The St.Emlyn’s Podcast

Today, we are discussing syncope, a common yet complex condition involving a transient loss of consciousness due to a temporary reduction in blood flow to the brain. This comprehensive guide aims to provide insights into diagnosing and managing syncope in the emergency department.

When patients present with collapse, it’s essential to differentiate between mechanical falls and syncope due to physiological reasons. The key to diagnosis lies in understanding whether the event was caused by a transient loss of consciousness or a mechanical fall. This distinction guides the diagnostic pathway and ensures the appropriate management of potential life-threatening conditions.

Syncope results from a temporary reduction in cerebral perfusion pressure, which can occur due to various physiological disruptions. Understanding the factors affecting cerebral perfusion, such as mean arterial pressure, cardiac output, and peripheral resistance, is crucial. Any significant deviation in these parameters can lead to syncope.

Cardiac syncope often involves rhythm disturbances like bradycardia (abnormally slow heart rate) or tachycardia (abnormally fast heart rate). Bradycardia can reduce cardiac output, while tachycardia can decrease stroke volume. Identifying these rhythm issues is vital as they can be life-threatening.

Structural heart diseases, such as aortic stenosis or hypertrophic cardiomyopathy, restrict blood flow, leading to syncope. Pulmonary embolism, although less common, can also cause syncope by obstructing pulmonary circulation.

The electrocardiogram (ECG) is a critical tool for diagnosing cardiac causes of syncope. It helps identify arrhythmias, conduction abnormalities, and other cardiac issues. Continuous ECG monitoring, or Holter monitoring, can capture transient arrhythmias not seen on a standard ECG.

Neurological conditions, such as seizures and transient ischemic attacks (TIAs), can present as syncope. Differentiating between these and true syncope is essential. Seizures often have specific signs like tongue biting, loss of bladder control, and post-ictal confusion. TIAs can cause temporary disruptions in blood flow to the brain, leading to syncope-like episodes.

Vasovagal syncope, triggered by stress, pain, or prolonged standing, involves a sudden drop in heart rate and blood pressure. It is a common and generally benign cause of syncope.

Orthostatic hypotension, a drop in blood pressure upon standing, can result from dehydration, medications, or autonomic dysfunction. It is a frequent cause of syncope, especially in elderly patients.

A thorough patient history is crucial for identifying the cause of syncope. Key elements include the circumstances of the episode, prodromal symptoms, witness accounts, and medical history. This information helps distinguish between different causes of syncope.

A comprehensive physical examination includes checking vital signs, cardiovascular examination, and neurological assessment. Identifying abnormalities during the physical exam can provide clues to the underlying cause of syncope.

• ECG: Identifies arrhythmias and conduction abnormalities.

Management of cardiac syncope focuses on stabilizing heart rhythm and function. Treatments may include pacemaker implantation for bradycardia, medications for tachycardia, and surgical interventions for structural heart diseases. Arrhythmias may require implantable cardioverter-defibrillators (ICDs).

Managing neurological causes involves addressing the underlying condition. Antiepileptic medications control seizures, while immediate interventions restore blood flow in strokes or control bleeding. TIAs require medications and lifestyle changes to reduce recurrence risk.

• Vasovagal Syncope: Management includes avoiding triggers, increasing fluid and salt intake, and using compression stockings. Severe cases may require medications.

Safety netting ensures patients receive appropriate follow-up care and instructions. Key elements include providing clear discharge instructions, scheduling follow-up appointments, and educating patients about syncope causes and management.

Reflex anoxic seizures, seen especially in children, involve shaking movements due to a drop in oxygenation. These can be misinterpreted as epileptic seizures but require different management.

Misdiagnosis of syncope as epilepsy or vice versa is common. Always consider both possibilities, especially when symptoms overlap.

Postural hypotension requires careful evaluation. Special considerations include ruling out abdominal aortic aneurysm in older men and ectopic pregnancy in younger women.

Syncope is a multifaceted condition that demands careful evaluation and management in the emergency department. By understanding the underlying causes, utilizing appropriate diagnostic tools, and implementing effective management strategies, healthcare professionals can optimize patient outcomes and reduce the risk of recurrent episodes.

This guide aims to provide valuable insights into the diagnosis and management of syncope, helping healthcare providers deliver high-quality care. For further information, examples, and case studies, visit the St Emlyn's blog, where we continue to share knowledge and expertise in emergency medicine.

