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1
Heart failure: Strategies to improve outcomes. Minneapolis, Minn: Cardiotext Publ., 2013.
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2
Stewart, Simon, and Lynda Blue, eds. Improving Outcomes in Chronic Heart Failure. London, UK: BMJ Publishing Group, 2004. http://dx.doi.org/10.1002/9780470750551.
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3
Simon, Stewart, and Blue Lynda, eds. Improving outcomes in chronic heart failure: Specialist nurse intervention from research to practice. 2nd ed. London: BMJ Books, 2004.
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4
Comparative guide to American hospitals: 4,383 hospitals with key personnel and 24 quality measures in treating heart attack, heart failure, pneumonia, pregnancy and surgical infection prevention. 4th ed. Millerton, N.Y: Grey House Pub., 2014.
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5
The Comparative guide to American hospitals: 4,693 hospitals with key personnel and 49 quality measures relating to heart attack, heart failure, pneumonia, childhood asthma, surgical care, medical imaging and patient experience. 3rd ed. Amenia, NY: Grey House Publishing, 2011.
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6
The fatal illness of Frederick the Noble. London: Keynes, 1987.
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7
Alpert, Joseph S., Lynne T. Braun, Elizabeth A. Madigan, Barbara J. Fletcher, and ileana L. Piña. Heart Failure: Strategies to Improve Outcomes. Cardiotext Publishing, 2013.
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8
(Editor), Debra K. Moser, and Barbara Riegel (Editor), eds. Improving Outcomes in Heart Failure: An Interdisciplinary Approach. Jones & Bartlett Publishers, 2001.
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9
(Contributor), Khalid Ashai, William Cohn (Contributor), Matthew Forrester (Contributor), Kelly Guglielmi (Contributor), Charles Herzog (Contributor), Rosemary Kelly (Contributor), Rakhi Khanna (Contributor), et al., eds. Cardiac Surgery in Chronic Renal Failure: Clinical Management and Outcomes. Blackwell Publishing Limited, 2007.
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10
Blue, Lynda, and Simon Stewart. Improving Outcomes in Chronic Heart Failure: A Practical Guide to Specialist Nurse Intervention. Wiley & Sons, Limited, John, 2007.
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11
Blue, Lynda, and Simon Stewart. Improving Outcomes in Chronic Heart Failure: A Practical Guide to Specialist Nurse Intervention. Wiley & Sons, Incorporated, John, 2008.
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12
Blue, Lynda, and Simon Stewart. Improving Outcomes in Chronic Heart Failure: A Practical Guide to Specialist Nurse Intervention. Wiley & Sons, Incorporated, John, 2008.
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13
Stewart, Simon, and Lynda Blue. Improving Outcomes in Chronic Heart Failure: A Practical Guide to Specialist Nurse Intervention. Bmj Publishing Group, 2001.
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14
Utili, Alberta Centre for Health Services. Rural and Urban Outcomes After Hospitalization for Congestive Heart Failure in Alberta. Alberta Centre for Health Services Utilizatio, 2003.
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15
Kamra, Komal, and Glyn D. Williams. Cardiomyopathy and Heart Failure. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0012.
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Congenital heart disease and cardiomyopathy are common causes of heart failure in children. Among cardiomyopathies, dilated cardiomyopathy is the most common cause of heart transplant in children. These patients with end-stage heart failure secondary to cardiomyopathy present for multiple interventions requiring anesthesia and may be challenging to manage because of their hemodynamic instability. Thoughtful, collaborative planning and execution of perioperative care is recommended to optimize patient outcomes. This includes good understanding of the patient’s clinical status and the relevant cardiac pathophysiology. Also, an appreciation of the implications of heart failure therapies and the invasive procedures for which the patient requires anesthesia care.
16
Stewart, Simon, and Lynda Blue. Improving Outcomes in Chronic Heart Failure: Specialist Nurse Intervention from Research to Practice. 2nd ed. Blackwell Publishing Limited, 2004.
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17
(Editor), Simon Stewart, and Lynda Blue (Editor), eds. Improving Outcomes in Chronic Heart Failure: A Practical Guide to Specialist Nurse Intervention. 3rd ed. Bmj Publishing Group, 2001.
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18
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.
19
Lameire, Norbert. Renal outcomes of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0238_update_001.
