Dissertations / Theses on the topic 'Early heart failure'

Heart failure affects 1-2% of the adult population in the United Kingdom and accounts for the majority of hospitalisations in patients with cardiovascular disease. The financial implications are enormous as it consumes 1-2% of the national health care budget with 70% of these costs relating to hospitalisation expenses. Prevention of these admissions may be possible by detecting early signs of decompensation in patients with chronic heart failure (CHF) and instituting interventions that may steer the course of disease back to stability without the need for a hospital inpatient stay. Further, Sleep Disordered Breathing (SDB) and in particular Central Sleep Apnoea (CSA) is found in patients with CHF and at any symptomatic stage of the condition. This may be associated with Cheyne-Stokes Respiration (CSR), which has been shown to be an independent predictor of mortality. In the first study of this thesis, I investigated the accuracy of the SleepMinderTM (SM) device; which is a non-contact monitor of nocturnal respiratory patterns; in diagnosing SDB by deriving measures of the Apnoea Hypopnea Index (AHI) and percentage overnight CSR from the SM signals. I found that SM was good in terms of diagnostic accuracy with an area under receiver operator characteristic curve (ROC) of 0.82 (p=0.02) for an AHI threshold >15, but only moderately so for % overnight CSR>0, with an area under ROC curve of 0.72 (p=0.06). In the second study, I examined the changes that occur in SM derived respiratory parameters over a long period of monitoring and found that the AHI, quantity of CSR, Total Sleep Time (TST) and Respiratory Rate (RR) were highly variable with Intra-Class Correlation (ICC) measures of 0.32, 0.39, 0.25, 0.36 respectively over a period of 12 months. Relying on data from a year rather than a single night resulted in misclassification of patients into a different severity group of SDB during 35% of the follow up period and placed patients into a different treatment group during 21% of this period. I also observed that a high proportion (59%) of patients studied had a mean AHI that was consistently above the accepted threshold for treatment (AHI>15). This was consistent even over a shorter follow up period of 2 weeks suggesting that a single night measure of the AHI may not be a sufficient risk assessment of SDB in heart failure patients. In the final study, I have investigated the predictive value of the SleepMinderTM for acute decompensation of heart failure (ADHF) using algorithms derived from its signals. I found that the SM was not accurate for this purpose, performing with a sensitivity and specificity of 0.38 and 0.71, respectively. In summary this study has demonstrated that the SleepMinderTM device provides a novel screening method, which is convenient for the detection of sleep disordered breathing in patients with CHF. It performs with a good diagnostic accuracy and is acceptable to these patients due to its non-contact operation. Algorithms derived from its signals however cannot be used to predict acute decompensation of chronic heart failure. Further, longitudinal analyses of nocturnal respiratory patterns in these patients have demonstrated that the Apnoea Hypopnea Index (AHI) is highly variable over a prolonged period of monitoring and a mean value rather that a single night measurement may be a more appropriate risk assessment tool for SDB. This requires confirmation.

