Mental Practice: A tool for skill training during COVID pandemic

mental practice

COVID-19 pandemic has caused drastic changes in personal and educational lives of medical students, who hold a unique position between being a student and a part of the health care workforce (1). The role of senior medical students who are on the brink of becoming licenced physicians, in particular, have been discussed thoroughly by experts from the perspective of safety, education and the need for skilled workforce. As the discussions continue, medical students got to stay home – as it should be, in my opinion – at least in most countries. Remote learning became the primary training modality all in a sudden.

Remote learning, even though the safest option, is not free of problems. Studying from home and continuing daily routine require a strong determination, especially when people have a lot on their minds. But most of all, clinical and procedural skills are hard, if not impossible, to translate into online learning. Medical students need alternative methods to physical practice of clinical and procedural skills, other than reading instructions and watching procedural videos. Mental practice may offer a solution for medical students who want to sharpen or at least retain procedural skills at home.

What is Mental Practice?

Mental practice refers to the introspective rehearsal or visualisation of psychomotor skills (2). It has been called many names including ‘‘imaginary practice,’’ ‘‘covert rehearsal,’’ ‘‘conceptualization,’’ or ‘‘mental imagery rehearsal’.’ It has been researched extensively in sports literature and is shown to provide both cognitive and motivational benefits (3). Can it do the same trick for medical training, though? At this point, being sceptical is perfectly normal. Let’s look into the literature.

 

The History of Mental Practice

Surprisingly, even as early as the 1900s, the scientists were discussing the effect of ideational elements in motor learning (4). In the 1930s, pioneer researchers had already experimented on rats that were deprived of kinesthetic impulses by sectioning of the cervical cord and discovered that even they could not run the maze as perfectly as normal rats in terms of motor skills, they still learned it (5, 6, 7). They asserted that kinesthetic impulses were neither sufficient nor necessary in learning of the motor skill. A few years later in 1940, researchers observed ideational clues helped human subjects to learn basic motor skills making fewer attempts, committing fewer errors, and spending less time (8). Subsequent studies tested mental practice against the physical in basketball free throws, dart games, and ring toss (9, 10). All reached the same conclusion: Mental practice was effective, even about as effective as physical practice in learning of motor skills.

What About Medical Training?

Experiments on the use of mental practice in the area of medical training started a few decades later. One of the first studies examined the use of mental practice in the pelvic examination. The students who did 5-minute audio-guided mental practices before and after the physical practice on a model performed significantly better at skill examination (11). Research in this area has gained momentum recently. Mental practice was shown to facilitate medical students’ learning of suturing, venipuncture, cricothyroidotomy, and lumbar puncture (12-15). In some studies, it performed as effective as physical practice, and superior to studying text (12, 16). 

The evidence shows that mental practice can be a strong and free learning tool. It can serve as a satisfactory substitute for physical practice in the days of the pandemic, which forces medical students to stay at home. But, let’s not get ahead of ourselves. Mental practice does not provide all of the answers. Remember the rats: They still needed motor practice to run perfectly and as fast as normal rats (7). In other words, you still need the train your muscles to operate smoothly what you have learned. Even after years of mental practice, one could never score a free throw if he or she is lacking the muscle strength to make the ball reach the basket. Admittedly, most medical procedures do not require large motor skills or much strength, but they still demand well-trained small muscles. However, until the world figures out how to put a medical student and a simulator together in the same room safely, the mental practice seems like a solid way of learning new procedures.

