Coda Change

In this podcast, Mervyn Singer talks about the link between stress and multiple organ failure. Often, the organs involved in multi-organ failure show no signs of structural damage or cell damage that would indicate these organs might be under stress. Stress might cause functional damage rather than structural damage. Stress is a normal coping mechanism which helps to deal with the various stressors we encounter. These mechanisms include changes in behaviour, as well as autonomic and hormonal modulation of various systems. These include inflammatory, immune, cardiovascular, respiratory and metabolic systems. Human bodies are not designed to cope with the stresses of prolonged life. These stresses include old age, co-morbidities, prolonged critical illness, modern lifesaving drugs, and organ support. Mervyn discusses the evolution of various theories associated with stress. Walter Cannon discovered acute stress response in 1915 when he noticed the manifestation of nervous exhaustion as physical illness in soldiers of World War I. Furthermore, Hans Seyle described the general adaptation syndrome in 1936, stating that when in distress, the physiological systems are functionally compromised. Moreover, Takotsubo identified cardiomyopathy in the early 90s in Japan – in this condition heart failure occurs due to emotional stress. Ultimately, Sterling and Eyer defined Allostasis in 1988 as "staying the same by being different." The body goes into allostatic overload when exposed to extreme stress conditions. Type 1 allostatic overload of stress causes the organism to switch off in order to regain energy balance. Hibernation, estivation, anoxia, and dormancy are all example of allostatic response to stress. Myocardial hibernation is an example of an allostatic response in humans. Multiple markers identify poor prognosis in stressed patients. Energy and metabolism are directly proportional to each other and a reduced level of either or both can be seen in critically stressed patients. An ICU patient is under multiple stressors. These include physiological, pharmacological, environmental, and psychological stress, all of which lead to chronic critical illnesses. Thus, multiple organ failure may be an allostatic response to the prolonged stress faced by an ICU patient. Mervyn ends the podcast by suggesting multiple pharmacological and non-pharmacological methods to de-stress the patients.

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Jon McCormack gives you what you need to know in the case of paediatric blunt traumatic cardiac arrest. This is a rare but deadly occurrence. Data shows that the population incidence for paediatric blunt traumatic arrest is 1 in 100 000. Of these, most are male, and most are involved in vehicle traffic accidents, along with falls and non-accidental injuries. The median age is 7 years old. The injuries are severe, and the survival numbers make for grim reading… around 1%. So, the numbers are low in both incidence and survival. However, the cases can be deeply personal and effect the clinician and bystanders for a long time. With that being the case, coupled with the enormous upside both socially and economically, surely emergency care should "go all in". Jon explains why this is the wrong approach. He discusses the reality of the presentation of a paediatric blunt traumatic cardiac arrest. He advises to limit unnecessary treatments and risks to yourself and team. There are potential survivors. Children who maintain a detectable cardiac rhythm and show signs of life have better survival prognostics. Children in asystole or without signs of life will not survive. Objectively assessing signs of life may be important so Jon recommends being well versed in roadside echocardiograms. However, given the fact that the vast majority of children will be in excellent health at the time of injury, if they are showing no signs of life or cardiac activity, they have likely exhausted their enormous physiologic reserve. In this instance, they are in a decompensated which will lead to death. Finally, Jon concludes with some advice. In a paediatric blunt trauma cardiac arrest, initiate CPR and basic life support early, do not resort to a thoracotomy, and organise rapid triage and transport to a trauma centre if there are signs of life. If not, be prepared to stop futile treatments.

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Stephen Bernard shares his thoughts and the current evidence for using oxygen for cardiac arrest patients. Oxygen is ubiquitous in society! You can buy it in bottles and there are even oxygen cafes. This is especially true in hospitals where oxygen is used frequently and often without much thought. Oxygen is a natural substance. So surely, a short time on 100% oxygen can't be harmful, right? Stephen wants to challenge that idea. In this talk he presents the data on why oxygen might be harmful to your patients, particularly following a cardiac arrest. Out-of-hospital cardiac arrest (OHCA) is common and carries a high mortality rate. In Victoria, Australia, approximately 50% of patients with an initial cardiac rhythm of VF achieve a return of spontaneous circulation (ROSC) and 30% overall survive to hospital discharge. The outcome for patients is improving. This is due mainly to faster ambulance response times and increased rates of bystander CPR. What is done in the hospital has altered the patient's outcomes in the same way. Currently, OHCA patients who have achieved ROSC but who remain unconscious routinely receive 100% oxygen for several hours in the ambulance, ED, cardiac catheterisation laboratory until admission to ICU. However, there is now evidence from laboratory studies and preliminary observational clinical studies that the administration of 100% oxygen during the first few hours following resuscitation may increase both cardiac and neurological injury. Clinical trials are underway to test whether titrated oxygen to a target oxygen saturation of 90-94% in the immediate hours after ROSC results in improved outcomes compared with 100% oxygen. Join Stephen as he makes you think twice about blindly using oxygen for patients following a cardiac arrest.

