The Resus Room

This is the first of a new series of Roadside to Resus podcasts. We've been joined by James Yates, a Critical Care Paramedic with the Great Western Air Ambulance to make it a truly multidisciplinary team. Each monthly episode we'll be discussing acute presentations, including the latest and most influential evidence base surrounding them. We really want to break down some barriers between pre-hospital and in hospital teams and it soon becomes evident in this first podcast that many of the problems we face are shared throughout the patient journey and across disciplines! We're starting off with Acute Heart Failure and in the podcast we run through; The underlying physiology and help explain the different problems we may find in each subset The keys to diagnosis, including the most predictive parts of history and examination We discuss the evidence base for treatment and the trends of use both pre and in-hospital We talk about CPAP and whether the evidence supports it's use Finally, the direction that further treatment in the UK may move Once again we hope you find the podcast useful. Get in touch with any comments, questions or suggestions for further topics. Most of all don't take our word for it, but make sure you delve into the references yourself and make up your own mind. Enjoy! Simon, Rob & James References & Further Reading Recommendations on pre-hospital & early hospital management of acute heart failure: a consensus paper from the Heart Failure Association of the European Society of Cardiology, the European Society of Emergency Medicine and the Society of Academic Emergency Medicine Understanding cardiac output. Jean-Louis Vincent. Crit Care. 2008. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure The pathophysiology of hypertensive acute heart failure. Viau DM. Heart. 2015 Meta-analysis: Noninvasive Ventilation in Acute Cardiogenic Pulmonary Edema. Weng. Annals Int Med. 2010 Does This Dyspneic Patient in the Emergency Department Have Congestive Heart Failure? Charlie S.JAMA 2005 Diagnosing Acute Heart Failure in the Emergency Department; A Systematic Review and Meta-analysis. Martindale. Academic Emergency Medicine. 2016 Noninvasive ventilation in acute cardiogenic pulmonary edema. Gray A. N Engl J Med. 2008 Life in the Fast Lane; severe heart failure management Emergency Medicine Cases; acute congestive heart failure REBEL.EM; morphine kills in acute decompensated heart failure EMCRIT 1; Sympathetic Crashing Acute Pulmonary Edema (SCAPE)

C-spine immobilisation is a controversial topic because of a lack of high quality evidence from clinical trials. Historical approaches have been challenged, however NICE guidance continues to recommend 3-point immobilisation for all patients with suspected spinal injury despite considerable clinical equipoise. In this episode we discuss the complexities of balancing the risks and harms when trying to provide a patient centred approach, rather than a "one-size fits all" model. As always, there are a number of papers, guidelines and resources that you should have a look at (it's not exhaustive, but a good place to start!) Enjoy! Rob References & Further Reading NICE Guidance Major trauma Spinal injury Faculty of prehospital care consensus statements Spinal immobilisation Minimal patient handling Cochrane reviews Spinal Immobilisation for Trauma Papers of interest Cowley et al 2017 Dixon et al 2015 Benger & Blackham 2009 Hauswald 2015 Hauswald 2013 Michaleff et al 2012 Podcasts RCEM Learning EMCrit

We're back with 3 superb topics this month! First off we have a look at the utility of ultrasound for the detection of pneumothoraces in the context of blunt trauma. Next we look at the need to scan facial bones when scanning a patient's head following trauma. Last of all we look at a paper reviewing the association between the use of a bougie and the first pass success when performing ED RSI. Have a listen to the podcast and most importantly make sure you have a look at the references and critically appraise the papers yourself. We'd love to hear your thoughts and comments at the bottom of the page. Enjoy! Simon & Rob References & Further Reading Detection of pneumothoraces in patients with multiple blunt trauma: use and limitations of eFAST. Sauter TC. Emerg Med J. 2017 Simultaneous head and facial computed tomography scans for assessing facial fractures in patients with traumatic brain injury. Huang LK. Injury. 2017 The Bougie and First-Pass Success in the Emergency Department. Driver B. Ann Emerg Med. 2017

