This patient presents to the emergency department with vague and nonspecific symptoms of nausea, fatigue, and palpitations. The initial EKG (EKG #1) demonstrates a wide-complex tachycardia (QRS >120msec) with a regular rhythm. The differential diagnosis for wide-complex tachyarrhythmias include ventricular tachycardia (monomorphic ventricular tachycardia), torsades de pointes (polymorphic ventricular tachycardia), coarse ventricular fibrillation, supraventricular tachycardias with aberrancy (i.e. underlying Wolf Parkinson White Syndrome or Ventricular Bundle Branch Block), electrolyte abnormalities (i.e., Hyperkalemia), and from medications (i.e., Na channel blocking agents). If the history is unclear or the patient shows signs of instability, Ventricular tachycardia should always be the assumed tachyarrhythmia. This is managed with electrical cardioversion or with medications (i.e., amiodarone, procainamide, lidocaine), depending on the patient’s symptoms and hemodynamic stability.
The prior EKG for the patient (EKG #2) is helpful in showing that the patient does not have a wide QRS complex at baseline. There also are no EKG signs of Wolf Parkinson White Syndrome (Choice B) on EKG #2, making this choice incorrect. Signs of this cardiac pre-excitation syndrome on EKG include a shortened PR interval and a delta wave (slurred upstroke at the beginning of the QRS complex). Anxiety (Choice D) can cause sinus tachycardia and be a symptom associated with any arrhythmia, but it is not the underlying cause for this patient’s bizarre wide-complex tachydysrhythmia. On a closer look, the patient’s EKG (EKG #1) demonstrates tall, peaked T waves in the precordial leads. This supports a diagnosis of hyperkalemia. Other signs of hyperkalemia on EKG include flattened or absent P waves, widened QRS complexes, or a sine wave morphology. A common underlying cause of hyperkalemia is renal disease (Choice C). Ischemic heart disease (Choice A) is a common underlying cause for ventricular tachycardia. Ventricular tachycardia is less likely in this case given the presence of peaked T waves and the lack of fusion beats, capture beats, or signs of AV dissociation on the 12-lead EKG. Correct Answer: C
This patient has a narrow-complex, regular tachycardia that is causing the sensation of palpitations. The clinical history, rapid heart rate, and 12-lead EKG provide enough information to diagnose this patient with supraventricular tachycardia, also known as “SVT.” Supraventricular tachycardias refer to a broad range of arrhythmias, including sinus tachycardia, atrial fibrillation, atrial flutter, multifocal atrial tachycardia, and AV nodal re-entry tachycardia. This scenario specifically depicts an AV nodal re-entry tachycardia (AVNRT). AVNRT is a common type of SVT that can occur spontaneously or is triggered by sympathomimetic agents (i.e., cocaine, amphetamines), caffeine, alcohol, exercise, or beta-2 agonists using in asthma treatment (i.e., albuterol, salbutamol). AVNRTs are narrow-complex tachycardias with rates that range from 120-280bpm. P waves are typically absent in AVNRTs, but rarely they may be present as retrograde inverted P waves located immediately before or after the QRS complex. Symptoms experienced by the AVNRT patient may include pre-syncope, syncope, dizziness, palpitations, anxiety, or mild shortness of breath. Patients with AVNRTs are more likely to be young and female over male.
QRS complexes in AVNRTs are often narrow (<120msec), however, wide QRS complexes may be present in AVNRTs if there is a concurrent bundle branch block or Wolff-Parkinson White Syndrome. AVNRTs are often stable and do not require electric cardioversion. Signs that indicate instability and necessitate cardioversion are hypotension (SBP <90mmHg), altered mental status, or ischemic chest pain (more common if known history of ischemic heart disease). This patient lacks all of these signs and symptoms.