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This chapter summarizes the accumulating evidence that incomplete or even apparent complete recovery of renal function after acute kidney injury (AKI) may be an important contributor to a growing number of incident chronic kidney disease (CKD) and end-stage renal disease (ESRD) cases, largely in excess of the global growth in CKD prevalence. Evidence based on epidemiologic studies supports the notion that even after adjustment for several important covariates AKI is independently associated with an increased risk for both CKD and ESRD. Several risk factors for the subsequent development of CKD among survivors of AKI have been identified. Besides well-known risk factors for CKD in general, such as hypertension, older age, congestive heart failure, diabetes, and proteinuria, AKIN staging and duration also predict longitudinal CKD development. These characteristics may identify a category of at-risk AKI patients at the time of hospital discharge that will need long follow-up times for appropriate screening and surveillance measures for CKD.
20
Wald, Ron, and Ziv Harel. The Long-Term Outcomes of Acute Kidney Injury. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0015.
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Recent research has provided important insights on the long-term outcomes of patients who develop acute kidney injury (AKI) in the setting of critical illness. Large epidemiologic studies have demonstrated compelling associations between episodes of AKI and progressive kidney disease and death, respectively, although such studies do not establish causality due to the potential for confounding. Whether AKI is intrinsically toxic or a mere by-product of serious comorbidities (e.g. prior chronic kidney disease, heart failure, diabetes), there is no doubt that AKI survivors are a high-risk group who would likely benefit from close post-discharge follow-up. Recent studies have shown that a minority of patients with AKI receive specialized nephrology follow-up after discharge, suggesting an opportunity for quality improvement. Emerging research is evaluating factors that predict chronic kidney disease, end-stage renal disease, and death among AKI survivors. This work will, it is hoped, suggest new targets for prevention and treatment, with the goal of enhancing the likelihood of recovery following AKI.
21
Ostermann, Marlies, and Ruth Y. Y. Wan. Diuretics in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0058.
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Fluid overload and chronic hypertension are the most common indications for diuretics. The diuretic response varies between different types and depends on underlying renal function. In patients with congestive heart failure, diuretics appear to reduce the risk of death and worsening heart failure compared with placebo, but their use in acute decompensated heart failure is questionable. Diuretics are also widely used in chronic kidney disease to prevent or control fluid overload, and treat hypertension. In acute kidney injury, there is no evidence that they improve renal function, speed up recovery, or change mortality. In patients with chronic liver disease and large volume ascites, paracentesis is more effective and associated with fewer adverse events than diuretic therapy, but maintenance treatment with diuretics is indicated to prevent recurrence of ascites. Mannitol has a role in liver patients with cerebral oedema and normal renal function. The use of diuretics in rhabdomyolysis is controversial and restricted to patients who are not fluid deplete. In conditions associated with resistant oedema (chronic kidney disease, congestive heart failure, chronic liver disease), combinations of diuretics with different modes of action may be necessary. Diuresis is easier to achieve with a continuous furosemide infusion compared with intermittent boluses, but there is no evidence of better outcomes. The role of combination therapy with albumin in patients with fluid overload and severe hypoalbuminaemia is uncertain with conflicting data.
22
De Sutter, Johan, Piotr Lipiec, and Christine Henri. Heart failure: preserved left ventricular ejection fraction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0028.
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Nearly half of all patients with heart failure present with a preserved left ventricular ejection fraction (HFPEF). HFPEF is a pathophysiologically and clinically heterogeneous disease with an overall similar outcome to heart failure patients with a reduced ejection fraction. It is predominantly seen in elderly patients and comorbidities such as obesity, diabetes, hypertension, a sedentary lifestyle, and myocardial ischaemia play important roles in its development. In this chapter the conventional echocardiographic hallmarks of HFPEF including a preserved ejection fraction, left ventricular hypertrophy, left atrial dilatation, diastolic dysfunction, and pulmonary hypertension are presented. For the evaluation of left ventricular diastolic dysfunction, it is important to keep in mind that no single echocardiographic parameter is sufficiently accurate and reproducible to be used in isolation to make a diagnosis of diastolic dysfunction. The value of newer techniques including three-dimensional echocardiography and longitudinal strain assessment for the diagnosis and follow-up of HFPEF patients are promising but require further evaluation. As exercise-induced dyspnoea may be the first manifestation of HFPEF, the role of exercise echo (or diastolic stress testing) with evaluation of exercise-induced changes in left ventricular filling pressure and pulmonary artery systolic pressure is also presented. This chapter ends with a discussion on the echocardiographic parameters that can be used for risk stratification and follow-up of HFPEF patients.