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John Myburgh speaks passionately about the use of oxygen in resuscitation, and clinical outcomes in critical care. For the 30 years, clinical understanding of haemodynamic resuscitation has been based on physiological paradigms that focus on convective oxygen delivery. Most of these emphasise the role of cardiac output, haemoglobin and recommend interventions using synthetic agents such as dobutamine, synthetic colloids and blood transfusions. However, markedly influenced by industry, these interventions and strategies hijacked critical thinking creating a belief in the utility of attaining short-term physiological surrogates for resuscitation that have little relevance in improving patient-centred outcomes. This 'physiological fallacy' has been demonstrated in high-quality RCTs of fluids, goal-directed therapy and catecholamines, that paradoxically inform the interpretation of new insights in the physiological basis of health and disease. In this talk John presents two halves. In the first half, he discusses oxygen delivery. He begins with the oxygen cascade and applies this to the current thinking by some on oxygen delivery in critical care. He believes the two are incongruous. Measuring and altering oxygen is achieved using expensive toys and is likely not having a great impact on patient outcomes. John questions the whole concept of driving P02 to influence patient outcomes and mortality. In the second half John talks about the 'physiological fallacy' – the clinical practice of relying on variables we cannot accurately measure and do not understand. He presents a different approach. Physiology and haemodynamics encompass complex processes under intense neurohormonal vasoregulation. There is no one simple metric to rely on, such as V02 or D02. When considering a patient, the clinician must use their brain. John stresses the importance of focusing on understanding the disease process in its entirety rather than chasing instant gratification by altering a number. Work out where your patient exists on a spectrum. Consider acute versus chronic presentation, as well as compensated versus decompensated patients. This will dictate treatment. The situation usually complex and dynamic… Treat it as such.

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Scott Weingart discusses the scientific aspects of meditation. He believes meditation is to the mind what exercise is to the body. There are two types of meditation: focussed attention meditation or vipassana, and contemplative meditation. Generally, people exist in a default mode network. This happens when we are not focussed on anything in particular and thoughts occur in our brain without us being aware of it. Spending a few minutes every day aware of what thoughts are occurring in our brain is highly beneficial. This helps with stress control, relaxation response control, slowing of telomere degradation, control over emotions and increased concentration. Scott, however, wants us to focus on a single objective benefit of meditation - controlling the stimulus-response gap. Viktor E. Frankl explains - "Between stimulus and response there is a space. In that space is our power to choose our response. In our response lies our growth and our freedom." Meditation helps to choose our responses to stimuli, both good and bad. Scott explains how to do mindfulness meditation or vipassana.

First, pay attention to your present circumstance by linking it to your breath.

Second, be non-judgemental and forgive yourself for the random thoughts that come up while meditating.

Finally, watch moment by moment as experiences unfold. A book written by William B. Irvine on Stoics, introduced Scott to contemplative mediation. Stoicism is based on a philosophy of happiness which tries to eliminate negative emotions like hate, envy, anxiety, and fear. Scott dedicates this podcast to John Hinds by explaining how he appreciated the moments he spent with John due to his practising of mindfulness. Meditation is a way to appreciate every moment that we have in our short life. Exercise is work to live longer, while meditation is work to live better.

