Modern Resident - The newsletter of AAEM/RSA
February/March 2014
Volume 5: Issue 5  |  FacebookTwitterLinkedIn

Your 2013-2014 Leaders:

Meaghan Mercer, DO

Vice President
Rachel Engle, DO

S. Terez Malka, MD

Immediate Past President
Leana Wen, MD MSc

At-Large Board Members
Michael Gottlieb, MD
Calvin Hwang, MD
Sean Kivlehan, MD
Nicole Piela, MD
Edward Siegel, MD
Victoria Weston, MD

Medical Student Council President
Mary Calderone

Modern Resident Contributors

Copy Editor: Victoria Weston, MD
Managing Editor: Lauren Johnson, AAEM/RSA Staff

Special thanks to this issue's contributors:
Thomas Doran, MSIV; Jenna Erickson, MSIIIl; Michael Gottlieb, MD; Ashley Grigsby, MSIV; Nathan Haas, MSIV; Maite Huis in 't Veld, MD; Alexandra Murray, MSIII; Matthew Pirotte, MD; Mignon Rademan, BA; Jennifer Stancati, MSIII; Marianne Wallis, MSIII; Michael Wilk, MSII

Interested in writing?

Email submissions to:

Please submit articles by March 25th for the February/March edition.

Articles appearing in Modern Resident are intended for the individual use of AAEM members. Opinions expressed are those of the authors and do not necessarily represent the official views of AAEM/RSA. Articles mey not be duplicated or distributed without the explicit permission of AAEM/RSA. Permission is granted in some instances in the interest of public education. Requests for reprints should be directed to the AAEM/RSA, 555 East Wells Street, Suite 1100, Milwaukee, WI 53202, Tel (800) 884-2236; Fax: (414) 276-3349, Email:

Discrepancies Between Urban and Rural Emergency Health Care
Marianne Wallis, MSIII
Loyola University Chicago Stritch School of Medicine

A recent study in Annals of Emergency Medicine came to the bold conclusion that large cities may be safer than rural areas for trauma victims. The overall safety metric used was total injury death rate which, to a significant degree, increased with how rural a given county was, as defined by an index that accounted for both population and distance from a major metropolitan area. A report by the Department of Transportation revealed that although only 19% of the U.S. population lives in rural areas, 55% of traffic fatalities in 2010 occurred there. While some of this can be accounted by higher speeds and the sheer number of miles traveled on rural roads, there are also areas for improvement in rural emergency health care that are evident. These disparities seem to be apparent both in patient transport at the hands of EMS, as well as within actual emergency departments. As a result, the reasons for differences in outcomes in rural areas and major metropolitan ones are complicated.

One reporter covering the issue in Colorado noted several main areas that must be examined to improve rural emergency medicine. The first is geography. In trauma, much is said about the “golden hour” after the injury has taken place. In rural areas, due to the sparseness of trauma centers, this hour may end up being a “golden day.” Unfortunately, this is the one item on the list that is the most difficult to change; in rural areas, things are simply more spread out. A car accident that might occur within 2 miles of a trauma center in a city, may happen 50 miles away from one in a rural area.

The reporter points out that some of the other factors that contribute to the disparity are more related to “philosophy,” and therefore, solutions to them may lend themselves more readily to change. For instance, in many rural areas there is room for improvement in EMS. Some areas lie outside of zones that are considered “covered” by standard EMS companies. These areas often fall into the care of volunteer EMS services, with personnel whose training and experience may differ from the professional EMT — though as the reporter states their “dedication is not in question.” Additionally, trauma centers tend to be concentrated in metropolitan areas — for instance, the only three level 1 trauma centers in Colorado are located in Denver, leaving 57 counties without a level 1 center.

Finally, the problem of physician shortages cannot be ignored. Currently, there are not enough board-certified emergency medicine physicians to meet the need of every emergency department in the country and this burden is especially felt in rural departments. As a result, alternative staffing models are required, utilizing the help of physicians in other fields as well as physician assistants. While there is much debate about whether this may affect health care outcomes, it confirms that the demand for emergency physicians is high and may continue to be for years.


