Involving relatives in ICU patient care: Critical care nursing challenges

Aims and objectives: To identify the barriers critical care nurses experience to relative involvement in intensive care unit patient care. Background: Previous studies have discussed the experiences of relatives visiting an intensive care unit, the needs of relatives in the intensive care environment, critical care nurse and relative interaction, intensive care unit visiting policies and the benefits of including relatives in patient care. The barriers that critical care nurses experience to relative involvement in patient care have received minimal exploration. Design: Critical care nurses were recruited for a mixed methods study. An explanatory mixed method design was used, with two phases. Phase 1 was Quantitative and Phase 2 was Qualitative. Methods: Data collection occurred over five months in 2012-2013. Phase 1 used an online questionnaire (n = 70), and semi-structured interviews (n = 6) were conducted in Phase 2. Phase 1 participants were 70 critical care nurses working in Australian intensive care units and six critical care nurses were recruited from a single Sydney intensive care unit for Phase 2. Through sequential data collection, Phase 1 results formed the development of Phase 2 interview questions. Results: Participants reported various barriers to relative involvement in critically ill patient care. Factors related to the intensive care unit patient, the intensive care unit relative, the critical care nurse and the intensive care environment contributed to difficulties encompassing relative involvement. Conclusions: This study has identified that when considering relative involvement in patient care, critical care nurses take on a paternalistic role. The barriers experienced to relative involvement result in the individual critical care nurse deciding to include or exclude relatives from patient care. Relevance to clinical practice: Knowledge of the barriers to relative involvement in critically ill patient care may provide a basis for improving discussion on this topic and may assist intensive care units to implement strategies to reduce barriers

Go Co-op: recent cases of Irish co-operative start-ups

This project aims to raise awareness of the role of co-operatives in Ireland and the practicalities involved in their establishment. This is achieved by means of detailing five case studies of new/emerging co-operatives. The focus of the case studies is on the motivations and experiences of these new co-operatives including factors facilitating and/or hindering their development. Cases cover a range of geographical locations, both urban and rural and a range of sectors from agri-food to retailing to environmental sustainability. It is hoped that the cases will be of benefit to: Individuals/groups wishing to establish a co-operative, whether in terms of inspiration or by way of practical example; Educators and researchers in need of relevant case studies to demonstrate the roles and practicalities as well as policy issues pertaining to co-operative development; Representative/apex bodies involved in the establishment and development of co-operatives. The co-operatives featured are: Aran Islands Energy; Co-operative/ Comharchumann Fuinnimh Oileáin Árann Teoranta; Donegal Woodland; Owners Co-operative: Ring of Kerry Quality; Lamb Co-operative; Courtmacsherry; Community Shop; Third Space Co-operative

Kruppel-like factor 15 is required for the cardiac adaptive response to fasting.

Cardiac metabolism is highly adaptive in response to changes in substrate availability, as occur during fasting. This metabolic flexibility is essential to the maintenance of contractile function and is under the control of a group of select transcriptional regulators, notably the nuclear receptor family of factors member PPARα. However, the diversity of physiologic and pathologic states through which the heart must sustain function suggests the possible existence of additional transcriptional regulators that play a role in matching cardiac metabolism to energetic demand. Here we show that cardiac KLF15 is required for the normal cardiac response to fasting. Specifically, we find that cardiac function is impaired upon fasting in systemic and cardiac specific Klf15-null mice. Further, cardiac specific Klf15-null mice display a fasting-dependent accumulation of long chain acylcarnitine species along with a decrease in expression of the carnitine translocase Slc25a20. Treatment with a diet high in short chain fatty acids relieves the KLF15-dependent long chain acylcarnitine accumulation and impaired cardiac function in response to fasting. Our observations establish KLF15 as a critical mediator of the cardiac adaptive response to fasting through its regulation of myocardial lipid utilization

National Audit of Hospital Mortality Annual Report 2019

This report shows that there has been a continuing decrease in crude mortality trends for AMI, haemorrhagic stroke, pneumonia and heart failure over the past 10 years. However, ischaemic stroke and COPD have seen an increase in mortality rates in 2019 compared with 2018. Hospitals and Hospital Groups continue to engage with NOCA around statistical outliers, and we thank them for their time and commitment to sharing their learnings in this report. The global COVID-19 pandemic has impacted on this fifth National Audit of Hospital Mortality Annual Report. Although data for 2019 continued to be collated and coded in the local HIPE offices, closure of the HIPE national file for 2019 was delayed by 1 month. The bigger impact, however, was on work which was planned to be carried out during the first half of 2020. As the virus continues to impact our society and businesses, NAHM is planning to release data to the NQAIS NAHM web-based tool in late 2020 with the inclusion of a flag to identify COVID-19 cases. The data for the National Audit of Hospital Mortality Annual Report 2020 will be more significantly impacted, and NAHM will continue to make efforts to ensure that meaningful data are produced in the NQAIS NAHM tool for 2020. NAHM has worked with stakeholders throughout the year, taking on board responses to issues as they arose. Work is planned for 2021 to analyse those hospitals which have been excluded from this public report due to the inclusion criteria for diagnoses. NAHM wishes to acknowledge the challenges faced by all contributors in writing this report; it could not have been written without the efforts of all staff in hospitals and HIPE offices nationwide. Thanks in particular go to members of the NAHM Report Writing Group, who have given up their time and shared their knowledge in the writing of this report.</p

