Taunton and Somerset Hospital

Taunton, United Kingdom

Taunton and Somerset Hospital

Taunton, United Kingdom
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Siassakos D.,Southmead Hospital | Fox R.,Taunton and Somerset Hospital | Crofts J.F.,Southmead Hospital | Hunt L.P.,University of Bristol | And 2 more authors.
Resuscitation | Year: 2011

Objectives: To determine whether team performance in a simulated emergency is related to generic teamwork skills and behaviours. Methods: Design - Cross-sectional analysis of data from the Simulation and Fire-drill Evaluation (SaFE) randomised controlled trial. Setting - Six secondary and tertiary Maternity Units in Southwest England. Participants - 140 healthcare professionals, in 24 teams. Assessment - Blinded analysis of recorded simulations. Main outcome measures - Correlation of team performance (efficiency conducting key clinical actions, including the administration of an essential drug, magnesium), and generic teamwork scores (using a validated tool that assesses skills and behaviours, by Weller et al.). Results: There was significant positive correlation between clinical efficiency and teamwork scores across all three dimensions; skills (Kendall's taub=0.54, p<0.001), behaviours (taub=0.41, p=0.001), and overall score (taub=0.51, p<0.001). Better teams administered the essential drug 2 1/2;min more quickly (Mann-Whitney U, p<0.001). Conclusions: The clinical conduct of a simulated emergency was strongly linked to generic measures of teamwork. Further studies are needed to elucidate which aspects of team working are critical for team performance, to better inform training programs for multi-professional team working. © 2010 Elsevier Ireland Ltd.

Fox R.,Taunton and Somerset Hospital | Walker J.J.,University of Leeds | Draycott T.J.,Southmead Hospital
BJOG: An International Journal of Obstetrics and Gynaecology | Year: 2011

From the earliest days of medical practice, when surgeons used cadavers to explore the possibilities of surgical intervention, simulation has been employed to advance the practice of health care. In the last 10 years, technological advances have allowed for a wider availability and greater realism of simulation, and this has encouraged a great expansion in its use. Simulation aims to create a virtuous cycle of professional development to improve patient outcomes. Although it seems eminently logical to believe that simulation will result in better outcomes, there is a need to test these new training interventions rigorously to be sure of their worth and to understand any limitations. The purpose of this BJOG supplement is to examine in depth several paradigms of medical simulation within maternity care and gynaecology, in different settings, looking at what can be achieved and how. In this opening review, we look at the potential use of medical simulation in broad terms and describe the types of evidence that can be employed to support its use. © 2011 The Authors BJOG An International Journal of Obstetrics and Gynaecology © 2011 RCOG.

Siassakos D.,Southmead Hospital | Draycott T.J.,Southmead Hospital | Crofts J.F.,Southmead Hospital | Hunt L.P.,Institute of Child Life and Health | And 2 more authors.
BJOG: An International Journal of Obstetrics and Gynaecology | Year: 2010

Objective To assess whether team performance in simulated eclampsia is related to the knowledge, skills and attitudes of individual team members. Design Cross-sectional analysis of data from the Simulation and Fire Drill Evaluation randomised controlled trial. Setting Six secondary and tertiary maternity units in south-west England. Participants One hundred and fourteen maternity professionals in 19 teams of six members; one senior and one junior obstetrician; two senior and two junior midwives. Methods We validated a team performance ranking scheme with respect to magnesium administration (Magnesium Administration Rank, MAR) by expert consensus (face validity) and correlation with clinical measures (construct validity). We tested for correlation between MAR and measures of knowledge, skills and attitudes. Main outcome measures Correlation between team performance (MAR) and scores in validated multiple-choice questionnaires (MCQs) (knowledge), a measure of individual manual skill to manage an obstetric emergency (skill) and scores in a widely used teamworksafety attitude questionnaire (attitude). Results There was no relationship between team performance and cumulative individual MCQs, skill or teamworksafety attitude scores. Conclusions The knowledge, manual skills and attitudes of the individuals comprising each team, measured by established methods, did not correlate in this study with the team's clinical efficiency in the management of simulated eclampsia. The inference is that unidentified characteristic(s) play a crucial part in the efficiency of teams managing emergencies. Any emphasis of training programmes to promote individual knowledge, skills and attitudes alone may have to be re-examined. This highlights a need to understand what makes a team efficient in dealing with clinical emergencies. © RCOG 2010 BJOG An International Journal of Obstetrics and Gynaecology.

