. AKI is accompanied by therapeutic interventions that alter intrinsic metabolism which is in turn complicated by kidney replacement therapy (KRT). So metabolism and removal are both altered and constantly changing. Drug management in AKI is exceedingly complex and is only beginning to be understood. Thus, we approach this discussion in a physiological manner. Critically ill patients pass through phases of illness, sometimes rapidly, other times slowly. The recognition of the phases and the need to adjust medication administration strategies is crucial to improving outcomes. An early phase involving supraphysiologic kidney function may be contributory to therapeutic failures that result in the complication of later AKI and kidney function failure.
42
Bellomo, Rinaldo, and John R. Prowle. Pathophysiology of oliguria and acute kidney injury. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0211.
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Oliguria and acute kidney injury (AKI) are common in critically-ill patients with studies reporting AKI affecting more than 50% of critically-ill patients. AKI is independently associated with increased mortality and is a potentially modifiable aspect of critical illness. The pathogenesis of AKI is complex and varies according to aetiology. The most common trigger in ICU patients is sepsis—the pathophysiology of septic AKI is poorly understood and probably involves intrarenal haemodynamic and inflammatory processes. In the setting of septic AKI, the classic acute tubular necrosis described in experimental models does not occur and histological changes are only minor. Activation of neurohormonal mechanisms is also important, particularly in the hepatorenal syndrome, where activation of the remain-angiotensin system appears to play a major role. The treatment of oliguria and AKI in ICU patients has traditionally relied on the administration of intravenous fluids. While such therapy is warranted in patients with a clear history, and physical examination suggestive of intravascular and extravascular volume depletion, its usefulness in other patients (e.g. septic patients) remains controversial. Removal of nephrotoxins, rapid treatment of the triggering factors, and attention to cardiac output and mean arterial pressure remain the cornerstones of the prevention and treatment of AKI in ICU.
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Benson, Carolyn, and G. Bryan Young. Ethical and end-of-life issues after cardiac arrest. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0067.
Full textAbstract:
Many survivors of cardiac arrest, especially out-of-hospital cardiac arrest, suffer varying degrees of anoxic-ischaemic brain injury. Accurate neurological prognostication to determine which patients will have poor neurological outcome is important to guide appropriate medical care and advise surrogate decision makers. Accurate prognostication generally requires the presence of two or more negative prognostic indicators, especially following treatment with therapeutic hypothermia. Medical care should be directed at achieving survival that the patient would consider acceptable. Poor quality survival is generally defined as severe disability with full dependency, minimally-conscious, or vegetative state. Discussions regarding prognosis and management of patients who remain unresponsive after resuscitation from cardiac arrest should be conducted in a professional manner and show respect for the individuals involved, their culture, and religion.
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Welsh, Sarah S., Geneviève Dupont-Thibodeau, and Matthew P. Kirschen. Neuroprognostication after severe brain injury in children: Science fiction or plausible reality? Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198786832.003.0010.
Full textAbstract:
Neuroprognostication is a complex process that spans the resuscitative, acute, and subacute phases of brain injury and recovery. Improvements over time have transitioned the task of outcome prediction after severe brain injury from estimating survival to providing a qualitative prognosis of functional neurologic recovery. This chapter follows the case of an 8-year-old boy who remained comatose following a cardiac arrest due to drowning. We describe and analyze novel applications of current technologies that could be used in the future to improve the accuracy, reliability, and confidence in the neuroprognostication process for physicians and families that are at the heart of ethical decision-making in medicine.
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Sever, Mehmet Şükrü, and Raymond Vanholder. Acute kidney injury in polytrauma and rhabdomyolysis. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0252_update_001.
