Implementation of an interdisciplinary tracheostomy care protocol to decrease rates of tracheostomy-related pressure ulcers and injuries.

OBJECTIVES: Tracheostomy-related pressure injuries (TRPI) have been demonstrated to occur in approximately 10% of tracheostomy patients. In this study, we present TRPI outcomes after implementation of a standardized tracheostomy care protocol. METHODS: A tracheostomy care protocol was developed by an interdisciplinary quality improvement program and implemented on July 1, 2016. The protocol was designed to minimize factors that contribute to the development of TRPI. Rates of TRPI over the subsequent 20 months were compared to the year before implementation. RESULTS: 9 out of 85 patients (10.6%) developed TRPI in the pre-protocol cohort compared to 0 of 137 (0%) in the post-protocol cohort, which was a statistically significant decrease by Fisher's exact test with a p-value of 0.0001. Pearson's correlation coefficient demonstrated a negative correlation between age and post-operative day of diagnosis (r = -0.641, p = 0.063), indicating that older patients develop TRPI more quickly. CONCLUSIONS: Interdisciplinary peri-operative tracheostomy care protocols can be effective in decreasing rates of TRPI.

Team-Based Intervention to Reduce the Impact of Nonactionable Alarms in an Adult Intensive Care Unit.

BACKGROUND: Nonactionable alarms comprise over 70% of alarms and contribute a threat to patient safety. Few studies have reported approaches to translate and sustain these interventions in clinical settings. PURPOSE: This study tested whether an interprofessional team-based approach can translate and implement effective alarm reduction interventions in the adult intensive care unit. METHODS: The study was a prospective, cohort, pre- and postdesign with repeated measures at baseline (preintervention) and post-phase I and II intervention periods. The settings for the most prevalent nonactionable arrhythmia and bedside parameter alarms were adjusted during phases I and II, respectively. RESULTS: The number of total alarms was reduced by 40% over a 14-day period after both intervention phases were implemented. The most prevalent nonactionable parameter alarms decreased by 47% and arrhythmia alarms decreased by 46%. CONCLUSIONS: It is feasible to translate and sustain system-level alarm management interventions addressing alarm fatigue using an interprofessional team-based approach.

Early versus delayed percutaneous coronary intervention for patients with non-ST segment elevation acute coronary syndrome: a meta-analysis of randomized controlled clinical trials.

BACKGROUND: Studies assessing the timing of percutaneous coronary interventions (PCI) in patients with Non-ST segment elevation Acute Coronary Syndromes (NSTE-ACS) have failed to generate a consensus on how early PCI should be performed in such patients. PURPOSE: This meta-analysis compares clinical outcomes at 30 days in NSTE-ACS patients undergoing PCI within 24 hours of presentation (early PCI) with those receiving PCI more than 24 hours after presentation (delayed PCI). DATA SOURCES: Data were extracted from searches of MEDLINE (1990-2010) and Google scholar and from scrutiny of abstract booklets from major cardiology meetings (1990-2010). STUDY SELECTION: Randomized clinical trials (RCTs) that included the composite endpoint of death and non-fatal myocardial infarction (MI) at 30 days after PCI were considered. DATA EXTRACTION: Two independent reviewers extracted data using standard forms. The effects of early and delayed PCI were analyzed by calculating pooled estimates for death, non-fatal MI, bleeding, repeat revascularization and the composite endpoint of death or non-fatal MI at 30 days. Univariate analysis of each of these variables was used to create odds ratios. DATA SYNTHESIS: Seven studies with a total of 13,762 patients met the inclusion criteria. There was no significant difference in the odds of the composite endpoint of death or non-fatal MI at 30 days between patients undergoing early PCI and those receiving delayed PCI (OR-0.83, 95%CI 0.62-1.10). Patients receiving delayed PCI experienced a 33% reduction in the odds of repeat revascularization at 30 days compared to those undergoing early PCI (OR-1.33, 95%CI 1.14-1.56, P=0.0004).Conversely, patients undergoing early PCI experienced lower odds of bleeding than those receiving delayed PCI (OR-0.76, 95%CI 0.63-0.91, P = 0.0003). CONCLUSIONS: In NSTE-ACS patients early PCI doesn't reduce the odds of the composite endpoint of death or non-fatal MI at 30 day. This strategy is associated with lower odds of bleeding and higher odds of repeat revascularization at 30 days than a strategy of delayed PCI.