Remember, accurate diagnosis and timely intervention are key to managing syncope effectively. Stay vigilant, consult with senior colleagues when needed, and always prioritize patient safety.

Thank you for reading. If you have any questions or need further information, please get in touch. We look forward to continuing the conversation and improving patient care together.

Welcome to the St. Emlyn's podcast. I'm Ian Beardsell and I'm Rick Bodden. This is part two of our troponin special where we delve deeper into high sensitivity troponins (hs-Tn) and their significance in emergency medicine. Today, we'll explore the nuances of hs-Tn assays and how they can enhance our work in the emergency department (ED).

High sensitivity troponins (hs-Tn) have transformed how we detect and manage myocardial infarctions (MI) in emergency settings. Unlike traditional assays, hs-Tn tests detect much lower concentrations of troponin, a protein released during myocardial injury, allowing for earlier and more accurate detection of cardiac events.

Understanding the difference between analytical and diagnostic sensitivity is crucial. Analytical sensitivity refers to the assay's ability to detect low concentrations of troponin, whereas diagnostic sensitivity relates to the test's performance in diagnosing acute myocardial infarctions (AMI).

Key Points on Analytical Sensitivity:

• Detection Threshold: High sensitivity troponin assays can detect troponin in over 50% of healthy individuals.

Diagnostic Sensitivity:

• Improved Detection: Studies show hs-Tn assays have a higher diagnostic sensitivity (90-92%) compared to older assays (80-85%).

To illustrate, let's focus on the Roche troponin T high sensitivity assay:

• 99th Percentile Cutoff: 14 nanograms per liter.

While hs-Tn assays improve sensitivity, they may reduce specificity:

• More Positives: Lowering the diagnostic threshold results in more positive results, increasing diagnostic sensitivity but reducing specificity.

Early Rule-Out Protocols: The most significant advantage of hs-Tn assays is their potential to expedite the rule-out process:

• Zero and Three-Hour Protocols: Studies suggest that hs-Tn assays can effectively rule out AMI with samples taken at 0 and 3 hours after arrival, instead of the traditional 6-hour wait.

Understanding Deltas: Delta refers to the change in troponin levels between tests:

• Absolute vs. Relative Deltas: Absolute changes (e.g., an increase of 10 nanograms per liter) are often more reliable than relative percentage changes.

Incidental Troponin Elevations: With increased testing at the front door, incidental findings are inevitable:

• Low Pre-Test Probability: In patients with a low pre-test probability of AMI (e.g., mechanical falls), a positive hs-Tn result often does not indicate AMI.

Patients with Comorbidities: Troponin levels can be elevated in patients with various comorbidities:

• Age and Chronic Conditions: Older patients and those with conditions like LV dysfunction may have higher baseline troponin levels.

Ongoing Research: Research and guidelines on hs-Tn usage are continually evolving:

• NICE Guidelines: Recommendations on using hs-Tn in clinical practice are expected to be published, providing clearer protocols for emergency physicians.

Point-of-Care Testing: While hs-Tn assays currently require large analyzers, point-of-care testing remains a goal:

• Future Developments: Advances in technology may eventually make hs-Tn testing available at the bedside, further streamlining ED workflows.

High sensitivity troponins represent a significant advancement in the early detection and management of myocardial infarctions in the emergency department. By understanding the nuances of analytical and diagnostic sensitivity, utilizing early rule-out protocols, and interpreting results within the clinical context, emergency physicians can leverage these assays to improve patient care. As always, ongoing research and adherence to evolving guidelines will be essential in optimizing the use of hs-Tn in clinical practice.

We hope this podcast helps you better understand the complexities and advantages of high sensitivity troponins. For more insights and updates, stay tuned to the St. Emlyn's blog and feel free to reach out with your questions and experiences. Together, we can continue to advance emergency medicine for the benefit of our patients.

Welcome to the St. Emlyne's blog, where we provide the latest updates and insights into the world of emergency medicine. Today, we're diving into the much-anticipated College of Emergency Medicine (CEM) Conference, set to take place in Exeter from September 9th to 11th. This conference is not only a hub for academic learning but also a celebration of the progress and future of emergency medicine.

Exeter, nestled in the scenic Southwest of England, offers an exciting venue for this year’s CEM Conference. The University of Exeter provides a fresh and dynamic backdrop, allowing attendees to experience a new environment. The choice of Exeter also aims to highlight the region's significant contributions to medical research and practice. Plus, the location promises better weather compared to other parts of the UK, making it a pleasant destination.

