BackgroundShared medical appointments (SMAs) are doctor-patient visits in which groups of patients are seen by one or more health care providers in a concurrent session. There is a growing interest in understanding the potential benefits of SMAs in various contexts to improve clinical outcomes and reduce healthcare costs. This study builds upon the existing evidence base that suggests SMAs are indeed effective. In this study, we explored how they are effective in terms of the underlying mechanisms of action and under what circumstances.MethodsRealist review methodology was used to synthesize the literature on SMAs, which included a broad search of 800+ published articles. 71 high quality primary research articles were retained to build a conceptual model of SMAs and 20 of those were selected for an in depth analysis using realist methodology (i.e.,middle-range theories and and context-mechanism-outcome configurations).ResultsNine main mechanisms that serve to explain how SMAs work were theorized from the data immersion process and configured in a series of context-mechanism-outcome configurations (CMOs). These are: (1) Group exposure in SMAs combats isolation, which in turn helps to remove doubts about one’s ability to manage illness; (2) Patients learn about disease self-management vicariously by witnessing others’ illness experiences; (3) Patients feel inspired by seeing others who are coping well; (4) Group dynamics lead patients and providers to developing more equitable relationships; (5) Providers feel increased appreciation and rapport toward colleagues leading to increased efficiency; (6) Providers learn from the patients how better to meet their patients’ needs; (7) Adequate time allotment of the SMA leads patients to feel supported; (8) Patients receive professional expertise from the provider in combination with first-hand information from peers, resulting in more robust health knowledge; and (9) Patients have the opportunity to see how the physicians interact with fellow patients, which allows them to get to know the physician and better determine their level of trust.ConclusionsNine overarching mechanisms were configured in CMO configurations and discussed as a set of complementary middle-range programme theories to explain how SMAs work. It is anticipated that this innovative work in theorizing SMAs using realist review methodology will provide policy makers and SMA program planners adequate conceptual grounding to design contextually sensitive SMA programs in a wide variety of settings and advance an SMA research agenda for varied contexts.

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Intermittent hypoxia (IH) resulting from sleep apnea can lead to pulmonary hypertension (PH) and right heart failure, similar to chronic sustained hypoxia (CH). Supplemental CO(2), however, attenuates hypoxic PH. We therefore hypothesized that, similar to CH, IH elicits PH and associated increases in arterial endothelial nitric oxide synthase (eNOS) expression, ionomycin-dependent vasodilation, and receptor-mediated pulmonary vasoconstriction. We further hypothesized that supplemental CO(2) inhibits these responses to IH. To test these hypotheses, we measured eNOS expression by Western blot in intrapulmonary arteries from CH (2 wk, 0.5 atm), hypocapnic IH (H-IH) (3 min cycles of 5% O(2)/air flush, 7 h/day, 2 wk), and eucapnic IH (E-IH) (3 min cycles of 5% O(2), 5% CO(2)/air flush, 7 h/day, 2 wk) rats and their respective controls. Furthermore, vasodilatory responses to the calcium ionophore ionomycin and vasoconstrictor responses to the thromboxane mimetic U-46619 were measured in isolated saline-perfused lungs from each group. Hematocrit, arterial wall thickness, and right ventricle-to-total ventricle weight ratios were additionally assessed as indexes of polycythemia, arterial remodeling, and PH, respectively. Consistent with our hypotheses, E-IH resulted in attenuated polycythemia, arterial remodeling, RV hypertrophy, and eNOS upregulation compared with H-IH. However, in contrast to CH, neither H-IH nor E-IH increased ionomycin-dependent vasodilation. Furthermore, H-IH and E-IH similarly augmented U-46619-induced pulmonary vasoconstriction but to a lesser degree than CH. We conclude that maintenance of eucapnia decreases IH-induced PH and upregulation of arterial eNOS. In contrast, increases in pulmonary vasoconstrictor reactivity following H-IH are unaltered by exposure to supplemental CO(2).

The purpose of this review was to summarize the findings of published reports that investigated quality-related outcomes and emergency department (ED) crowding. Of 276 data-based articles, 23 reported associations between patient outcomes and crowding. These articles were grouped into 3 categories: delay in treatment, decreased satisfaction, and increased mortality. Although these studies suggest that crowding results in poor outcomes, it is possible that other factors such as nursing care contribute to these adverse outcomes. Nursing care has been shown to contribute to both positive and negative patient outcomes in other settings. Building an understanding of how ED crowding affects the practice of the emergency nurse is essential to examining how nursing care, surveillance, and communication impact outcomes of emergency patients. Investigation into nurse-sensitive quality indicators in the ED has potential to develop strategies that deliver high quality of care, regardless of crowded conditions.