MacIver D.H.,Taunton and Somerset Hospital | Clark A.L.,University of Hull
The American journal of cardiology | Year: 2015

The development of acute pulmonary edema involves a complex interplay between the capillary hydrostatic, interstitial hydrostatic, and oncotic pressures and the capillary permeability. We review the pathophysiological processes involved and illustrate the concepts in a number of common clinical situations including heart failure with normal and reduced ejection fractions, mitral regurgitation, and arrhythmias. We also describe other rarer causes including exercise, swimming, and diving-induced acute pulmonary edema. We suggest a unifying framework in which the critical abnormality is a mismatch or imbalance between the right and left ventricular stroke volumes. In conclusion, we hypothesize that increased right ventricular contraction is an important contributor to the sudden increase in capillary hydrostatic pressure, and therefore, a central mechanism involved in the development of alveolar edema. Copyright © 2015 Elsevier Inc. All rights reserved.

MacIver D.H.,Taunton and Somerset Hospital | Dayer M.J.,Taunton and Somerset Hospital | Harrison A.J.I.,University of Bristol
International Journal of Cardiology | Year: 2013

Current concepts of heart failure propose multiple heterogeneous pathophysiological mechanisms. Recently a theoretical framework for understanding chronic heart failure was suggested. This paper develops this framework to include acute heart failure syndromes. We propose that all acute heart failure syndromes may be understood in terms of a relative fall in left ventricular stroke volume. The initial compensatory mechanism is frequently a tachycardia often resulting in a near normal cardiac output. In more severe forms a fall in cardiac output causes hypotension or cardiogenic shock. In chronic heart failure the stroke volume and cardiac output is returned to normal predominantly through ventricular remodeling or dilatation. Ejection fraction is simply the ratio of stroke volume and end-diastolic volume. The resting stroke volume is predetermined by the tissue's needs; therefore, if the ejection fraction changes, the end-diastolic volume must change in a reciprocal manner. The potential role of the right heart in influencing the presentation of left heart disease is examined. We propose that acute pulmonary edema occurs when the right ventricular stroke volume exceeds left ventricular stroke volume leading to fluid accumulation in the alveoli. The possible role of the right heart in determining pulmonary hypertension and raised filling pressures in left-sided heart disease are discussed. Different clinical scenarios are presented to help clarify these proposed mechanisms and the clinical implications of these theories are discussed. Finally an alternative definition of heart failure is proposed. © 2012 Elsevier Ireland Ltd.

MacIver D.H.,Taunton and Somerset Hospital
European Journal of Echocardiography | Year: 2011

Aims Left ventricular ejection fraction (EF) is a suboptimal measure of ventricular function. Recent mathematical modelling of left ventricular contraction has shown that the EF is determined by both myocardial shortening (strain) and by end-diastolic wall thickness. Increasing end-diastolic wall thickness resulted in augmented radial wall thickening. This may result in a significant 'overestimation' of ventricular systolic function as assessed by the EF. This study proposes a new measure of ventricular systolic function, the corrected EF (EFc) to allow for the presence of concentric left ventricular hypertrophy (LVH). Methods and results The study uses a new two-layer, three-dimensional mathematical model of ventricular contraction. Changes in end-diastolic wall thickness in addition to long-axis and mid-wall circumferential strain were modelled. Iso-strain lines were obtained where myocardial shortening (strain) is constant; EF increases with increasing end-diastolic wall thickness. The corrected EF is determined by following the iso-strain lines to the equivalent EF in the absence of hypertrophy (e.g. 9 mm thickness). For example, an individual with a mean end-diastolic wall thickness of 20 mm and measured EF of 60 has a corrected EF (EFc) of 37. Conclusion The study shows that the EF is determined by absolute wall thickening and provides a nomogram for comparing EF when LVH is present. The EFc is a potential new measure of left ventricular systolic function. Its possible role will need validating in mortality trials. © 2010 The Author.