23
Croskerry, Pat. The Cognitive Autopsy. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190088743.001.0001.
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Behind heart disease and cancer, medical error is now listed as one of the leading causes of death. Of the medical errors that lead to injury and death, diagnostic failure is regarded as the most significant. Generally, the majority of diagnostic failures are attributed to the clinicians directly involved with the patient, and to a lesser extent, the system in which they work. In turn, the majority of errors made by clinicians is due to decision making failures manifested by various departures from rationality. Of all the medical environments in which patients are seen and diagnosed, the emergency department is the most challenging. It has been described as a ‘wicked’ environment where illness and disease may range from minor ailments and complaints to severe, life-threatening disorders. The Cognitive Autopsy is a novel strategy towards understanding medical error and diagnostic failure in 42 clinical cases with which the author was directly involved or became aware of at the time. Essentially, it describes a cognitive approach towards root cause analysis of medical adverse events or near misses. Whereas root cause analysis typically focuses on the observable and measurable aspects of adverse events, the cognitive autopsy attempts to identify covert cognitive processes that may have contributed to outcomes. In this clinical setting, no cognitive process is directly observable but must be inferred from the behaviour of the individual clinician. The book illustrates unequivocally that chief among these cognitive processes are cognitive biases and other flaws in decision making, rather than knowledge deficits.
24
Caroline, Mara, Ryan Bradley, and Mimi Guarneri. Cardiovascular Disease. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190466268.003.0013.
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The older population is challenging to treat for numerous reasons, including comorbid conditions and increased susceptibility to adverse drug reactions, limiting medical therapy. They are at increased risk for loneliness and depression, which strongly impacts their cardiovascular outcomes, and they also have different values, usually prioritizing quality of life over mortality objectives. Finally, the elderly are underrepresented in cardiovascular clinical trials, thus limiting the applicability of guideline recommendations. This chapter emphasizes the importance of a comprehensive assessment of individual circumstances when assessing cardiovascular health in the elderly population. The chapter focuses on the role of nutrition, resiliency, and exercise for the prevention and treatment of cardiovascular disease. Nutrient deficiencies commonly seen with cardiovascular drugs are also discussed, as well as specific integrative strategies for optimizing dyslipidemia, atrial fibrillation, and heart failure in this population.
25
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.
26
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0045.
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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
27
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_001.
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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
28
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_002.
Full textAbstract:
Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
29
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_003.
Full textAbstract:
Mechanical complications after an acute infarction involve different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies occurring in <1% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment (Ibanez et al, 2017). Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
30
Joyce, David L., and Lyle D. Joyce. Mechanical Circulatory Support. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190909291.001.0001.
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Mechanical circulatory support (MCS) offers life-saving treatment options for patients with advanced heart failure, cardiogenic shock, and acute cardiopulmonary failure. With the development of short-term, long-term, left-sided, right-sided, biventricular, and cardiopulmonary support options, the complexity surrounding this field has evolved substantially in the past decade. This textbook seeks to provide a logical and systematic framework for managing patients who require MCS therapies. In chapters 2–9, a comprehensive approach to selecting and preparing patients for MCS interventions is described. In chapters 10–23, the range of currently available devices is reviewed with updates on the most up-to-date clinical experiences based on recently published outcomes. Chapters 24–30 describe the current state of the art in perioperative strategies for achieving long-term success. Finally, chapters 31–46 outline the myriad of clinical challenges that often occur in the postoperative period, including some of the frequently encountered adverse events that are unique to the physiology associated with this technology. The fundamental principles included in this textbook will provide a framework for the MCS provider that can serve as a road map amidst the rapidly evolving landscape created by the technology pipeline within this industry.
31
Kelley, Roger E. Cardiac Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0188.
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Heart disease is a major contributor to stroke and other neurologic disorders in adults. Cardioembolic stroke accounts for roughly 15% of all stroke, and the most common mechanism is cardiac arrhythmia, with atrial fibrillation the leading contributor. Anticoagulation such as using aspirin or warfarin is chosen based on the presence of associated risk factors including congestive heart failure, hypertension, age, and diabetes mellitus. Heart failure ranks second in the incidence of stroke from cardioembolism, with other risk factors being endocarditis, severe cardiomyopathy, acute myocardial infarction, and patent foramen ovale. Recent clinical trials indicate that induction of total body hyopthermia after cardiac arrest to a target temperature of 32°C to 34°C, for 24 hours, had a more favorable neurological outcome compared with a normothermia group.