Identifying people with advanced illnesses whose health is deteriorating, assessing their needs and planning care proactively with them are healthcare priorities given the demographic trend of ageing populations in the UK and internationally. Over the past 10 years (2004-2014), I have led a series of research studies that have made an important academic contribution to improving palliative care services for patients with heart disease and advanced multimorbidity. My first paper reported secondary analysis of data generated from a qualitative study of the illness and care experiences of patients with advanced heart failure. This work used innovative, qualitative research methods to explore and understand patient, carer and health professional perspectives over time. My second study then evaluated whether health and social care services were configured and delivered in response to the needs of people with heart failure and their families. This led me to recommend an anticipatory care framework which integrated a palliative care approach with other aspects of treatment and care. Around this time, advance care planning (planning ahead to facilitate end-of-life care aligned with people’s goals and preferences) was being strongly advocated by NHS health policy makers despite limited research in the UK. For my third study, I evaluated an evidence-based, educational intervention for general practitioners while also exploring barriers and facilitators to advance care planning in primary care for patients with cancer or other advanced conditions. It was becoming increasingly clear that failure to identify people with deteriorating health and a high risk of dying in a timely way was a major barrier to more effective palliative care. The problem was greatest for patients with non-malignant conditions whose illness trajectory is much less easy to predict than in cancer populations. I therefore started to research and develop a new clinical tool designed to prompt early, proactive patient identification in routine clinical practice – the Supportive and Palliative Care Indicators Tool (SPICT). My fourth research paper reported an evaluation of the SPICT in a mixed-methods study in a large tertiary care hospital. The SPICT was then used to identify people with multimorbidity for my fifth study, a longitudinal exploration of patient and carer experiences of hospital admission and ongoing community care. In my final paper, I drew on my previous research and combined this with well-developed approaches to timely identification and effective communication. I described the design of a successful pilot randomised trial of future care planning with people who had advanced heart disease and their carers. This thesis presents a critical review of these six research studies setting them in context and demonstrating the impact they have had in ensuring that high quality research evidence informs current and future developments in palliative care policy and clinical practice.

Intraaortic balloon counterpulsation (IABP) is the most widely used mechanical support in the assistance of a failing heart.1 Despite extensive research in this field no experimental or clinical studies have been undertaken to evaluate the most effective manner to wean IABP.2 The research reported in this thesis examines early recognition of cardiac decompensation and the management of IABP weaning. Conducted in three phases, the aim of this research programme was to determine the best manner by which to wean IABP. Phase 1 utilised a comparative descriptive design to examine IABP practice at a single cardiothoracic tertiary referral hospital. The majority of data collection was prospective, however, the required sample size saw inclusion of some retrospective data. This single centre data were than compared with an international registry to contrast IABP management and outcome. Phase 2 utilised a questionnaire survey to audit all Australasian intensive care units. Survey results were combined and statistically analysed to describe Australasian IABP management, weaning and outcome. Phase 3 utilised a quasi-experimental, one-group, posttest-only design to clinically validate a tool designed to monitor a patient's cardiac function - the 'cardiac decompensation tool'. Phase 1 saw data collected for 669 IABP insertions over an 11 year period at a single Australian hospital. This cohort was compared against the 38,606 patient dataset of The Benchmark Counterpulsation Outcomes Registry. Australian IABP practice saw later application of the device in a higher acuity patient. Australian practice demonstrated a prejudice toward intraoperative use (34.2% versus 16.6%; p=< 0.0001) and an aversion to catheter laboratory support (10.6% versus 19%; p=< 0.0001). Australian mortality while slightly higher, remained comparable (22% versus 20.8%; p=ns). Phase 2 response rate was 60%. The most common Australasian method of IABP support withdrawal was ratio reduction only (61%). Units with a documented weaning policy were less likely to require balloon reinsertion or pharmacologic escalation following IABP removal (p=0.06). Indicators most likely to demonstrate a patient's readiness for IABP weaning were blood pressure (92%), heart rate (76%) and wedge pressure (59%). Phase 3 revealed cardiac decompensation tool scores to increase immediately prior to a treatment escalation (p=0.022) and decrease immediately following this escalation in therapy (p=0.0096). There was also some indication of decreasing scores prior to treatment minimisation (p=0.005). Tool scores demonstrated a corresponding treatment fluctuation up to three hours prior to the treatment intervention. With Phase 1 and 2 revealing many aspects of IABP practice to vary, the need for some direction regarding weaning is evident. Timely recognition of cardiac decompensation during IABP weaning allows an opportunity for the earlier escalation of treatment and consequent provision of increased cardiac support. Application of the Phase 3 cardiac decompensation tool can only assist in ensuring the best manner by which to support IABP weaning.