Guidelines. Algorithms. Evidence based medicine. These all play a significant part in the safe and effective management of the majority of our patients. As a result there is a danger that treatment pathways are followed blindly without critiquing their use and there is real risk we can loose sight of what's best for the patient in front of us. Guidelines encourage inflexible decision making, which creates further challenge when we are met by patients who do not fit standard treatment pathways. If this is the case then the management of cardiac arrest, which is taught and delivered in a didactic and protocol driven fashion, is surely the pinnacle of the problem. Standard Advanced Life Support (ALS) is totally appropriate for the majority of cardiac arrests, but what happens when it fails our patients? Refractory ventricular fibrillation (rVF) is, by its very nature, defined by the failure of ALS, but frustratingly there is very little evidence, or guidance, surrounding how to manage this patient group. I was faced with this situation when called to support an ambulance crew who were resuscitating an out-of-hospital VF arrest. When benchmarked against the ALS guidelines their management had been exemplary, but the patient remained in VF after eight shocks. So what now? The UK Resuscitation Council doesn't specifically discuss rVF, but offers the advice that it is "usually worthwhile continuing" if the patient remains in VF. Not a particularly controversial statement, but not much help either. They do discuss the potential for ECMO use, but this is currently a very rare option in UK practice, or thrombolysis for known or suspected pulmonary embolism. Other potential interventions not in the guidelines include IV magnesium and placing defibrillator pads in the anterior-posterior orientation. PCI can also be considered if there is a suitable receiving centre available and the patient can be delivered in a safe and timely fashion. A final option is the use of double sequential defibrillation (DSD), using two defibrillators, charged to their maximum energy setting, to deliver two shocks in an almost simultaneous fashion.DSD was first described in human subjects in 1994 when it was used to successfully defibrillate five patients who entered rVF during routine electrophysiologic testing. These patients were otherwise refractory to between seven and twenty single shocks. Looking at the available literature there has been little interest in DSD since then, until the last two to three years when it appears to have undergone a small revival. Sadly, there is no evidence for its use beyond case reports and small case series. The case reports appear to show good results with four in the last two years reporting survival to discharge with good neurological outcome. There are also a handful of other cases discussed in online blogs and articles with good outcomes. But these case reports and articles almost certainly represent an excellent example of publication bias. The most recent case series reviewed the use of DSD by an American ambulance service over a period of four years. During this time DSD was written into their refractory VF protocol, with rVF defined as failure of five single shocks. The study included twelve patients, three of whom survived to discharge with two of these demonstrating a cerebral performance score of 1. Despite appearing to demonstrate reasonable outcomes for DSD, sadly this study has a number of significant limitations. One important point the authors fail to discuss is that the two neurologically intact survivors received their DSD shocks after two and three single shocks respectively, not after five shocks which would have been per-protocol and consistent with the authors definition of refractory VF. This highlights a further problem with analysing the use of DSD. Not only is there a dearth of high-level evidence, but the literature that is available is highly inconsistent. There are a range of definitions for refractory VF, different orientations for the second set of pads, variable interventions prior to using DSD, a variety of timings between the shocks and so on. This means that comparison between studies and drawing meaningful conclusions is nearly impossible. Given these challenges, what are the explanations for why DSD might work? The first theory is that by using DSD the myocardium is defibrillated with a broader energy vector compared to a single set of pads resulting in a more complete depolarisation