The systematic approach to improving care for Frail Older Patients (SAFE) study: A protocol for co-designing a frail older person's pathway.

Background: Frailty is the age-accelerated decline across multiple organ systems which leads to vulnerability to poor resolution of homeostasis after a stressor event. This loss of reserve means that a minor illness can result in a disproportionate loss of functional ability. Improving acute care for frail older patients is now a national priority and an important aspect of the National Programme for Older People in Ireland. Evidence suggests that an interdisciplinary approach incorporating rapid comprehensive geriatric assessment and early intervention by an interdisciplinary team can reduces susceptibility to hospitalisation related functional decline. The aim of the Systematic Approach to Improving Care for Frail Older Patients (SAFE) is to develop and explore the process of implementing a model of excellence in the delivery of patient-centred integrated care within the context of frail older people's acute admissions. Methods: The SAFE study will employ a mixed methodology approach, including a rapid realist review of the current literature alongside a review of baseline data for older people attending the emergency department. Semi-structured interviews will be undertaken to document the current pathway. The intervention processes and outcomes will be jointly co-designed by a patient and public involvement (PPI) group together with the interdisciplinary healthcare professionals from hospital, community and rehabilitation settings. Successive rounds of Plan-Do-Study-Act cycles will then be undertaken to test and refine the pathway for full implementation. Discussion: This research project will result in a plan for implementing an integrated, patient-centred pathway for acute care of the frail older people which has been tested in the Irish setting. During the process of development, each element of the new pathway will be tested in turn to ensure that patient centred outcomes are being realised. This will ensure the resulting model of care is ready for implementation in the context of the Irish health service.

The accuracy of anatomical landmarks for locating the carotid sinus.

BACKGROUND: carotid sinus massage (CSM) is a valuable clinical test for carotid sinus syndrome (CSS) and relies on accurately locating the carotid sinus (CS). OBJECTIVE: in this study, we sought to examine the accuracy of using anatomical landmarks for locating the CS. METHODS: consecutive patients (n = 20) were recruited prospectively. Two clinicians, trained in CSM, were asked to locate the CS using anatomical landmarks. A point on the skin overlying the CS was then marked by a vascular technician using ultrasound. Accuracy of techniques was compared using intra-class correlation coefficients and Bland-Altman statistics. RESULTS: anatomical landmarks underestimated the CS location by 1.5 ± 1.3 cm. Error extremes ranged from 4 cm below to 2 cm above CS using anatomical landmarks. A moderate correlation between ultrasound and anatomical landmarks was found, r = 0.371 (P = 0.031). CONCLUSION: this is the first study to characterise the accuracy of standard anatomical landmarks used in CSM. Results suggest that the point of maximal pulsation has the lowest associated error. Future work should examine CSM yield across this and a range of other methodological factors.

Walking the cognitive "minefield" between high and low blood pressure.

Vascular risk factors are implicated in the pathogenesis of Alzheimer's disease (AD). There is an age-dependent relationship between blood pressure and the risk of AD. Given the potential temporal lag that can exist between the two conditions, longitudinal population studies offer the best opportunity to identify a causal relationship. Midlife hypertension increases the risk for AD, yet later-life hypertension does not appear to confer the same risk and may in fact be protective. Low diastolic blood pressure, especially in later-life, is associated with an increased risk of AD. Orthostatic hypotension and other neurocardiovascular syndromes may increase the risk for cognitive impairment and AD. Several physiopathological mechanisms may contribute to this increased risk. Dynamic blood pressure changes and impaired cerebrovascular autoregulation may result in cerebral hypoperfusion. Hypertensive patients also develop cerebral infarcts, resulting in diminished perfusion. Subsequent hypoxia driven pathways result in increased cerebral amyloid-ß and phosphorylated tau protein accumulation. Treatment of elevated blood pressure with antihypertensive medications attenuates the risk of AD attributable to elevated midlife hypertension. Certain antihypertensive compounds have neuroprotective properties that may reduce the risk of AD, independent of their effects on blood pressure.

Parasympathetic autonomic dysfunction is common in mild cognitive impairment.

Components of the central autonomic network attract the greatest neurofibrillary degeneration and related cell death during the course of Alzheimer's disease (AD). The insular cortex and brainstem are affected from the early stages of disease. Acetylcholine, the main neurotransmitter of the parasympathetic system may be deficient in mild cognitive impairment (MCI). Hence, autonomic dysfunction may be a novel biomarker of neurodegeneration. Autonomic function was examined in 97 MCI participants and 36 controls using beside cardiovascular reflex tests and heart rate variability. The association between dysautonomia and neuropsychiatric deficits was examined. This observational study was conducted in a clinical setting. MCI participants showed significant parasympathetic deficits in bedside cardiovascular reflex tests and heart rate variability compared with controls. Those with more significant autonomic dysfunction had more severe neuropsychological deficits. MCI participants were 5.60 (95% confidence interval, 1.6-27.2) times more likely than a control to have autonomic dysfunction. Autonomic dysfunction, particularly parasympathetic dysfunction is prevalent in MCI. This may be due to early neuroanatomical and neurochemical changes in the central autonomic network in Alzheimer's disease. This may accelerate cognitive decline via proinflammatory mechanisms and/or hypotension-induced cerebral hypoperfusion. This provides insight into the pathophysiological mechanisms that contribute to cognitive decline, and may lead to the development of effective therapeutic interventions.