Intraaortic balloon counterpulsation (IABP) is the most widely used mechanical support in the assistance of a failing heart.1 Despite extensive research in this field no experimental or clinical studies have been undertaken to evaluate the most effective manner to wean IABP.2 The research reported in this thesis examines early recognition of cardiac decompensation and the management of IABP weaning. Conducted in three phases, the aim of this research programme was to determine the best manner by which to wean IABP. Phase 1 utilised a comparative descriptive design to examine IABP practice at a single cardiothoracic tertiary referral hospital. The majority of data collection was prospective, however, the required sample size saw inclusion of some retrospective data. This single centre data were than compared with an international registry to contrast IABP management and outcome. Phase 2 utilised a questionnaire survey to audit all Australasian intensive care units. Survey results were combined and statistically analysed to describe Australasian IABP management, weaning and outcome. Phase 3 utilised a quasi-experimental, one-group, posttest-only design to clinically validate a tool designed to monitor a patient's cardiac function - the 'cardiac decompensation tool'. Phase 1 saw data collected for 669 IABP insertions over an 11 year period at a single Australian hospital. This cohort was compared against the 38,606 patient dataset of The Benchmark Counterpulsation Outcomes Registry. Australian IABP practice saw later application of the device in a higher acuity patient. Australian practice demonstrated a prejudice toward intraoperative use (34.2% versus 16.6%; p=< 0.0001) and an aversion to catheter laboratory support (10.6% versus 19%; p=< 0.0001). Australian mortality while slightly higher, remained comparable (22% versus 20.8%; p=ns). Phase 2 response rate was 60%. The most common Australasian method of IABP support withdrawal was ratio reduction only (61%). Units with a documented weaning policy were less likely to require balloon reinsertion or pharmacologic escalation following IABP removal (p=0.06). Indicators most likely to demonstrate a patient's readiness for IABP weaning were blood pressure (92%), heart rate (76%) and wedge pressure (59%). Phase 3 revealed cardiac decompensation tool scores to increase immediately prior to a treatment escalation (p=0.022) and decrease immediately following this escalation in therapy (p=0.0096). There was also some indication of decreasing scores prior to treatment minimisation (p=0.005). Tool scores demonstrated a corresponding treatment fluctuation up to three hours prior to the treatment intervention. With Phase 1 and 2 revealing many aspects of IABP practice to vary, the need for some direction regarding weaning is evident. Timely recognition of cardiac decompensation during IABP weaning allows an opportunity for the earlier escalation of treatment and consequent provision of increased cardiac support. Application of the Phase 3 cardiac decompensation tool can only assist in ensuring the best manner by which to support IABP weaning.

This thesis focuses on the development of machine learning tools to better characterize the cardiac anatomy and function in the context of heart failure, and in particular their extension to consider multiple parameters that help identifying the pathophysiological aspects underlying disease. This advanced and personalized characterization may eventually allow assigning patients to clinically-meaningful phenogroups with a uniform treatment response and/or disease prognosis. Specifically, the thesis copes with the technical difficulties that multivariate analyses imply, paying special attention to properly combine different descriptors that might be of different nature (e.g., patterns, continuous, or categorical variables) and to reduce the complexity of large amounts of data up to a meaningful representation. To this end, we implemented an unsupervised dimensionality reduction technique (Multiple Kernel Learning), which highlights the main characteristics of complex, high-dimensional data into fewer dimensions. For our computational analysis to be useful for the clinical community, it should remain fully interpretable. We made special emphasis in allowing the user to be aware of how the input to the learning process models the obtained output, through the use of multi-scale kernel regression techniques among others.