Treatment of AVNRT focuses on restoring the patient to normal sinus rhythm, which leads to resolution of symptoms. First-line medications for AVNRTs are short-acting AV nodal blocking agents, like adenosine (Choice A). Beta-blockers or calcium channel blockers act as second-line agents for patients who do not respond to adenosine. Metoprolol is a beta-blocker (Choice C) and Diltiazem is a calcium channel clocker (Choice D). Prior to any medications, vagal maneuvers should always be attempted first in a stable patient with AVNRT. The Valsalva maneuver (Choice B), or “bearing down,” is a commonly used vagal maneuver in the termination of AVNRTs. Other vagal maneuvers include the carotid massage or the Diving reflex (place bag of ice and water on face). Correct Answer: B
This patient presents to the emergency department with palpitations, a narrow complex tachycardia (<120msec), and an irregularly irregular rhythm. A close look at this patient’s EKG reveals the absence of discrete P waves and QRS complexes that are spaced at varying distances from each other (most apparent in lead V6). These signs support a diagnosis of Atrial Fibrillation, or “AFib.” Atrial Fibrillation is an arrhythmia characterized by an irregularly irregular rhythm, the absence of P waves with a flat or undulating baseline, and narrow QRS complexes. Wide-QRS complexes may be present in AFib if there is a concurrent bundle branch block or Wolff-Parkinson White Syndrome. AFib is caused by the electric firing of multiple ectopic foci in the atria of the heart. This condition is triggered by a multitude of causes, including ischemic heart disease, valvular heart disease, dilated or hypertrophic cardiomyopathies (likely related to this patient’s congestive heart failure history), sepsis, hyperthyroidism, excess caffeine or alcohol intake, pulmonary embolism, and electrolyte abnormalities.
The main risk in AFib is the creation of thrombi in the atria as they fibrillate, resulting in emboli that travel to the brain and cause a stroke. The CHA2DS2VASc scoring system is used to risk stratify patients and determine if they require anticoagulation to prevent against thrombo-embolic phenomenon (i.e. stroke). This patient has a high CHA2DS2VASc score, so she would require anticoagulation. In addition to anticoagulation, A fib is treated with rate control (i.e. beta blockers or calcium channel blockers), rhythm control (i.e. anti-arrhythmic agents), or electrical cardioversion. Electrical cardioversion (choice A) is typically avoided when symptoms occur greater than 48 hours, since the risk of thrombo-emboli formation is higher in this scenario. An exception to this would be a patient with “unstable” AFib. Signs of instability in any tachyarrhythmia are hypotension, altered mental status, or ischemic chest pain. This patient lacks all of these signs and symptoms. Although this patient lacks signs of instability, this patient’s marked tachycardia should be addressed with medical treatment. General observation (Choice C) is not the best choice for this reason. Intravenous adenosine (Choice D) is the best choice for a patient with supraventricular tachycardia (SVT). This is a narrow-complex AV nodal re-entry tachycardia with rates that range from 120-280bpm. SVT also lacks discrete P waves. A key factor that differentiates A fib from SVT is that SVT has a regular rhythm, while AFib has an irregular rhythm. Intravenous metoprolol (Choice B) is the best treatment option listed in order to decrease the patient’s heart rate.
As Dan Sanberg once said; “Emergency Medicine is the most interesting 15 minutes of all specialties”. Indeed, if we were to recommend one textbook to a newly graduated physician, it would probably make the most sense for it to be an Emergency Medicine textbook. So which one?
I asked this question in Turkish and English to the Twitterverse recently. The responses showed once again the diversity of emergency medicine resources and the importance of basic textbooks.
Justin Hensley reminded the fallacy of the sentence “I’ll read it just on the Internet” and the importance of keeping up-to-date as follows: “I’m not sure there’s a right answer to this. Honestly, I would say the one that has the most recent new addition, because it will be the least out of date. The fundamentals need to come out of a text and not #FOAMed though. Can’t build a pyramid without a base.“
Shehni Nadeem said:
“It’s hard to pick ONE. Here’s why: 1) Textbooks are critical to forming that foundation of knowledge but must be kept current 2) Ea textbook has a slightly different read to it. I would encourage the learner to try out each one and see which fits the best (did this as an intern)”
Isn’t it a great idea to leave the preference to the reader by giving general information about the books rather than ranking the best for “me” or “person x”?
Let’s do it like this.
We will discuss the books included in this article in two groups according to book sizes.
Hand and Pocket Size Textbooks
You cannot see a doctor standing at the bedside with a large reference book in his/her hands. In fact, most textbooks are not even suitable to keep in your bag and take it wherever you go (Hello, back pains, hello!). Hand and pocket books have been prepared to solve this problem. TL; DR (Too long, didn’t read), the small ones of these books are called “pocket books” and the bigger ones are called “handbooks”. Isn’t that great? Yes, but please remember that “only” studying handbooks may not be enough if you haven’t read the topics from a broader source before. It is best to move on to these books after doing the basic reading. Or, as we all did when we first turned the pages of Tarascon, you’ll stare at the pages for a long time and try to understand whether it is English or Klingon.
