Monday, March 30, 2015

EKG Challenge No. 12: Once Upon a Time in Triage

You are working as the "triage physician" in a busy city emergency department when a 34 yo female presents with chest pain.   The pain is retrosternal and burning in nature and has been persistent for 3 hrs.  It is associated with some nausea, but no shortness of breath or diaphoresis.  You order a GI cocktail and get an EKG:

 What is your differential diagnosis?  What would you do next?
 Read the case conclusion here

Wednesday, March 25, 2015

How Do You "FOAM," Anyway?

Last fall, I had the honor and opportunity of delivering a lecture about FOAMed to my fellow residents and faculty during our Tuesday didactic conferences. During this lecture, I had about 40 minutes to try my best to give a broad overview of what FOAMed is, how it’s impacting our specialty, and how to incorporate it into one’s practice.

The lecture can be viewed on Vimeo here.

Today, I want to focus on a specific part of the lecture: “How do you ‘FOAM,’ anyway?” For those following along at home, it starts about 15 minutes in, and lasts for about 15 minutes.

In my experience – and I think this sentiment is shared by others – one of the major hurdles faced by those looking to jump in to the FOAMed world is information overload. The sheer number of blogs and podcasts has exploded in recent years and has reached the point of being overwhelming, as seen in this figure from a paper by Mike Cadogan and Brent Thoma chronicling the rise of the FOAM:

From Emerg Med J. 2014 Oct;31(e1):e76-7

For FOAMed to be used as a learning tool, especially for the EM physician in training, I think two important points must be kept in mind. First, learning can only occur in an environment in which there is a positive cognitive margin. Basically, when you have the time, energy, and focus to be able to sit down and really dive into something, retention is maximized. If the environment is not conducive to cognitive functioning – from fatigue, distraction, intoxication, what-have-you – true active learning from a FOAMed resource is going to be very difficult.

Second, while we are in general andragogical learners who want to seek out the information we want and need rather than having it all spoon-fed to us, it is exceptionally inefficient and difficult to wade out into the FOAM world and attempt to “pull in” everything of interest to you. Much more efficient and comprehensive to have everything that’s new “pushed” to you, for your perusal at a time in which you have a positive cognitive margin.

And this is where Chris Nickson’s chosen vernacular comes in. Replace “information overload” with “filter failure” in your lexicon. Particularly when you’re first starting out, you don’t want every new item posted from every FOAMed world pushed to your brain all at once. You need a way to improve the signal-to-noise ratio, to pare down the breadth of content to those things that are highest-yield to you.

Having gone through the painful process of trying to “pull” FOAMed information to me, and then subsequently being drowned in knowledge from filter failure after learning how to “push” information, I’d like to do what I can today to help my fellow EM learners ease their transition to “push” information and filtering.

How To Do It:

1. Familiarize yourself with RSS feeds. This is basically a piece of computer code that indexes all of the posts of a particular blog. They’re usually signified with the following icon:

In and of themselves, they’re useless. If you happened to click on one, your screen would be filled with incomprehensible programming code. BUT, if only there were a piece of software that knew what to do with them…

2. Learn how to use an RSS feed aggregator. This is a program into which you can upload RSS feeds for whatever blogs you want to follow, and then those posts from all of those blogs will be listed out for you in a chronological digest format. I prefer Feedly, which you can download [here]. It integrates into PC & Mac browsers, and I believe there are both Apple & Android apps for mobile devices. Adding blogs to Feedly is pretty simple; I go over it in the video, right at the 19-minute mark.

3. But how do I know which blogs to add? How do I know where to start? Well, this is what I’m going to try to help you with. There is actually another way to add blogs to your Feedly feed, and you can do it en masse. This is via an OPML file, which is just a file 
cataloging the RSS feeds from whichever blogs you want. Upload the OPML file to Feedly, and *BOOM* all of those blogs are instantly added. Here’s a couple screencaps showing you how to do this in Feedly.

Clicking your e-mail address in the bottom left corner will take you to the "Organize" screen.