Esta tesis se centra en el desarrollo de herramientas de aprendizaje automático para mejorar la caracterización de la anatomía y la función cardíaca en el contexto de insuficiencia cardíaca, y, en particular, su extensión para considerar múltiples parámetros que ayuden a identificar los aspectos pato-fisiológicos subyacentes a la enfermedad. Esta caracterización avanzada y personalizada podría en última instancia permitir asignar pacientes a fenogrupos clínicamente relevantes, que demuestren una respuesta uniforme a un determinado tratamiento, o un mismo pronóstico. Específicamente, esta tesis lidia con las dificultades técnicas que implican los análisis multi-variable, prestando especial atención a combinar de forma apropiada diferentes descriptores que pueden ser de diferente naturaleza (por ejemplo, patrones, o variables continuas o categóricas), y reducir la complejidad de grandes cantidades de datos mediante una representación significativa. Con este fin, implementamos una técnica no supervisada de reducción de dimensionalidad (Multiple Kernel Learning), que destaca las principales características de datos complejos y de alta dimensión utilizando un número reducido de dimensiones. Para que nuestro análisis computacional sea útil para la comunidad clínica debería ser enteramente interpretable. Por eso, hemos hecho especial hincapié en permitir que el usuario sea consciente de cómo los datos entrantes al algoritmo de aprendizaje modelan el resultado obtenido mediante el uso de técnicas de regresión kernel multi-escala, entre otras.

Tese de mestrado, Doenças Metabólicas e Comportamento Alimentar, Universidade de Lisboa, Faculdade de Medicina, 2019
The present thesis is based on the premise that chronic heart failure patients have a high morbidity and mortality due to the fact that cardiac insufficiency per se evolves inexorably, and that it affects an elder and frail population, suffering from multiple pathologies, polymedicated and even socio-economically vulnerable. The increase of life expectancy, inherent to the improvement of health care, determined a parallel augment of chronic heart failure patients. Albeit we have assisted to a consistent decline in the rate of heart failure hospitalizations, surprisingly, short-term readmission and mortality persist high, irrespective of clinical innovations and guideline directed management, representing a tremendous health care burden. It urges to define a short-term prognosis for these patients in order to reduce the readmission and premature mortality rates due to its socio-economic impact. The main purpose of this dissertation is to characterize at risk patients for early (defined as a period of 90 days post-discharge) readmission, due to heart failure, and overall death. The putative role of biochemical cardiovascular markers in clinical decision making, principally in recognizing high risk patients that could benefit from therapeutic intensification and stricter surveillance is also addressed. To characterize the population we addressed disease related risk factors [namely the etiology, the New York Heart Association Functional (NYHA) Class, left ventricular ejection fraction (LVEF), right ventricular function, signs and symptoms], non-modifiable cardiovascular risk factors, modifiable cardiovascular risk factors, comorbidities [chronic kidney disease (CKD), anemia, iron deficiency, thyroid function], therapeutic and biomarkers [specifically troponins, proBNP-Aminoterminal B-type Natriuretic Peptide (NT-proBNP), Galectin-3 (Gal-3), Suppression of Tumorigenicity 2 (ST2), Mid-Regional pro-Adrenomedullin (pro-ADM)] and Erythropoietin (EPO).
