Development of the Leapfrog Group's Bar Code Medication Administration Standard to Address Hospital Inpatient Medication Safety.

ABSTRACT: Medication errors are the most common type of error in hospitals and reflect a leading cause of avoidable harm to patients. Bar code medication administration (BCMA) systems are a technology designed to help intercept medication errors at the point of medication administration. This article describes the process of developing, testing, and refining a standard for BCMA adoption and use in U.S. hospitals, as measured through the Leapfrog Hospital Survey. Building on the published literature and an expert panel's collective experience in studying, implementing, and using BCMA systems, the expert panel recommended a standard with 4 key domains. Leapfrog's BCMA standard provides hospitals with a "how-to guide" on what best practice looks like for using BCMA to ensure safe medication administration at the bedside.

La implementación de la administración de medicamentos con código de barras y las bombas de infusión inteligentes es sólo el comienzo del camino seguro para prevenir los errores de administración / Implementing barcode medication administration and smart infusion pumps is just the beginning of the safety journey to prevent administration errors

INTRODUCCIÓN: La tecnología sanitaria se ha convertido en la solución más aceptada para reducir los eventos adversos provocados por los medicamentos, minimizando los posibles errores humanos. La introducción de la tecnología puede mejorar la seguridad y permitir una mayor eficiencia en la clínica. Sin embargo, no elimina todos los tipos de error y puede crear otros nuevos. La administración de medicamentos con código de barras y la utilización de bombas de infusión inteligentes son dos estrategias que pueden emplearse durante la administración de medicamentos para evitar errores antes de que estos lleguen al paciente. OBJETIVO: En este artículo se han revisado diferentes tipos de errores relativos a la administración de medicamentos con código de barras y las bombas de infusión inteligentes, y se ha examinado la forma en la que se producían dichos errores al emplear la tecnología. También se exponen las recomendaciones encaminadas a evitar este tipo de errores. CONCLUSIÓN: Los hospitales deben comprender la tecnología, su funcionamiento y los errores que pretende evitar, así como analizar de qué manera cambiará los procesos clínicos. Es esencial que la dirección del hospital establezca las métricas necesarias y las monitorice regularmente para garantizar el uso óptimo de estas tecnologías. También es importante identificar y evitar desviaciones en los procesos que puedan eliminar o disminuir los beneficios de seguridad para los que fue diseñada. De igual forma, es necesario recopilar periódicamente las opiniones del profesional que la utiliza para detectar los posibles problemas que pudieran surgir. Sin embargo, la dirección debe ser consciente de que incluso con la implementación completa de la tecnología pueden surgir errores a la hora de administrar la medicación

INTRODUCTION: Healthcare-related technology has been widely accepted as a key patient safety solution to reduce adverse drug events by decreasing the risk of human error. The introduction of technology can enhance safety and support workflow; however, it does not eliminate all error types and may create new ones. Barcode medication adminis-tration and smart infusion pumps are two technologies utilized during medication administration to prevent medication errors before they reach the patient. OBJECTIVE: This article reviewed different error types with barcode medi-cation administration and smart infusion pumps and examined how these errors were able to occur while using the technology. Recommendations for preventing these types of errors were also discussed. CONCLUSION: Hospitals must understand the technology, how it is desig-ned to work, which errors it is intended to prevent, as well as understand how it will change staff workflow. It is essential that metrics are set by hospital leadership and regularly monitored to ensure optimal use of these technologies. It is also important to identify and avoid workarounds which eliminate or diminish the safety benefits that the technology was designed to achieve. Front line staff feedback should be gathered on a periodic basis to understand any struggles with utilizing the technology. Leaders must also understand that even with full implementation of technology, medication errors may still occur

Implementing barcode medication administration and smart infusion pumps is just the beginning of the safety journey to prevent administration errors.

INTRODUCTION: Healthcare-related technology has been widely accepted as a key  patient safety solution to reduce adverse drug events by decreasing the risk  of human error. The introduction of technology can enhance safety and  support workflow; however, it does not eliminate all error types and may create  new ones. Barcode medication administration and smart infusion pumps are two  technologies utilized during medication administration to prevent medication  errors before they reach the patient. OBJECTIVE: This article reviewed different error types with barcode medication administration and smart infusion pumps and examined how these errors were able to occur while using the technology. Recommendations for preventing these types of errors were also discussed. CONCLUSION: Hospitals must understand the technology, how it is designed to  work, which errors it is intended to prevent, as well as understand how it will  change staff workflow. It is essential that metrics are set by hospital leadership  and regularly monitored to ensure optimal use of these technologies. It is also  important to identify and avoid workarounds which eliminate or diminish the  safety benefits that the technology was designed to achieve. Front line staff  feedback should be gathered on a periodic basis to understand any struggles  with utilizing the technology. Leaders must also understand that even with full  implementation of technology, medication errors may still occur.