References

  1. Miller, D. G., Pierson, L., & Doernberg, S. (2020). The role of medical students during the COVID-19 pandemic. Annals of Internal Medicine.
  2. Oxendine, J.B. (1968). Psychology of motor learning. Englewood Cliffs, New York: Prentice-Hall.
  3. Rogers, R. G. (2006). Mental practice and acquisition of motor skills: examples from sports training and surgical education. Obstetrics and Gynecology Clinics33(2), 297-304.
  4. Watson, J. B. (1907). Kinæsthetic and organic sensations: Their role in the reactions of the white rat to the maze. The Psychological Review: Monograph Supplements8(2), i.
  5. Lashley, K. S., & Ball, J. (1929). Spinal conduction and kinesthetic sensitivity in the maze habit. Journal of Comparative Psychology9(1), 71.
  6. Ingebritsen, O. C. (1932). Maze learning after lesion in the cervical cord. Journal of Comparative Psychology14(2), 279.
  7. Honzik, C. H. (1936). The role of kinesthesis in maze learning. Science84(2182), 373-373.
  8. Buegel, H. F. (1940). The effects of introducing ideational elements in perceptual-motor learning. Journal of Experimental Psychology27(2), 111.
  9. Vandell, R. A., Davis, R. A., & Clugston, H. A. (1943). The function of mental practice in the acquisition of motor skills. The Journal of General Psychology29(2), 243-250.
  10. Twining, W. E. (1949). Mental practice and physical practice in learning a motor skill. Research Quarterly. American Association for Health, Physical Education and Recreation20(4), 432-435.
  11. Rakestraw, P. G., Irby, D. M., & Vontver, L. A. (1983). The use of mental practice in pelvic examination instruction. Journal of Medical Education58(4), 335.
  12. Sanders, C. W., Sadoski, M., Bramson, R., Wiprud, R., & Van Walsum, K. (2004). Comparing the effects of physical practice and mental imagery rehearsal on learning basic surgical skills by medical students. American journal of obstetrics and gynecology191(5), 1811-1814.
  13. Sanders, C. W., Sadoski, M., Wasserman, R. M., Wiprud, R., English, M., & Bramson, R. (2007). Comparing the effects of physical practice and mental imagery rehearsal on learning basic venipuncture by medical students. Imagination, Cognition and Personality27(2), 117-127.
  14. Bathalon, S., Martin, M., & Dorion, D. (2004). Cognitive task analysis, kinesiology and mental imagery: Challenging surgical attrition. Journal of the American College of Surgeons199(3), 73.
  15. Bramson, R., Sanders, C. W., Sadoski, M., West, C., Wiprud, R., English, M., … & Xenakis, A. (2011). Comparing the effects of mental imagery rehearsal and physical practice on learning lumbar puncture by medical students. Annals of Behavioral Science and Medical Education17(2), 3-6.
  16. Sanders, C. W., Sadoski, M., van Walsum, K., Bramson, R., Wiprud, R., & Fossum, T. W. (2008). Learning basic surgical skills with mental imagery: using the simulation centre in the mind. Medical Education42(6), 607-612.
Cite this article as: Elif Dilek Cakal, Turkey, "Mental Practice: A tool for skill training during COVID pandemic," in International Emergency Medicine Education Project, June 8, 2020, https://iem-student.org/2020/06/08/mental-practice-a-tool-for-skill-training-during-covid-pandemic/, date accessed: September 30, 2020

Acute Management of Supraventricular Tachycardias

Acute management of SVT

The term “supraventricular tachycardia (SVT)” expresses all kinds of rhythms that meet two criteria: Firstly, the atrial rate must be faster than 100 beats per minute at rest. Secondly, the mechanism must involve tissue from the His bundle or above. Mechanism-wise, atrial fibrillation resembles SVTs. However, supraventricular tachycardia traditionally represents tachycardias apart from ventricular tachycardias (VTs) and atrial fibrillation (1,2).

Supraventricular tachycardias are frequent in the ED!

The SVT prevalence is 2.25 per 1000 persons. Women and adults older than 65 years have a higher risk of developing SVT! SVT-related symptoms include palpitations, fatigue, lightheadedness, chest discomfort, dyspnea, and altered consciousness.

How to manage supraventricular tachycardia?

In clinical practice, SVTs are likely to present as narrow regular complex tachycardias. Concomitant abduction abnormalities may cause SVTs to manifest as wide complex tachycardias or irregular rhythms. However, 80% of wide complex tachycardias are VTs. Most importantly, SVT drugs may be harmful to patients with VTs. Therefore, wide complex tachycardias should be treated as VT until proven otherwise (1,2).

The chart below summarizes acute management of regular narrow complex tachycardias:

Acute Management of Regular Narrow Tachycardias

References and Further Reading

  1. Brugada, J., Katritsis, D. G., Arbelo, E., Arribas, F., Bax, J. J., Blomström-Lundqvist, C., … & Gomez-Doblas, J. J. (2019). 2019 ESC Guidelines for the management of patients with supraventricular tachycardia: the Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). European Heart Journal, 00, 1-66.
  2. Page, R. L., Joglar, J. A., Caldwell, M. A., Calkins, H., Conti, J. B., Deal, B. J., … & Indik, J. H. (2016). 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Journal of the American College of Cardiology67(13), e27-e115.

Pacemaker-Related Emergencies – Part 1

pacemaker related emergencies

After the initial implementation of a pacemaker in the 1950s, implanted cardiac devices have become the mainstay therapy for life-threatening arrhythmias and severe congestive heart failure (1). Thanks to technological advancements, the devices become cheaper and smaller, now improving the lives of millions of patients (2). As physicians who serve in an acute setting, we started to take care of patients with implanted cardiac devices on a daily basis. Therefore, we must know how to manage implanted cardiac devices-related emergencies.