1- Oxford Handbook of Emergency Medicine
The Oxford Handbook of Emergency Medicine, whose 5th edition has been released recently, is a starter book prepared for medical students, paramedics and physicians. The manual-sized work is still 800 pages long and contains basic information on many subjects from life-threatening emergencies to ENT, analgesia to toxicology. The fourth edition of the book was released in 2012. Emergency Medicine professor Richard Body also recommends this book to our readers as a starter book.
2- Emergency Medicine Secrets
Unlike many resource books, Emergency Medicine Secrets deals with questions and answers on every subject. For example, when you look at the Pneumonia section, you can find various questions (and answers, of course) such as, “Why should I learn about Pneumonia?”, “How does pulmonary infection develop?”, “What are the differences between the presentations of typical and atypical pneumonia?”. The book that can really benefit to the reader in this respect is 768 pages long.
3- Avoiding Common Errors in the Emergency Department
This work by Amal Mattu et al., One of the well-known names in FOAMed world, discusses 365 common mistakes in emergency medicine practice in a chatty, easy-to-read style, and offers practical, easy-to-remember tips to avoid these pitfalls. The fact that the chapters are short and understandable allows easy reading even when you are working. The second edition published in 2017 has a total of 1080 pages.
4- EM Fundamentals: The Essential Handbook for Emergency Medicine Residents
This pocket guide, prepared by EMRA (Emergency Medicine Residents Association) for Emergency Medicine residents, is one of the ideal books you can take with you during your emergency department shifts. On 366 pages, it summarizes common situations that may be encountered in the emergency room, in clear language and without missing the necessary emphasis.
5- Tarascon Adult Emergency Pocketbook
I do not think there is an emergency medicine physician unfamiliar with Tarascon (at least in Turkey). We know that on many Emergency Medicine Clinics those who do not have Tarascon in their pockets at bedside visits are condemned. As someone who is always amazed at how many things fit into this 240-page pocket book, I say, “If you haven’t found what you are looking for in basic emergency medicine in this book, look again, there is for sure.” Tarascon published books in a series style from Pediatric Emergency to Orthopedics. I recommend especially Adult Emergency and Medical Procedures pocket books. Character sizes may spoil the taste of those who like to read books written in big fonts and large line spacings. But the goal here is to be as small as possible, so it is understandable.
6- Tintinalli’s Emergency Medicine Manual
Would there be an Emergency Medicine list without Tintinalli? Tintinalli book appears with large-small-median dimensions. The last version of this book, which is easy to read and will not let the reader down with its structure containing plenty of pictures, tables and graphics, is the 8th edition published in 2017. It covers every subject an Emergency physician may need, and Palliative Care is no exception. The preface to the latest edition is also giving a glimpse of Emergency Medicine’s history.
Large textbooks that might be expected not to leave “anything missing” in their field often have a serious volume and a long list of authors. These works that will have a dedicated spot in your library to grab and read from time to time over the years may be too much for a medical student or a newly graduated physician. But if it is necessary to prepare a presentation or learn a subject in depth, the address is clear.
1- Adams Emergency Medicine: Clinical Essentials
This 1888-page “tome”, which weighs nearly 5 kilograms, provides extensive information on any subject you may need in a visually rich and easily understandable language. The disadvantage is that the second original edition is dated 2012. So it may be partly outdated. Elsevier is sharing the book online (for a fee) under the title Adams Emergency Medicine Review. However, even that was published in 2015.
2- Clinical Emergency Medicine
Clinical Emergency Medicine contains information on the diagnosis and treatment of 98 changes and condition in 400 pages. Each chapter starts with the Key Points. It also continues with Introduction, Clinical Presentation (History and Physical Examination), Diagnostic Studies, Medical Decision Making, Treatment and Discharge, and Reading Recommendations. The printing date is a bit old. The last edition was published in 2014.
3- Diagnosis And Management Emergency Medicine
The 556-page work by Mike Cadogan is not only practical, but also includes a very comprehensive content. The eighth edition has been completely revised and updated. the book covers all emergencies as well as procedures and administrative and legal issues.
4- First Aid For The Emergency Medicine Boards
Published for those who want to prepare for the Emergency Medicine Boards exams organized by the American Board of Emergency Medicine, this book offers a great option for those who want concise summaries with reminder boxes, notes, mnemonics and clinical pearls. Each subject is briefly described in subheadings such as Symptoms, Diagnosis, and Treatment in this approximately 1000-page book.