  1. Myers, Sage R, et al. “Safety in numbers: are major cities the safest places in the United States?” Annals of Emergency Medicine. 62.4 (2013): 408-418.e3.
  2. NHTSA National Center for Statistical Analysis. 2010 Data Rural/Urban Comparison. 2012.
  3. Vaughan, Kevin. "Is a Rural Emergency More Fatal." The Durango Herald. N.p., 31 Aug. 2013.
  4. Camargo, Carlos A, et al. “Assessment of emergency physician workforce needs in the United States, 2005.” Academic Emergency Medicine. 15.12 (2008): 1317-20.

Mental Health Visits to the ED
Jennifer Stancati, MSIII
Loyola University Chicago Stritch School of Medicine

In Wake County, North Carolina, a study was recently performed in an attempt to reduce the number of mental health related visits to local emergency departments (EDs). The program involved training paramedics to perform mental health exams by asking a series of questions to patients who were deemed not in need of emergency medical care. The paramedics then gave the patient the option of going to an emergency department or to another facility, such as a commercial psychiatric facility.1 After reading about this experiment, I was left thinking: what is going on in our EDs to necessitate such an undertaking and what can we do about it?

Visits to EDs for mental health care are on the rise. This trend reflects the pattern of the ED used as a safety net for the community’s primary care needs.2 However, there is another consistently cited reason for the increase: the deinstitutionalization of mental illness. This attempt, headed by President John F. Kennedy in the 1960s, was intended to decrease stigma and provide patients with better care. However, by decreasing the number of inpatient psychiatric wards, there have been increasing numbers of patients with mental health needs out in the communities, and consequently, in our EDs.2

The ED environment lends to a lack of privacy and comfort for any type of patient. For a mentally ill patient, this environment can be particularly unnerving, exacerbating his or her illness. Furthermore, patients often receive care without the proper continuity or follow up that they need, which can lead to higher costs and unnecessary tests. Emergency staff is trained to handle psychiatric emergencies; however, they must often rely on outside services to evaluate the patient. Coverage for inpatient psychiatric admissions can vary with insurance and for some patients, leads to a prolonged wait for an inpatient bed. All of these factors contribute to a length of stay that is often double that of other patients.2

Most EDs have developed mental health teams composed of licensed clinical social workers, advanced practice nurses, psychiatrists and psychologists. There is huge variation in how these teams work and how they are organized. With increasing demands, EDs are attempting to develop new systems and new approaches. Some EDs report attempts to make the psychiatric rooms more inviting, while maintaining appropriate safety precautions (e.g., murals, TVs, chairs and tables).2 Another approach was to develop a “co-management” model where a patient’s complete care, including medications and testing, is transferred to mental health teams after they have been medically cleared. These “co-management” systems have been associated with decreased length of stay.2 Other EDs have developed separate psychiatric ED spaces with low-stimulation waiting rooms and family-friendly interviewing rooms.2 A task force established by the Illinois Hospital Association has proposed the development of ED beds designed and reserved for 24-48 hour stays for crisis stabilization.2

When President Kennedy originally developed his plan for deinstitutionalization of mental illnesses 50 years ago, the aim was to efficiently treat patients in their own communities. We still have a long way to go in accomplishing this goal.


  1. Creswell J. E.R. Costs for mentally ill soar, and hospitals seek better way. The New York Times. 2013.
  2. Slade M, Taber D, Clarke MM, et al. Best practices for the treatment of patients with mental and substance use illnesses in the emergency department. Dis Mon. 2007; 53: 536-580.
  3. Polevoi SK, Shim JJ, McCulloch CE, Grimes B, Govindarajan P. Marked reduction in length of stay for patients with psychiatric emergencies after implementation of a comanagement model. Acad Emerg Med. 2013; 20: 338-343.

Toxicology Board Review
Michael Gottlieb, MD
Cook County Emergency Medicine Residency

Which of the following dermatologic findings and potential causes is INCORRECT?