A presente tese baseia-se na premissa de que os doentes que padecem de insuficiência cardíaca crónica apresentam uma morbilidade e mortalidade elevadas fruto da evolução per se inexorável da insuficiência cardíaca e do facto de afetar uma população maioritariamente idosa, frágil, que sofre de múltiplas patologias, polimedicada e, inclusive, socioeconomicamente desprovida. O aumento da esperança de vida, inerente à melhoria dos cuidados de saúde, determinou um incremento paralelo da prevalência da insuficiência cardíaca crónica. Apesar de se ter assistido a um declínio das taxas de internamento por insuficiência cardíaca, surpreendentemente, as taxas de reinternamento e mortalidade precoces mantêm-se elevadas, independentemente dos avanços clínicos e abordagem em conformidade com as directrizes preconizadas, sobrecarregando tremendamente o sistema de saúde. Atendendo ao seu impacto socioeconómico urge definir o prognóstico a curto prazo destes doentes a fim de reduzir a taxa de readmissão e mortalidade precoces. Trata-se de um estudo de coorte prospetivo observacional, unicêntrico, com um único braço, de utilidade diagnóstica. O objetivo principal do estudo foi caracterizar os doentes de risco para readmissão e mortalidade precoces (definido como o período até 90 dias pós-alta) por insuficiência cardíaca. Apesar do propósito deste estudo ser, primeiramente, definir o prognóstico a curto prazo da insuficiência cardíaca, o seguimento prolongado permitiu-nos caracterizar, também, a mortalidade a longo prazo. Consideramos a mortalidade global atendendo a que a maioria dos doentes não faleceu no hospital, pelo que não tivemos acesso às certidões de óbito. O objetivo secundário foi avaliar a importância de biomarcadores emergentes no prognóstico da insuficiência cardíaca. Para caracterizar a população abordamos fatores de risco relacionados com a insuficiência cardíaca per se (nomeadamente a etiologia, a classe funcional da NYHA, a fração de ejecção do ventrículo esquerdo, a função do ventrículo direito, sinais e sintomas), fatores de risco cardiovasculares não-modificáveis, factores de risco cardiovasculares modificáveis, comorbilidades (tais como a doença renal crónica, a anemia, a deficiência de ferro, a função tiroideia), a terapêutica e biomarcadores (troponinas, NT-proBNP, galectina-3, ST2, pro-ADM e EPO).

Impedance has been used as a tool for cardiac research since the early 1940’s. Recently there have been many advances in this field in the diagnosis of human heart failure through the measurement of pacemaker and ICD coupled impedance detection to determine the state of pulmonary edema in patients through drops in lung impedance. These new detection methods are far downstream of the initial changes in physiology, which signify heart failure risk, namely, an increased left ventricular (LV) end-diastolic volume (also known as preload). This dissertation presents the first formal validation of the complex admittance technique for more accurate blood volume measurement in vivo in mice. It aims to determine a new configuration of admittance measurement in a large scale animal model (pigs). It also aims to prove that “piggybacking” an admittance measurement system onto previously implanted AICD and bi-ventricular pacemakers is a feasible and practical measurement that will serve as an early warning system for impending heart failure through the measurement of LV preload, which appears before the currently measured drop in lung impedance using previous techniques.
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Myocardial fibrosis is a common pathological finding in patients with cardiovascular disease and is believed to be a major contributing factor in the development of end stage organ failure. Early events that promote the development of myocardial fibrosis are not well understood. Rapid cellular infiltration into the cardiac tissue is evident in fibrosis but the infiltrating populations and their functions have yet to be completely elucidated. The aim of this thesis was to characterize the phenotype and function of this cellular population in a model of hypertension mediated myocardial fibrosis. Furthermore, we intended to explore therapies that target this population and ameliorate fibrosis. We characterized a novel population of infiltrating cells as circulating fibroblast progenitor cells, termed fibrocytes. We determined that this population does not appear to specifically migrate in response to previously established chemotactic signals (CCL2 or CXCL12). We found that fibrocytes respond to fibrogenic stimuli (AngII and CTGF) by increasing the expression of collagen and CTGF, an early molecular mediator of fibrosis, while also promoting fibrocyte differentiation. Using an anti-hypertension treatment, we found that hypertension as a physiologic stimulus likely promotes cellular infiltration and corresponding fibrosis. We also established that treatment with activated protein C (aPC) conferred protection against the development of myocardial fibrosis, potentially by inhibiting fibrocyte recruitment and/or activation. Lastly, to assess fibrocyte involvement in the progression of human myocardial fibrosis we assessed fibrocytes in levels in the circulation of patients with ischemic heart disease compared to healthy controls. We found that patients with ischemic heart disease had an increase of circulating cells that have the potential to become fibrocytes compared to healthy controls and therefore likely contribute to myocardial fibrosis. From this data, we propose that fibrocytes are a key effector cell that directly promotes pathologic fibrosis within the injured myocardium. Understanding their migration and function is therefore essential to the development of future therapies targeting this cell type to inhibit their role in fibrosis.