5- CURRENT Medical Diagnosis And Treatment
This book can be considered as an Internal Medicine textbook. However, in addition to Internal Medicine subspecialties such as geriatrics, preventive medicine and palliative care; it offers detailed reviews of all internal medicine disciplines such as gynecology and obstetrics, dermatology, ophthalmology, neurology, psychiatry, and infectious diseases. The book includes the diagnosis and treatment of more than 1000 diseases and is about 2000 pages. It is ALWAYS up-to-date due to its yearly updates.
6- Rosen & Barkin’s 5-Minute Emergency Medicine Consult
In this textbook, each subject is summarized in 2 pages divided into three sections. The last edition of the chapter, in which every subject is explained systematically in Introduction, Diagnosis, Treatment, Follow-up, Tips, Reading, ICD Codes sections. Its last edition was published in 2019 with a length of 1256 pages.
7- Rosen’s Emergency Medicine: Concepts And Clinical Practice
This book is one of the “brand”s of our field. The original version is 2688 pages long. When you think about it yu will realise that even if you read 10 pages a day, it will be over in 9 months. Due to its size, its suitability for colleagues who do not intend to acquire an Emergency Medicine profession can be discussed, but making a list that Rosen is not included will also upset every Emergency physician.
8- Tintinalli’s Emergency Medicine
I think it would suffice to say that it is the best selling Emergency Medicine book worldwide. Tintinalli’s word is deed, wherever Emergency Medicine is experienced, from in-clinic trainings to certification exams. The 9th edition, published very recently, is 2160 pages long. Pre-hospital care, disaster preparedness and resuscitation techniques… You can find everything you can think of in this book, from all major medical, traumatic and environmental conditions that require urgent treatment in adults, children and neonates.
Suppose you are going to Antarctica as a “team doctor”. You will be completely isolated from the outside world for 3 months. Neither a plane nor a ship will bring aid. Which textbook would you choose to take with you? In my opinion, the answer to this question for every physician is an Emergency Medicine textbook.
Due to the nature of our expertise, every textbook will undoubtedly help Emergency in at least one way. If you choose to read a good Dermatology or a good ENT textbook, you will definitely benefit. From another angle, even the most comprehensive Emergency Medicine textbook will not enable you to learn everything, for example, a thorough understanding of all heart rhythms or interventional procedures. You should refer to thousands of pages of books written specifically for these.
Therefore, our aim in this article was to present a collection of textbooks that examine Emergency Medicine as a whole. While choosing from hundreds of textbooks, we got the great support of the Twitter #FOAMed world. Most of the photos above were provided by the physicians mentioned below. I thank them very much.
If knowledge is a flower garden, textbooks are honeycombs prepared by “master” bees by roaming around those flowers. Rather than visiting thousands of flowers one by one and trying to distinguish between good and bad; it would be most logical to set the foundation on these “honeycombs” and set sail to new gardens.
What did Justin Hensley say? “You can’t build a pyramid without a base.”
We would like to thank the following names for their contributions to this article (alphabetical order):
Ali Kemal Yıldız, Arif Alper Çevik, Ayhan Özhasenekler, Barış Murat Ayvacı, Berika Kavaz Kuru, Bora Çekmen, Burak Özkan, Cem Turam, Ener Çağrı Dinleyici, Fatih Beşer, Gizem Altınsoy, Göksu Afacan Öztürk, Haldun Akoğlu, İbrahim Varol, Justin Hensley, Mehmet Çulha, Mike Cadogan, Nevrez Koylan, Nurettin Özgür Doğan, Oğuzhan Aytepe, Onurcan Kaya, Richard Body, Salahi Engin, Shehni Nadeem, Yonca Bulut, Yusuf Ali Altuncı, Zeynep Kekeç.
You can read the Turkish version of this article on Acilci.net:“Hangi Acil Tıp Kitabı?”
This patient has marked bradycardia on exam with a borderline low blood pressure. These vital sign abnormalities are likely the cause of the patient’s dizziness. Bradycardia is defined as any heart rate under 60 beats/min. The most common cause of bradycardia is sinus bradycardia (Choice A). Other types of bradycardia include conduction blocks (i.e. type 2 or type 3 AV blocks), junctional rhythms (lack of P waves with slow SA nodal conduction), idioventricular rhythms (wide QRS complex rhythms that originate from the ventricles, not atria), or low atrial fibrillation or atrial flutter. About 80% of all bradycardias are caused by factors external to the cardiac conduction system, such as hypoxia, drug effects (i.e., beta block or calcium channel blocker use or overdose), or acute coronary syndromes.