Introducción: La tecnología sanitaria se ha convertido en la solución más  aceptada para reducir los eventos adversos provocados por los medicamentos, minimizando los posibles errores humanos. La introducción de la tecnología puede mejorar la seguridad y permitir una mayor eficiencia en la clínica. Sin embargo, no elimina todos los tipos de error y puede crear otros nuevos. La administración de medicamentos con código de  barras y la utilización de bombas de infusión inteligentes son dos estrategias que  pueden emplearse durante la administración de medicamentos para evitar  errores antes de que estos lleguen al paciente.Objetivo: En este artículo se han revisado diferentes tipos de errores relativos a  la administración de medicamentos con código de barras y las bombas de  infusión inteligentes, y se ha examinado la forma en la que se producían dichos  errores al emplear la tecnología. También se exponen las recomendaciones  encaminadas a evitar este tipo de errores.Conclusión: Los hospitales deben comprender la tecnología, su funcionamiento y los errores que pretende evitar, así como analizar de qué manera cambiará los procesos clínicos. Es esencial que la dirección del hospital establezca las métricas necesarias y las monitorice regularmente para garantizar el uso óptimo de estas tecnologías. También es  importante identificar y evitar desviaciones en los procesos que puedan eliminar  o disminuir los beneficios de seguridad para los que fue diseñada. De igual forma, es necesario recopilar periódicamente las opiniones del profesional que la utiliza para detectar los posibles problemas que pudieran surgir. Sin embargo, la dirección debe ser consciente de que incluso con la implementación completa de  la tecnología pueden surgir errores a la hora de administrar la medicación.

Regulation of cardiomyocyte signaling by RGS proteins: differential selectivity towards G proteins and susceptibility to regulation.

Many signals that regulate cardiomyocyte growth, differentiation and function are mediated via heterotrimeric G proteins, which are under the control of RGS proteins (Regulators of G protein Signaling). Several RGS proteins are expressed in the heart, but so far little is known about their function and regulation. Using adenoviral gene transfer, we conducted the first comprehensive analysis of the capacity and selectivity of the major cardiac RGS proteins (RGS2-RGS5) to regulate central G protein-mediated signaling pathways in adult ventricular myocytes (AVM). All four RGS proteins potently inhibited Gq/11-mediated phospholipase C beta stimulation and cell growth (assessed in neonatal myocytes). Importantly, RGS2 selectively inhibited Gq/11 signaling, whereas RGS3, RGS4 and RGS5 had the capacity to regulate both Gq/11 and Gi/o signaling (carbachol-induced cAMP inhibition). Gs signaling was unaffected, and, contrary to reports in other cell lines, RGS2-RGS5 did not appear to regulate adenylate cyclase directly in AVM. Since RGS proteins can be highly regulated in their expression by many different stimuli, we also tested the hypothesis that RGS expression is subject to G protein-mediated regulation in AVM and determined the specificity with which enhanced G protein signaling alters endogenous RGS expression in AVM. RGS2 mRNA and protein were markedly but transiently up-regulated by enhanced Gq/11 signaling (alpha1-adrenergic stimulation or Galphaq* overexpression), possibly by a negative feedback mechanism. In contrast, the other negative regulators of Gq/11 signaling (RGS3-RGS5) were unchanged. Endogenous RGS2 (but not RGS3-RGS5) expression was also up-regulated in cells with enhanced AC signaling (beta-adrenergic or forskolin stimulation). Taken together, these findings suggest diverse roles of RGS proteins in regulating myocyte signaling. RGS2 emerged as the only selective and highly regulated inhibitor of Gq/11 signaling that could potentially become a promising target for ameliorating Gq/11-mediated signaling and growth.

Expression of ten RGS proteins in human myocardium: functional characterization of an upregulation of RGS4 in heart failure.

OBJECTIVE: RGS proteins (regulators of G protein signalling) negatively regulate G protein function as GTPase activating proteins. By controlling heterotrimeric G proteins they may regulate myocardial hypertrophy and contractility. We investigated the expression of RGS proteins in the human heart and whether they take part in the pathophysiological changes of heart failure. METHODS AND RESULTS: Using RNase protection assays (RPAs) RGS2, 3L, 3S, 4, 5 and 6 were identified in the myocardium from terminally failing human hearts with dilated (DCM, n=22) or ischemic (ICM, n=18) cardiomyopathy and from nonfailing donor hearts (NF, n=9). With reverse transcriptase polymerase chain reaction in addition mRNA of RGS1, 9, 12, 14 and 16 were detectable. Compared to NF in failing LV myocardium RGS4 mRNA and protein was upregulated 2-3-fold (mRNA, 10(-21) mol/microg+/-S.E.M.: NF: 22+/-5, DCM: 51+/-10*, ICM: 37+/-8; P<0.05 vs. DCM+ICM, *P<0.05 vs. NF, P<0.05 vs. DCM+ICM; protein, % of NF+/-S.E.M.: NF: 100+/-35, DCM 266+/-60*, ICM: 205+/-64, n=5, *P<0.05 vs. NF). In contrast, RGS2, 3L, 3S, 5, 6, and 16 protein and mRNA levels did not vary between failing and NF hearts. In order to investigate the impact of RGS4 on Gq/11 mediated signalling, PLC activity was measured in human LV membranes. Recombinant RGS4 blunted the endothelin-1 (ET-1) stimulated PLC activity. When overexpressed by adenoviral mediated gene transfer in rabbit ventricular myocytes RGS4 abolished the inotropic effect of ET-1. CONCLUSION: The upregulation of RGS4 in failing human myocardium diminishes Gq/11-mediated signalling and can be involved in the desensitization of Gq/11-mediated positive inotropic effects.

