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1.
Ann Am Thorac Soc ; 2024 Sep 05.
Artículo en Inglés | MEDLINE | ID: mdl-39236274

RESUMEN

ICU strain, characterized by a discrepancy between perceived or actual intensive care resources and demand, significantly impacts patient outcomes and healthcare worker well-being. The COVID-19 pandemic exacerbated ICU strain, leading to increased mortality and extended hospital stays, affecting both critically ill COVID-19 and non-COVID-19 patients. A systematic review identified 16 leading and lagging indicators of ICU capacity strain, including queuing, premature and after-hours ICU discharge, use of temporary space, length of stay, burnout, staffing and nurse-to-patient ratio, ICU census, acuity and turnover, standardized mortality ratio (SMR), readmissions, availability of critical supplies, ventilator use and surgery cancellation. However, variability in operational definitions and limited evidence regarding the reliability, validity, usability, and feasibility limit the value of single indicators for informed strategic planning and policy guidance. Regional and national policies and programs are essential to enhance real-time monitoring for effective management of critical care resources and mitigate the impact of ICU strain, facilitating complex interhospital transfers to reduce strain, and ensuring comprehensive strategies for enhancing ICU resilience. Proactive regional cooperation is advocated for policy formulation, knowledge exchange, and resource allocation to anticipate and mitigate ICU strain, ensuring equitable healthcare access during global health crises. The policy implications for future preparedness emphasize the importance of evidence-based triage and adaptable patient management strategies, alongside ethical considerations in resource allocation and the role of behavioral economic insights in optimizing resource utilization and collaborative healthcare practices. This multifaceted approach for addressing ICU strain comprehensively and effectively during pandemics would promote health equity and enhance healthcare system resilience under both routine operations and crisis conditions. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/).

2.
MDM Policy Pract ; 7(1): 23814683221099454, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35592271

RESUMEN

Background: Discordance with well-known sepsis resuscitation guidelines is often attributed to rational assessments of patients at the point of care. Conversely, we sought to explore the impact of choice architecture (i.e., the environment, manner, and behavioral psychology within which options are presented and decisions are made) on decisions to prescribe guideline-discordant fluid volumes. Design: We conducted an electronic, survey-based study using a septic shock clinical vignette. Physicians from multiple specialties and training levels at an academic tertiary-care hospital and academic safety-net hospital were randomized to distinct answer sets: control (6 fluid options), time constraint (6 fluid options with a 10-s limit to answer), or choice overload (25 fluid options). The primary outcome was discordance with Surviving Sepsis Campaign fluid resuscitation guidelines. We also measured response times and examined the relationship between each choice architecture intervention group, response time, and guideline discordance. Results: A total of 189 of 624 (30.3%) physicians completed the survey. Time spent answering the vignette was reduced in time constraint (9.5 s, interquartile range [IQR] 7.3 s to 10.0 s, P < 0.001) and increased in choice overload (56.8 s, IQR 35.9 s to 86.7 s, P < 0.001) groups compared with control (28.3 s, IQR 20.0 s to 44.6 s). In contrast, the relative risk of guideline discordance was higher in time constraint (2.07, 1.33 to 3.23, P = 0.001) and lower in choice overload (0.75, 0.60, to 0.95, P =0.02) groups. After controlling for time spent reading the vignette, the overall odds of choosing guideline-discordant fluid volumes were reduced for every additional second spent answering the vignette (OR 0.98, 0.97, to 0.99, P < 0.001). Conclusions: Choice architecture may affect fluid resuscitation decisions in sepsis regardless of patient conditions, warranting further investigation in real-world contexts. These effects should be considered when implementing practice guidelines. Highlights: Time constrained clinical decision making was associated with increased proportion of guideline-discordant responses and relative risk of failure to prescribe guideline-recommended intravenous fluids using a sepsis clinical vignette.Choice overload increased response times and was associated with decreased proportion of guideline-discordant responses and relative risk of guideline discordance.Physician odds of choosing to prescribe guideline-discordant fluid volumes were reduced with increased deliberation as measured by response times.Clinicians, researchers, policy makers, and administrators should consider the effect of choice architecture on clinical decision making and guideline discordance when implementing guidelines for sepsis and other acute care conditions.