of the myocardium. A second theory is that the first shock reduces the ventricular defibrillation threshold meaning that the second shock is more effective. A third explanation may simply be the large amount of energy delivered to the myocardium. These theories should be tempered by the fact that studies have demonstrated increasing defibrillation energy to result in increased defibrillation success, but only up to a plateau. After this the success of defibrillation drops sharply. Increased energy use has also been demonstrated to cause an increase in A-V block but without an associated increase in shock success or patient outcome. The use of double sequential defibrillation is clearly an area that would benefit from further research, but despite this it is interesting to note that London Ambulance Service have enabled their Advanced Paramedic Practitioners to use DSD and some American EMS systems have written DSD into their protocols. So returning to the case in point what did I choose to do with my patient? After changing the pad position, administering magnesium and continuing defibrillation they remained in VF. I considered transport to a hospital with interventional cardiology but the patient was several stories up in a property with an inherently complex extrication. So I chose to use DSD because I felt that all other avenues had been explored. The patient had suffered a witnessed arrest, received bystander CPR immediately and throughout the resuscitation they had maintained a high end tidal CO2 and a coarse VF. I felt that this was a patient who could still respond to non-standard cardiac arrest management in the absence of a response to guideline directed treatment. After two DSD shocks a return of spontaneous circulation was achieved and the patient survived to hospital admission, but sadly didn't survive to hospital discharge. We're left with a even bigger question: if we accept that DSD is a potentially useful intervention in rVF, when should we consider using it? Would the outcome for this patient have been different if DSD had been used earlier? The European Resuscitation Council states that the use of double sequential defibrillation cannot be recommended for routine use. But treating rVF is not routine and the guidelines have otherwise failed our patient. It is said that insanity is defined as doing the same thing over and over again, without changing anything, and expecting a different result. Is this not what the guidelines preach in rVF? It is up to you, the clinician, to determine whether DSD is appropriate for each rVF case you encounter. But I urge you to consider the patient in front of you and tailor your resuscitation to their needs, whether that includes DSD or an alternative option. Personally, I believe DSD does have a place in the management of rVF patients, after considering the other interventions previously discussed. Given that shock success declines over time, DSD could be used as early as the sixth shock, because at this point the guidelines have nothing further to add. Or maybe it's me who's insane… James Yates (Critical Care Paramedic GWAAC) References Double sequential Defibrillation therapy for out-of-hospital cardiac arrests: the London experience. Emmerson AC, et al. Resuscitation. 2017 A Case Series of Double Sequence Defibrillation. Merlin MA. Prehosp Emerg Care. 2016 Double sequential external shocks for refractory ventricular fibrillation. Hoch DH. J Am Coll Cardiol. 1994 Double Sequential External Defibrillation in Out-of-Hospital Refractory Ventricular Fibrillation: A Reportof Ten Cases. Cabañas JG. Prehosp Emerg Care. 2015 Double Sequential Defibrillation for Refractory Ventricular Fibrillation: A Case Report. Lybeck AM. Prehosp Emerg Care. 2015 Double simultaneous defibrillators for refractory ventricular fibrillation. Leacock BW. J Emerg Med. 2014 Simultaneous use of two defibrillators for the conversion of refractory ventricular fibrillation. Gerstein NS. J Cardiothorac Vasc Anesth. 2015 Use of double sequential external defibrillation for refractory ventricular fibrillation during out-of-hospital cardiac arrest. Cortez E. Resuscitation. 2016 Double Sequential External Defibrillation and Survival from Out-of-Hospital Cardiac Arrest: A CaseReport. Johnston M. Prehosp Emerg Care. 2016 Dual defibrillation in out-of-hospital cardiac arrest: A retrospectivecohort analysis. Ross EM. Resuscitation. 2016 Refractory Ventricular Fibrillation Successfully Cardioverted With Dual Sequential Defibrillation. Sena RC. J Emerg Med. 2016 Dual sequential defibrillation: Does one plus one equal two? Deakin CD. Resuscitation. 2016 Magnesium therapy for refractory ventricular fibrillation. Baraka A. J Cardiothorac Vasc Anesth. 2000