  1. Cyanosis - Methemoglobinemia
  2. Erythroderma - Boric Acid
  3. Pallor - Carbon Monoxide
  4. Jaundice - Hypercarotinemia (excess carrot intake)
  5. Brightly flushed skin - Niacin

C is incorrect. Methemoglobinemia causes cyanosis due to the oxidation of the iron molecule in hemoglobin, thereby reducing its oxygen carrying capacity. Boric acid (commonly found in a variety of products, but classically, pesticides) is well-known to cause a "boiled lobster" skin rash. Carbon monoxide causes normal appearing or pink-colored skin due to its ability to increase hemoglobin's affinity for oxygen, resulting in hyper-oxygenated red blood cells. Hypercarotinemia, classically seen among anorexic and bulimic teenagers replacing high calorie foods with low calorie carrots, results in excessive beta-carotene, a yellow-pigmented vitamin which mimics jaundice. Note: hypercarotinemia, as opposed to hyperbilirubinemia, does not result in scleral icterus. Niacin (occasionally used to increase HDL in hypercholesterolemia) is well-known to cause prostaglandin-mediated flushing, which may be mitigated by pre-treating with aspirin before each dose.


  1. Wright RO, et al. Methemoglobinemia: etiology, pharmacology, and clinical management. Ann Emerg Med. 1999 Nov;34(5):646-56.
  2. Schillinger BM, et al. Boric Acid Poisoning. J Am Acad Dermatol. 1982 Nov;7(5):667-73.
  3. Piantadosi CA. Carbon monoxide poisoning. N Engl J Med. 2002 Oct 3;347(14):1054-5.
  4. Mazzone A, Dal Canton A. Image in clinical medicine. Hypercarotenemia. N Engl J Med. 2002 Mar 14;346(11):821.
  5. Hochholzer W. The facts behind niacin. Ther Adv Cardiovasc Dis. 2011 Oct;5(5):227-40.

Nitroglycerin and Chest Pain: It Provides Relief, but Does it Provide Data?
Thomas Doran, MSIV
Lake Erie College of Osteopathic Medicine

Overheard in the ED: “Given your cardiac history, your relief from pain after nitroglycerin is a ‘slam dunk.’ This chest pain is most likely your heart.”

As recently as 2000, Braunwald's Heart Disease referred to the subjective presentation of ACS as “diffuse substernal chest pressure that starts gradually, radiates to the jaw or arms, and is worsened by exertion and relieved by rest or nitroglycerin.” However, this statement is amended in the 2011 edition to reflect research in the intervening years: “Studies have suggested that response to nitroglycerin may not reliably discriminate cardiac chest pain from non-cardiac chest pain.”

There are at least four studies which have examined the utility of nitroglycerin as a diagnostic tool.1,2,3,4 Some studies have shown that of the subset of patients who experienced pain relief after nitroglycerin, a majority were found to have a non-cardiac source of chest pain. Henrikson et al., performed a prospective study of 459 patients and found that in patients for whom CAD was the subsequent diagnosis, nitroglycerin relieved the chest pain in 35% of cases, whereas 41% of patients whose chest pain was determined to be other than CAD also found relief.3 In other words, pain relief with nitroglycerin was not predictive of CAD, and more people without cardiac chest pain found relief than those with cardiac chest pain.

Further, Steele et al., found that the Positive Likelihood Ratio for nitroglycerin was approximately one.5 This means that both the pre-test probability (if nitroglycerin administration is to be a diagnostic test) and post-test probability for cardiac origin were unchanged after administration. In sum, pain relief from nitroglycerin was not predictive of CAD.

In short, each of these studies concludes that nitroglycerin is at best unsubstantiated as a diagnostic tool to support a diagnosis of chest pain of cardiac origin. Although it is at times useful in relieving the pain associated with angina, it should be used as a treatment rather than as a diagnostic measure.


  1. Bonow: Braunwald's Heart Disease - A Textbook of Cardiovascular Medicine, 9th ed., CH. 53, Approach to the Patient with Chest Pain.
  2. Shry EA, Dacus J, Van De Graaff E, et al. Usefulness of the response to sublingual nitroglycerin as a predictor of ischemic chest pain in the emergency department. Am J Cardiol. 2002;90:1264-6.
  3. Henrikson C, Howell E, Bush D, et al. Chest pain relief does not predict active coronary artery disease. Ann Intern Med. 2003;139:979-86.
  4. Diercks D, Boghos E, Guzman H, et al. Changes in the numeric descriptive scale for pain after sublingual nitroglycerin do not predict cardiac etiology of chest pain. Ann Emerg Med. 2005;45:581-5.
  5. Steele R; McNaughton T, McConahy M, Lam J. Chest pain in emergency department patients: If the pain is relieved by nitroglycerin, is it more likely to be cardiac chest pain? CJEM. 2006;8(3):164-169.