Select the appropriate OPML file for import.

Can you feel the power?

There are a variety of options to view and organize posts from your chosen FOAMed resources.

I have created a set of OPML files to help you get started. The file names should be relatively self-explanatory. “Getting Started” includes just a few of the most popular and highest quality resources out there for those just dipping their toes in the FOAMed kiddie pool. “The Basics” adds a few more resources, and it goes up from there. The “Advanced Practice” file includes every blog on my Feedly, which is every active EM-relevant blog I know about. I’m sure I've missed a few, but it should be the lion’s share of what’s out there. You can download these at will and upload them to your Feedly.

I. Getting Started
II. The Basics
III. Intermediate Level
IV. Advanced Practice

If you load “Getting Started” but later want to see more, you can upload one of the other files. Only the new additions will be added to your feed; it won’t duplicate what you already have. Pretty neat.

5. Go get FOAMy! Remember: there’s no “right” or “wrong” way to do this. I still struggle with filter failure. Just remind yourself there’s no possible way to read everything. Find the things that look interesting to you, and bookmark those to read in detail later. Don’t be afraid to let some other things pass you by – if you stay active in the FOAMed Twitter world and keep up with high-quality FOAMed digests like those from Life in the Fast Lane and EM Curious, you’ll catch the most-important, highest-quality stuff. Hopefully the organization of the OPML files will help those of you just getting started, or those of you struggling with “push” information gathering and filter failure.

I’m always open to comments and questions! Feel free to comment here on the blog, or catch me on Twitter: @CSamSmithMD.

Never stop learning,

C. Sam Smith, PGY-3

Wednesday, March 18, 2015

Sprinkle on a little ketamine

A middle aged patient with a longstanding history of asthma (multiple intubations and ICU stays) presents with 3 days of worsening dyspnea, refractory to home bronchodilators, speaking in 2 word sentences and in tripod position. As oxygen saturations hover in the low 90s, the patient is transferred to critical care area for BiPAP.  As the patient rolls by you plan on BiPAP, solumedrol, epinephrine, and magnesium, and you and your attending think “why don’t we try some ketamine?” 

Severe Respiratory distress (Source imgkid)

Clinical Question: Can ketamine be used as a bronchodilator improve outcomes in patients with severe asthma?

Literature Review: In the review article from 2013 by Goyat et al, 20 articles were examined looking at ketamine for bronchospasm (case series, RCTs, observational, retrospective studies) 3 of which were in the ED.  Ketamine was used as a rescue agent in all studies; general doses were 0.1-0.2mg/kg IVP followed by infusion at 0.15-0.25mg/kg/hr.  Eighteen articles showed a “favorable response”, and 2 studies showed insufficient response.  No major adverse events were reported.  

To review, ketamine has 2 enantiomers: the S is more potent and faster acting, and the R enantiomer may be associated with more emergence reactions.  Most preparations are 1:1 S:R. Peak onset is at 60 seconds with a duration of 10-15 minutes. The distribution half-life is approximately 7-11 minutes and is cleared via the hepatic route with half life of 2-3 hours.  Several mechanisms have been proposed for its effect on bronchospasm: improved airway mechanics, anti-inflammatory properties, airway relaxation, reduction of nitric oxide, inhibition of reuptake of catecholamines at the synapse, and anticholinergic effects.

The first case report of ketamine use for reactive airway disease was in 1972 of a child who had anaphylaxis during skin testing that improved after ketamine, followed by a non-controlled trial in children intubated for asthma that showed a significant difference in PaO2/FiO2 and dynamic compliance after initiation of ketamine infusion.  The first controlled double blind trial in 1994 showed an improvement in “stethoscopic exam” and in Po2 and PCO2.  While it is worth noting the significant change in these objective data points, they are not exactly patient centered outcomes.

One observational study looked at pediatric ED patients. It enrolled 10 patients who were unresponsive to traditional therapy; no change in peak expiratory flow (PEF) was noted at 1 hour, but a significant change in the patients’Asthma Scores and respiratory rates (RR) was noted. 