The three most common implanted cardiac devices are pacemakers (PMs), implantable cardioverter-defibrillators (ICDs), and left ventricular assist devices (LVADs). PMs generate rhythmic electrical stimuli and consequent heart contractions when the intrinsic electrical activity is below a threshold. ICDs recognize and treat ventricular tachyarrhythmias electrically. Newer generation ICDs also function as pacemakers (3). While the PMs and ICDs mainly support the cardiac electrical function, LVADs support the mechanical function of the heart.

Pacemaker related emergencies are divided into two broad groups as complications of implantation and device malfunction. In this post (part 1), we will summarize complications of implantation.

Complications of Implantation

Although modern technology and technique have significantly decreased the complication rates., we as acute care providers still must be aware of the perioperative complications related to pacemaker implantation. Relatively common complications include pocket, lead-related, thromboembolic, mechanical complications, and pacemaker syndrome (1,4).

Hematomas

Hematomas are formed by perioperative arterial and venous bleeding and can spread tracking the pacemaker leads (5). Palpable hematomas require surgical evacuation as needle aspiration is ineffective, poses pacemaker damaging risk, and does not reveal the underlying source (6). Hematomas increase infection risk.

Pocket Infections

The infections of pocket or leads can occur, mostly due to cutaneous flora, namely, Staphylococcus aureus and Staphylococcus epidermidis (4). The presence of foreign bodies and hematomas contribute to the infectious process (4). Local infections may progress to lung infections, sepsis, skin erosion, and wound dehiscence. The clinical picture may vary from local inflammation and fluctuation to vague systemic complaints and even to sepsis/septic shock without origin (1, 5). Therefore, a clinician should always suspect pacemaker and lead-related infections as a source in patients with a pacemaker. In the ED, after taking blood cultures, intravenous wide-spectrum antibiotics should be started. Pocket cultures should be obtained under fluoroscopy (4). Pocket infections generally necessitate long admissions with IV antibiotics therapy and removal of the pacemaker (7).

Lead-related complications

Lead-related complications include lead malposition, dislodgment, fracture, and damage to the insulation, all of which cause various malfunctions (8, 9). Among them, lead malposition and dislodgement have some additional clinical implications.

Lead malposition

Lead malposition refers to when a lead is inadvertently placed into the left ventricle (9). Lead may land in the left ventricle through a natural orifice of intracardiac variants and defects (atrial-septum defect, patent foramen ovale, sinus venosus defect, malpositioned coronary sinus or its tributaries) or perforation of the intraventricular septum (9). Also, the operator may erroneously place the lead through the subclavian artery and aortic valve.

Lead malposition significantly increases thromboembolic event risk, including transient ischemic attack and stroke (9). Even though there are rare nonpathological right bundle branch block causes, in the acute care setting, if pacing rhythm is right bundle branch block, especially in a patient, whose previous rhythm is known to be left bundle branch block, lead malposition should be suspected (9, 10). A chest X-ray shows the lead position.

 Lead dislodgement

Leads can be dislodged from the endocardial interface, mostly, days or months after implantation (11). In dual-chamber pacemakers, atrial leads get more frequently dislodged than the ventricular leads (11). Such dislodgement produces various rhythm problems due to malfunctions. Additionally, two lead dislodgement-related syndrome is defined below:

  • Lead displacement dysrhythmia refers to when free-floating ventricular leads cause episodes of malignant arrhythmias (12). When a lead is dislodged from the endocardial interface, the patient’s pacemaker dependency determines the symptoms (11). While pacemaker-dependent patients experience episodes of bradycardia- and ventricular tachyarrhythmia-related symptoms, if the native rhythm is favorable, lead dislodgement may stay unknown until malignant arrhythmia episode. Additionally, hiccups may occur due to vagal pacing (11).
  • Macrodislocation lead-dysfunctioning syndromes include Twiddler’s syndrome (coiling of the pacemaker leads due to rotation of the pacemaker generator on its long axis), Reel syndrome (coiling of the pacemaker leads around the pacemaker generator due to rotation of the pacemaker generator on its transverse axis) and Rachet syndrome (13). For further information, please check links 13 – 14.

Thromboembolic complications

The presence of leads in the venous system may cause thrombosis in axillary, subclavian, innominate, and upper arm veins or the superior vena cava up to varying degrees (4). Extensive collateralization masks symptoms. The most common symptoms include swelling and pain of the arm on the lead insertion side (5). However, pacemaker induced thrombosis may even lead to superior vena cava syndrome (5). Standard diagnostic and therapeutic measures apply.