Trabalho Final do Curso de Mestrado Integrado em Medicina, Faculdade de Medicina, Universidade de Lisboa, 2016
Heart Failure (HF) is an increasingly prevalent syndrome and a leading cause of both first hospitalization and readmissions. Strikingly, up to 25% of the patients are readmitted within 30 to 60-days, accounting for HF as the primary cause for readmission in the adult population. Given its poor prognosis, one could describe it as a “malignant condition”. Acute decompensation is intrinsically related to increased right heart tele-diastolic pressures, converging into congestive manifestations independently of precipitant(s). In-hospital strategies to adequately compensate and timely discharge patients are limited. Conversely, the fragile early postdischarge phase is a vulnerable period when one could potentially intervene cost-effectively to improve survival and to reduce morbidity. Promising transitional hospital-to-home programs may have a broader role in the near future, namely for selected higher risk patients. However, identifying patients at risk for hospital readmission has been challenging. Novel approaches, such as ferric carboxymaltose and valsartan/sacubitril, and reemerging drugs, particularly digoxin, may reduce hospitalizations. Despite this, optimizing the use of “older” therapies is still warranted. Right heart pressures monitoring may provide novel insights into promptly outpatient management. Unfortunately, randomized trials in the specific ADHF population are scarce. A novel paradigmatic approach is needed in order to suitably improve the currently poor prognosis of ADHF. Both improving survival and reducing hospitalizations are, therefore, primordial therapy goals. Lastly, no single drug has consistently proved to improve survival in HF with preserved ejection fraction (HFpEF); yet, some approaches may efficiently reduce hospitalizations. Awareness on HFpEF management beyond the failing heart is imperative.
Actualmente, a Insuficiência Cardíaca (IC) é uma síndrome cada vez mais prevalente, com uma morbilidade e mortalidade consideráveis. Esta é frequentemente comparada a doenças malignas na literatura médica pelo seu prognóstico reservado. A IC é a causa mais frequente de readmissão hospitalar de entre os adultos. Inclusive, até 25% dos doentes são readmitidos no espaço de 30 a 60 dias. Os estudos têm indicado que a descompensação aguda está relacionada com o aumento das pressões tele-diastólicas do coração direito. Apesar dos vários factores precipitantes identificados, estes poderão promover tal descompensação por mecanismos fisiopatológicos comuns, convergindo em manifestações congestivas. As estratégias intra-hospitalares para promover a subsequente compensação adequada e aquelas para preparar a alta em tempo oportuno são ainda limitadas. Por outro lado, o período de tempo que segue à alta, em que o doente com IC se encontra vulnerável, poderá demonstrar-se como oportuno para intervir, com os objectivos de reduzir a mortalidade, impedir readmissões evitáveis, e fazê-lo de modo custo-eficaz, dado que grande partes dos custos na IC são atribuíveis ao peso das readmissões hospitalares. Neste âmbito, os programas de transição hospital-ambulatório poderão vir a ter um papel promissor no futuro, nomeadamente em doentes identificados como sendo de alto risco para tais eventos após a alta. Contudo, a identificação destes doentes em risco tem-se ainda demonstrado um desafio. Recentemente, outras abordagens terapêuticas poderão alterar o prognóstico da IC, tais como a carboximaltose férrica e o valsartan/sacubitril, ou inclusive terapêuticas reemergentes, como a digoxina na IC com fracção de ejecção reduzida, tema de controvérsia actual. No futuro torna-se premente melhorar a utilização das terapêuticas já disponíveis para a IC, além da procura de novos alvos terapêuticos. Recentemente, a monitorização das pressões cardíacas direitas demonstrou reduzir as hospitalizações ao permitir intervenções atempadas no doente em ambulatório com doença estável. Ainda assim, os ensaios clínicos controlados que incidem especificamente nos pacientes com descompensação aguda de IC são escassos. Torna-se então fundamental estudar esta população tendo por objectivo uma nova abordagem paradigmática, ou seja, deverá ter-se em consideração a problemática da mortalidade mas também das hospitalizações e da qualidade de vida diminuída. Por fim, a IC é verdadeiramente uma síndrome, em que a heterogeneidade dos pacientes é evidente. Especificamente, deve salientar-se que nenhum fármaco ainda demonstrou reduzir a mortalidade nos pacientes com IC com fracção de ejecção preservada, ainda que algumas abordagens poderão demonstrar-se eficaz na redução de hospitalizações. Este subgrupo da IC precisa de um estudo que deverá ir além do coração em falência, o qual é apenas uma peça do puzzle incompleto deste “quebra-cabeças”.