Signalling components involved in the coupling of alpha 1-adrenoceptors to phospholipase D in neonatal rat cardiac myocytes.

Activation of phospholipase D (PLD) is assumed to be one major pathway by which alpha(1)-adrenoceptors (alpha(1)ARs) induce hypertrophic responses in cardiac myocytes. Heterotrimeric G proteins, protein kinase C (PKC) isoforms, protein tyrosine kinases, monomeric GTPases of the ADP-ribosylation factor (ARF) and Rho families, and as important cofactor phosphatidylinositol 4,5-bisphosphate (PIP(2)) seem to participate in the G protein-coupled receptor dependent regulation of PLD. We therefore studied the role of these components in the coupling of alpha(1)ARs to PLD in neonatal rat cardiac myocytes (NRCM). Stimulation of alpha(1)ARs, most likely of the alpha(1A) subtype, by noradrenaline increased PLD activity three- to fourfold concomitant with the stimulation of phospholipase C (PLC). In contrast, the partial agonist phenylephrine stimulated PLC, but failed to increase PLD activity. The PLC and PLD responses were pertussis toxin insensitive and treatment of the cells with the G(q)-activating toxin of Pasteurella multocida stimulated both phospholipases about fourfold. Over-expression of the G(q)-and G(i)-type-specific regulator of G protein signalling RGS4 blunted alpha(1)AR-induced PLC and PLD stimulation. Ro 31-8220, known to inhibit Ca(2+)-dependent and -independent PKC isoforms, strongly inhibited PLD activity, whereas Gö 6976, known to inhibit preferentially Ca(2+)-dependent PKC isozymes, was without effect. The ARF signalling inhibitor brefeldin A, protein tyrosine kinase inhibitors and the Rho-inactivating toxin B of Clostridium difficile blunted alpha(1)AR-induced PLD stimulation and largely reduced the cellular PIP(2) content. In membranes of toxin B-treated NCRM, PLD activity was similarly reduced, but was fully restored by addition of exogenous PIP(2). We conclude, that alpha(1A)ARs stimulate PLD activity via a G(q/11)-PLCbeta-novel PKC isoform-dependent pathway in NRCM. ARF and Rho GTPases as well as protein tyrosine kinases contribute to PLD stimulation in NRCM, most likely by regulating the supply of PIP(2).

Distinct signaling pathways mediate cardiomyocyte phospholipase D stimulation by endothelin-1 and thrombin.

Several G protein-coupled receptors which stimulate phospholipase C (PLC) also activate phospholipase D (PLD) in cardiomyocytes. Here, we characterized PLD activation in neonatal rat cardiomyocytes by the PLC-stimulatory thrombin receptor PAR1, in comparison to the endothelin-1 receptor ET(A)R, which induces PLD stimulation by activation of protein kinase C (PKC) delta and epsilon. Similar to ET(A)R, activation of PAR1 induced PLD stimulation, which, however, was insensitive to PKC inhibition. Furthermore, in contrast to ET(A)R, PLD stimulation by PAR1 was suppressed by overexpression of regulators of G protein signaling specific for G(12)-type G proteins and treatment with brefeldin A, an inhibitor of guanine nucleotide exchange factors for ADP-ribosylation factor (ARF) GTPases. On the other hand, inactivation of Rho GTPases by Clostridium difficile toxin B and treatment with general tyrosine kinase inhibitors suppressed PAR1- and ET(A)R- as well as phorbol ester-induced PLD stimulation and was associated with a fall in the cellular level of phosphatidylinositol 4,5-bisphosphate (PIP(2)). We conclude that, in contrast to ET(A)R-PLD coupling, PAR1-induced cardiomyocyte PLD stimulation is PKC-independent and mediated by G(12)-type G proteins and ARF GTPases, while Rho and tyrosine kinases regulate PLD stimulation by either receptor, apparently by controlling the cellular level of PIP(2), a common regulator of PLD activity.