Mechanical complications

Pacemaker and leads implantation may cause many mechanical complications, including tricuspid regurgitation, pneumothorax, hemothorax, air embolism, pericarditis, cardiac tamponade, and perforation (1, 7). All entities have distinct clinical courses and treatments. However, acute care providers should keep in mind all these differential diagnoses when a patient with a pacemaker presents with chest pain and shortness of breath.

Pacemaker Syndrome

It refers to when a patient’s symptoms progressively worsen after pacemaker implantation due to loss of AV synchrony and subsequent reduced cardiac output (15). These symptoms include fatigue, exertional dyspnea, paroxysmal nocturnal dyspnea, orthopnea, orthostatic hypotension, presyncope, and syncope (16). The syndrome is more frequent in patients with single-chamber ventricular pacing systems; however, it also occurs in patients with dual-chamber systems. If the patient has a single-chamber device, the treatment is upgrading the pacemaker to a dual-chamber system. If the patient has a dual-chamber device, the pacemaker programming should be adjusted (17).

References and Further Reading

  1. Cabrera, D., & Decker, W.W. (2013). Management of Emergencies Related to Implanted Cardiac Devices. In: J.G. Adams, E.D. Barton, J.L. Collings, P.M.C. DeBlieux, M.A. Gisondi, E.S. Nadel (Eds.), Emergency Medicine: Clinical Essentials (2nd ed., pp. 547-557). Philadelphia: Elsevier. 
  2. Birnie, D., Williams, K., Guo, A., Mielniczuk, L., Davis, D., Lemery, R., … & Tang, A. (2006). Reasons for escalating pacemaker implants. The American journal of cardiology98(1), 93-97.
  3. Beyerbach, D. M. (2019). Pacemakers and Implantable Cardioverter-Defibrillators. Retrieved October 20, 2019 from https://emedicine.medscape.com/article/162245-overview.
  4. Niemann, J. T. & Squire, B. Implantable cardiac devices. (2014). In: J. A. Marx, R. S. Hockberger, R. M. Walls (Eds.), Rosen’s emergency medicine: Concepts and clinical practice (8th ed., pp. 1064-1074). Philadelphia: Elsevier. 
  5. McMullan, J., Valento, M., Attari, M., & Venkat, A. (2007). Care of the pacemaker/implantable cardioverter defibrillator patient in the ED. The American Journal of Emergency Medicine25(7), 812-822.
  6. Trohman, R. G., Kim, M. H., & Pinski, S. L. (2004). Cardiac pacing: the state of the art. The Lancet364(9446), 1701-1719.
  7. Mulpuru, S. K., Madhavan, M., McLeod, C. J., Cha, Y. M., & Friedman, P. A. (2017). Cardiac pacemakers: function, troubleshooting, and management: part 1 of a 2-part series. Journal of the American College of Cardiology69(2), 189-210.
  8. Aguilera, A. L., Volokhina, Y. V., & Fisher, K. L. (2011). Radiography of cardiac conduction devices: a comprehensive review. Radiographics31(6), 1669-1682.
  9. Ohlow, M. A., Roos, M., Lauer, B., Von Korn, H., & Geller, J. C. (2015). Incidence, predictors, and outcome of inadvertent malposition of transvenous pacing or defibrillation lead in the left heart. Ep Europace18(7), 1049-1054.
  10. Erdogan, O., & Aksu, F. (2007). Right bundle branch block pattern during right ventricular permanent pacing: Is it safe or not?. Indian pacing and electrophysiology journal7(3), 187.
  11. Fuertes, B., Toquero, J., Arroyo-Espliguero, R., & Lozano, I. F. (2003). Pacemaker lead displacement: mechanisms and management. Indian pacing and electrophysiology journal3(4), 231.
  12. Burns, E. (2019). Pacemaker Malfunction. Retrieved October 20, 2019 from https://litfl.com/pacemaker-malfunction-ecg-library/
  13. Alvarez-Acosta, L., Garrido, R. R., Farrais-Villalba, M., & Afonso, J. H. (2014). Reel syndrome: a rare cause of pacemaker malfunction. British Medical Journal Case Reports2014, bcr2014204545.
  14. Munawar, M., Munawar, D. L., Basalamah, F., & Pambudi, J. (2011). Reel syndrome: A variant form of Twiddler’s syndrome. journal of arrhythmia27(4), 338-342.
  15. Prinzen, F. W., Vernooy, K., Lumens, J., Auricchio, A.(2017). Physiology of Cardiac Pacing and Resynchronization. In: K. A. Ellenbogen, B. L. Wilkoff, G. N. Kay, C. Lau, A. Auricchio. (Eds.), Clinical Cardiac Pacing, Defibrillation and Resynchronization Therapy (5th Ed., pp. 213-248). Philadelphia: Elsevier. 
  16. Gillis, A. M. (2017). Pacing for Sinus Node Disease. In: K. A. Ellenbogen, B. L. Wilkoff, G. N. Kay, C. Lau, A. Auricchio. (Eds.), Clinical Cardiac Pacing, Defibrillation and Resynchronization Therapy (5th Ed., pp. 375-398). Philadelphia: Elsevier. 
  17. Stephenson, E. A. & Davis, A. M. (2009). Electrophysiology, Pacing, and Devices. In: R. H. Anderson, E. J. Baker, D. Penny, A. N. Redington, M. L. Rigby, G. Wernovsky (Eds.), Paediatric Cardiology (3rd Ed., pp. 379-413). Philadelphia: Churchill Livingstone.
Cite this article as: Elif Dilek Cakal, Turkey, "Pacemaker-Related Emergencies – Part 1," in International Emergency Medicine Education Project, November 20, 2019, https://iem-student.org/2019/11/20/pacemaker-related-emergencies-part-1/, date accessed: September 30, 2020