The conference is packed with sessions designed to engage and educate emergency medicine professionals. Here are some highlights to look forward to:

• Ann Marie Kelly from Australia will share her expertise on arterial and venous blood gases, offering critical insights for daily medical practice.

The conference features a variety of sessions tailored to different interests within emergency medicine:

• Dragon's Den: Watch as grant applicants pitch their projects to a panel of emergency medicine experts, competing for a share of £1000 to fund their innovative ideas.

Balancing work with social activities is a key theme of the conference. Highlights include:

• Gala Dinner at Exeter Castle: An opportunity to unwind and network in a historic setting.

The conference boasts a robust academic programme with four tracks running simultaneously on some days, ensuring there's something for everyone, whether you're a trainee, an established consultant, or involved in cutting-edge emergency medicine research.

Sessions focus on essential topics in emergency medicine, aiming to reconnect professionals with the fundamentals that make this field vital and rewarding. The goal is to address rising attendances and increasing pressures in emergency departments by reinforcing core knowledge and practices.

Attendees will engage with the latest research and innovations in emergency medicine. The programme is designed to be both educational and academically stimulating, attracting participants with its high-quality content.

The CEM Conference in Exeter offers numerous benefits:

• Professional Development: Enhance your knowledge and skills through sessions led by top experts in the field.

If you haven't booked your place yet, it’s not too late! There are still a few spots available, but they are filling up fast. Visit the college website to secure your place and register for the explore Devon activities, which are also in high demand.

For those who can’t attend in person, the conference will share video excerpts of key sessions. Follow the #CEMEXETER2014 hashtag on Twitter and check out the college's YouTube channel for updates and highlights.

The CEM Conference in Exeter is shaping up to be an unmissable event for anyone in the field of emergency medicine. With its combination of high-quality academic content, inspirational speakers, and engaging social activities, it promises to be both educational and enjoyable. Whether you're attending for the learning opportunities, the chance to network, or simply to enjoy the vibrant atmosphere, this conference has something to offer everyone.

Don't miss out on this fantastic opportunity to advance your career and connect with the emergency medicine community. Book your place today and join us in Exeter for an unforgettable experience!

Shortness of breath, or dyspnoea, is an alarming symptom because it can signify a wide range of serious conditions. From acute respiratory diseases to cardiac emergencies, the differential diagnosis is vast. For new doctors, encountering a patient with dyspnea can be particularly challenging due to the multitude of potential causes and the urgent nature of the symptom.

In the ED, our primary focus is to rule out the most serious conditions first. This approach ensures that we address potentially fatal diagnoses promptly. The key life-threatening causes of shortness of breath include:

These conditions require immediate attention and demand different management strategies. Let's break down each one and discuss the clinical approach.

When a patient presents with shortness of breath, one of the first steps is to administer oxygen. This intervention is typically beneficial, as it addresses potential hypoxia, a common denominator in many serious conditions. While long-term oxygen therapy may have contraindications in specific situations, such as COPD exacerbations, the immediate goal is to stabilize the patient.

For patients with severe dyspnea, resuscitation measures might be necessary. These individuals should be placed in a monitored area with nursing support and close physician oversight. In cases where respiratory distress is evident, ensure that resuscitation equipment and personnel are readily available.

A thorough history is critical in identifying the underlying cause of shortness of breath. Key aspects to explore include:

It's also helpful to ask the patient if they have experienced similar symptoms before. This question can provide immediate insight, especially if the patient has a known condition like LVF.

The physical examination should be comprehensive, focusing on:

Continuous monitoring is vital for patients presenting with shortness of breath. Vital signs, including oxygen saturation and respiratory rate, should be closely observed. Frequent reassessment allows for timely adjustments in the treatment plan, ensuring optimal patient outcomes.

In the ED, working alongside senior colleagues and consulting other specialties can significantly enhance patient care. Junior doctors should proactively seek guidance, especially in complex or uncertain cases. This collaborative approach not only enhances patient safety but also serves as a valuable educational experience.

Dealing with shortness of breath can be stressful, especially when the cause is not immediately apparent. Developing a systematic approach, or mental model, can help clinicians efficiently manage these cases. Practicing this approach mentally, perhaps during a commute, can prepare one for real-life scenarios. This mental rehearsal fosters a more confident and effective response when faced with an actual patient.