Sinus bradycardia (Choice A) occurs when the electrical impulse originates from the SA node in the atria. Signs of sinus bradycardia on EKG are the presence of a P wave prior to every QRS complex. This EKG shows P waves prior to each QRS complex, but there are extra P waves that are not followed by QRS complexes. Some P waves are “buried” within QRS complexes or within T waves. The EKG below marks each P wave with a red line and each QRS complex with a blue line.
First-degree AV Block (Choice B) is a benign arrhythmia characterized by a prolonged PR interval. This patient’s EKG has variable PR intervals (some prolonged, some normal). This is a result of a more severe AV conduction block. Second-Degree AV Blocks are divided into Mobitz type I and Mobitz Type II. Mobitz type I, also known as Wenckebach, is characterized by a progressive lengthening PR interval followed by a dropped QRS complex. This can be remembered by the phrase, “longer, longer, longer, drop.” Wenckebach is a benign arrhythmia that does not typically require any treatment. Mobitz type II (Choice C) is characterized by a normal PR interval with random intermittent dropping of QRS complexes. This patient’s EKG has consistent spacing between each QRS complex (blue lines) and consistent spacing between each P wave (red lines). However, the P waves and QRS complexes are not associated with each other. This phenomenon is known as AV dissociation. These EKG changes are signs of a complete heart block, also known as Third-Degree AV Block (Choice D). Both Second-Degree AV block- Mobitz type II (Choice C) and Third-Degree AV Block (Choice D) are more serious conduction blocks that require cardiac pacemakers. Correct Answer: D
This patient is suffering from severe bradycardia with signs of poor cardiac output, shock, and diminished perfusion to the brain. Bradycardia is defined as any heart rate under 60 beats/min. Many individuals may be bradycardic at rest with no danger to the patient (i.e. young patients or athletes). Bradycardia in these scenarios is physiologic and is not associated with difficulty in perfusing the brain and other organs. This patient’s 12-lead EKG shows sinus bradycardia since there is a P wave prior to every QRS complex. Sinus bradycardia is the most common type of bradycardia. Other types of bradycardia include conduction blocks (i.e. type 2 or type 3 AV blocks), junctional rhythms (lack of P waves with slow SA nodal conduction), idioventricular rhythms (wide QRS complex rhythms that originate from the ventricles, not atria), or slow atrial fibrillation or atrial flutter. About 80% of all bradycardias are caused by factors external to the cardiac conduction system, such as hypoxia, drug effects (i.e. beta block or calcium channel blocker use or overdose), or acute coronary syndromes.
For any patient with a bradyarrhythmia or tachyarrhythmia, it is crucial to determine if the arrythmia is “stable” or “unstable”. Signs that an arrhythmia is unstable include altered mental status, hypotension with systolic blood pressure under 90mmHg, chest pain, or shortness of breath. Patients with a stable arrhythmia can be managed supportively with observation and less invasive medical management. Patients with unstable arrhythmia are managed more aggressively with the use of electricity, often in combination with other medical treatments. This patient has an unstable bradyarrhythmia, given her altered mental status and hypotension. Intravenous metoprolol (Choice D) would make the patient more bradycardic since this medication blocks beta-adrenergic receptors of the heart that control heart rate and contractility. Intravenous Amiodarone (Choice C) is an antiarrhythmic agent used often in wide complex tachyarrhythmias (i.e. Ventricular Tachycardia). Intravenous atropine or epinephrine are agents that can be used in this patient prior to preparing for electric pacing. Transcutaneous pacing (Choice A) should always be attempted prior to Transvenous pacing (Choice B), as Transcutaneous pacing is less invasive and quicker to set up. If Transcutaneous pacing does not result in electrical “capture” or change the heart rate, the next step is Transvenous pacing. Correct Answer: A
This patient presented to the emergency department with acute pleuritic chest pain, dyspnea, and experienced a cardiac arrest prior to a detailed physical examination. The cardiac monitor shows a narrow complex sinus rhythm morphology. In the setting of a cardiac arrest and pulselessness, this cardiac rhythm is known as pulseless electric activity (PEA). PEA includes any cardiac rhythm that is not asystole, ventricular fibrillation, or pulseless ventricular tachycardia. The ACLS algorithm divides the management of patients with pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) and patients with pulseless electric activity (PEA) or asystole. Assuming adequate staff and medical resources are present, patients with all of these rhythms receive high-quality CPR, IV epinephrine, and airway management. Patients with pVT or VF receive electrical cardioversion, while patients with PEA or asystole do not receive electrical cardioversion. Patients with PEA or asystole generally have a poorer prognosis than those with pVT or VF. Out of hospital cardiac arrests that present to the emergency department with PEA or asystole on initial rhythm have a survival rate of under 3%. The etiology of PEA in cardiac arrest includes a wide variety of causes. A traditional approach to remembering the reversible causes of PEA are the “Hs & Ts”. The list of the “Hs & Ts” along with their individual treatments are listed in the table below.