Evidence-based Approach: Introduction

Acquiring solid history-taking and physical examination skills, the ability to use and interpret them in the right way are essential for physicians.

The literature shows the physical examination, in general, is considered in decline while the use of laboratory and imaging testing has markedly increased (1-3). Indeed, physicians tend to over-rely on the test results, instead of history and physical examination findings. A reason for this trend may be physicians’ lack of knowledge or confidence (4,5). However, not every institution has the optimal resources and even if they have, extensively testing every patient for every disease possible is not cost-effective or free of complications (5). Therefore, acquiring solid history-taking and physical examination skills, the ability to use and interpret them in the right way are still essential for physicians.

Learning and performing history-taking and physical examination techniques is one thing, applying the findings to reach a diagnosis is another (6). Early learners tend to focus on mastering the skills itself so much that often they may fail to notice how to utilize it, its strengths and weaknesses. iEM Education Project’s new series “Evidence-based Approach to History-taking and Physical Examination” aims to support this learning gap.

In a way, evidence-based history-taking and physical examination challenge traditional habits in an attempt to curate them; gives us the information needed to abandon the invalid techniques and nourish the beneficial ones. However, interpreting the findings relies on understanding the evidence. Therefore, before analyzing each disease from the perspective of evidence-based diagnostic skills, we need to review the biostatistical terms such as pre-test probability, sensitivity and specificity, positive and negative likelihood ratios (LR).

Below is a simple reminder about how to interpret these values. You may refer to the links provided to reach more information.

Pre-test Probability

Pre-test probability is the probability of the disease before implementing any results (7,8). In other words, it is how likely the physician thinks a patient with a chief complaint may have a specific condition. There are three main ways to estimate pretest probability; first, prevalence studies; second, validated clinical prediction rules; and third, physicians’ gestalt based on their own clinical experience (9).

Sensitivity

Sensitivity is a feature (symptom, sign or test) with a high sensitivity is positive more frequently in patients compared to healthy population and selects patients accurately when it is positive (positivity in disease) (7). Therefore, when a highly sensitive feature is absent, the probability of the disease decreases. (SnNout = a Sensitive test, when Negative, rules out disease) (7).

Specificity

Specificity is a feature (symptom, sign or test) with a high specificity is negative more frequently in the health population compared to patients and selects healthy people accurately when it is negative (negativity in health) (7). Therefore, when a highly specific test is positive, the probability of the disease increases. (SpPin = a Specific test, when Positive, rules in disease) (7).

Positive Likelihood Ratio (LR+)

LR+ describes how the probability of a disease changes when a feature (symptom, sign or test) is present (10).

      • If LR+ > 1, the presence of the feature, increases the probability of the disease. The bigger the LR+, the more strongly it favors the diagnosis.
      • If LR+ = 1, the presence of the feature does not change the probability. Therefore, it does not have diagnostic value. 
      • If LR+ = 0-1, the presence of the feature decreases the probability of the disease. The smaller the LR+, the more strongly it opposes the diagnosis (10).

Negative Likelihood Ratio (LR-)

LR- describes how the probability of a disease changes when a feature (symptom, sign or test) is absent (10).

      • If LR- > 1, the absence of the feature, increases the probability of the disease. The bigger the LR-, the more strongly it favors the diagnosis.
      • If LR- = 1, the absence of the feature does not change the probability. Therefore, it does not have diagnostic value.
      • If L- = 0-1, the absence of the feature decreases the probability of the disease. The smaller the LR-, the more strongly it opposes the diagnosis (10).

How to combine all?