Adiponectin abates diabetes-induced endothelial dysfunction by suppressing oxidative stress, adhesion molecules, and inflammation in type 2 diabetic mice.

Adiponectin (APN) can confer protection against metabolism-related illnesses in organs such as fat, the liver, and skeletal muscle. However, it is unclear whether APN improves endothelial-dependent nitric oxide-mediated vasodilation in type 2 diabetes and, if so, by what mechanism. We tested whether exogenous APN delivery improves endothelial function in type 2 diabetic mice and explored the mechanisms underlying the observed improvement. To test the hypothesis, we injected adenovirus APN (Ad-APN) or adenovirus ß-galactosidase (Ad-ßgal; control virus) via the tail vein in control (m Lepr(db)) and diabetic (Lepr(db); db/db) mice and studied vascular function of the aorta ex vivo. Ad-APN improved endothelial-dependent vasodilation in db/db mice compared with Ad-ßgal, whereas Ad-APN had no further improvement on endothelial function in control mice. This improvement was completely inhibited by a nitric oxide synthase inhibitor (N(G)-nitro-l-arginine methyl ester). Serum triglyceride and total cholesterol levels were increased in db/db mice, and Ad-APN significantly reduced triglyceride levels but not total cholesterol levels. Immunoblot results showed that interferon-γ, gp91(phox), and nitrotyrosine were markedly increased in the aorta of db/db mice. Ad-APN treatment decreased the expression of these proteins. In addition, mRNA expression of TNF-α, IL-6, and ICAM-1 was elevated in db/db mice, and Ad-APN treatment decreased these expressions in the aorta. Our findings suggest that APN may contribute to an increase in nitric oxide bioavailability by decreasing superoxide production as well as by inhibiting inflammation and adhesion molecules in the aorta in type 2 diabetic mice.

The link between metabolic abnormalities and endothelial dysfunction in type 2 diabetes: an update.

Despite abundant clinical evidence linking metabolic abnormalities to diabetic vasculopathy, the molecular basis of individual susceptibility to diabetic vascular complications is still largely undetermined. Endothelial dysfunction in diabetes-associated vascular complications is considered an early stage of vasculopathy and has attracted considerable research interests. Type 2 diabetes is characterized by metabolic abnormalities, such as hyperglycemia, excess liberation of free fatty acids (FFA), insulin resistance and hyperinsulinemia. These abnormalities exert pathological impact on endothelial function by attenuating endothelium-mediated vasomotor function, enhancing endothelial apoptosis, stimulating endothelium activation/endothelium-monocyte adhesion, promoting an atherogenic response and suppressing barrier function. There are multiple signaling pathways contributing to the adverse effects of glucotoxicity on endothelial function. Insulin maintains the normal balance for release of several factors with vasoactive properties. Abnormal insulin signaling in the endothelium does not affect the whole-body glucose metabolism, but impairs endothelial response to insulin and accelerates atherosclerosis. Excessive level of FFA is implicated in the pathogenesis of insulin resistance. FFA induces endothelial oxidative stress, apoptosis and inflammatory response, and inhibits insulin signaling. Although hyperglycemia, insulin resistance, hyperinsulinemia and dyslipidemia independently contribute to endothelial dysfunction via various distinct mechanisms, the mutual interactions may synergistically accelerate their adverse effects. Oxidative stress and inflammation are predicted to be among the first alterations which may trigger other downstream mediators in diabetes associated with endothelial dysfunction. These mechanisms may provide insights into potential therapeutic targets that can delay or reverse diabetic vasculopathy.

Cardiovascular mortality in dialysis patients.

In their broad spectrum, cardiovascular diseases are, collectively, the major cause of death in patients on dialysis. The population of patients treated with peritoneal dialysis and hemodialysis are not only subject to the traditional risk factors for heart disease, but also to certain uremia-associated risk factors that are unique in this population. In the dialysis population, data regarding the effectiveness of routine pharmacologic and procedural interventions on cardiovascular outcomes are limited. Most dialysis patients are excluded from clinical trials, and so data from randomized controlled trials investigating outcomes in patients undergoing peritoneal dialysis or hemodialysis are almost absent. In this review, we discuss some of the major cardiovascular problems in the dialysis population, the impact of those problems on survival, and when data are available, the impact of therapeutic strategies.

Exercise training improves endothelial function via adiponectin-dependent and independent pathways in type 2 diabetic mice.