The next prospective, double blind RCT (Howton, 1996) showed no benefit with ketamine.  Fifty-three consecutive patients with peak flows less than 40% after 3 does of albuterol were enrolled, all were given continuous albuterol, methylpredisolone and oxygen and then either a 0.2mg/kg ketamine bolus followed by 0.5mg/kg/hr x 3 hours, or an equivalent saline dose.  While there was a significant improvement in PEF, RR, FEV-1 in both groups over time, there was no difference between the groups. 

Similarly, a follow up RCT in kids (Allen, 2005), looked at 62 consecutive patients randomized to saline or the same ketamine doses as above, without improvement in pulmonary scores.

 Take-Home Points:
The conclusions of the above review are that ketamine is cheap, has a physiologic rationale, has few adverse effects and has been shown to improve asthma in case series and observational trials, though this has not been born out in the two small RCTs undertaken.  Their suggestion is that it should remain in the ED physicians armamentarium for refractory status asthmaticus and, as always, “further well-designed studies are warranted”.  It is probably not unreasonable for ketamine to be the induction agent of choice for asthmatics, and should be considered whenever NPPV is considered for status asthmaticus. 

Allen JY, Macias CG. The efficacy of ketamine in pediatric emergency department patients who present with acute severe asthma. Annals of Emergency Medicine 2005, 46 (1): 43-50

Howton JC, Rose J, Duffy S, Zoltanski T, Levitt MA. Randomized, double-blind, placebo-controlled trial of intravenous ketamine in acute asthma. Annals of Emergency Medicine 1996, 27 (2): 170-5

Shweta Goyal, Amit Agrawal.  Ketamine in status asthmaticus: A review.  Indian Journal of Critical Care Medicine 2013, 17 (3): 154-61

Submitted by Wes Watkins, PGY-4 
Edited by Louis Jamtgaard, PGY-3 @Lgaard

Faculty Review by Joan Noelker

Wednesday, March 11, 2015

Hippocratic medicine No. 3: A Prescription for Honesty, Conversation and Compassion

Clinical Scenario: You are taking care of a middle-aged female who was brought to the emergency department by her family for altered mental status.  She has stage IV ovarian cancer and is undergoing chemotherapy which has caused persistent nausea, vomiting, and diarrhea.  According to her husband, she was conversant and fully oriented this morning.  During the day, she suddenly became very confused.  Per the patient’s husband, the patient has had multiple episodes like this in the past, usually associated with electrolyte abnormalities in the context of her persistent poor PO intake.  You review the patient's electronic chart and note that she has been admitted approximately every two weeks for electrolyte replacement over the course of the last several months.  You call the patient's oncologist, who states that they had been trying to manage her as an outpatient, but agrees that she needs admission again.  You inform the husband of this plan, and he notes, reluctantly, that he is "used to the routine.

It takes a while to get the bed upstairs.  In the meantime, you correct the patient's electrolytes and her mentation improves.  When you go in to check on her, you assess the patient's understanding of her disease.  The patient and her husband are aware of her poor prognosis from cancer, but they are considering another round of chemotherapy and seem resigned to continued aggressive medical interventions.

Despite the busy ED around you, you take time to talk to them about their life.  The patient says that what she actually wants to do is spend as much time at home as possible.  The patient and her husband are not familiar with hospice care and state that she is not ready to "just give up and die."

After your conversation, you walk away and wonder what is (and what should be) the role of emergency providers in initiating end of life conversations with patients and families?  What are the harms of avoiding these difficult subjects and what benefits can be gained by doing so? 

Literature Review:
"End-of-life" is not a rarity in emergency medicine.  Before starting in this field, many of us may have assumed naively that our experience with end-of-life situations would come acutely in the form of sudden cardiac arrests, terrible car accidents, or  gun shot wounds to the chest.  The reality, however, is that emergency medicine also encompasses oncology, geriatrics, end-stage organ failure, debilitating co-morbidities, and social work nightmares.  We take care of the chronically (and newly chronically) ill, and it is our duty as physicians to discuss their medical options with them in a way that they can understand.