In the traditional sense, the pretest probability is used to mean the prevalence of a disease before ordering a test (8). Basically, it is another way of saying physicians used to combine symptoms and signs intuitively, based on their experience to reach a pretest probability. However, evidence-based medicine encourages the physicians and the literature to reflect on the practice, break it into pieces and review the individual and collective value of each part. Accordingly, each individual feature from history or examination can be considered “tests.” (8)

You may think reviewing the value of each feature from the history and physical examination is mentally exhausting. Validated clinical prediction rules are here to help! Similar to the traditional sense, but in an evidence-based and standardized way, the validated clinical prediction rules combine some elements to reach a more straightforward calculation of pretest (9).

Overall, interpreting the findings is as important as performing the skill itself. Interpretation requires biostatistical knowledge as much as clinical ability. When applied analytically, history-taking and physical examination can safely accelerate the diagnostic process and limit overtesting (5).

References and Further Reading

  1. Smith-Bindman, R., Miglioretti, D. L., & Larson, E. B. (2008). Rising use of diagnostic medical imaging in a large integrated health system. Health Affairs, 27(6), 1491-1502.
  2. O’Sullivan, J. W., Stevens, S., Hobbs, F. R., Salisbury, C., Little, P., Goldacre, B., … & Heneghan, C. (2018). Temporal trends in use of tests in UK primary care, 2000-15: retrospective analysis of 250 million tests. British Medical Journal, 363, k4666.
  3.  Bergl, P., Farnan, J. M., & Chan, E. (2015). Moving toward cost-effectiveness in physical examination. The American Journal of Medicine, 128(2), 109-110.
  4. Cook, C. (2010). The lost art of the clinical examination: an overemphasis on clinical special tests. The Journal of Manual & Manipulative Therapy, 18(1), 3.
  5. Greenberg, J., & Green, J. B. (2014). Over-testing: why more is not better. The American Journal of Medicine, 127(5), 362-363.
  6. Chi, J., Artandi, M., Kugler, J., Ozdalga, E., Hosamani, P., Koehler, E., … & Verghese, A. (2016). The five-minute moment. The American Journal of Medicine, 129(8), 792-795.
  7. McGee, S. (2018). Evidence-based Physical Diagnosis (4th Ed., Kindle Ed.). Philadelphia: Elsevier.
  8. Parikh, R., Parikh, S., Arun, E., & Thomas, R. (2009). Likelihood ratios: clinical application in day-to-day practice. Indian Journal of Ophthalmology, 57(3), 217.
  9. Shaneyfelt, T. (2012). Diagnostic Process. [Online Lecture]. Retrieved April 25, 2019 from https://www.youtube.com/watch?v=6qgnrXELoo4.
  10. McGee, S. (2002). Simplifying likelihood ratios. Journal of General Internal Medicine, 17(8), 647-650.
Cite this article as: Elif Dilek Cakal, Turkey, "Evidence-based Approach: Introduction," in International Emergency Medicine Education Project, April 29, 2019, https://iem-student.org/2019/04/29/evidence-based-medicine/, date accessed: September 30, 2020

Five Tips About Well-being During and After Medical School

Even the best of us suffer from burnout from time to time. It is utterly human as training in medicine is very demanding itself and combined with the life issues it can be weary. Well, we can control the chaos. Here are five tips for creating a system to support long term-term success and a happy life.

1

Adopt a healthy lifestyle and be persistent: Back to basics: Embrace a sustainable, healthy diet; drink approximately eight glass of water; sleep at least eight hours a day and exercise regularly. You need to take care of your body: A healthy diet and adequate water enhance stamina; regular and enough sleep promotes learning, memory, stress relief and performance; exercising helps you to relieve stress and increases endurance. Sacrificing any of these for studying more does not miraculously help you reach success. Building a career is a long path: You have to stay strong.

For more on this topic: National Health Service, Why We Sleep by Matthew Walker 

2

Regulate your time wisely: Have you ever met an astonishingly successful professional who seems to be participating in every social activity? Do not fret! Learning how to manage your time will get you there. Let me share a few tricks with you: Decide your priorities and learn to say “no” to the rest. Spending ten minutes to planning your day will sometimes save you a few hours – hours that you may spend on your hobbies or with your family or friends. Conquer procrastination and do it now! Create a study area and be minimalist about it. Get rid of your phone (and your social media accounts!) while studying. If you feel you lose your focus, it is probably time for a break. A bullet journal is an excellent way to plan your day, month and future.