Shortness of breath is a common yet potentially life-threatening symptom that demands a structured and thorough approach. By prioritizing the exclusion of critical diagnoses, employing appropriate diagnostic tools, and initiating targeted treatments, emergency physicians can significantly improve patient outcomes. Remember, early intervention and continuous monitoring are key, as is the willingness to consult senior colleagues and use available resources.

For more detailed discussions and educational resources, visit our blog site. Keep learning, stay curious, and continue to provide compassionate care to all patients. Thank you for joining us on the St. Emlyn's podcast. We look forward to sharing more insights and discussions in future episodes. Good luck in your practice, and always strive to heal the sick! See you soon!

Shortness of breath is a common yet potentially life-threatening presentation in the emergency department. A structured approach to assessment and management, including a thorough primary survey, focused history, physical examination, and targeted investigations, is essential. Early initiation of oxygen therapy, appropriate use of diagnostic tools, and timely management of underlying conditions can significantly impact patient outcomes. Collaboration with senior colleagues and continuous education through simulation and practice are key to improving care for these patients.

Breathless patients are a challenge in the ED. Shortness of

• Pneumonia
• Asthma/COPD
• Pulmonary Embolism
• Acute left ventricular failure
• Pneumothorax

In

 For

http://vimeo.com/35310564

• Oxygen should be used in the patient with shortness of breath and the patient monitored closely. Hypoxia kills
• Always rule out life threatening causes first
• These patients are sick - do not be afraid to ask advice from a senior colleague early
• Look for clues - you don't have to wait until the penultimate page of the story to solve the mystery.

 Oxygen - or no oxygen??

Where do I begin?
A focused history, including asking the patient about previous conditions and whether they know what's going on!

What treatments might be useful?

Which investigations might help me find out more?

• A

One

Headaches can be tricky. Many patients experience them as part of various symptomatologies, but our focus here is on those for whom headache is the primary complaint. Our objective is to rule out serious conditions while providing effective management. The major diagnoses to consider include subarachnoid haemorrhage, meningitis, brain tumours, and temporal arteritis.

Every emergency physician must be vigilant about subarachnoid haemorrhage (SAH). The classic presentation is a sudden-onset severe headache, often described as being hit on the back of the head with a baseball bat. However, not all patients present with this textbook description. Many just report an incredibly severe headache, sometimes developing over minutes rather than instantaneously.

In such cases, the threshold for investigation should be low. Studies indicate that about 10% of patients presenting to the ED with headaches have a potentially life-threatening condition such as SAH, tumor, or meningitis. This high hit rate underscores the importance of being thorough. Early CT scans are critical. They are more diagnostic the earlier they are performed, and a negative CT can often effectively rule out SAH.

Meningitis is another serious condition that can cause a headache. The classic signs include a recent infection, high temperature, neck stiffness, and altered consciousness. However, like SAH, meningitis doesn’t always follow the textbook. Patients may present with milder symptoms, such as neck pain without severe rigidity or general discomfort with light without pronounced photophobia.

Blood tests like white cell count and CRP are not always reliable when considering meningitis. The absence of abnormalities doesn’t rule out the disease. Therefore, empirical treatment with antibiotics is often warranted if there’s any suspicion of meningitis. It’s better to administer antibiotics and later find out they weren’t necessary than to miss a diagnosis and face dire consequences.

Brain tumours can present subtly, often with non-specific signs like headaches, which can be easily overlooked. First-time seizures in young adults are a common presentation that warrants a thorough evaluation for tumours. CT scans are typically sufficient to detect most tumours, although in some cases, additional imaging such as MRI or CT angiography may be necessary.

Temporal arteritis is another condition to consider, particularly in patients over 50. Symptoms include headache, jaw claudication, and visual disturbances. Blood tests such as ESR and CRP are useful here. Early treatment with steroids can prevent irreversible vision loss, making prompt diagnosis and intervention crucial.

Migraines are a common yet often overlooked cause of severe headaches that bring patients to the ED. While not life-threatening, they can be debilitating. Effective management involves hydration, analgesics, anti-emetics, and sometimes 5HT3 receptor antagonists. It’s important to distinguish between first-time migraine presentations and recurrent migraines, especially in older patients, to rule out more serious underlying conditions.

The advent of CT scanning has revolutionized the management of headaches in the ED. Today, the threshold for performing a CT scan is much lower than it was 15 years ago. Despite concerns about radiation, the benefit of identifying serious conditions outweighs the risks, particularly when about 10% of patients have significant pathology.