Sodium bicarbonate (Choice A) would be the correct choice for a patient whose PEA arrest was caused by severe acidosis. This can occur in severe lactic acidosis (i.e. sepsis), diabetic ketoacidosis, certain toxic ingestions (i.e. iron, salicylates, tricyclic antidepressants), as well as other causes. Calcium gluconate (Choice B) would be the correct choice for a patient whose PEA arrest was caused by hyperkalemia. This can occur in renal failure, in the setting of certain medications, rhabdomyolysis (muscle tissue breakdown), and other causes. Blood products (Choice D) would be the correct choice for a patient whose PEA arrest was due to severe hemorrhage, such as gastrointestinal bleeding or in the setting of traumatic injuries. This patient has symptoms and risk factors for pulmonary embolism, including pleuritic chest pain, dyspnea, and a cancer history. These details make pulmonary embolism the most likely cause of PEA arrest in this scenario. The best treatment for this diagnosis would be thrombolysis (Choice C).
This patient presents to the Emergency Department after a cardiac arrest with an unknown medical history. Important components of Basic Life Support (BLS) include early initiation of high-quality CPR at a rate of 100-120 compressions/minute, compressing the chest to a depth of 5 cm (5 inches), providing 2 rescue breaths after every 30 compressions (30:2 ratio), avoiding interruptions to CPR, and allowing for adequate chest recoil after each compression. In the Advanced Cardiovascular Life Support (ACLS) algorithm, intravenous epinephrine is administered every 3-5 minutes and a “pulse check” is performed after every 2 minutes of CPR. The patient’s cardiac rhythm, along with the clinical history, helps decide if the patient should receive additional medications or receive unsynchronized cardioversion (defibrillation, or “electrical shock. The ACLS algorithm divides management in patients with pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) and patients with pulseless electric activity (PEA) or asystole.
The cardiac rhythm seen during the pulse check for this patient is ventricular fibrillation. The ACLS algorithm advises unsynchronized cardioversion at 150-200 Joules for patients with pVT or VF. Continuing chest compressions (Choice A) with minimal interruptions is a crucial component of BLS, however, this patient’s cardiac rhythm is shockable. Defibrillation (Choice B) takes precedence over CPR in this scenario. Amiodarone (Choice C) is an antiarrhythmic agent that is recommended in patients with pVT, in addition to unsynchronized cardioversion. This patient has VF, not pVT. Sodium bicarbonate (Choice D) is an alkaline medication that is helpful in cardiac arrests caused by severe acidosis or certain toxins (i.e. salicylates or tricyclic antidepressants). The next best step in this patient scenario would be defibrillation for the patient’s VF (Choice B).
For medical students! – Question of The Day – A 68-year-old man presents to the Emergency department after a witnessed collapse. ❓Which of the following is the most appropriate next step in management for this patient’s condition ❓ pic.twitter.com/N5HIjINtpx
This patient experienced a witnessed cardiac arrest at home, after which pre-hospital providers initiated cardiopulmonary resuscitation (CPR, or “chest compressions”) and Advanced Cardiovascular Life Support (ACLS). ACLS includes the tenets of Basic Life Support (BLS), such as early initiation of high-quality CPR at a rate of 100-120 compressions/minute, compressing the chest to a depth of 5 cm (2 inches), providing 2 rescue breaths after every 30 compressions (30:2 ratio), avoiding interruptions to CPR, and allowing for adequate chest recoil after each compression. In the ACLS algorithm, intravenous epinephrine is administered every 3-5 minutes and a “pulse check” is performed after every 2 minutes of CPR. The patient’s cardiac rhythm, along with the clinical history, helps decide if the patient should receive defibrillation (“electrical shock”) or additional medications. The ACLS algorithm divides management into patients with pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) and patients with pulseless electric activity (PEA) or asystole.