For more on this topic: Eat that Frog by Brian Tracy, Bullet Journal, Work Life Balance

3

Regulate your Energy Wisely: Managing your time is essential but not enough. If you have ever struggled not to sleep in the second half of a 2-hour lecture, then you are not alone. Energy management, a newer concept than time management, is about to change our beliefs related to performance and happiness. Here are a few basics: According to Jim Loehr and Tony Schwartz, you must be physically energized, emotionally connected, mentally focused and spiritually aligned for long-term performance, health and happiness. Overuse and underuse will hinder your energy, you need to balance your energy expenditure by intentional challenges and resting in between. Studying continuously will damage your performance in the long term.

For more on this topic: The Power of Full Engagement by Jim Loehr & Tony Schwartz

4

Recognize and change your values: Identify your priorities. If you are prioritizing medicine over your health and happiness, you are in the wrong. You and your well-being are your top priorities. Your job or your academic performance does not define you, you are more than that. Determine your personal and professional long-term goals, then create a road map. Check and update your goals regularly. Do not let the first bump on the road demotivate you; if you stay persistent, you will reach your goals sooner or later.

For more on this topic: How To Make Work-Life Balance Work by Nigel Marsh

5

Spend quality time with your family and friends: If you think that you can accomplish all by yourself, think again. Spending quality time with your friend and family has numerous personal and professional benefits: It helps you to relieve stress, create an early network and a supportive net, diversify your area of interests, rest your mind by distracting it away from medicine. Always remember: “If you want to go fast, go alone. If you want to go far, go together.”

For more on this topic: Why It’s Important to Spend More Time with Friends and Family, 4 Reasons Friends And Family Are Good For Your Health

Is Troponin Enough?

You are the emergency doc working in a rural ED. It is the Saturday night at 23:25 and you have three patients with chest pain. All have unchanged ECGs and normal troponins. All feel well now and want to go home if you think their results are okay. What is your plan for each of them?

Patient 1. Isabel D. is a 45-year old female with a history of hypertension. She presented to the emergency department with left-sided sharp chest pain. Her pain started after his evening run, and she vomited once. Her pain continued for one hour, but then it lessened spontaneously. Now she is feeling well, and she wants to go home. Her ECG is completely normal. Her 0- and 3-hour troponins are negative.

Paint 2. Daniel B. Is a 65-year old male with a history of smoking, hypotension and left bundle branch block (LBBB). He is obese. He presented to the emergency department with left-sided heavy chest pain, radiating to his left arm, chin, and back. He went to bed early today, and his chest pain woke him up. For half an hour, he has felt sweaty and nauseated but now he is feeling well, and he wants to go home. His ECG shows LBBB, unchanged compared to his previous ECGs and without Sgarbossa Criteria. His 0- and 3- hour troponins are negative.

Patient 3. Hank P. is a 54-year old male with a history of hypertension, diabetes mellitus and prior stroke with no sequel. For twenty minutes, he experienced a sharp pain in the middle of his chest. His pain had started while he was watching TV and he felt sweaty all in a sudden. he had His ECG shows findings related to left ventricular hypertrophy.  His 0- and 3- hour troponins are negative.

HEART Score

HEART Score was developed to predict the 6-week risk of a major adverse cardiac event of patients with chest pain, precisely in the emergency department setting (1). It outperformed the others, especially in exclusion of low-risk patients (2) Patients with a combination of HEART score of 0-3 and two negative troponins can be safely discharged from ED with no major adverse cardiac events (3). Patients with HEART Score of 4-6 requires admission and are candidates for further noninvasive investigations (1). Patients with HEART Score of ≥7 requires admission and are candidates for early invasive strategies (1).

HEART Score

CategoryScoreExplanationRisk Features
HistoryHigh-risk features
• Middle- or left-sided chest pain
• Heavy chest pain
• Diaphoresis
• Radiation
• Nausea and vomiting
• Exertional
• Relief of symptoms by sublingual nitrates

Low-risk features
• Well localized
• Sharp pain
• Non-exertional
• No diaphoresis
• No nausea and vomiting
Slightly Suspicious 0Mostly low-risk features
Moderately Suspicious+1Mixture of high-risk and low-risk features
Highly Suspicious+2Mostly high-risk features
ECG
Normal0Completely Normal
Non-specific Repolarization Disturbance+1Non-specific repolarization disturbance• Repolarization abnormalities
• Non-specific T wave changes
• Non-specific ST wave depression or elevation
• Bundle branch blocks
• Pacemaker rhythms
• Left ventricular hypertrophy
• Early repolarization
• Digoxin effect
Significant ST Depression+2Significant ST depression• Ischemic ST-segment depression
• New ischemic T wave inversions
Age
<450
45-64+1
≥ 65+2
Risk Factors• Obesity (Body-Mass Index ≥ 30)
• Current or recent (≤ 90 days)smoker
• Currently treated diabetes mellitus
• Family history of coroner artery disease (1st degree relative < 55 year old)
• Hypercholesterolemia

OR

Any history of atherosclerotic disease earn 2 points:
• Know Coroner artery Disease: Prior myocardial infarctions, percutan coronary intervention (PCI) or coronary artery bypass graft
• Prior stroke or transient ischemic attack
• Peripheral arterial disease
No known risk factors0
1-2 risk factors+1
≥ 3 risk factors or history of atherosclerotic disease+2
Initial Troponin
≤ normal limit0
1-3 x normal limit+1
> 3x normal limit+2
Please read articles 1,2,4 for more information.