Type 2 diabetes (T2D) is a leading risk factor for a variety of cardiovascular diseases including coronary heart disease and atherosclerosis. Exercise training (ET) has a beneficial effect on these disorders, but the basis for this effect is not fully understood. This study was designed to investigate whether the ET abates endothelial dysfunction in the aorta in T2D. Heterozygous controls (m Lepr(db)) and type 2 diabetic mice (db/db; Lepr(db)) were either exercise entrained by forced treadmill exercise or remained sedentary for 10 wk. Ex vivo functional assessment of aortic rings showed that ET restored acetylcholine-induced endothelial-dependent vasodilation of diabetic mice. Although the protein expression of endothelial nitric oxide synthase did not increase, ET reduced both IFN-γ and superoxide production by inhibiting gp91(phox) protein levels. In addition, ET increased the expression of adiponectin (APN) and the antioxidant enzyme, SOD-1. To investigate whether these beneficial effects of ET are APN dependent, we used adiponectin knockout (APNKO) mice. Indeed, impaired endothelial-dependent vasodilation occurred in APNKO mice, suggesting that APN plays a central role in prevention of endothelial dysfunction. APNKO mice also showed increased protein expression of IFN-γ, gp91(phox), and nitrotyrosine but protein expression of SOD-1 and -3 were comparable between wild-type and APNKO. These findings in the aorta imply that APN suppresses inflammation and oxidative stress in the aorta, but not SOD-1 and -3. Thus ET improves endothelial function in the aorta in T2D via both APN-dependent and independent pathways. This improvement is due to the effects of ET in inhibiting inflammation and oxidative stress (APN-dependent) as well as in improving antioxidant enzyme (APN-independent) performance in T2D.

Comparative analysis of telmisartan and olmesartan on cardiac function in the transgenic (mRen2)27 rat.

Telmisartan, an angiotensin receptor blocker, may have unique benefits as it possesses partial peroxisome proliferator-activated receptor (PPAR)-γ agonist activity in addition to antihypertensive effects. In this study, we test whether treatment with telmisartan ameliorates cardiovascular abnormalities to a greater extent than olmesartan, which has little PPAR-γ activity. The hypertensive rodent model of tissue renin-angiotensin system activation, transgenic (mRen2)27 (Ren2) rats and their littermate Sprague-Dawley controls were used. Rats were treated with telmisartan (2 mg · kg(-1) · day(-1)), olmesartan (2.5 mg · kg(-1) · day(-1)), or vehicle via drinking water for 3 wk; these doses achieved similar blood pressure control, as measured by telemetry. Ren2 rats displayed impaired diastolic and systolic function using left ventricular (LV) pressure-volume (P-V) analysis. Load-independent diastolic indexes, including the time constant of isovolumic relaxation and the slope of the end-diastolic P-V relationship, as well as systolic indexes, including preload recruitable stroke work, the dP/dt(max)-end-diastolic volume (EDV) relationship, and the P-V area-EDV relationship, were elevated in Ren2 rats compared with Sprague-Dawley controls (P < 0.05). The Ren2 myocardium exhibited parallel increases in the oxidant markers NADPH oxidase and 3-nitrotyrosine. The increase in the prohypertrophic protein Jak2 in Ren2 rats was associated with cardiac structural abnormalities using light microscopic and ultrastructural analysis, which included interstitial fibrosis, cardiomyocyte and LV hypertrophy, and mitochondrial derangements. Both angiotensin receptor blockers attenuate these abnormalities to a similar extent. Our data suggest that the beneficial effect of telmisartan and olmesartan on cardiac structure and function may be predominantly pressor-related or angiotensin type 1 receptor dependent in this model of renin-angiotensin system activation.

Isolated dynamic left ventricular outflow tract obstruction can cause hypotension that rapidly responds to intravenous beta blockade.

Dynamic left ventricular outflow tract obstruction occurs in hypertrophic cardiomyopathy, stress cardiomyopathy, acute coronary syndromes, and with inotrope use. We describe three critical care patients who developed "isolated" left ventricular outflow tract obstruction with hypotension in the absence of these precipitants. Systolic anterior motion of anterior mitral valve leaflet with peak left ventricular outflow tract gradients of greater than 120 mmHg was noted in Cases 1 and 2. Under close supervision, intravenous (IV) ß blocker was initiated with 5 mg metoprolol repeated every 5 minutes up to 15 mg and continued to maintain heart rate less than 70 beats/min. IV fluids were replaced aggressively. Bedside Doppler echocardiogram confirmed near normalization of left ventricular outflow tract gradient with improvement in systolic anterior motion and hypotension within minutes after IV ß blocker confirming its specific therapeutic effect. Isolated left ventricular outflow tract obstruction can occur in the absence of recognized precipitants. Early recognition is crucial because this potentially fatal condition responds well to adequate ß blocker and IV fluids with rapid relief of hypotension and symptoms.