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Paul Young discusses remote ischaemic preconditioning and along he delves into the pitfalls of clinical research. 2016 was the 30th anniversary of ischaemic preconditioning. Remote ischaemic preconditioning is the magical offspring of ischaemic preconditioning and refers to the phenomenon whereby brief periods of ischaemia in one organ can protect other organs from subsequent prolonged ischaemic insults. Ischaemic preconditioning rose to prominence after a seminal paper in 1986 that demonstrated the protective effects of ischaemic preconditioning in dogs who had coronary ischaemia. This effect had been appreciated in humans. For instance, pre-infarct angina leads to smaller infarcts that in heart attacks without preceding angina. Remote preconditioning is for more magical. Paul takes you through the basics. The idea is simple enough. Blockage to one site leading to ischaemia preconditions another site to subsequent ischaemia. This was first demonstrated by blocking the circumflex artery in the first instance with a series of temporary occlusions. The left anterior descending was then blocked for a prolonged period. This preconditioned the heart to the prolonged ischaemia and decreased deleterious effects. This effect was then repeated with transient renal ischaemia protecting the heart from prolonged cardiac ischaemia. This effect was demonstrated with different organs – with almost any organ being able to protect another organ. The clinical application? Inflate a blood pressure cuff on an arm (to above systolic blood pressure) for five minutes and you will protect the opposite limb… or the heart. Remote ischaemic preconditioning is a reproducible phenomenon. However, as Paul explains, no one knows how it works. In this talk Paul describes his research – a double blind trial on remote ischaemic preconditioning; the first of its kind. He also describes a systematic review and meta-analysis he conducted. He found conflicting results in his trial and heterogeneity across other studies. When considering further research Paul concluded that it nothing was convincing and there were many pitfalls in the papers. What matters? What the patient can do, how they feel, whether they live and to a lesser extent does the intervention save money. In the end it seems that it is the relationship between ischaemia and reperfusion that makes a difference. That is, apply the remote ischaemic preconditioning after the primary ischaemia but before the reperfusion.

This has potential clinical implications for the following:

1. Heart surgery with cardiopulmonary bypass

2. Planned percutaneous coronary interventions

3. Acute myocardial infarction

4. CBA being treated with lysis or clot retrieval

5. Carotid endarterectomy surgery

6. Hypoxic ischaemic encephalopathy

7. Organ transplantation

8. abdominal aortic aneurysm surgery While this technique is not yet ready for clinical application, it remains an exciting potential therapeutic modality for the future. Finally, Paul finished with his top tips. Don't believe single centre studies, consider biological plausibility, be sceptical about secondary endpoints and don't be misled by surrogate endpoints.

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Marius Rehn examines the difficulties and importance of evidence based medicine in prehospital resuscitation. Notably, combining academic activity with pre- and in-hospital clinical practice is hard work. Being an academic in a flight suit can be quite lonely. Marius wants this to change and is passionate about increasing the quantity and quality of prehospital research. Prehospital research that examines patient pathophysiology should dictate care – as it does in the hospital environment. However, Evidence based practice pertaining to the prehospital environment is minimal. This needs to change. Evidence based medicine in the prehospital setting can dictate care, critically appraise practice and enable improvements in process and cost effectiveness whilst decreasing harms. Evidently, in-hospital evidence is different to the field application. Ultimately, prehospital research is critical, 5.8 million people die from injury every year – around 10% of the world's deaths. Unfortunately, pre-hospital research is underfunded. So, how can we take interventions from the hospital to the streets? Marius shares three important steps: The research that is needed How to interpret the evidence Why all research is important to consider (from case studies to randomised controlled trials) Moreover, Marius highlights the need to lean on other members of the scientific community when conducting your own research. For example, a statistician is worth their weight in gold in observational studies when fleshing out regression analysis. Finally, Marius discusses the importance of information dissemination across all platforms, including peer reviewed journals and informal FOAMed platforms such as Twitter. They all have their place.

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Anand Swaminathan brings precision emergency medicine and outcomes in critical care into the light.

He will convince you to start calling diseases for what they are and as a result start offering the proper treatments and care. All disease exists on a spectrum. You can't treat one end of the spectrum the same way you treat the other end.

This talk is inspired by a case of Anand's. An older man presented to the ED with acute onset shortness of breath and crackles. He was treated with Lasix. More and more Lasix – even though he wasn't improving.

Anand knew this presentation was more than just an exacerbation of heart failure. This was acute pulmonary oedema and this man needed a different treatment. Disease is on a spectrum with 'urgent' on one end and 'critical' on the other.