Now, let’s look back on our patients.

Isabel’s pain has both high-risk (exertional, left-sided pain with vomiting) and (sharp pain, no diaphoresis) features; therefore, her pain is moderately suspicious. (H: +1) Her ECG is completely normal. (E: 0) She is 45 years old. (A: +1). She has one risk factor, hypertension. (R: +1) Her troponins are normal. (T: 0) Her HEART score is 3, and she can safely go home from the emergency department. The expected MACE rate in 30 days is 0%.

Daniel’s pain has mostly high-features (left-sided, radiating heavy chest pain with nausea and vomiting); therefore his pain is highly suspicious. (H: +2) His ECG is not completely normal but free of new ischemic changes. (E: +1) He is 65 years old. (A: +2). He has three risk factors, smoking, obesity, and hypertension. (R: +2) His troponins are normal. (T: 0) His HEART score is 7, and he is a candidate for early invasive intervention. You should admit him and call the cardiologist.

Hank’s pain has both high-risk (middle-sided chest pain with diaphoresis) and low-risk (non-exertional, sharp pain) features; therefore, his pain is moderately suspicious. (H: +1) His ECG is not completely normal but free of new ischemic changes. (E: +1) He is 54 years old. (A: +1). He has three risk factors, hypertension, diabetes mellitus and prior stroke. (Note that prior stroke alone earns two points) (R: +2) His troponins are normal. (T: 0) His HEART score is 5, and he is a candidate for noninvasive investigation. You should admit him.

PEARLS and PITFALLS

  1. ECG: If the ECG shows STEMI, do not wait for troponin or consider the HEART score. Call the cardiologist and consider activating angiography unit for the primary PCI.
  2. Troponins: If you first troponin is highly abnormal, do not wait for the second troponin or consider the HEART score. Call the cardiologist and consider activating angiography unit for the primary PCI. Additionally, the magnitude of change between the first and the second troponin is important in diagnosing acute myocardial infarction (5).
  3. Clinical Gestalt: You will gain a clinical gestalt over the years. If your clinical gestalt and any scoring disagree, always stay on the safe side for the patient’s benefit (4).
  4. Patient Safety: In the original study, the HEART score was combined with only one troponin. The adverse event rate was 2.5% for the HEART score 0-3 patients, 20.3% for the HEART score 4-6 patients and 72.7% for the HEART score ≥7 patients. Therefore, the author believes, the HEART score combined with two troponins is safer in the discharge of low-risk patients. Low-risk patients (i.e., HEART Score 0-3) with negative two troponins had no MACE within 30 days (3).

Suggested Chapters

Chest Pain by Asaad S Shujaa

Acute Coronary Syndrome (ACS)

by Khalid Mohammed Ali, Shirley Ooi

REFERENCES

  1. Six, A. J., Backus, B. E., & Kelder, J. C. (2008). Chest pain in the emergency room: value of the HEART score. Netherlands Heart Journal, 16(6), 191-196. – link
  2. Radecki, R. (2013). Time to Move to the HEART Score. Available at: http://www.emlitofnote.com/?p=440 (Accessed: 17/07/2018) – link
  3. Mahler, S. A., Riley, R. F., Hiestand, B. C., Russell, G. B., Hoekstra, J. W., Lefebvre, C. W., … & Herrington, D. M. (2015). The Heart Pathway Randomized Trial: Identifying Emergency Department Patients With Acute Chest Pain for Early Discharge. Circulation: Cardiovascular Quality and Outcomes, 8(2), 195-203. – link
  4. Hyunjoo, L., & Rodriguez, C. (n.d.). HEART Score for Major Cardiac Events. Available at: https://www.mdcalc.com/heart-score-major-cardiac-events#evidence (Accessed: 17/07/2018) – link
  5. Roffi, M., Patrono, C., Collet, J. P., Mueller, C., Valgimigli, M., Andreotti, F., … & Gencer, B. (2016). 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). European heart journal, 37(3), 267-315. – link

FURTHER READING