Heart Failure Transition of Care: An Educational Program for Nurses

Heart failure (HF) is becoming an epidemic as people are living longer and surviving cardiovascular events. According to the 2015 to 2018 data the American Heart Association estimates 6 million American adults aged twenty or older are living with HF (AHA, 2021). Heart failure is the nation\u27s leading 30-day readmission diagnosis costing the nation an estimated $30.7 billion according to the Division of Heart Disease and Stroke Prevention. Heart failure is a chronic progressive disease that if not managed correctly will lead to increased morbidity and decreased quality of life. A review of the literature on transition of care frameworks for HF patients validated the most effective interventions and best practices to reduce hospitalization in patients with heart failure. Nurses need to possess knowledge of heart failure care best practices to optimize patient outcomes. The purpose of this quality improvement project was to determine if implementation of a Heart Failure Transition of Care education program increased nurses’ knowledge of heart failure and heart failure transition of care best practices. The results of the educational program demonstrated improvement in nurses\u27 knowledge in all three categories; Heart failure facts and pathophysiology, best practice nursing interventions, and Heart failure assessment and goal directed medical therapy

Heart Failure Transition of Care: An Educational Program for Nurses

Heart failure (HF) is becoming an epidemic as people are living longer and surviving cardiovascular events. According to the 2015 to 2018 data the American Heart Association estimates 6 million American adults aged twenty or older are living with HF (AHA, 2021). Heart failure is the nation\u27s leading 30-day readmission diagnosis costing the nation an estimated $30.7 billion according to the Division of Heart Disease and Stroke Prevention. Heart failure is a chronic progressive disease that if not managed correctly will lead to increased morbidity and decreased quality of life. A review of the literature on transition of care frameworks for HF patients validated the most effective interventions and best practices to reduce hospitalization in patients with heart failure. Nurses need to possess knowledge of heart failure care best practices to optimize patient outcomes. The purpose of this quality improvement project was to determine if implementation of a Heart Failure Transition of Care education program increased nurses’ knowledge of heart failure and heart failure transition of care best practices. The results of the educational program demonstrated improvement in nurses\u27 knowledge in all three categories; Heart failure facts and pathophysiology, best practice nursing interventions, and Heart failure assessment and goal directed medical therapy

Regulation of macrophage polarization and plasticity by complex activation signals

Macrophages are versatile cells of the immune system that play an important role in both advancing and resolving inflammation. Macrophage activation has been described as a continuum, and different stimuli lead to M1, M2, or mixed phenotypes. In addition, macrophages expressing markers associated with both M1 and M2 function are observed in vivo. Using flow cytometry, we examine how macrophage populations respond to combined M1 and M2 activation signals, presented either simultaneously or sequentially. We demonstrate that macrophages exposed to a combination of LPS, IFN-γ, IL-4, and IL-13 acquire a mixed activation state, with individual cells expressing both M1 marker CD86 and M2 marker CD206 instead of polarizing to discrete phenotypes. Over time, co-stimulated macrophages lose expression of CD86 and display increased expression of CD206. In addition, we find that exposure to LPS/IFN-γ potentiates the subsequent response to IL-4/IL-13, whereas pre-polarization with IL-4/IL-13 inhibits the response to LPS/IFN-γ. Mathematical modeling of candidate regulatory networks indicates that a complex inter-dependence of M1- and M2-associated pathways underlies macrophage activation. Specifically, a mutual inhibition motif was not by itself sufficient to reproduce the temporal marker expression data; incoherent feed-forward of M1 activation as well as both inhibition and activation of M2 by M1 were required. Together these results corroborate a continuum model of macrophage activation and demonstrate that phenotypic markers evolve with time and with exposure to complex signals