32
Randerath, Winfried J., and Shahrokh Javaheri. Sleep and the heart. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0040.
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Heart function and sleep are closely associated. While NREM sleep reduces cardiac workload, phasic REM sleep increases sympathetic activity and cardiac vulnerability. Heart failure (HF) patients suffer from disturbed sleep due to frequent awakenings, periodic limb movements, sleep apnea, and depression. Insomnia seems to be associated with incident HF, and, when comorbid, results in a vicious circle. There is much evidence of a relationship between breathing disturbances during sleep and heart diseases. At least 50% of HF patients suffer from obstructive (OSA) or central (CSA) sleep apnea, both associated with impaired prognosis. OSA is a risk factor for arterial hypertension, atrial fibrillation, and HF. Continuous positive airway pressure devices reduce adverse cardiac events and improve outcome in severe OSA in compliant subjects. Adaptive servoventilation (ASV) is superior to other therapeutic options for CSA. However, the use of ASV is contraindicated in severe HF with reduced, but not preserved, ejection fraction.
33
Goldsmith, David J. Cardiovascular disease and chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0098.
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Even after as full a statistical adjustment as can be made for traditional cardiovascular risk factors has been undertaken, impaired kidney function and raised concentrations of albumin in urine each increase the risk of cardiovascular disease (CVD) by two- to fourfold, the degree increasing with severity. If the patient is also suffering from diabetes (as either the cause of CKD or a complication of it), the risks of CVD increase two- to fourfold again. CKD patients should, therefore, be acknowledged as having perhaps the highest cardiovascular risk of any patient cohort. CVD is underdiagnosed and undertreated in these patients. In early CKD the manifestations of CVD are similar to those of other patients. In late CKD and particularly in patients on dialysis the epidemiology is different. Left ventricular hypertrophy is very common and sudden cardiac death is greatly increased in incidence. Heart failure is a common complication. Calcification of valves and vessels becomes increasingly common and bad CVD outcomes are associated with hyperphosphataemia and other manifestations. The mechanisms by which risks are increased are not fully understood. The evidence base for the effectiveness of established therapies for CVD is relatively light in patients with CKD, but there is evidence for benefit of lipid-lowering therapies and most nephrologists believe that blood pressure and volume control are important for good long-term outcomes. Evidence of impact on CVD of interventions to alter mineral bone disease is disappointingly weak.
34
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.
35
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.
Full textAbstract:
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.
36
Paneni, Francesco, and Massimo Volpe. Co-morbidity (HFrEF and HFpEF): hypertension. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198784906.003.0415_update_001.
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Hypertensive heart disease is a major cause of heart failure (HF) and mortality. Hypertension precedes HF occurrence in 75% of cases, and carries a sixfold increase in HF risk as compared to non-hypertensive individuals. Most importantly, a minority of patients survive 5 years after the onset of hypertensive HF. In hypertensive patients, the heart may present different patterns of adaptive remodelling: concentric remodelling, concentric hypertrophy, and eccentric hypertrophy. Although most hypertensive patients are at high risk of developing concentric hypertrophy, a growing proportion of subjects display a concentric-to-eccentric progression eventually leading to left ventricular dilation and systolic dysfunction. Several factors including myocardial ischaemia, ethnicity, genetic background, history of diabetes, and blood pressure pattern may significantly influence the pathway from hypertension to left ventricular dilation. Patients with a concentric hypertrophy usually develop HF with preserved ejection fraction (HFpEF), whereas those with an eccentric (dilated) phenotype develop HF with reduced ejection fraction (HFrEF). Lowering blood pressure has a striking effect in reducing the risk of HF. Although available antihypertensive drugs are all successful in lowering blood pressure, angiotensin-converting enzyme inhibitors, angiotensin receptor blocker (ARBs), and diuretics are more effective than other drug classes in preventing HF. The combination of the neprilysin inhibitor sacubitril with the ARB valsartan (LCZ696) has recently been shown to be highly effective in reducing HF-related outcomes in hypertensive subjects. An individualized treatment scheme taking into account blood pressure levels, type of HF (HFpEF or HFrEF), and relevant co-morbidities (i.e. renal disease, diabetes) is currently the best approach to improve morbidity and mortality in hypertensive patients with HF.