The majority of people would prefer to die at home [1,2].  Despite this, over 75% of Americans die in an institution [3].   One in five Americans dies in or soon after a stay in the ICU[4].  In a study done by Teno et al. looking at over 1500 patients who were at the end of life,  67% ended up in a nursing home or hospital [5].  Even for those who go to hospice, the option may be offered late, as many patients die within days (not months) of starting hospice. 

Studies have also shown that we spend more money in a patient’s last 6 months of life than at any other point in their life [2]. States that have had more emphasis on end of life support tend to have fewer ICU days in the last 6 months per the CDC analysis (ranging from 1.6 to 4.3 ICU days). La Crosse, Wisconsin is well known for starting Respecting Choices, a program which encourages participation in end of life discussions and advance directive cares. A Dartmouth program compared the amount of money spent in the last 6 months by patients living in La Crosse, WI to averages across the country and noted that the money spent in the last 6 months in La Crosse was significantly less [6]. 

Aggressive care for the dying is more than an issue of monetary cost in an already-strapped healthcare system.  When studied in two separate populations of patients with metastatic cancer, aggressive care for the dying was associated with reduced quality of life at its end, and worse bereavement adjustment in caregivers [7,8].  End-of-life discussions have been shown to reduce both the incidence of aggressive intervention and the subsequent psychological stress amongst surviving family members[7]. 

In addition, good end-of-life care has been shown to benefit both quality and quantity of life in the terminally ill.  The goals of hospice care are to alleviate suffering and promote the best quality of life for patients and families facing a  prognosis of six months (not days) or less.  Of those admitted to hospice, family members perceived a significant increase of emotional support and respect for their dying loved one. (96% compared to 68%) [5]. Family members were more satisfied with the overall quality of care with hospice services, rating hospice services “excellent” 70% of the time compared to those admitted to the institution setting (less than 50% “excellent” ratings).   According to a 2007 retrospective chart review of Medicare records, patients with CHF, lung cancer, and pancreatic cancer who received hospice care had an increased length of survival (29 days for hospice patients with) when compared with patients who did not [9]. 

Perhaps most importantly, we should consider what constitutes a “good death.”  Zhang et al performed a prospective, longitudinal cohort study of 396 advanced cancer patients and their  caregivers to try and assess what constitutes quality of life at the end of life. They found the factors that were associated with the highest quality of life were fewer hospitalizations, fewer ICU stays, meditation, and therapeutic alliance with their physicians [10]. 

Good end-of-life decisions require honest discussion of goals, but this can be difficult.  Multiple studies have shown that physicians often avoid these conversations [6], and patients may be overly optimistic about their family members understanding of their wishes [2].  Advanced care planning and better communication surrounding end-of-life has the potential to improve patient care.   For example,  Detering et. al. carried out a prospective randomized controlled study of 309 adults over the age of 80  looking at the effect of advance care planning support versus standard care [11]. Of the 56 patients who died within the 6 month study period, those in the advance care planning support group were much more likely to have end of life wishes known (86% vs 30%). in addition, both patients and family of the intervention group had significantly less stress, anxiety, and depression than control group.

Most studies looking at end-of-life communication have been based in the outpatient or ICU setting.  However, we as emergency providers must ask ourselves what role we should play in this process. End of life discussions in the ED, especially for the chronically ill, can be challenging, but like it or not, they occur.  It can be frustrating to talk to a patient with an advanced cancer diagnosis who seems unaware of her prognosis.  How does one get the medical story, communicate with the primary care provider and oncologist, and then talk with the patient and family, all while adhering to the demanding ED timetable?   In the busy ED, it is often easier to avoid such problems than to address them.  However, an abundance of research has demonstrated that an honest and compassionate conversation about goals of care, even if brief,  may be the most beneficial thing that we as an emergency physician can provide to these patients. 