Full textAbstract:
The term ‘polytrauma’ refers to blunt (or crush) trauma that involves multiple body regions or cavities, and compromises physiology to potentially cause dysfunction of uninjured organs. Polytrauma frequently affects muscles resulting in rhabdomyolysis. In daily life, it mostly occurs after motor vehicle accidents, influencing a limited number of patients; after mass disasters, however, thousands of polytrauma victims may present at once with only surgical features or with additional medical complications (crush syndrome). Among the medical complications, acute kidney injury (AKI) deserves special mention, since it is frequent and has a substantial impact on the ultimate outcome.Several factors play a role in the pathogenesis of polytrauma (or crush)-induced AKI: (1) hypoperfusion of the kidneys, (2) myoglobin-induced direct nephrotoxicity, and intratubular obstruction, and also (3) several other mechanisms (i.e. iron and free radical-induced damage, disseminated intravascular coagulation, and ischaemia reperfusion injury). Crush-related AKI is prerenal at the beginning; however, acute tubular necrosis may develop eventually. In patients with crush syndrome, apart from findings of trauma, clinical features may include (but are not limited to) hypotension, oliguria, brownish discoloration of urine, and other symptoms and findings, such as sepsis, acute respiratory distress syndrome, disseminated intravascular coagulation, bleeding, cardiac failure, arrhythmias, electrolyte disturbances, and also psychological trauma.In the biochemical evaluation, life-threatening hyperkalaemia, retention of uraemic toxins, high anion gap metabolic acidosis, elevated serum levels of myoglobin, and muscle enzymes are noted; creatine phosphokinase is very useful for diagnosing rhabdomyolysis.Early fluid administration is vital to prevent crush-related AKI; the rate of initial fluid volume should be 1000 mL/hour. Overall, 3–6 L are administered within a 6-hour period considering environmental, demographic and clinical features, and urinary response to fluids. In disaster circumstances, the preferred fluid formulation is isotonic saline because of its ready availability. Alkaline (bicarbonate-added) hypotonic saline may be more useful, especially in isolated cases not related to disaster, as it may prevent intratubular myoglobin, and uric acid plugs, metabolic acidosis, and also life-threatening hyperkalaemia.In the case of established acute tubular necrosis, dialysis support is life-saving. Although all types of dialysis techniques may be used, intermittent haemodialysis is the preferred modality because of medical and logistic advantages. Close follow-up and appropriate treatment improve mortality rates, which may be as low as 15–20% even in disaster circumstances. Polytrauma victims after mass disasters deserve special mention, because crush syndrome is the second most frequent cause of death after trauma. Chaos, overwhelming number of patients, and logistical drawbacks often result in delayed, and sometimes incorrect treatment. Medical and logistical disaster preparedness is useful to improve the ultimate outcome of disaster victims.
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Fayet, Cristina. Role of cardiac valve interstitial cells in valve repair: Deposition of fibronectin and formation of fibrillar adhesions in response to injury. 2004.
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Merry, Alan F., Simon J. Mitchell, and Jonathan G. Hardman. Hazards in anaesthetic practice: general considerations, injury, and drugs. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0044.
Full textAbstract:
The hazards of anaesthesia should be considered in the context of the hazard of surgery and of the pathology for which the surgery is being undertaken. Anaesthesia has become progressively safer since the successful demonstration of ether anaesthesia in Boston, Massachusetts, United States in 1846 and the first reported death under anaesthesia in 1847. The best estimation of the rate of anaesthesia-related mortality comes from the anaesthesia mortality review committees in Australia and New Zealand, where data have been collected under essentially consistent definitions since 1960, and reports are amalgamated under the auspices of the Australian and New Zealand College of Surgeons. An internationally accepted definition of anaesthetic mortality is overdue. Extending the time for inclusion of deaths from 24 h to 30 days or longer substantially increases estimated rates of mortality. Attribution of cause of death may be problematic. Even quite small degrees of myocardial injury in patients undergoing non-cardiac surgery increase the risk of subsequent mortality, and in older patients, 30-day all-cause mortality following inpatient surgery may be surprisingly high. Patients should be given a single estimate of the combined risk of surgery and anaesthesia, rather than placing undue emphasis on the risk from anaesthesia alone. Hazards may arise from equipment or from drugs either directly or through error. Error often underlies harmful events in anaesthesia and may be made more likely by fatigue or circadian factors, but violations are also important. Training in expert skills and knowledge, and in human factors, teamwork, and communication is key to improving safety.
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Salerno, Tomas A., and Marco Ricci. Myocardial Protection. Wiley & Sons, Incorporated, John, 2008.
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A, Salerno Tomas, and Ricci Marco, eds. Myocardial protection. Elmsford, N.Y: Blackwell Pub., 2004.
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Salerno, Tomas A., and Marco Ricci. Myocardial Protection. Wiley & Sons, Incorporated, John, 2008.
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