For junior doctors, it’s essential to involve senior colleagues in the evaluation and management of patients presenting with headaches. Discussing cases with experienced physicians helps in understanding the rationale behind investigations and management decisions. This collaborative approach ensures comprehensive care and aids in professional development.

Managing headaches in the emergency department requires a careful, systematic approach to rule out life-threatening conditions while providing effective symptom relief. Subarachnoid haemorrhage, meningitis, brain tumours, and temporal arteritis are critical diagnoses that must not be missed. Early CT scans, judicious use of blood tests, and prompt empirical treatment when necessary are key strategies. Remember, thorough evaluation and timely intervention can significantly improve patient outcomes.

We've all had headaches, but not often severe enough to prompt us to seek help in an Emergency Department.

In

• Subarachnoid Haemorrhage
• Meningitis
• Tumours and Space Occupying Lesions
• Temporal Arteritis

Listen to Simon and Iain discuss how to approach these patients here

Headaches at Life in the Fast Lane - a great summary from the LiTFL crew

NICE Guidelines (NCG150) - diagnosis and management of headaches; there's a flowchart and some red flags although you could read the St Emlyn's summary here!

Headache from the Flipped EM Classroom

Welcome to the St. Emlyn's podcast! In this episode, we're exploring the fascinating world of troponins, vital biomarkers essential for diagnosing myocardial injury. Whether you're a seasoned clinician or a medical student, understanding troponins is crucial for effective patient care. We'll cover everything from the basics to advanced concepts, ensuring you have a comprehensive grasp of this critical topic.

Troponins are proteins found in muscle tissue, playing a key role in muscle contraction. Often misunderstood as cardiac enzymes, troponins are actually proteins involved in the contractile apparatus within muscle cells. They exist in three forms: Troponin I, Troponin T, and Troponin C, which work together within muscle fibers to regulate muscle contractions.

Troponins are crucial biomarkers for diagnosing myocardial injury. When heart muscle is damaged, troponins are released into the bloodstream. This release can occur due to various conditions, including myocardial infarction (heart attack) and other forms of stress on the heart. Measuring troponin levels in the blood helps clinicians determine the extent of myocardial injury and make informed decisions about patient care.

Troponins are present in both skeletal and cardiac muscle. However, cardiac-specific isoforms of Troponin I and Troponin T can be detected through blood tests, allowing clinicians to specifically identify myocardial damage. This specificity is a significant advancement over previous markers like CK, LDH, and ALT, which were not cardiac-specific and took longer to rise in the bloodstream.

Troponins are released into the bloodstream when there is myocardial injury. This injury can result from various causes, such as acute myocardial infarction, physical stress, or other conditions that strain the heart. Understanding that troponins indicate myocardial injury rather than just myocardial infarction is crucial for accurate diagnosis and treatment.

Following myocardial injury, troponin levels typically peak in the blood within 12 to 24 hours. The time it takes for troponin levels to fall depends on several factors, including the severity of the injury, the patient's renal function, and whether there is ongoing troponin release into the blood. For example, patients with significant myocardial infarction might take weeks to clear troponins from their bloodstream, while those with smaller injuries might clear them within a day.

A common question is whether troponin tests are useful in patients with renal failure. The answer is a resounding yes. Although patients with renal failure may have elevated baseline troponin levels due to reduced clearance, troponin testing remains a valuable diagnostic tool. It's essential to interpret these levels in the context of the patient's renal function and look for trends in troponin levels through serial testing.

Troponin tests are immunoassays, which means they use antibodies to target specific parts of the troponin molecule. These antibodies are attached to a signal that emits light, allowing for the quantification of troponin levels in the blood. While lab-based assays are highly accurate, point-of-care testing devices are also available, though they may not be as sensitive or precise as lab tests.

Point-of-care testing devices, such as handheld analyzers, offer quick results and can be used at the bedside. However, they may not match the sensitivity and precision of lab-based assays. Some portable devices provide qualitative results, similar to a home pregnancy test, while others offer quantitative measurements. Clinicians should be aware of these differences and use point-of-care devices appropriately.