3.
Crit Care Med ; 49(3): 490-502, 2021 03 01.
Artículo en Inglés | MEDLINE | ID: mdl-33405409

RESUMEN

OBJECTIVES: Prone position ventilation is a potentially life-saving ancillary intervention but is not widely adopted for coronavirus disease 2019 or acute respiratory distress syndrome from other causes. Implementation of lung-protective ventilation including prone positioning for coronavirus disease 2019 acute respiratory distress syndrome is limited by isolation precautions and personal protective equipment scarcity. We sought to determine the safety and associated clinical outcomes for coronavirus disease 2019 acute respiratory distress syndrome treated with prolonged prone position ventilation without daily repositioning. DESIGN: Retrospective single-center study. SETTING: Community academic medical ICU. PATIENTS: Sequential mechanically ventilated patients with coronavirus disease 2019 acute respiratory distress syndrome. INTERVENTIONS: Lung-protective ventilation and prolonged protocolized prone position ventilation without daily supine repositioning. Supine repositioning was performed only when Fio2 less than 60% with positive end-expiratory pressure less than 10 cm H2O for greater than or equal to 4 hours. MEASUREMENTS AND MAIN RESULTS: Primary safety outcome: proportion with pressure wounds by Grades (0-4). Secondary outcomes: hospital survival, length of stay, rates of facial and limb edema, hospital-acquired infections, device displacement, and measures of lung mechanics and oxygenation. Eighty-seven coronavirus disease 2019 patients were mechanically ventilated. Sixty-one were treated with prone position ventilation, whereas 26 did not meet criteria. Forty-two survived (68.9%). Median (interquartile range) time from intubation to prone position ventilation was 0.28 d (0.11-0.80 d). Total prone position ventilation duration was 4.87 d (2.08-9.97 d). Prone position ventilation was applied for 30.3% (18.2-42.2%) of the first 28 days. Pao2:Fio2 diverged significantly by day 3 between survivors 147 (108-164) and nonsurvivors 107 (85-146), mean difference -9.632 (95% CI, -48.3 to 0.0; p = 0·05). Age, driving pressure, day 1, and day 3 Pao2:Fio2 were predictive of time to death. Thirty-eight (71.7%) developed ventral pressure wounds that were associated with prone position ventilation duration and day 3 Sequential Organ Failure Assessment. Limb weakness occurred in 58 (95.1%) with brachial plexus palsies in five (8.2%). Hospital-acquired infections other than central line-associated blood stream infections were infrequent. CONCLUSIONS: Prolonged prone position ventilation was feasible and relatively safe with implications for wider adoption in treating critically ill coronavirus disease 2019 patients and acute respiratory distress syndrome of other etiologies.


Asunto(s)
COVID-19/complicaciones , Evaluación de Procesos y Resultados en Atención de Salud , Posicionamiento del Paciente , Respiración Artificial/métodos , Síndrome de Dificultad Respiratoria/terapia , Insuficiencia Respiratoria/terapia , Centros Médicos Académicos , Adulto , Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Posición Prona , Síndrome de Dificultad Respiratoria/etiología , Insuficiencia Respiratoria/etiología , Estudios Retrospectivos , Estados Unidos/epidemiología
4.
Crit Care ; 24(1): 25, 2020 01 28.
Artículo en Inglés | MEDLINE | ID: mdl-31992351

RESUMEN

RATIONALE: There remains significant controversy regarding the optimal approach to fluid resuscitation for patients in shock. The magnitude of care variability in shock resuscitation, the confounding effects of disease severity and comorbidity, and the relative impact on sepsis survival are poorly understood. OBJECTIVE: To evaluate usual care variability and determine the differential effect of observed and predicted fluid resuscitation volumes on risk-adjusted hospital mortality for mechanically ventilated patients in shock. METHODS: We performed a retrospective outcome analysis of mechanically ventilated patients admitted to intensive care units using the 2013 Premier Hospital Database (Premier, Inc.). Observed and predicted hospital mortality were evaluated by observed and predicted day 1 fluid administration, using the difference in predicted and observed outcomes to adjust for disease severity between groups. Both predictive models were validated using a second large administrative database (Truven Health Analytics Inc.). Secondary outcomes included duration of mechanical ventilation, hospital and ICU length of stay, and cost. RESULTS: Among 33,831 patients, observed hospital mortality was incrementally higher than predicted for each additional liter of day 1 fluid beginning at 7 L (40.9% vs. 37.2%, p = 0.008). Compared to patients that received expected (± 1.5 L predicted) day 1 fluid volumes, greater-than-expected fluid resuscitation was associated with increased risk-adjusted hospital mortality (52.3% vs. 45.0%, p < 0.0001) among all patients with shock and among a subgroup of shock patients with comorbid conditions predictive of lower fluid volume administration (47.1% vs. 41.5%, p < 0.0001). However, in patients with shock but without such conditions, both greater-than-expected (57.5% vs. 49.2%, p < 0.0001) and less-than-expected (52.1% vs. 49.2%, p = 0.037) day 1 fluid resuscitation were associated with increased risk-adjusted hospital mortality. CONCLUSIONS: Highly variable day 1 fluid resuscitation was associated with a non-uniform impact on risk-adjusted hospital mortality among distinct subgroups of mechanically ventilated patients with shock. These findings support closer evaluation of fluid resuscitation strategies that include broadly applied fluid volume targets in the early phase of shock resuscitation.