High quality manual cardiopulmonary resuscitation (CPR) with minimal delays has been shown to improve outcomes following out-of-hospital cardiac arrest (OHCA). There are concerns that the quality of CPR can diminish over time and as little as 1 minute of CPR can lead to fatigue and deviation from the current recommended rate and depth of compressions. With this in mind, a mechanical device to provide chest compressions at a constant rate, depth and without tiring has considerable theoretical benefits to patients, yet clinical equipoise remains about the role for this treatment modality. In this podcast, we discuss and critically appraise 2 randomised controlled trials (RCTs) set out to answer exactly that question and give our take on the role for mechanical CPR devices in the future Hope you enjoy and feel free to leave any feedback below! Rob References Mechanical versus manual chest compression for out-of-hospital cardiac arrest (PARAMEDIC): a pragmatic, cluster randomised controlled trial. Perkins GD. Lancet. 2015 Mechanical chest compressions and simultaneous defibrillation vs conventional cardiopulmonary resuscitation in out-of-hospital cardiac arrest: the LINC randomized trial. Rubertsson S. JAMA. 2014

We're back with another look at the papers most relevant to our practice in and around The Resus Room. The WOMAN trial was a huge trial that looked at tranexamic acid in post partum haemorrhage, it's gained a lot of attention online and we kick things off having a look at the paper ourselves. Next up, and following on nicely from our previous Cardiac Arrest Centres podcast, we have a look at a systematic review and meta-analysis on whether prolonged transfer times in patients following cardiac arrest affects outcomes. Finally we have a look at a paper on management of PEs in cardiac arrest which draws some very interesting conclusions on the management of such cases and the associated outcomes! Please make sure you go and have a look at the papers yourself and as ever huge thanks to our sponsors ADPRAC for making this all possible. Enjoy! Simon & Rob References & Further Reading Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-controlled trial. WOMAN Trial Collaborators.Lancet 2017 Does transport time of out-of-hospital cardiac arrest patients matter? A systematic review and meta-analysis. Geri G. Resuscitation 2017 Pulmonary embolism related sudden cardiac arrest admitted alive at hospital: Management and outcomes. Bougouin W. Resuscitation. 2017 The Woman Trial; The Bottom Line

Oxygen is probably the drug that we give the most but possibly has the least governance over. More has got to be good except in those at high risk of type II respiratory failure right?? Well as we know the evidence base has swung to challenge that idea in recent years and the new BTS guidelines for Oxygen use in Healthcare and Emergency Settings has just been published with a few things that are worth reviewing since the original publication in 2008. No apologies that this may be predominantly old ground here, this is an area we're all involved with day in and day out that is simple to correct and affects mortality Historically oxygen has been given without prescription; 42% of patients in the 2015 BTS audit had no accompanying prescription When it is prescribed this doesn't always correlate with delivery 1/3 of patients were outside of target SpO2 range (10% below & 22% above) If nothing else is taken from this document then reinforcement of the fact that we need to keep oxygen saturations normal/near normal for all patients, except groups at risk of type II respiratory failure Prescribe and delivery oxygen by target oxygen saturations What is normal? Normal Oxygen saturations for healthy young adults is approximately 96-98%, there is minor decrease with increasing age. Healthy subjects desaturate to 90% SpO2 during night time; be cautious interpreting a single oximetry reading from a sleeping patient, short duration overnight dips are normal Will mental status give me an early indication of hypoxaemia? No, impaired mental function at a mean value of SaO2 64%, no evidence above SaO2 84% Loss of consciousness at a mean SaO2 56% Aims of oxygen therapy Correct potentially harmful hypoxia Alleviate breathlessness only in those hypoxic