Chronic kidney disease (CKD) and its cardiac complications represent a large and growing problem in Canada. The progression of CKD is driven by the activation of several final common pathways of injury, including fibrosis and oxidative stress. If left unchecked, these inter-connected processes lead to progressive damage and subsequent organ dysfunction. Current clinical therapies, consisting of aggressive blood pressure control and blockade of the renin-angiotensin system, fail to arrest this progressive injury in a significant number of patients. Early outgrowth cells (EOCs) represent a novel bone marrow-derived cell population that have been recently described to have tissue protective activity. In this work, we examined the effects of intravascular EOC infusion in two independent models of CKD, demonstrating potent anti-fibrotic renoprotective effects in the subtotally nephrectomized (SNX) rat, a well-established model of non-diabetic progressive CKD, and anti-fibrotic and anti-oxidant effects in the db/db mouse, a commonly used model of type 2 diabetic nephropathy. In the SNX rat, which is characterized by impaired cardiac relaxation reminiscent of a common and high risk clinical CKD phenotype, EOC infusion was also associated with improved cardiac structure and function. In both cases, infused EOCs were not retained in significant numbers within the diseased kidney or heart, but rather localized to distant organs such as the liver, spleen, and bone marrow. We further demonstrated that EOCs release soluble factors with anti-oxidant and anti-fibrotic activity in vitro, and that a cell-free preparation of EOC-derived factors can mimic the reno- and cardiac protective effects of the cells themselves when infused into the SNX rat. Taken together, our results demonstrate the therapeutic potential of an EOC-based strategy for the treatment of CKD and its cardiac complications, and provide the preclinical rationale for the design of clinical trials of EOC-based therapies for this devastating disease.

Indiana University-Purdue University Indianapolis (IUPUI)
Lithium-ion batteries are widely used for portable electronics due to high energy density, mature processing technology and reduced cost. However, their applications are somewhat limited by safety concerns. The lithium-ion battery users will take risks in burn or explosion which results from some internal components failure. So, a practical method is required urgently to find out the failures in early time. In this thesis, a new method based on temperature difference between internal point and surface (TDIS) of the battery is developed to detect the thermal failure especially the thermal runaway in early time. A lumped simple thermal model of a lithium-ion battery is developed based on TDIS. Heat transfer coefficients and heat capacity are determined from simultaneous measurements of the surface temperature and the internal temperature in cyclic constant current charging/discharging test. A look-up table of heating power in lithium ion battery is developed based on the lumped model and cyclic charging/discharging experimental results in normal operating condition. A failure detector is also built based on TDIS and reference heating power curve from the look-up table to detect aberrant heating power and bad parameters in transfer function of the lumped model. The TDIS method and TDIS detector is validated to be effective in thermal runaway detection in a thermal runway experiment. In the validation of thermal runway test, the system can find the abnormal heat generation before thermal runaway happens by detecting both abnormal heating power generation and parameter change in transfer function of thermal model of lithium ion batteries. The result of validation is compatible with the expectation of detector design. A simple and applicable detector is developed for lithium ion battery catastrophic failure detection.