The cardiac rhythm seen during the pulse check for this patient is a wide complex tachycardia with a regular rhythm. In the setting of cardiac arrest, chest pain prior to collapse, and a history of acute coronary syndrome, ventricular tachycardia is the most likely cause. The ACLS algorithm advises unsynchronized cardioversion at 150-200 Joules for patients with pVT or VF. Watching the cardiac monitor for a rhythm change (Choice A) or checking for a pulse (Choice D) are not recommended after defibrillation. A major priority of both BLS and ACLS is to avoid interruptions to CPR, so the best next step in management is to continue CPR (Choice B) after defibrillation. Administration of intravenous adrenaline (Choice C) is helpful for cardiac arrests to initiate shockable rhythm and should be repeated every 3-5 minute or every 2 cycle of CPR, particularly valuable in asystole patients. Calcium gluconate is another drug that can be used in patients with hyperkalemia and indicated in a patient with known kidney disease, missed hemodialysis sessions, or a history of usage of medications that can cause hyperkalemia. Magnesium can be used for patients who show polymorphic VT, particularly Torsades de Pointes. The next best step in this scenario is to continue CPR, regardless of the etiology of the cardiac arrest. Correct Answer: B.
This patient’s EKG demonstrates alternating amplitudes of QRS complexes, a phenomenon known as electrical alternans. This is caused by the heart swinging back and forth within a large pericardial effusion. The patient is tachycardic and borderline hypotensive, which should raise concern over impending cardiac tamponade. The next best investigation to definitively diagnose a large pericardial effusion with possible tamponade would be a cardiac sonogram (Choice B). This investigation could also guide treatment with pericardiocentesis in the event of hemodynamic decompensation and the development of obstructive shock. Other EKG signs of a large pericardial effusion are diffusely low QRS voltages and sinus tachycardia. Chest radiography (Choice C) may show an enlarged cardiac silhouette in this case and evaluate for alternative diagnoses (i.e. pneumothorax, pleural effusions, pneumonia, atelectasis), however, cardiac echocardiography is the best next investigation. CT pulmonary angiography (Choice D) would demonstrate the presence of a pericardial effusion along with differences in cardiac chamber size indicative of tamponade. Still, bedside cardiac sonogram is a faster test that prevents a delay in diagnosis. Sending a potentially unstable patient for a CT scan may also be dangerous. Arterial blood gas testing (Choice A) has no role in diagnosing pericardial effusion or cardiac tamponade. Correct Answer: B
Cough is one of the most common complaints presenting to any emergency physician or primary care practitioner – whether it is the chief complaint or an associated symptom. An acute cough is one that has been present for less than three weeks. In the era of COVID-19, a patient presenting with an acute cough can be alarming and scary. So, now more than ever, it is important to develop a strong diagnostic approach to the acute cough, which is largely a clinical diagnosis.
Differential Diagnosis of Acute Cough
*Indicates the most common causes of acute cough.
Symptoms / warning signs
Upper respiratory tract infection aka common cold*
Rhinorrhea, nasal obstruction, sneezing, scratchy/sore throat, malaise, headache, and no
signs of consolidation
Recent upper respiratory tract infection, and absence of COPD, and absence of high fever or other systemic signs
Fever, sore throat, nasal congestion, myalgia, headache, and no signs of consolidation
Fever, tachycardia, tachypnea, consolidation signs on respiratory exam, and mental status change in patients >75y old
Whooping cough and cough-emesis
Fever, non-productive cough, fatigue, dyspnea, and/or other less common symptoms such as sore throat, diarrhea, headache, skin rash, and anosmia
drip aka upper airway cough syndrome
Post-nasal drainage sensation, need to clear throat, and rhinorrhea
rhinitis aka hay fever
Itching and watering of eyes, rhinorrhea, pruritis
of a pre-existing chronic disease
Exacerbation of Asthma
History of episodic wheezing, non-productive cough, dyspnea, reversible air-flow obstruction, allergen exposure or triggered by exercise
Exacerbation of COPD
Smoking history, dyspnea, signs of obstruction on respiratory exam i.e. decreased
breath sounds, and irreversible air-flow obstruction
Exacerbation of CHF
Dyspnea, orthopnea, peripheral edema, gallop rhythm on cardiac exam, and elevated JVP
ACE inhibitor use
Non-productive cough, tickling or scratchy sensation in throat typically arising within 1 week of starting medication
reflux disorder (GERD)
Heartburn, regurgitation, dysphagia, and cough is more prominent at night
Other pulmonary causes
Clinical signs and symptoms of DVT, dyspnea, tachypnea, tachycardia, pleuritic chest pain,
immobilization for 3 or more days, surgery in the past 4 weeks, history of DVT/PE, hemoptysis, and malignancy with active treatment in the past 6 months
Smoking history, new change in cough, hemoptysis, dyspnea, night sweats, weight loss, and signs of focal obstruction on respiratory exam i.e. decreased breath
Foreign body aspiration
Dyspnea, inspiratory stridor, choking, and elevated risk in children
Acute inhalation injury
History of exposure to smoke (e.g. in firefighters, thermal burn victims) or chemicals (e.g. chlorine, ammonia)
Large volumes of purulent sputum, dyspnea, wheezing, and chest pain
Interstitial lung disease
Non-productive cough, dyspnea, fatigue, weight loss
Picture the scene: A 23-year-old female presents to the emergency department with a cough that has been ongoing for one week. What are your next steps?