Case Study: Pulmonary Embolism Masked as an ST-Segment Elevation Myocardial Infarction
Matthew Pirotte, MD
Michael Wilk, MSII
Loyola University Chicago Stritch School of Medicine

A 50-year-old man arrives to the emergency department complaining of recent onset chest pain and progressively worsening dyspnea over the past week. An EKG showed ST-elevation in leads V1-V4 and a point-of-care Troponin I test revealed a slightly elevated value. The clinician quickly made the diagnosis of an acute ST-segment elevation myocardial infarction (STEMI) and the patient was urgently rushed to the catherization lab. However, catherization failed to identify any angiographic evidence of an AMI.

What other diagnoses should be investigated? Important considerations include Prinzmetal’s angina, pericarditis, early repolarization, left bundle branch block, hyperkalemia and pulmonary embolism (PE).1

EKGs can be of significant diagnostic value in identifying false-positive STEMIs. Most importantly, EKGs from false-positive STEMIs are more likely to lack ST-segment reciprocal changes (PPV 95.1%) and have a concave morphology (PPV 93.1%) than true-positive STEMIs.2

In this case, Prinzmetal’s angina (coronary spasm) could be a plausible diagnosis given the signs of coronary ischemia with a normal angiogram. This particular patient, however, was ultimately diagnosed with a sub-massive PE. Despite usual EKG changes seen during PEs such as the classic S1Q3T3 pattern, they can uncommonly present with ST elevations. If ST elevations develop during PE, they are most likely to be found in the anteroseptal leads.3,4 The etiology underlying EKG changes due to sub-massive PEs remains uncertain, but may be caused by hypoperfusion and increased right ventricular afterload.5 Moreover, nearly half of patients diagnosed with PE may have positive Troponin I values, making a definitive diagnosis of PE difficult.6

False-positive STEMIs present a diagnostic dilemma for clinicians. ST-elevation of the anteroseptal leads remains a rare, but possible explanation of PE.


  1. Wang K, Asinger RW, Marriott HJ. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med. 2003 Nov 27;349(22):2128-35. Review.
  2. Chung SL, Lei MH, Chen CC, Hsu YC, Yang CC. Characteristics and prognosis in patients with false-positive ST-elevation myocardial infarction in the ED. Am J Emerg Med. 2013 May;31(5):825-9. doi: 10.1016/j.ajem.2013.02.009. Epub 2013 Mar 9.
  3. Wilson GT, Schaller FA. Pulmonary embolism mimicking anteroseptal acute myocardial infarction. J Am Osteopath Assoc. 2008 Jul;108(7):344-9.
  4. Falterman TJ, Martinez JA, Daberkow D, Weiss LD. Pulmonary embolism with ST segment elevation in leads V1 to V4: case report and review of the literature regarding electrocardiographic changes in acute pulmonary embolism. J Emerg Med. 2001 Oct;21(3):255-61. Review.
  5. Lin JF, Li YC, Yang PL. A case of massive pulmonary embolism with ST elevation in leads V1-4. Circ J. 2009 Jun;73(6):1157-9. Epub 2008 Dec 19.
  6. Mehta NJ, Jani K, Khan IA. Clinical usefulness and prognostic value of elevated cardiac troponin I levels in acute pulmonary embolism. Am Heart J. 2003 May;145(5):821-5.

Scribes in the ED: A Scribe's Point of View
Jenna Erickson, MSIII
Chicago Medical School
Mignon Rademan, BA

For the past two years I have worked as a scribe in a fast-paced, level 1 trauma center. Before training, my motivation was to build my resume and to witness the exciting events that are notorious to EM. I never imagined my value as a scribe or the necessity of my role for the smooth functioning of such a busy environment.