Cardiac specific deletion of KLF15 alters lipid profile.

<p>Metabolomic analysis of long chain acylcarnitines in cardiac tissue from control (MHC-Cre) vs. KLF15-cKO with and without 48 hour fast, (n = 5), *P<0.05 by one-way analysis of variance (ANOVA) with the Tukey post hoc test.</p

Short-chain diet rescues the KLF15-dependent attenuation of cardiac function in response to fasting.

<p>(A) qPCR analysis of expression of transporter genes in MHC-Cre vs. KLF15-cKO under fed vs. 48 hour fasting conditions. *P<0.05 vs. Cre Fed, **P<0.05 vs. CKO Fed, # P<0.05 vs. Cre Fast. Values normalized to <i>Ppib</i>. (B) <i>Slc25a20</i> expression (qPCR) in MHC-Cre vs. KLF15-cKO under fed vs. 48 hour fasting conditions. *P<0.05 vs. Cre Fed, **P<0.05 vs. CKO Fed, # P<0.05 vs. Cre Fast. Values normalized to <i>Ppib</i>. (C) Western blot analysis of CACT levels in MHC-Cre vs KLF15-cKO under fed and 48 hour fasting conditions. α-tubulin used as loading control. (D) Quantification of data in C (n = 3 per group). Two-tailed Student's <i>t</i>-test for unpaired data was used. *P<0.05. (E) Left ventricular fractional shortening from echocardiography performed in control (MHC-Cre) vs. KLF15-cKO under fed vs. 48 hours fasting conditions following 10 weeks of short-chain fatty acid diet, (n = 10). (F) Representative echocardiography image from MHC-Cre vs. KLF15-cKO following 48 hours fasting and 10 weeks of short-chain fatty acid diet. (G) Tabular representation of echocardiography data in MHC-Cre vs. KLF15-cKO under fed vs. 48 hour fasting conditions following 10 weeks of short-chain fatty acid diet.</p

Cardiac specific deletion of KLF15 alters tissue and plasma levels of free fatty acids and triglycerides.

<p>Cardiac FFA (A) and TG (B) levels in control (MHC-Cre) vs. KF15-cKO following 48 hours fasting, (n = 5), *P<0.05 vs. Cre Fed, **P<0.05 vs. CKO Fed, # P<0.05 vs. Cre Fast. Plasma FFA (C) and TG (D) levels in control (MHC-Cre) vs. KLF15-cKO following 48 hours fasting, (n = 5), *P<0.05 vs. Cre Fed, **P<0.05 vs. CKO Fed, # P<0.05 vs. Cre Fast.</p

Cardiac KLF15 is required for the heart’s functional adaptation in response to fasting.

<p>(A) Left ventricular fractional shortening from echocardiography performed in control (MHC-Cre) vs KLF15-cKO under fed vs. 48 hours fasting conditions, (n = 5), *P<0.05 vs. MHC-Cre Fast. (B) Representative echocardiography image from MHC-Cre vs. KLF15-cKO following a 48 hour fast. (C) Tabular representation of echocardiography data in MHC-Cre vs. KLF15-cKO under fed vs. 48 hour fasting conditions.</p

Systemic KLF15 is required for the heart’s functional adaptation in response to fasting.

<p>(A) Left ventricular fractional shortening from echocardiography performed in wild-type (WT) vs. systemic <i>Klf15</i>-null (<i>Klf15-/-</i>) under fed vs. 48 hours fasting conditions, (n = 5), *P,0.05 vs. WT Fast. (B) Representative echocardiography image from WT vs. <i>Klf15-/-</i> following a 48 hour fast. (C) Tabular representation of echocardiography data in WT vs. <i>Klf15-/-</i> under fed vs. 48 hour fasting conditions.</p

Change in long chain acylcarnitine profiles after loss of cardiac KLF15 expression.

<p>Change in long chain acylcarnitine profiles after loss of cardiac KLF15 expression.</p