When discussing troponin assays, it's crucial to differentiate between analytical sensitivity and diagnostic sensitivity. Analytical sensitivity refers to the assay's ability to detect low concentrations of troponin reliably. In contrast, diagnostic sensitivity pertains to the assay's ability to correctly identify patients with the condition being tested for, such as acute myocardial infarction. High-sensitivity troponin assays have improved both analytical and diagnostic sensitivity, enabling earlier and more accurate diagnosis.

In the UK, troponin testing typically starts from the time of symptom onset. This approach differs from other countries where testing begins upon the patient's arrival in the emergency department. The timing of troponin testing is crucial, as early testing can lack sensitivity. Serial sampling over several hours helps ensure accurate diagnosis, with a common practice being to test initially and then again at intervals such as six, ten, or twelve hours after symptom onset.

Interpreting troponin levels requires considering the clinical context and pre-test probability. A positive troponin test in a patient with low pre-test probability of myocardial infarction may not indicate a true positive. Conversely, a negative test in a high-risk patient does not entirely rule out disease, especially if there is potential for a late troponin rise. Clinicians must integrate troponin results with other diagnostic information to make informed decisions.

Patients with renal failure often have elevated baseline troponin levels due to impaired clearance. However, troponin testing remains valuable for diagnosing myocardial injury in these patients. It's essential to understand the baseline level for each patient and focus on changes in troponin levels over time, rather than a single measurement. Serial sampling helps differentiate chronic elevation from acute myocardial injury.

It's important to recognize that unstable angina can occur without elevated troponin levels. These patients may not show a rise and fall in troponin but still have significant coronary artery disease that requires attention. Clinical judgment, along with other diagnostic tools like ECG and patient history, is vital in diagnosing and managing unstable angina.

Understanding troponins and their role in diagnosing myocardial injury is essential for clinicians. From the basics of what troponins are to the nuances of interpreting test results, this knowledge is crucial for providing the best care to patients with suspected cardiac conditions. Stay tuned for our next episode, where we'll delve deeper into high-sensitivity troponin assays and their impact on emergency medicine.

For any questions or further discussion, feel free to comment on the blog post or email us. We're here to help and look forward to continuing this conversation. Until next time, take care and keep learning!

This blog post is brought to you by the team at St. Emlyn's, dedicated to providing high-quality education and resources for emergency medicine professionals.

Do you remember when it took three days to 'rule in' or 'rule out' an acute myocardial infarction (AMI)?  When I was a medical student doing my first clinical attachments, I remember doing ward rounds on the CCU seeing patients with suspected AMI.  The way they were managed is a million miles from what we do now.  Back then, patients would have serial ECGs and then be admitted for cardiac enzyme evaluation over the course of the next 3 days.  We'd measure CK, AST and LDH.  'CK' was the so-called 'early marker', which would rise early after the start of an AMI.  Today we use CK as a marker of skeletal muscle damage (e.g. rhabdomyolysis).  AST and LDH (today we think of these as liver function tests, I know) were the 'late markers' - and by late I really mean late - we might see a rise on days 2 and 3.

Could you imagine for a second, in today's world, ruling out AMI because their CK and LFTs were normal?  It's completely unthinkable.  That's how much cardiac troponin has changed our practice.  We rely on it so completely to diagnose AMI.  And yet, it's one of the most misunderstood tests in medicine.  Given how much we use it, I guess we feel that we all should know lots about this test.  But doctors still have so many questions.  Here are just a few:

• What is cardiac troponin?
• Why is it a marker of AMI?
• What else causes a raised troponin and how?
• Should we be doing troponins at 3 hours, 6 hours, 12 hours?  What's the difference and what's the evidence?
• What is a 'delta troponin'?
• What do you need to 'rule in' AMI?
• How do you use cardiac troponin in patients with renal failure?

This is just a brief list.  With the research I do in this area and my experience developing protocols/guidelines, people get in touch to ask questions like this quite a lot.  There are loads of questions that people ask - but there are lots of themes in common.  We thought it was about time we produced a handy run down in the true spirit of #FOAMed.

Take a listen to Part 1 of our troponin podcast.  While Simon and Iain have been prolifically churning out spectacular stuff for some time now, this is my debut on the St. Emlyn's podcast.  I really enjoyed talking about troponin with Iain - and I hope we covered some useful stuff.

We'll cover more in part 2, when we'll move on to discussing high sensitivity troponins, what they are, how to use them and how to speak the troponin lingo.  Please get in touch if there's anything we haven't covered that you'd like us to, or if there's anything you'd like us to elaborate on some more!

Rick