The use of scribes in emergency medicine has been growing, and the necessity to provide accurate, detailed EMR continues to drive the demand for our services. In 2009, Tri-City Medical Center reported that scribes accounted for an increase in productivity equaling a $600,000 gain for the hospital.1 A retrospective study in 2010 analyzed 243 emergency physician shifts with and without scribe usage, reporting a statistically significant improvement in productivity per physician.2 Editorial accounts of scribes in EM vouch for their value as well, stating personal stories of increased productivity, higher job satisfaction and reduction in burnout.3 The popularity of scribe use in EM is discussed in a two-part podcast series by Dr. Joseph Guarisco, American Academy of Emergency Medicine Operations Management Committee Chair, verifying the claims and educating the community of emergency physicians.4

When asked if I think scribes are worth the time, training and resources, I think back on one of the rare times when a scribe was unable to make her shift. The physician, though competent at creating a chart, was completely disoriented. Rather than seeing the usual four patients an hour he spent most of his shift facing a computer screen. This resulted in excess workload for the other physicians, who were equipped with a scribe, to maintain productivity.

With a scribe taking ownership of documentation, the physician is free to spend much more time in the patient room. This is not only a better work environment for the doctor, but also the patient. When physicians are not occupied with data entry and note taking, they are free to spend more time conversing with patients, shifting the atmosphere from a rushed interview to a genuine conversation. Documentation improves as the scribe records real-time events and data. The doctors’ lives also improve since they spend more time practicing medicine and less time managing records.

My experience verifies the benefits scribes provide for physicians, patients and even us. As a college student, firsthand exposure to traumas and routines in EM has cemented my decision to pursue a career in medicine. Along with the numerous analytical reports quantifying improvement in time and money, scribe services are a big win for emergency medicine. It is my hope that more emergency physicians will embrace the role of scribes and incorporate them into their practice to keep up with the changing times.


  1. Scribes, EMR Please Docs, Save $600,000. ED Manag. (2009) Oct; (21)10: 117-8.
  2. Arva R, Salovich DM, Ohman-Strickland P, Merlin MA. Impact of scribes on performance indicators in the emergency department. Acad Emerg Med. (2010) May; 17(5): 490-4.
  3. Shadofax MD. My experience with a scribe in the emergency department. blog (2012) Dec 6. Accessed 4 Jan 2014.
  4. Guarisco J, Taylor T. Scribes in the ED Part 1. The American Academy of Emergency Medicine. December 16, 2013.

Evaluation of Apparent Life-Threatening Events (ALTEs)
Ashley Grigsby, MSIV
Arizona College of Osteopathic Medicine

An apparent life-threatening event (ALTE) is defined as an acute change in an infant that frightens the parent or caregiver. ALTEs are frequently described by parents as changes in color, changes in muscle tone or episodes of choking.1 As you can imagine, the broad definition of an ALTE leads to a broad differential diagnosis for its etiology. An ALTE is not a diagnosis, but more a symptom that must be investigated. Often, the true etiology of the episode will not be determined in the emergency department; however, it is important for the emergency medicine physician to do a thorough evaluation to best determine disposition. Here is a short list of the possible causes of an ALTE:1

  • Normal behavior — periodic breathing, respiratory pauses
  • Infectious — RSV, pertussis, sepsis
  • GI — intussusception, volvulus, reflux
  • Primary inborn errors of metabolism
  • Electrolyte disturbances
  • Non-accidental trauma (child abuse)
  • Cardiac — arrhythmia, cardiomyopathy
  • Respiratory — laryngomalacia, airway obstruction, vascular ring
  • Neurologic — seizure, syncope, CNS hemorrhage
  • Accidental or intentional ingestions

As you can see, the possible etiologies are endless and encompass all organ systems. It would be impossible for an EM physician to rule out all of the possibilities in the ED. Diagnostic studies should be focused after a careful history and physical examination. There are six warning signs, that if present, increase the likelihood that the ALTE is medically significant, and should prompt further investigation.1

  • Symptoms at time of evaluation
  • Bruising or evidence of trauma
  • History of prior ALTE, especially within the last 24 hours
  • Unexpected death in a sibling
  • Dysmorphic features or known syndrome
  • Need for resuscitation by caregiver