According to the Choosing Wisely campaign "Top Ten" for Emergency Medicine, we should not delay palliative or hospice services for patients who are likely to benefit:

In many cases, for patients whose goal is to be comfortable and avoid hospitalization, hospice care at home can be arranged directly from the emergency department.   For patients who require more care than they can receive at home, an admission may be warranted, but starting a conversation about goals in the ED can smooth the transition.  According to 2012 statistics from the Center to Advance Palliative Care, almost 2/3 of hospitals in the US with more than 50 beds have inpatient palliative care services, and there were over 3500 hospice agencies throughout the US []  .  Emergency physicians should be aware of the resources  available in their area.  For our own hospital, BJH in St. Louis, information about hospice and home care services can be found at the  BJC Hospice website. 

Take home points:  While many people express a desire to die at home, the majority of Americans die in acute or extended care facilities.  The US has a robust system for helping people access aggressive medical care in emergency situations.  This is a tremendous asset for many Americans, but for those dying of serious illness, it may not be the best pathway.  When aggressive care is seen as the default option for dying patients, it may confer significant harm in the form of decreased quality of life and increased long term psychological stress on caregivers.  Despite the pressures of working in the ED,  emergency physicians are well-positioned to help patients, families, and our colleagues in other areas of healthcare begin conversations addressing end-of-life care.    

Submitted by Melissa Kroll (@misskrll) PGY-2
Edited by Maia Dorsett (@maiadorsett)
Faculty reviewed by Maria Dans (Palliative Care) and Douglas Char and Ryan Schneider (Emergency Medicine)

[1] Field, M. J., & Cassel, C. K. (2010). Approaching death: improving care at the end of life. Palliative Care: Transforming the Care of Serious Illness, 79.
[2] Halpern, S. D. (2012, August). Shaping end-of-life care: behavioral economics and advance directives. In Seminars in respiratory and critical care medicine (No. 33, pp. 393-400).
[3] Health, United States. 2010. With special features on death and dying. National Center for Health Statistics [on-line]. Available at Accessed February 13, 2014.
[4] Angus, D. C., Barnato, A. E., Linde-Zwirble, W. T., Weissfeld, L. A., Watson, R. S., Rickert, T., ... & Robert Wood Johnson Foundation ICU End-Of-Life Peer Group. (2004). Use of intensive care at the end of life in the United States: An epidemiologic study*. Critical care medicine, 32(3), 638-643.
[5]Teno JM, Clarridge BR, Casey V, et al. Family perspectives on end-of-life care at the last place of care. JAMA. 2004;291:88–93.
[6] The Dartmouth Atlas of Health Care. The Dartmouth Institute for Health Policy and Clinical Practice [on-line]. Available at Accessed February 13, 2014.
[7]Wright, A. A., Zhang, B., Ray, A., Mack, J. W., Trice, E., Balboni, T., ... & Prigerson, H. G. (2008). Associations between end-of-life discussions, patient mental health, medical care near death, and caregiver bereavement adjustment. Jama, 300(14), 1665-1673.
[8]Wright, A. A., Keating, N. L., Balboni, T. A., Matulonis, U. A., Block, S. D., & Prigerson, H. G. (2010). Place of death: correlations with quality of life of patients with cancer and predictors of bereaved caregivers' mental health. Journal of Clinical Oncology, JCO-2009.
[9] Connor, S. R., Pyenson, B., Fitch, K., Spence, C., & Iwasaki, K. (2007). Comparing hospice and nonhospice patient survival among patients who die within a three-year window. Journal of pain and symptom management, 33(3), 238-246.
[10] Zhang B, Nilsson ME, Prigerson HG. Factors important to patients' quality of life at the end of life. Arch Intern Med. 2012 Aug;172(15):1133-42. 
[11] Detering KM, Hancock AD, Reade MC, et al. The impact of advance care planning on end of life care in elderly patients: Randomised controlled trial. BMJ. 2010;340:c1345. 
 The Hippocratic Medicine series is modeled after the Do No Harm project pioneered at the University of Colorado, the aim of this (hopefully) monthly installment will be on the avoidance of avoidable care i.e. raising awareness for how medical overuse has the potential to do patient harm.   Because every test or intervention we do has the potential for not just benefit but also harm, we should seek that our patients do better because of the care we provide instead of despite it.  The WUSM Hippocratic Medicine Series is supported by a grant provided by the Foundation for Barnes Jewish Hospital. 