Dobutamine stress echocardiography Doppler estimation of cardiac diastolic function: a simultaneous catheterization correlation study.

BACKGROUND: Doppler echocardiography using the ratio of early diastolic transmitral velocity to early diastolic mitral annular tissue velocity (E/E') is routinely used to evaluate left ventricular (LV) filling pressures at rest. We tested the hypothesis that measurement of E/E' in patients undergoing dobutamine stress echocardiography (DSE) will detect changes in LV filling pressures. METHODS: In this prospective study, 16 patients with normal LV ejection fraction and normal coronary arteries by angiography underwent a standard DSE protocol with simultaneous LV filling pressure monitoring with a fluid filled pigtail catheter. Doppler echocardiographic assessment of LV diastolic function was performed using E/E' at rest and during DSE. RESULTS: The average age of the study participants was 57 ± 8 years. Average heart rate was 61 ± 11 bpm at baseline and 141 ± 12 bpm at peak stress. LV mean diastolic pressure decreased from 12.3 ± 2.6 mmHg at baseline to 9.0 ± 2.3 mmHg at peak stress (P = 0.0001). Baseline E/E' at the septum and lateral annulus were 8.7 ± 2.2 and 7.5 ± 1.9 and during peak stress were 8.3 ± 3.1 and 7.9 ± 3.5, respectively. There was no significant change in E/E' at either the septum or the lateral annulus (P = 0.55, P = 0.66). There was no significant correlation between LV mean diastolic pressure and E/E' with dobutamine stress. CONCLUSIONS: In patients with normal LV ejection fraction and no significant coronary artery disease undergoing DSE, the ratio of early diastolic transmitral velocity to early diastolic tissue velocity (E/E') at peak stress with dobutamine does not predict changes in LV filling pressures.

Update on cardiorenal Syndrome: a clinical conundrum.

Our understanding of the cardiorenal syndrome continues to progress. Decades of research have led to a better definition of the clinical cardiorenal syndrome and have laid the groundwork for understanding its pathophysiology. Although improvements have been made, there are still knowledge gaps concerning the interactions of these two organ systems. In the present review, we examine those interactions in the setting of acute and chronic cardiac decompensation and the resulting impacts on renal dysfunction. Recognition and prevention of this syndrome may help to better serve a growing patient population.

Resveratrol improves left ventricular diastolic relaxation in type 2 diabetes by inhibiting oxidative/nitrative stress: in vivo demonstration with magnetic resonance imaging.

Resveratrol is a natural phytophenol that exhibits cardioprotective effects. This study was designed to elucidate the mechanisms by which resveratrol protects against diabetes-induced cardiac dysfunction. Normal control (m-Lepr(db)) mice and type 2 diabetic (Lepr(db)) mice were treated with resveratrol orally for 4 wk. In vivo MRI showed that resveratrol improved cardiac function by increasing the left ventricular diastolic peak filling rate in Lepr(db) mice. This protective role is partially explained by resveratrol's effects in improving nitric oxide (NO) production and inhibiting oxidative/nitrative stress in cardiac tissue. Resveratrol increased NO production by enhancing endothelial NO synthase (eNOS) expression and reduced O(2)(·-) production by inhibiting NAD(P)H oxidase activity and gp91(phox) mRNA and protein expression. The increased nitrotyrosine (N-Tyr) protein expression in Lepr(db) mice was prevented by the inducible NO synthase (iNOS) inhibitor 1400W. Resveratrol reduced both N-Tyr and iNOS expression in Lepr(db) mice. Furthermore, TNF-α mRNA and protein expression, as well as NF-κB activation, were reduced in resveratrol-treated Lepr(db) mice. Both Lepr(db) mice null for TNF-α (db(TNF-)/db(TNF-) mice) and Lepr(db) mice treated with the NF-κB inhibitor MG-132 showed decreased NAD(P)H oxidase activity and iNOS expression as well as elevated eNOS expression, whereas m-Lepr(db) mice treated with TNF-α showed the opposite effects. Thus, resveratrol protects against cardiac dysfunction by inhibiting oxidative/nitrative stress and improving NO availability. This improvement is due to the role of resveratrol in inhibiting TNF-α-induced NF-κB activation, therefore subsequently inhibiting the expression and activation of NAD(P)H oxidase and iNOS as well as increasing eNOS expression in type 2 diabetes.