Why the fuss about hyperoxia? Hyperoxia has been shown to be associated with Risk to COPD patients and those at risk of type II respiratory failure Increased CK level in STEMI and increased infarct size on MR scan at 3 months Association of hyperoxaemia with increased mortality in several ITU studies Worsens systolic myocardial performance Absorption Atelectasis even at FIO2 30-50% Intrapulmonary shunting Post-operative hypoxaemia Coronary vasoconstriction Increased Systemic Vascular Resistance Reduced Cardiac Index Possible reperfusion injury post MI In patients with COPD studies have showed most hypercapnia patients arriving at hospital with the equivalent of SpO2 > 92% were acidotic, high concentration O2has been associated with more than double the mortality rate in those with acute exacerbations of COPD. Titrate O2 delivery down smoothly Which patients are at risk of CO2 retention and acidosis if given high dose oxygen? Chronic hypoxic lung disease COPD/CF/Bronchiectasis Chest wall disease Kyphoscoliosis Thoracoplasty Neuromuscular disease Morbid obesity with hypo ventilatory syndrome What is the oxygen target? Oxygen titrated to an SpO2 of 94-98% Except in those at risk of hypercapnia respiratory failure, then 88-92%(or specific SpO2 on patient's alert card) What about in Palliative Care? Most breathlessness in cancer patients is caused by airflow obstruction, infections or pleural effusions and in these cases the issues need to be addressed. Oxygen does relieve breathlessness in hyperaemic cancer patients but not if SpO2 >90%. Midazolam and morphine also relieve breathlessness and are more likely to be effective. Delivery Devices Reservior masks can deliver O2 concentrations between 60-80% Nasal cannualae at 1-6L/min can deliver 24-50% Venturi masks allow accurate delivery of O2 If tachypnoeic over 30 breaths per minute an increase over the marked flow rate should be delivered, note this won't increase the FiO2! Equivalent doses of O2 24% venturi = 1L O2 28 % venturi = 2L O2 35% venturi = 4L O2 40% venturi = nasal/facemask 5-6LO2 60% venturi = 7-10L simple face mask Approach to oxygen delivery Firstly determine if at risk of type II respiratory failure If not; SpO2 Perform an ABG If high PCO2 consider invasive ventilation, in the interim aim SpO2 94-98% If PCO2 normal or low aim SpO2 94-98% and repeat ABG in 30-60 minutes If at risk of type II respiratory failure Obtain ABG if hypoxic or already on oxygen If a respiratory acidosis consider NIV, address medical condition and senior review. Treat with the lowest FiO2 via venturi or nasal specs to maintain an SpO2 88-92% If hypercapnia but not acidotic, titrate the lowest FiO2 via venturi or nasal specs to maintain an SpO2 88-92%. Repeat ABG after change of treatment/deterioration. Consider reducing FiO2 if PO2 on ABG >8kPa If PCO2 Points specific to prehospital oxygen use A sudden reduction in 3% of SpO2 within the target range should prompt a fuller assessment of the patient Pulse oximetry must be available in all locations in which oxygen is being used Some patients over the age of 70 when clinically stable may have SpO2 between 92-94%, these patients don't require O2 therapy unless the SpO2 falls below the level that is known to be normal for that individual Patients with COPD should initially be given oxygen via 24% venturi at 2-4L/min or 28% mask at a flow rate 4L/min, or nasal cannulae at 1-2L/min aiming for 88-92% Patients over 50 years of age and long term smoker with a history of SOB on exertion and no other cause for their breathlessness should be treated as having COPD. Limit O2 driven nebs, if no air driven nebs available, to 6 minutes in duration in patients known to have COPD In summary.... So the bottom line? Well just like Goldielock's porridge, with oxygen we don't want too little, we don't want too much but we want just the right amount! There is no doubt that hypoxia kills but beware that too much of anything is bad for you and in the same way we need to be vigilant to targeting oxygen delivery to our patients target SpO2 References BTS Guideline for oxygen use in healthcare and emergency settings