The umbrella term that identifies the disease needs to be spread out so that it can be placed on this spectrum by you and others around you. Calling a presentation an exacerbation of CHF when it is in fact acute pulmonary oedema is wrong and leads to harm for the patient. We have the medications and treatments for both end of the spectrum. However, they aren't always used.

Too often disease gets miscategorised on the wrong, milder end of the spectrum. Why? First, more patients exist at this end, and we therefore default back to this presentation of the illness. Secondly, there is an inverse relationship between the severity of disease and the research guiding treatment. Therefore, the temptation is to use this research to guide management all along the spectrum. Finally, time and resources are precious. The sicker a patient is, the more of these commodities they use up so err towards an approach for milder disease.

To counteract these points Anand wants you to understand the diseases better. How? First, educate yourself and those around you to assess and treat disease properly. Call the disease the right thing and ensure proper allocation of proper and adequate treatment and resources. Secondly, spend more time at the bedside – especially early in your training. This is how you rapidly identify sick patient, and rapidly determine what needs to be done. After this talk Anand hopes you are inspired and can walk into work tomorrow and make a change. Empower each other to act by calling things what they are!

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Sue Mason gives you her take on Geriatric Emergency Medicine. Sue's bread and butter is managing the elderly in the Emergency Department. It is not a sexy topic and there are few gizmos and gadgets. Nevertheless, it is very important. How big is the problem? Patients over 65 years represent about a quarter of the patients that attend Sue's Emergency Department. However, most of these patients arrive by ambulance and the vast majority of visits in this age group are deemed necessary. This culminates with 50% of these patients being admitted. Attendance and admissions in the elderly age group are both going up. What are we doing about it? Advances have been made in prehospital care. In Sue's region, paramedics have been trained in assessing and managing elderly falls. This found a reduction in ED attendance by 25% and decreased admissions by 6%. Approaching the management of the elderly with a multidisciplinary team has proved to be effective in a ward setting. This has not been replicated in the Emergency Department. Within the ED there is potential for the inclusion of a pharmacist to improve admission rates. However there has not been any other "in department" interventions involving a broader team. The initiation of interventions from the ED to continue in the community has been looked at, although the evidence is mixed. How can we do it better? Sue explores the question of whether all Emergency physicians should be trained in Geriatric Medicine. Or whether there should be sub-specialists in Geriatric Emergency Medicine. She also explores other strategies. Simple things such as not putting elderly patients on beds/trolleys unless clinically indicated and ensuring they have fluids on board. Overriding all decisions should be the question – does this patient need this investigation, treatment, and admission.

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Dr Michelle Johnston talks about dystopian futures and the relevance of emergency medicine in forming such futures. Literature can provide insights into the two types of future we can expect: an optimistic, technologically advanced future as showcased in the movie "Blade Runner" or a dystopian future as envisioned by George Orwell in the novel "1984".

She discusses how different authors have written along similar dystopian themes with government controlling all aspects of human life. Some examples are novels like "Brave New World" by Aldous Huxley and "The Handmaid's Tale" by Margaret Atwood. Or, "The Hunger Games", "The Maze Runner", and movies like "Brazil". The common theme of these stories is oppression of the individual, non-existence or illusion of freedom, poverty, and police societies.

Michelle believes that dystopian literature is based on the tiny fears of individuals and how they react to it, shaping the future.

Therefore, she asks the question: what are the things that we do today that might lead to a dystopian future?

She begins with discussing technology in emergency medicine that already exists and points towards a bright utopia. This includes augmented reality, smart glasses, shmeat, 3-D printed replacement parts, robots, nano-robots and genome mapping. Michelle next discusses factors in emergency medicine that might lead us to a dystopian future. Over use of broad-spectrum antibiotics combined with uncontrolled use of antibiotics in agriculture, and international travel has led to increased microbial resistance. Unnecessary tests and treatments are another factor contributing to a dystopian future.

Economic inequity in emergency medicine. One side of society spend huge amounts on sustaining the last years of a patient's life. Meanwhile, on the other side, huge populations are deprived of basic needs. Increased waste production by hospitals due to increased usage of disposable tools is contributing to climate change.

Administrative bureaucracy is another factor which though necessary, might be restricting creativity and individuality. Michelle concludes by quoting Immanuel Kant: "Even small decisions ought to be made as if we were choosing for all of humanity, not just our paltry self."

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