Asunto(s)
Fluidoterapia/métodos , Evaluación de Resultado en la Atención de Salud/estadística & datos numéricos , Choque/tratamiento farmacológico , Anciano , Anciano de 80 o más Años , Análisis de Varianza , Área Bajo la Curva , Femenino , Fluidoterapia/instrumentación , Fluidoterapia/normas , Humanos , Masculino , Persona de Mediana Edad , Curva ROC , Respiración Artificial/métodos , Resucitación/instrumentación , Resucitación/métodos , Resucitación/normas , Estudios Retrospectivos , Ajuste de Riesgo/métodos , Choque/fisiopatología
7.
J Mol Cell Cardiol ; 46(5): 739-47, 2009 May.
Artículo en Inglés | MEDLINE | ID: mdl-19233194

RESUMEN

Mutations in cardiac troponin T (TnT) are a cause of familial hypertrophic cardiomyopathy (FHC). Transgenic mice expressing a missense mutation (R92Q) or a splice site donor mutation (Trunc) in the cardiac TnT gene have mutation-specific phenotypes but mice of both models have smaller hearts compared to wild type and exhibit hemodynamic dysfunction. Because growth-related signaling pathways in the hearts of mice expressing TnT mutations are not known, we evaluated the impact of increased Akt or glycogen synthase kinase-3beta (GSK-3beta) activity in both mutant TnT mice; molecules that increase heart size via physiologic pathways and block pathologic growth, respectively. Expression of activated Akt dramatically augments heart size in both R92Q and Trunc mice; however, this increase in heart size is not beneficial, since Akt also increases fibrosis in both TnT mutants and causes some pathologic gene expression shifts in the R92Q mice. Activated GSK-3beta results in further decreases in left ventricular size in both R92Q and Trunc hearts, but this decrease is associated with significant mutation-specific phenotypes. Among many pathologic consequences, activating GSK-3beta in R92Q hearts decreases phosphorylation of troponin I and results in early mortality. In contrast, increased GSK-3beta activity in Trunc hearts does not significantly impact cardiac phenotypes. These findings demonstrate that increased Akt and its downstream target, GSK-3beta can impact both cardiac size and phenotype in a mutation-specific manner. Moreover, increased activity of these molecules implicated in beneficial cardiac phenotypes exacerbates the progression of disease in the R92Q TnT mutant.


Asunto(s)
Cardiomiopatía Hipertrófica Familiar/enzimología , Glucógeno Sintasa Quinasa 3/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Transducción de Señal , Sustitución de Aminoácidos , Animales , Peso Corporal , Cardiomiopatía Hipertrófica Familiar/genética , Activación Enzimática , Regulación de la Expresión Génica , Glucógeno Sintasa Quinasa 3 beta , Ventrículos Cardíacos/enzimología , Ventrículos Cardíacos/patología , Hipertrofia/genética , Masculino , Ratones , Ratones Mutantes , Mutación/genética , Miocardio/patología , Tamaño de los Órganos , Fenotipo , Fosforilación , Análisis de Supervivencia , Troponina T/metabolismo
8.
Am J Physiol Heart Circ Physiol ; 292(2): H838-45, 2007 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-17012357

RESUMEN

Mutations in myosin heavy chain (MyHC) can cause hypertrophic cardiomyopathy (HCM) that is characterized by hypertrophy, histopathology, contractile dysfunction, and sudden death. The signaling pathways involved in the pathology of HCM have not been elucidated, and an unresolved question is whether blocking hypertrophic growth in HCM may be maladaptive or beneficial. To address these questions, a mouse model of HCM was crossed with an antihypertrophic mouse model of constitutive activated glycogen synthase kinase-3beta (caGSK-3beta). Active GSK-3beta blocked cardiac hypertrophy in both male and female HCM mice. However, doubly transgenic males (HCM/GSK-3beta) demonstrated depressed contractile function, reduced sarcoplasmic (endo) reticulum Ca(2+)-ATPase (SERCA) expression, elevated atrial natriuretic factor (ANF) expression, and premature death. In contrast, female HCM/GSK-3beta double transgenic mice exhibited similar cardiac histology, function, and survival to their female HCM littermates. Remarkably, dietary modification from a soy-based diet to a casein-based diet significantly improved survival in HCM/GSK-3beta males. These findings indicate that activation of GSK-3beta is sufficient to limit cardiac growth in this HCM model and the consequence of caGSK-3beta was sexually dimorphic. Furthermore, these results show that blocking hypertrophy by active GSK-3beta in this HCM model is not therapeutic.


Asunto(s)
Cardiomiopatía Hipertrófica/metabolismo , Cardiomiopatía Hipertrófica/fisiopatología , Glucógeno Sintasa Quinasa 3/metabolismo , Cadenas Pesadas de Miosina/metabolismo , Remodelación Ventricular , Actinas/metabolismo , Animales , Factor Natriurético Atrial/metabolismo , Proteínas de Unión al Calcio/metabolismo , Cardiomiopatía Hipertrófica/dietoterapia , Cardiomiopatía Hipertrófica/patología , Cruzamientos Genéticos , Proteínas en la Dieta/administración & dosificación , Modelos Animales de Enfermedad , Femenino , Fibrosis , Glucógeno Sintasa Quinasa 3/genética , Glucógeno Sintasa Quinasa 3 beta , Ventrículos Cardíacos/metabolismo , Ventrículos Cardíacos/fisiopatología , Estimación de Kaplan-Meier , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Transgénicos , Mutación , Contracción Miocárdica , Cadenas Pesadas de Miosina/genética , Fosforilación , ARN Mensajero/metabolismo , ATPasas Transportadoras de Calcio del Retículo Sarcoplásmico/metabolismo , Factores Sexuales , Factores de Tiempo
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