Confirm the duration and timing of cough
Nature of cough, i.e. whooping, hemoptysis, and productive vs non-productive?
Presence of the following associated symptoms: fever, dyspnea, sore throat, headache, chest pain, heartburn, rhinorrhea, facial pressure/pain, nasal congestion, or weight loss
History of any chronic lung disease (i.e. asthma, COPD), allergies, CHF, or immunosuppression?
Medication history, i.e. ACE inhibitor use?
HEENT exam (head, eyes, ears, nose, and throat)
Cardiac exam, including JVP
Send for COVID-19 swab according to your hospital’s guidelines
Order CBC if suspecting infection
Order ABG if dyspnea present or life-threatening cause of acute cough suspected
Order sputum culture if suspecting bacterial pneumonia
Spirometry if need to differentiate between obstructive lung disease (e.g., asthma, COPD) and restrictive lung disease (e.g., interstitial lung disease)
Consider starting with a Chest X-ray if red flags for serious pathology are present >> dyspnea, hemoptysis, chest pain, weight loss, immunosuppression, significant smoking history, elderly or at risk of aspiration, tachypnea or hypoxemia, abnormal cardiac or respiratory exam, or sepsis.
If suspecting foreign body aspiration, need to order bronchoscopy
Please note that treatment of the conditions that may cause acute cough are not discussed in this blog post, but can be found through medical resources such as those in the references section. Treatment for acute cough often requires treating the underlying cause.
Boujaoude ZC, Pratter MR. Clinical approach to acute cough. Lung. 2010;188 Suppl 1(Suppl 1):S41-S46. doi:10.1007/s00408-009-9170-6
Holzinger F, Beck S, Dini L, Stöter C, Heintze C. The diagnosis and treatment of acute cough in adults. Dtsch Arztebl Int. 2014;111(20):356-363. doi:10.3238/arztebl.2014.0356
Madison JM, Irwin RS. Cough: A worldwide problem. Otolarynogol Clin North Am. 2010 Feb;43(1):1-13, vii.
All patients who present to the emergency department with chest pain should be evaluated for the top life-threatening conditions causing chest pain. Some of these include myocardial infarction, pulmonary embolism, esophageal rupture, tension pneumothorax, cardiac tamponade, and aortic dissection. Many of these diagnoses can be ruled-out or deemed less likely with a detailed history, physical exam, EKG, and sometimes imaging and blood testing. This patient presents with vague, burning chest pain, nausea, and tachycardia on exam. Pulmonary embolism (Choice A) is hinted by the patient’s tachycardia, but the patient has no tachypnea or risk factors mentioned for PE. Additionally, the chest X-ray findings demonstrate an abnormality that can explain the patient’s symptoms. Pancreatitis (Choice B) and Gastroesophageal reflux disorder (Choice D) are also possible diagnoses, especially with the location and description of the patient’s pain. However, Chest X-ray imaging offers an explanation for the patient’s symptoms. The patient’s Chest X-ray demonstrates the presence of pneumoperitoneum. In the presence of NSAID use, this radiological finding raises concern over a perforated viscus from advanced peptic ulcer disease (Choice C). Peptic ulcer disease (PUD) is most commonly caused by Helicobacter pylori infection, but NSAIDs, iron supplements, alcohol, cocaine, corrosive substance ingestions, and local infections can cause PUD. PUD is a clinical diagnosis which can be confirmed visually via endoscopy. The treatment for PUD includes initiation of a proton pump inhibitor (H2-receptor blockers are 2nd line), avoiding the inciting agent, and H.pylori antibiotic regimens in confirmed H.pylori cases. The treatment for a perforated peptic ulcer with pneumoperitoneum is IV fluids, IV antibiotics, Nasogastric tube placement, and surgical consultation for repair.