Monday, March 9, 2015

Hypertensive Encephalopathy

A middle age woman with  a history of chronic kidney disease and hypertension presents with chest pain and altered mental status. Paramedics note that she is having decreased responsiveness, moaning to questions, and stating only that she has pain everywhere.  Her blood pressure is 230/165 on arrival.  She is alert and oriented only to self with an otherwise nonfocal neurologic exam.  Head CT is negative for intracranial hemorrhageAs you work through your differential, you wonder how should the diagnosis of hypertensive encephalopathy be made?  How should it be managed in the emergency department and what is the prognosis for patients who have a hypertensive crisis like this patient?

Literature Review:
In a patient with altered mental status in the setting of severe hypertension (systolic >180 or diastolic >120), a hypertensive emergency needs to be on the differential, which is defined by signs of acute end-organ damage in the setting of severe hypertension.  Examples of end-organ damage include altered mental status, pulmonary edema, elevated troponins, and acute kidney injury.  Approximately 1-2% of people with HTN will have an episode of hypertensive encephalopathy in their lifetime, which may manifest as headache, nausea, vomiting, and confusion [1].

There is little evidence in the management of a hypertensive emergency; differences in medicine choices appear mostly based on symptoms of the crisis.  Initial management of hypertensive encephalopathy is to rule out other causes for encephalopathy (ischemic stroke accounts for 25% of all hypertensive encephalopathy cases), other considerations are intracranial bleed (SAH, IPH), posterior reversible encephalopathy syndrome (PRES) or even carotid or vertebral-basilar dissection. After ruling out other causes focus should be on treating the blood pressure with a IV anti-hypertensive that can be quickly titrated, such as nicardipine or nitroprusside [2].  Blood pressure should be lowered approximately 10-20% in the emergency department, and should not be lowered more than 25% in the first day due to the risk of ischemia from dropping pressures below the brain's autoregulatory range.  Keep in mind that the diagnosis of hypertensive encephalopathy is a diagnosis of exclusion and is only confirmed retrospectively with resolution of symptoms after treating the blood pressure [3]. 

Prognosis for hypertensive emergencies is variable.  In 2009 Katz et al. looked at 1,568 patients presenting with SBP >180 or DBP >110 or those with SAH and SBP >140 to evaluate practice patterns, mortality, and complications. Over 50% required more than one anti-hypertensive for blood pressure control. In-hospital mortality in this group was 6.9%, with 90 day mortality of 11%.  59% had acute worsening of end organ damage during the hospitalization. Hypertension has a high health burden, as 37% of the patients analyzed were re-admitted with-in 90 days, of which over 25% were due to repeat “severe hypertension” [4].  Of course, patients do much better if they can take their blood pressure medicines consistently, and this was demonstrated as far back as 1958 where an old study by Dustan showed that without any anti-hypertensive treatment, the survival at 1 year for those admitted for hypertensive encephalopathy was 10-20%.  However, with adherent treatment, 5 year survival rates were 70% [5].

Take-home Points:

Hypertensive encephalopathy is a diagnosis of exclusion, retroactively diagnosed after symptoms resolve with lowering blood pressure. BP should only be lowered 10-20% in the ED. Patients with HTN encephalopathy have an in hospital mortality between 6-11% at 90 days. Mortality reduction is related to long term compliance with antihypertensives. 


1.  Vaughan C, Delanty N. Hypertensive emergencies. Lancet. 2000;356:411–7.
2.  Price RS, Kasner SE. Hypertension and hypertensive encephalopathy. Handb Clin Neurol. 2014;119:161-7.