Frequently, the following diagnostic tests are done for ALTE evaluation: complete blood count, basic metabolic profile, calcium, magnesium, chest radiograph and EKG.1 RSV and pertussis testing can be considered if clinically indicated.1 However, one systemic review showed no place for these diagnostic studies for routine use.2 Instead, testing should be guided by history and physical examination.2

Final disposition is dependent on history, physical exam and social situation. If the event resulted in physiologic compromise or if any of the six warning signs are present, the infant should be admitted for cardiopulmonary monitoring and/or observation.1 Some argue that all ALTEs should be admitted for 24 hour observation, although more studies are necessary to determine the safety of discharging well-appearing infants after an ALTE.2

Although ALTEs can be difficult to investigate in the inpatient setting, the management from an emergency medicine physician’s standpoint can be fairly simple. A careful history and complete physical exam should be performed and diagnostic studies guided by these exams. Warning signs should prompt further investigation and observation. The majority of patients will benefit from limited diagnostics and a period of observation.3


  1. Corwin, MJ. Apparent life-threatening event in infants. Up to Date [Internet]. 2013 [cited 2013 19 January].
  2. Tieder JS et al. Management of apparent life-threatening events in infants: a systematic review. J of Pediatrics. 2013: 163 (1).
  3. De Peiro AD et al. ED Evaluation of infants after an apparent life-threatening event. Amer J of Emer Med. 2004: 22(2).

Analgesia for Corneal Abrasions: An Evidence-Based Approach
Nathan Haas, MSIV
Loyola University Chicago Stritch School of Medicine

Corneal abrasions are a commonly encountered problem in any emergency department, and are the source of significant pain in countless patients. The emergency physician’s approach to managing this pain is based more on tradition than sound evidence.

Traditionally, the approach to analgesia for corneal abrasions has varied significantly, but often consists of topical tetracaine or proparacaine administered in the ED with strict prohibition of providing similar topical anesthetics upon discharge.1 Contrary to previous belief, eye patching does not reduce pain in patients with corneal abrasions.2 Topical NSAID solutions show promise for managing the pain associated with corneal abrasions, and a Cochrane Review addressing this concept is currently underway.3,4

Although corneal abrasions can heal quickly with resolution of pain within a few days, pain control upon discharge from the ED is often not adequately achieved with systemic analgesics. Patients frequently request topical anesthetics for home use. Extended use of the “-caine” class of topical anesthetics has long been avoided based on fear of adverse ophthalmologic events, including corneal ulceration, delayed healing or epithelial thickening. However, this practice is based primarily on a series of small case reports, with an overall lack of strong data supporting or reputing this treatment modality.5

One such case series from 1968 consisted of five patients using topical anesthetics at higher concentrations (5%), more frequently (up to every six minutes) and for longer durations (up to three months) than typically is required for a corneal abrasion.6 Another case series of three patients from 1978 includes one patient that used a topical anesthetic every 30 minutes for six weeks.7

Clearly, prolonged courses of concentrated topical anesthetics used frequently can lead to adverse events. However, case reports such as these fail to address the safety and efficacy of much abbreviated (i.e., 48 hour) treatment regimens. A large randomized controlled trial has yet to be conducted addressing this topic, and until this is completed, practice patterns will likely continue to be dictated more by tradition than evidence.


  1. Calder L, Balasubramanian S, Stiell I. Lack of Consensus on Corneal Abrasion Management: Results of a National Survey. CJEM. 6.6 (2004): 402-07. Online.
  2. Fraser S. Corneal Abrasion. Clinical Ophthalmology. (2010): 387-90. Online.
  3. Weaver CS, Terrell KM. Evidence-based Emergency Medicine. Update: Do Ophthalmic Nonsteroidal Anti-inflammatory Drugs Reduce the Pain Associated with Simple Corneal Abrasion without Delaying Healing? Annals of Emergency Medicine. 41.1 (2003): 134-40. Online.
  4. McCabe A, Awan JA, Walsh CD, Brown MD, Lawrenson JG, Lawrenson AL, Wakai A. Topical non-steroidal anti-inflammatory drugs for analgesia in traumatic corneal abrasions. Cochrane Database of Systematic Reviews. 2012, Issue 4. Art. No.: CD009781. DOI: 10.1002/14651858.CD009781.
  5. Swaminathan A, Orman R. Mythbusting 1 - Corneal Abrasions and Topical Anesthetics. 2014. EM:RAP. Web. 21 Jan. 2014.
  6. Epstein DL, Paton D. Keratitis from Misuse of Corneal Anesthetics. New England Journal of Medicine. 279.8 (1968): 396-99. Online.
  7. Henkes H E, Waubke TN. Keratitis from Abuse of Corneal Anaesthetics. British Journal of Ophthalmology. 62.1 (1978): 62-65. Online.