Advances in percutaneous coronary intervention in patients with chronic kidney disease.

Coronary artery disease is the number one cause of death in patients with chronic kidney disease (CKD). However,patients with impaired renal function are much less likely than patients with normal renal function to undergo left heart catheterization and coronary intervention. Patients that do receive invasive strategies experience more bleeding and higher rates of ischemic events. In this review, we examine advances in percutaneous coronary intervention--including antiplatelet therapy and drug-eluting stents--and their impact on patients with CKD.

Cardiovascular problems in dialysis patients: impact on survival.

Cardiovascular diseases, in their broad spectrum, are collectively the major cause of death in patients on dialysis. The population of patients treated with peritoneal and hemodialysis are not only subject to the traditional risk factors for heart disease, but also to certain uremia-associated risk factors that are unique in this population. Limited data are available on the effectiveness of routine interventions on cardiovascular outcomes in dialysis patients. Because most dialysis patients are excluded from clinical trials, data from randomized controlled trials regarding outcomes in patients undergoing peritoneal dialysis are almost absent. The present review discusses some of the major cardiovascular problems in the dialysis population, the impact of those problems on survival, and the available therapeutic strategies.

Rosuvastatin ameliorates the development of pulmonary arterial hypertension in the transgenic (mRen2)27 rat.

We have recently reported that transgenic (mRen2)27 rats (Ren2 rats) exhibit pulmonary arterial hypertension (PAH), which is, in part, mediated by oxidative stress. Since 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors (statins) exhibit beneficial vascular effects independent of cholesterol synthesis, we hypothesized that rosuvastatin (RSV) treatment ameliorates PAH and pulmonary vascular remodeling in Ren2 rats, in part, by reducing oxidative stress. Six-week-old male Ren2 and Sprague-Dawley rats received RSV (10 mg x kg(-1) x day(-)1 ip) or vehicle for 3 wk. After treatment, right ventricular systolic pressure (RVSP) and mean arterial pressure (MAP) were measured. To evaluate treatment effects on pulmonary arteriole remodeling, morphometric analyses were performed to quantitate medial thickening and cell proliferation, whereas whole lung samples were used to quantitate the levels of 3-nitrotyrosine, superoxide, stable nitric oxide (NO) metabolites [nitrates and nitrites (NO(x))], and expression of NO synthase isoforms. In the Ren2 rat, RVSP is normal at 5 wk of age, PAH develops between 5 and 7 wk of age, and the elevated pressure is maintained with little variation through 13 wk. At 8 wk of age, left ventricular function and blood gases were normal in the Ren2 rat. Ren2 rats exhibited elevations in medial hypertrophy due to smooth muscle cell proliferation, 3-nitrotyrosine, NO(x), NADPH oxidase activity, and endothelial NO synthase expression compared with Sprague-Dawley rats. RSV significantly blunted the increase in RVSP but did not reduce MAP in the Ren2 rat; additionally, RSV significantly attenuated the elevated parameters examined in the Ren2 rat. These data suggest that statins may be a clinically viable adjunct treatment of PAH through reducing peroxynitrite formation.

Unexplained hypotension: the spectrum of dynamic left ventricular outflow tract obstruction in critical care settings.

OBJECTIVE: To illustrate the clinical and hemodynamic abnormalities caused by dynamic left ventricular outflow tract obstruction (LVOTO) in critical care setting. DESIGN: We reviewed cases referred to Cardiology with echocardiographic evidence of LVOTO and their clinical presentations. We present those cases where LVOTO can transiently occur without hypertrophic cardiomyopathy when inotropic agents are used for hypotension. MEASUREMENTS AND MAIN RESULTS: Five women in the 50-70 age range and prior history of hypertension presented with various symptoms like chest discomfort, fatigue, dizziness, atrial fibrillation, and hypotension. An ejection systolic murmur was noted most often in the left third intercostal space and ECG revealed ST-T wave abnormalities. LVOTO caused by mitral systolic anterior motion was detected by echocardiography and catheterization excluded acute coronary disease. In critical care setting, LVOTO can occur due to apical ballooning syndrome, coronary disease, medications, volume depletion, and valvular abnormalities. Because this condition mimics acute coronary syndrome or other etiologies of hypotension in medical and surgical intensive care units, appropriate treatment can be delayed. Nonhypertrophic cardiomyopathy LVOTO usually responds well to fluid replacement, beta blockers, and medication changes. CONCLUSIONS: LVOTO should be suspected especially in women presenting with hypotension and systolic murmur in critical care settings. Clinical acumen and timely echocardiography are required to effectively counter this transient but potentially lethal problem.