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Salvatori, Daniela, Harsha D. Devalla, and Robert Passier. Cells to repair the infarcted myocardium. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0030.
Full textAbstract:
The adult mammalian heart has poor regenerative capacity. Loss of functional cardiomyocytes following myocardial infarction leads to the replacement of functional muscle by scar tissue. This has a detrimental effect on cardiac function and may lead to heart failure. Potential regeneration of severe cardiac damage would require replacement of dead and damaged cardiomyocytes by transplantation, recruitment of endogenous progenitor cells, or induction of cardiomyocyte proliferation. For more than a decade, clinical trials to ameliorate the injured heart have been under way. However, after evaluation of the outcome of these trials it is evident that the beneficial effects of these cell-based transplantations are only marginal, and beneficial effects, if any, are not caused by regeneration of cardiomyocytes. In recent years, alternative approaches and various cell sources have been studied and suggested for cardiac repair. Recent advances in these cell-based therapies or strategies to activate endogenous cardiac repair are discussed.
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Fagard, Robert, Giuseppe Mancia, and Renata Cifkova. Blood pressure. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0014.
Full textAbstract:
Prevention of hypertension can help prevent cardiovascular disease and renal complications. Obesity, a high sodium and low potassium intake, physical inactivity, and high alcohol consumption all contribute to the development of hypertension, and randomized controlled trials have shown that appropriate lifestyle modifications are able to reduce blood pressure and/or prevent the development of hypertension. The major complications of hypertension are stroke, coronary heart disease, heart failure, peripheral artery disease, and chronic kidney disease. Multiple randomized controlled trials and their meta-analyses have shown that treatment with antihypertensive drugs reduces the incidence of fatal and non-fatal cardiovascular events. In addition, meta-analyses have shown that there are no clinically relevant differences in the effects of the five major drug classes on outcome, so all of them are considered suitable for the initiation and maintenance of antihypertensive therapy. Nevertheless, the therapeutic approach in the elderly, women, and patients with diabetes, cerebrovascular, cardiac, or renal disease deserves special attention.
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Waldek, Stephen. Fabry disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0335_update_001.
Full textAbstract:
Fabry disease is a rare X-linked disorder of glycosphingolipid metabolism caused by a deficiency of the lysosomal acid hydrolase enzyme, alpha-galactosidase A. The resulting accumulation of substrate, mostly globotriaosylceramide, leads to a progressive, multiorgan disease affecting predominantly the kidneys, skin, heart, and nervous system. It is one of over 50 lysosomal storage diseases. It is typically diagnosed in young men after many years of ‘acral pain’ syndrome, when the diagnosis is made through identification of characteristic abnormalities of skin, kidney or heart, or of other organs. Renal failure has been a common outcome. Females may also develop manifestations, usually later in life. Renal biopsy shows vacuoles/deposits in podocytes and other renal cell types with progressive scarring. The diagnosis can be made by measuring enzyme levels in men, or by genetic testing. This latter is the more reliable test in women. Fabry disease can now be treated where affordable by regular (every 2 weeks) intravenous infusions of recombinant preparations of the deficient enzyme. These are burdensome and expensive, but are transforming the outlook for the condition.
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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.
Full textAbstract:
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.
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Sinagra, Gianfranco, Marco Merlo, and Davide Stolfo. Dilated cardiomyopathy: clinical diagnosis and medical management. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0356.
Full textAbstract:
Dilated cardiomyopathy (DCM) is a relatively rare primary heart muscle disease with genetic or post-inflammatory aetiology that affects relatively young patients with a low-risk co-morbidity profile. Therefore, DCM represents a particular heart failure model with specific characteristics and long-term evolution. The progressively earlier diagnosis derived from systematic familial screening programmes and the current therapeutic strategies have greatly modified the prognosis of DCM with a dramatic reduction of mortality over recent decades. A significant number of DCM patients present an impressive response to pharmacological and non-pharmacological evidence-based therapy in terms of haemodynamic improvement with subsequent left ventricular reverse remodelling, which confer a favourable long-term prognosis. However, in some DCM patients the outcome is still severe. This prognostic heterogeneity is possibly related to the aetiological variety of this disease. Maximal effort towards an early aetiological diagnosis of DCM, by using all diagnostic available tools (including cardiovascular magnetic resonance imaging, endomyocardial biopsy, and genetic testing when indicated), as well as the individualized long-term follow-up appear crucial in improving the prognostic stratification and the clinical management of these patients.
