ObjectivesThere has been little research conducted to understand the essential meaning of quality, community-based, end-of-life (EOL) care, despite the expansion of these services. The purpose of this study was to define what matters most for EOL care from the perspective of a diverse range of palliative care providers in the community who have daily encounters with death and dying.MethodsWe used interviews to explore the perceptions of providers and administrators from 14 specialised palliative care teams in Ontario, Canada. Participants were prompted with the question ‘What matters most for EOL care?’ Responses were analysed using a phenomenological approach to derive themes depicting the universal essence of EOL care.ResultsData from 107 respondents were obtained and analysed, from which 40 formulated concepts emerged; these were further grouped into 9 themes. Of the respondents, 39% were nurses, 19% physicians, 27% were supervisors or executives and 15% other. The most predominate concept was that Patient's Wishes are Fulfilled, cited by almost half the respondents. The most prominent themes were Addressing the Non-physical Needs, Healthcare Teams’ Nature of Palliative Care Delivery, Patient Wishes are Honoured, Addressing the Physical Needs, Preparing for and Accepting Death, Communication and Relationship Development, and Involving and Supporting the Family.Conclusions9 critical domains of EOL care evolved from the interviews, indicating that quality EOL care extends beyond managing physical pain, but includes a holistic perspective of care, a healthcare team dedicated to the EOL journey and a patient-centred pathway. Tailoring the provision of care to consider these important elements plays a critical role in supporting a positive EOL experience for patients and families.

We investigated the effects of reducing sarcoplasmic reticular (SR) Ca(2+) stores using the Ca(2+)-ATPase inhibitor cyclopiazonic acid (CPA) in Langendorff-perfused mouse hearts exposed to different pro-arrhythmic agents all known to produce Ca(2+)-mediated arrhythmogenesis. CPA (100 and 150 nM) produced progressive (beginning over approximately 1 min) and significant (P<0.0001) reductions in peak amplitudes of Ca(2+) transients evoked by regular stimulation in isolated Fluo-3 loaded myocytes from F/F(0)=3.2+/-0.16 (n=12 cells) to 1.62+/-0.012 (n=6 cells) and 1.53+/-0.06 (n=12 cells), respectively, consistent with previous reports describing reductions of store Ca(2+) in other cell systems. The corresponding effects of CPA were then examined in intact hearts exposed to isoproterenol (100 nM), elevated extracellular [Ca(2+)] (5mM) and caffeine (1mM). All three agents produced ventricular tachycardia either when added alone or simultaneously with CPA during programmed electrical stimulation. However, arrhythmogenicity was not observed when such agents were added approximately 10 min after introduction of CPA. CPA thus antagonized this Ca(2+)-mediated arrhythmogenesis but only under circumstances of SR Ca(2+) depletion. These alterations in arrhythmogenic tendency took place despite an absence of alterations in electrogram and monophasic action potential characteristics. This was in sharp contrast to previous observations in murine, DeltaKPQ-Scn5a (LQT3) and KCNE1(-/-) (LQT5), systems where re-entry has been implicated in arrhythmogenesis.