Shock Review
Alexandra Murray, MSIII
Ohio University College of Osteopathic Medicine

Shock is classically defined as circulatory insufficiency that creates an imbalance between tissue oxygen supply and demand.1 In the emergency department, over 1 million cases of shock present each year with the source of the shock falling into one of four major categories and over 15 different subcategories. Due to the wide variety of causes of shock, the emergency physician is often faced with a large spectrum of possible presentations that requires immediate recognition and action to avoid morbidity and mortality. The four major categories of shock can be classified as hypovolemic, cardiogenic, distributive/vasodilatory and obstructive.1-3

Hypovolemic Shock
Hypovolemic shock is due to inadequate venous return to the heart caused by lack of circulating volume. Causes of hypovolemic shock include hemorrhage (i.e., trauma, childbirth, GI bleeding), dehydration (i.e., burns, diarrhea, vomiting), third spacing, widespread vasoplegia (postperfusion syndrome), or lack of vascular tone.1-3 Clinical manifestations of hypovolemic shock include signs of hypoperfusion such as altered mental status, oliguria, cool and clammy skin, mottling, low jugular venous pressure, poor capillary refill, and narrow pulse pressure. Treatment includes rapid and appropriate replacement of fluids in order to restore organ perfusion.1-4

Cardiogenic Shock
Cardiogenic shock is caused by inadequate cardiac pump function due to loss of cardiac contractility. Causes of cardiogenic shock include myocardial infarction and resulting complications, atrial and ventricular arrhythmias, valvular heart defects, atrial myxomas, and ventricular free wall aneurysms.1-3 Clinical manifestations of cardiogenic shock include evidence of global hypoperfusion such as altered mental status, mottled extremities, oliguria, narrow pulse pressure and elevated jugular venous pressure. Other clinical signs may include pulmonary edema and cardiac gallop.2,5 Treatment includes inotropic and vasopressor medications and fluid resuscitation, if patients do not display signs of volume overload. Dobutamine may be considered for systolic blood pressure (SBP) between 70-100mmHg and Norepinephrine may be considered for patients whose SBP is <70mmHg.1,4

Distributive/Vasodilatory Shock
Distributive or vasodilatory shock is caused by maldistribution of blood flow. Examples of distributive/vasodilatory shock include septic shock (most common), systemic inflammatory response syndrome, toxic shock syndrome, anaphylaxis and anaphylactoid reactions, drug or toxin reactions, Addisonian crisis, myxedema coma, neurogenic shock after a CNS or spinal cord injury, acute systemic inflammation following acute MI, post-resuscitation syndrome, and post-cardiopulmonary bypass.1-3 Clinical findings are usually similar to patients with hypovolemic shock except that these patients will not respond as well to fluid replacement. Low blood pressure, altered mental status, and oliguria usually fail to respond to several liters of fluids. Instead, patients may develop hyperemic extremities, bounding pulses, brisk capillary refill, hyperdynamic heart sounds, and a wide pulse pressure in response to fluids.2,3 The 2012 guidelines for the Surviving Sepsis Campaign suggest that initial resuscitation efforts for distributive shock include keeping CVP between 8-12mmHg, MAP≥65mmHg, urine output ≥0.5mL/kg/hr, SVO2 at 65%, and efforts to normalize lactate levels. Antibiotics, fluid resuscitation, inotropes and/or vasopressor therapy may be indicated.4,6

Obstructive Shock
Obstructive shock is the result of extracardiac obstruction to blood flow such as massive pulmonary embolism, tension pneumothorax, severe constrictive pericarditis, pericardial tamponade and Eisenmenger’s syndrome.1-3 Treatment varies with etiology. For example, thrombolysis can be considered in patients with pulmonary, tension pneumothorax is treated with needle decompression followed by chest tube placement and cardiac tamponade is treated with pericardiocentesis.8 Maintenance of intravascular volume is of vital importance in all forms of obstructive shock; however, fluid resuscitation may only improve the patient’s cardiac output and hypotension temporarily.