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Detering, Karen, Elizabeth Sutton, and Scott Fraser. Advance care planning in chronic disease: finding the known in the midst of the unknown. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198802136.003.0025.
Full textAbstract:
People are living longer lives with a greater burden of disease. Diseases which contribute significantly to this burden are chronic kidney disease; chronic obstructive pulmonary disease and heart failure. Technologies exist that can sustain life for patients with these disease, however patients and their families/loved ones need to know the likely outcome of their disease, its course, and all management options. Advance care planning (ACP) can assist with this process as well as ensuring that patients, families, and health care teams are aware of what treatment a patient wants—or does not want. ACP also enables the appointment of a decision maker to act on behalf of the patient should they lose capacity to make medical decisions. This chapter discusses the benefits of ACP and why it needs to be introduced early in the course of any life-limiting illness.
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Lara-Millán, Armando. Redistributing the Poor. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780197507896.001.0001.
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This book argues that the changes taking place in the United States’ largest jails and public hospitals have been drastically misunderstood. And more generally, the way that states govern urban poverty at the turn of the twenty-first century has been misunderstood as well. It is widely believed that because US society has divested in public health, the sick and poor now find themselves subject to powerful criminal justice institutions. Rather than focus on the underinvestment of health and overinvestment of criminal justice, this book argues that the fundamental problem of the state is a persistent crisis between budgetary catastrophe and expansive new legal rules. Redistributing the Poor pushes the reader to think about the circulation of people for the purposes of generating absent revenue, absolving new legal demands, and projecting illusions that crisis have been successfully resolved. This book delves into the heart of the state: the day-to-day operations of the largest hospital and jail system in the world. It is only by centering the state’s use of redistribution that one can understand how certain forms of social suffering—the premature death of mainly poor, people of color—are not a result of the state’s failure to act, but instead are the necessary outcome of so-called successful policy.
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Jacquemyn, Yves, and Anneke Kwee. Antenatal and intrapartum fetal evaluation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0006.
Full textAbstract:
Antenatal and intrapartum fetal monitoring aim to identify the beginning of the process of fetal hypoxia before irreversible fetal damage has taken place. Fetal movement counting by the mother has not been reported to be of any benefit. The biophysical profile score, incorporating ultrasound and fetal heart rate monitoring, has not been proven to reduce perinatal mortality in randomized trials. Doppler ultrasound allows the exploration of the perfusion of different fetal organ systems and provides data on possible hypoxia and fetal anaemia. Maternal uterine artery Doppler can be used to select women with a high risk for intrauterine growth restriction and pre-eclampsia but does not directly provide information on fetal status. Umbilical artery Doppler has been shown to reduce perinatal mortality significantly in high-risk pregnancies (but not in low-risk women). Adding middle cerebral artery Doppler to umbilical artery Doppler does not increase accuracy for detecting adverse perinatal outcome. Ductus venosus Doppler demonstrates moderate value in diagnosing fetal compromise; it is not known whether its use adds any value to umbilical artery Doppler alone. Cardiotocography (CTG) reflects the interaction between the fetal brain and peripheral cardiovascular system. Prelabour routine use of CTG in low-risk pregnancies has not been proven to improve outcome; computerized CTG significantly reduces perinatal mortality in high-risk pregnancies. Monitoring the fetus during labour with intermittent auscultation has not been compared to no monitoring at all; when compared with CTG no difference in perinatal mortality or cerebral palsy has been noted. CTG does lower neonatal seizures and is accompanied by a statistically non-significant rise in caesarean delivery. Fetal blood sampling to detect fetal pH and base deficit lowers caesarean delivery rate and neonatal convulsions when used in adjunct to CTG. Determination of fetal scalp lactate has not been shown to have an effect on neonatal outcome or on the rate of instrumental deliveries but is less often hampered by technical failure than fetal scalp pH. Analysis of the ST segment of the fetal ECG (STAN®) in combination with CTG during labour results in fewer vaginal operative deliveries, less need for neonatal intensive care, and less use of fetal blood sampling during labour, without a change in fetal metabolic acidosis when compared to CTG alone.