3.  Manning L, Robinson TG, Anderson CS. Control of blood pressure in hypertensive neurological emergencies. Curr Hypertens Rep. 2014 Jun;16(6):436.
4.  Katz JN, et al. Practice patterns, outcomes, and end-organ dysfunction for patients with acute severe hypertension: the Studying the Treatment of Acute hyperTension (STAT) registry.  Am Heart J. 2009 Oct;158(4):599-606.
5.  Dustan HP, Schneckloth RE, Corcoran AC, Page IH. The effectiveness of long-term treatment of malignant hypertension. Circulation. 1958 Oct;18(4 Part 1):644-51.

Submitted by Melissa Kroll, PGY-2

Edited by Philip Chan, PGY-2 & Louis Jamtgaard, PGY3 @lgaard
Faculty reviewed by Joan Noelker

Thursday, March 5, 2015

EKG Challenge No. 11 Case Conclusion: It's Wide! It's Fast! It's a Wide Complex Tachycardia!

You are working one evening in the emergency department when a 60-something year old female is slotted for a room.  Her chief complaint?  "Fever, weakness, vomiting".    Seeing that her triage heart rate was 157, you leave your granola bar where it is and immediately walk into the room to assess her.  You see an elderly-appearing female in moderate respiratory distress.  Her temperature is 38.2,  blood pressure is 125/87, RR is 32, oxygen saturation is 93% on 5L NC.  She has a history of a bone-marrow transplant and is chronically immunosuppressed. She endorses poor PO intake and several episodes of emesis over the last few days.  She says that she came in today when she developed some shortness of breath as well.  She denies any chest pain or palpitations.  On exam, her mucous membranes are dry, her abdomen non-tender, and her breath sounds are decreased in the right base.  You are a bit disturbed by the looks of her rhythm strip on the monitor so you get a 12-lead EKG:
The EKG above features a regular tachycardia (rate of 162) with a QRS complex duration of > 120 ms with LBBB morphology.  This leads you to an initial EKG diagnosis of a regular wide complex tachycardia, which has the following differential [1,2,3]:  

Originates in the ventricle:
            1. Ventricular tachycardia

Originates above the ventricle, but has abnormal ventricular conduction:
            2. Supraventricular tachycardia (AVRNT) with delayed ventricular conduction 
            3. Atrial flutter with 2:1 block and delayed ventricular conduction
            4. Sinus tachycardia with delayed ventricular conduction 

Delayed ventricular conduction can be due to a pre-existing bundle branch block, a toxicologic insult leading to QRS widening (such as Na-channel blockade), electrolyte abnormality (such as hyperkalemia), or aberrancy.  Aberrancy refers to the situation in which one bundle branch is ready to conduct another beat, but the other has not had time to fully repolarize and occurs in the setting of tachycardias in which there is a very short interval between electrical impulses.

So how and why does one differentiate between these three scenarios?  Since we are emergency providers in the business of saving lives, the important consideration at each step of working through an EKG differential is considering  how making the "EKG diagnosis" will alter patient management.   

Since the management of sinus tachycardia is to treat the underlying cause (and not electricity or anti-arrythmmics), the first step of working through the differential is differentiate Sinus tachycardia with abnormal conduction from SVT with aberrancy and Vtach by asking
                                                    Are there sinus p-waves?  

We underline the term sinus here because with SVT and Vtach you can get retrograde or abnormal p-waves.   To remind everyone, p-waves need to meet the following criteria for the rhythm to be considered sinus:

                                  - a p-wave in front of every QRS
                                  - Normal p wave axis:  upright in I, II; inverted in aVR; biphasic in V1.
If you can find a prior EKG for the patient with the same bundle branch block morphology, this lends further evidence to your cause.

If it is sinus tachycardia, then identify and treat the underlying cause.  If it is not sinus tachycardia, then you are left with two possibilities:  SVT with aberrancy or Vtach.  