How many patients are admitted from your ED with suspected cardiac chest pain? What strategy of testing do you employ to rule out acute myocardial infarction? When and why do you send troponins in this process? In this podcast Ed Carlton, Emergency Medicine Consultant at North Bristol Hospital and Troponin Researcher, talks to us about troponin rule out strategies, recent publications on the topics, where the future of troponin research is heading and most importantly what this all means for our practice. Our previous podcast on troponins acts as a good introduction to this episode. Have a listen to both and we'd love to hear your comments at the bottom of the page and we hope you found this as useful as we did! Enjoy Simon References Rapid Rule-out of Acute Myocardial Infarction With a Single High-Sensitivity Cardiac Troponin TMeasurement Below the Limit of Detection: A Collaborative Meta-analysis. Pickering JW. Ann Intern Med. 2017 Effect of Using the HEART Score in Patients With Chest Pain in the Emergency Department: A Stepped-Wedge, Cluster Randomized Trial. Poldervaart JM. Ann Intern Med. 2017 Comparison of the Efficacy and Safety of Early Rule-Out Pathways for Acute Myocardial Infarction. Chapman AR. Circulation. 2017

This month we've got a good variety of topics. We look at an recent systematic review and meta analysis on the prognostic value of echo in life support, an update from Blyth's paper in 2012. We review a paper looking at testing gin patients presenting to the emergency department in SVT. Finally we cover a paper looking at different methods employed when running an Emergency Department. As always make sure you go and have a read of the papers yourselves and come up with your own conclusions, we'd love to hear your feedback. Enjoy! Simon & Rob References & Further Reading Accuracy of point-of-care focused echocardiography in predicting outcome of resuscitation in cardiac arrest patients: A systematic review and meta-analysis. Tsou PY. Resuscitation. 2017 Usefulness of laboratory and radiological investigations in the management of supraventricular tachycardia. Ashok A. Emerg Med Australas.2017 What do emergency physicians in charge do? A qualitative observational study. Hosking I. Emerg Med J. 2017

This podcast is taken from a talk I gave at Grand Rounds at The Bristol Royal Infirmary on the Top 10 Papers in EM over the last 12 months. Many of these have been covered in previous podcasts, but running through them gives a good opportunity for further recap and reflection. Papers Covered; Chest wall thickness and decompression failure: A systematic review and meta-analysis comparing anatomic locations in needle thoracostomy. Laan DV1. Injury. 2015 Dec 13. pii: S0020-1383(15)00768-8. doi: 10.1016/j.injury.2015.11.045. [Epub ahead of print] (more in February'sPapers of the month) Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy (PATCH): a randomised, open-label, phase 3 trial. Baharoglu MI. Lancet.2016 May 9. pii: S0140-6736(16)30392-0. doi: 10.1016/S0140-6736(16)30392-0. [Epub ahead of print] (more in July's Papers of the month) Causes of Elevated Cardiac Troponins in the Emergency Department and Their Associated Mortality. Meigher S. Acad Emerg Med. 2016 (more in our Troponins podcast) Propofol or Ketofol for Procedural Sedation and Analgesia in Emergency Medicine-The POKER Study: A Randomized Double-Blind Clinical Trial. Ferguson I, et al. Ann Emerg Med. 2016. (more in September's Paper's of the month) Prevalence of Pulmonary Embolism among Patients Hospitalized for Syncope. Prandoni P. N Engl J Med. 2016 (more in our podcast PE The Controversy) Association Between Tracheal Intubation During Adult In-Hospital Cardiac Arrest and Survival. Andersen LW. JAMA. 2017 (more in March's Papers of the month) Review article: Why is there still a debate regarding the safety and efficacy of intravenous thrombolysis in the management of presumed acute ischaemic stroke? A systematic review and meta-analysis. Donaldson L. Emerg Med Australas. 2016 Aug 25 (more in our Stroke Thrombolysis podcast) Prophylactic hydration to protect renal function from intravascular iodinated contrast material in patients at high risk of contrast-induced nephropathy (AMACING): a prospective, randomised, phase 3, controlled, open-label, non-inferiority trial. Nijssen EC. Lancet. 2017 (more in April's Papers podcast) Immediate total-body CT scanning versus conventional imaging and selective CT scanning in patients with severe trauma (REACT-2): a randomised controlled trial. Sierink JC. Lancet. 2016 Jun 28 (more in August's Papers podcast) Accuracy of point-of-care focused echocardiography in predicting outcome of resuscitation in cardiac arrest patients: A systematic review and meta-analysis. Tsou PY. Resuscitation. 2017 (more coming up in May's Papers podcast!) Enjoy and we'll be back with our papers of the month next week! Simon