Role of TNF-alpha in vascular dysfunction.

Healthy vascular function is primarily regulated by several factors including EDRF (endothelium-dependent relaxing factor), EDCF (endothelium-dependent contracting factor) and EDHF (endothelium-dependent hyperpolarizing factor). Vascular dysfunction or injury induced by aging, smoking, inflammation, trauma, hyperlipidaemia and hyperglycaemia are among a myriad of risk factors that may contribute to the pathogenesis of many cardiovascular diseases, such as hypertension, diabetes and atherosclerosis. However, the exact mechanisms underlying the impaired vascular activity remain unresolved and there is no current scientific consensus. Accumulating evidence suggests that the inflammatory cytokine TNF (tumour necrosis factor)-alpha plays a pivotal role in the disruption of macrovascular and microvascular circulation both in vivo and in vitro. AGEs (advanced glycation end-products)/RAGE (receptor for AGEs), LOX-1 [lectin-like oxidized low-density lipoprotein receptor-1) and NF-kappaB (nuclear factor kappaB) signalling play key roles in TNF-alpha expression through an increase in circulating and/or local vascular TNF-alpha production. The increase in TNF-alpha expression induces the production of ROS (reactive oxygen species), resulting in endothelial dysfunction in many pathophysiological conditions. Lipid metabolism, dietary supplements and physical activity affect TNF-alpha expression. The interaction between TNF-alpha and stem cells is also important in terms of vascular repair or regeneration. Careful scrutiny of these factors may help elucidate the mechanisms that induce vascular dysfunction. The focus of the present review is to summarize recent evidence showing the role of TNF-alpha in vascular dysfunction in cardiovascular disease. We believe these findings may prompt new directions for targeting inflammation in future therapies.

The role of echocardiography in cardiac structural and functional assessment in dialysis patients.

In recent decades, echocardiography has evolved into a useful tool in the assessment of cardiovascular anatomy, physiology, and pathology. Its use has enabled the measurement of structural parameters such as left ventricular mass, which has both diagnostic and prognostic value. Doppler measurements have allowed for accurate hemodynamic assessment that can help to guide therapy. Newer methods have also been used and proposed to evaluate systolic and diastolic function. Here, we review the use of echocardiography in cardiac structural and functional assessment, providing insights into the challenges and limitations of these techniques in dialysis patients.

A Health System's Pilot Experience with Using Social Knowledge Networking (SKN) Technology to Enable Meaningful Use of EHR Medication Reconciliation Technology.

Similar to issues faced in health systems across USA, AU Health, based in Augusta, Georgia, faced a scenario of low physician engagement in, and limited-use of its Electronic Health Record (EHR) Medication Reconciliation (MedRec) technology, which translated to high rates of medication discrepancies and low accuracy of the patient's active medication list, during transitions of care. In fall 2016, a two-year grant was secured from the U.S. Agency for Healthcare Research and Quality (AHRQ), to pilot a Social Knowledge Networking (SKN) system pertaining to "EHR-MedRec," to enable AU Health to progress from "limited use" of EHR MedRec technology, to "meaningful use." The rationale behind an SKN system, is that it could provide a platform for inter-professional knowledge exchange on practice issues related to EHR MedRec, across diverse provider subgroups and care settings, to highlight adverse consequences of gaps in practice for patient safety, and emphasize the value of adhering to best-practices in EHR MedRec. This, in turn, is expected to increase provider engagement in addressing issues related to EHR MedRec, and promote inter-professional learning of best-practices, to create a foundation for practice change or improvement (e.g., Meaningful Use of EHR MedRec technology). This Case Report describes AU Health's experiences with this novel initiative to pilot an SKN system for enabling Meaningful Use of EHR MedRec technology. It also discusses lessons learned in regard to the potential of an SKN system to enable inter-professional learning and practice improvement in the context of EHR MedRec, which, in turn, helps identify strategies and practice implications for healthcare managers.