The mechanisms of heart failure are ill understood with multiple, heterogeneous hypotheses proposed to describe the condition. This study examines the individual effects of left ventricular hypertrophy, long-axis shortening and the effect of left ventricular remodeling on ejection fraction, end-diastolic volume and stroke volume using a mathematical model of left ventricular contraction. Reducing long-axis shortening caused a decline in stroke volume independently of hypertrophy. Increasing concentric left ventricular hypertrophy resulted in an increase in ejection fraction secondary to augmented wall thickening. A decline in stroke volume occurred despite a preserved ejection fraction when concentric hypertrophy was present. Normalization of stroke volume by remodeling resulted in a marked increase in end-diastolic volume in the absence of hypertrophy and an end-diastolic volume similar to normal in the presence of concentric hypertrophy. The model predicts that the dominant compensatory mechanism in chronic heart failure is remodeling with normalization of stroke volume. Observational data cited supports this conclusion.

MacIver D.H.,Taunton and Somerset Hospital
Experimental and Clinical Cardiology | Year: 2012

In vivo data have been unable to provide conclusive results with regard to the relative impact of circumferential and longitudinal shortening on stroke volume. The objective of the present study was to assess the relative contribution of circumferential and longitudinal myocardial shortening to left ventricular stroke volume and ejection fraction, and to evaluate the effect of left ventricular hypertrophy. A two-shell, three-dimensional mathematical model was used to assess the individual contributions of longitudinal and midwall circumferential shortening (or strain) to stroke volume and ejection fraction. Reducing either circumferential or longitudinal shortening resulted in a reduced ejection fraction and stroke volume. The stroke volume fell by 43% when circumferential strain was reduced from -20% to -5%, but only by 19% when longitudinal strain was similarly reduced. The sole contribution of circumferential and longitudinal shortening to stroke volume was 67% and 33%, respectively. These proportions were independent of wall thickness. The present study demonstrated that both longitudinal and midwall circumferential shortening contribute to different extents depending on the degree of abnormality of myocardial shortening. Contrary to most previous studies, the present study shows that circumferential shortening has a relatively greater contribution to stroke volume (ie, two-thirds) and ejection fraction than longitudinal shortening. These observations have important clinical and research implications in the assessment of left ventricular function. ©2012 Pulsus Group Inc. All rights reserved.

MacIver D.H.,Taunton and Somerset Hospital
Future Cardiology | Year: 2010

Heart failure with a preserved ejection fraction is a fascinating and multifaceted condition that has provoked enormous debate and a wealth of mechanistic studies. Controversies exist with regard to its nomenclature. If its nomenclature is questioned, one can be certain the pathogenesis is ill understood. If the pathogenesis is disputed, the diagnosis becomes difficult and inconsistent. These diagnostic challenges result in inappropriate recruitment to clinical trials. Therefore, the trials may be underpowered and difficult to interpret. This paper examines contemporary theories of heart failure with a preserved ejection fraction, clarifies the controversies and attempts to resolve the divergences of opinion. Copyright © 2010 Future Medicine Ltd.

MacIver D.H.,Taunton and Somerset Hospital | Dayer M.J.,Taunton and Somerset Hospital
International Journal of Cardiology | Year: 2012

No single well established hypothesis for the mechanisms of heart failure currently exists. Those definitions that do exist are either not universally applicable or are not exclusive to heart failure. The pathogenesis of heart failure has been considered by some to be too complex to define with multiple pathophysiological processes being implicated. The many clinical and neurohumoral features of heart failure may be more dependent on the severity of the condition and its speed of onset rather than its etiology. This suggests a potential single common pathway or pathogenic mechanism in all forms of heart failure regardless of cause. This viewpoint uses the framework of myocardial mechanics and energetics to propose an alternative, simplified definition and unifying hypothesis for the pathogenesis of chronic heart failure. Chronic heart failure may be understood as follows. Cardiac output and stroke volume are determined by the tissues' requirements; the ejection fraction is determined by both myocardial shortening and degree of end-diastolic wall thickness; the end-diastolic volume is determined by the requirement to normalize stroke volume. We will argue that chronic heart failure can be viewed as a condition where the dominant compensatory mechanism is through regulation of ventricular end-diastolic volume. Consequently, in conditions where there is a fall in tissue perfusion, stroke volume and tissue perfusion are returned toward normal predominantly via this feedback mechanism. It is important for researchers, clinicians and their patients that we strive for a comprehensive, inclusive and unambiguous unifying hypothesis for pathophysiological mechanisms of heart failure. © 2011 Elsevier Ireland Ltd. All rights reserved.

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