Presentation and Physical Exam
It is important to note that while there may be certain clinical findings that are characteristic of a particular type of shock, there are several clinical features that are common to all types of shock. Clinical signs can also vary widely depending on the stage of presentation.1 There is no one vital sign or lab value that can diagnose a specific type of shock, nor is there any particular vital sign or value that can accurately determine the severity of shock.1 Mortality secondary to shock remains high; however, quick and accurate recognition of the causes of shock can improve patient outcomes.


  1. Tintinalli J. (2000). Approach to the patient in shock. In Emergency Medicine: A Comprehensive Study Guide (5th ed., pp. 215–250). New York: McGraw-Hill.
  2. Holmes C. (2003). The evaluation and management of shock. Clin Chest Med. 24, 775–789.
  3. Kelley D. (2005). Hypovolemic shock: An overview. Critical Care Nurse. 28 (1), 2–19.
  4. Moranville M. (2011). Evaluation and Management of Shock States: Hypovolemic, Distributive, and Cardiogenic Shock. Journal of Pharmacy Practice. 24 (1), 44–60.
  5. Dubey L. (2011). Cardiogenic Shock Complicating an Acute Myocardial Infarction - A review. Acta Cardiol. 66 (6), 691–699.
  6. Dellinger RP. (2013). Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock, 2012. Intensive Care Med. 39, 165–228.
  7. Meyer G. (2000). Acute circulatory failure caused by primary pulmonary hypertension or pulmonary embolism. Rev Mal Respir. 17 (1), 51–65.
  8. Society of Critical Care Medicine. (2007). Diagnosis and Management of Shock. In Fundamental Critical Care Support (pp. 1–12).

Board Review Question
Maite Huis in 't Veld, MD
University of Maryland

A 28-year-old male presents to the emergency department after a mechanical fall while ice skating. You notice an open fracture of his right ankle. The patient is placed on a stretcher and when the patient is connected to the monitor you see the rhythm strip illustrated below.

Board Review Question

Patient reports he has a lot of pain at his ankle but denies any other symptoms at this time. Vital signs are: BP 135/90, pulse rate 75/min, respiratory rate 20/min, O2 sat 100%, T 36.9.

Which of the following is true regarding this patient’s condition?

  1. This patient needs immediate synchronized cardioversion.
  2. Cardiology should be consulted for pacemaker implantation.
  3. This condition does not need any specific treatment at this time.
  4. Atropine should be administered to treat this condition.

C is correct. This condition does not need any specific treatment. This is second degree atrioventricular (AV) block, Mobitz type I (Wenkebach). Mobitz type I AV block (Wenkebach) is progressive prolongation of the PR-interval, until a P-wave is not conducted. The PR-interval is longest immediately before the dropped beat and shortest immediately following the dropped beat. The pattern is typically repeated in a 3:2, 4:3 or 5:4 ratio. Causes include increased vagal tone, myocarditis, acute inferior myocardial infarction, following cardiac surgery and drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone).

In Mobitz type II AV block there are P-waves that, intermittently, are not conducted, without progressive prolongation of the PR-interval. Causes include anterior myocardial infarction, myocarditis, hyperkalemia, auto-immune (SLE, systemic sclerosis), Lenegre’s or Lev’s disease, amyloidosis, sarcoidosis, and drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone).

Mobitz type I AV block is typically transient and asymptomatic. This condition does not need any specific treatment. Symptomatic patients usually respond to atropine. Outpatient follow up with a cardiologist is indicated. This in comparison to Mobitz type II AV block, which typically requires pacing.


  1. Life in the Fast Lane Blog.
  2. Life in the Fast Lane Blog.
  3. UpToDate: Second degree atrioventricular block: Mobitz type I (Wenckebach block).