The important thing here to realize is that if you treat SVT with aberrancy like Vtach (with electricity or amiodarone and admission) then you have caused no harm.  If you treat Vtach like SVT with aberrancy, then you have vastly under-estimated your patient's mortality and may do harm.  Adenosine can be given if a regular ventricular tachycardia is in the differential, but it does not reliably distinguish between SVT with aberrancy and Ventricular tachycardia, as there are a subset of Ventricular tachycardias (especially in young patients) that are adenosine sensitive [4].  If a patient with a wide complex tachycardia converts with adenosine, do not send them home (unless they have a previous EKG demonstrating a pre-existing bundle branch block with the exact same morphology).

Many algorithms have been developed to differentiate between these two conditions [5,6,7].  For those of you who are interested, more detailed descriptions of these algorithms are included at the very end of this post. 

The truth of the matter is that when there are more than five algorithms (and there are!) to differentiate between two conditions, it is likely that none of them are good enough to use in a life and death situation such as this one.  Indeed, one recent study by Szelenyi et. al. compared the "real life" sensitivity of two different recently developed algorithms (RWPT in II and Vereckei's avR algorithm) when applied by cardiologists, internists and emergency physicians [8].  Both algorithms were insufficiently sensitive for Ventricular tachycardia in this real life application:


Similarly, another study published by Kastrzebski et. al. found that the performance of multiple algorithms, including those cited above, was sub-par for real life use:
Image source: Reference 8

Therefore, if you are an "EP" as in Emergency Provider rather than Electrophysiologist, you should probably subscribe to the Mattu algorithm for management of wide complex tachycardias which he presented in this episode of the ECG case of the week:

Getting back to our case, you apply the Mattu algorithm to your patient.

Step 1:  Is the rhythm sinus?

You examine the EKG and find upright p-waves in lead II:

After 1 liter of fluid her heart rate comes down and you can see this even more clearly:

                       Your EKG diagnosis? sinus tachycardia with LBBB.
                       Your emergency department management?  Treat the underlying cause.

Given that this is an immunosuppressed patient with fever and tachycardia,  you have high suspicion for sepsis.   Blood and urine cultures sent.  A CXR reveals an underlying right-sided pneumonia.

The patient is started on broad spectrum antibiotics and ultimately does well.   Score: EP 1, Sepsis 0.

Take home Points: Wide complex tachycardias have an important differential diagnosis.  Start by determining if the rhythm is sinus, because this requires treating the underlying cause such as sepsis, PE, dehydration or pain.  If the rhythm is not sinus, assume its ventricular tachycardia because even if you had the time, no algorithm is sensitive or specific enough to rule out Vtach.  Electricity helps both and should be used in the unstable patient.  Remember, it's safer in the long run to assume it's T-rex and not a Tweety bird: 

Submitted by Maia Dorsett (@maiadorsett), PGY-3
Faculty reviewed by  Douglas Char

[1]Goldberger, Z. D., Rho, R. W., & Page, R. L. (2008). Approach to the diagnosis and initial management of the stable adult patient with a wide complex tachycardia. The American journal of cardiology, 101(10), 1456-1466.
[2]Brady, W. J., & Skiles, J. (1999). Wide QRS complex tachycardia: ECG differential diagnosis. The American journal of emergency medicine, 17(4), 376-381.
[3]Hollowell, H., Mattu, A., Perron, A. D., Holstege, C., & Brady, W. J. (2005). Wide-complex tachycardia: beyond the traditional differential diagnosis of ventricular tachycardia vs supraventricular tachycardia with aberrant conduction. The American journal of emergency medicine, 23(7), 876-889.
[4]Brugada, P., Brugada, J., Mont, L., Smeets, J. L. R. M., & Andries, E. W. (1991). A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation, 83(5), 1649-1659.
[5] Pava, L. F., Perafán, P., Badiel, M., Arango, J. J., Mont, L., Morillo, C. A., & Brugada, J. (2010). R-wave peak time at DII: a new criterion for differentiating between wide complex QRS tachycardias. Heart Rhythm, 7(7), 922-926.
[6]Vereckei, A., Duray, G., Szénási, G., Altemose, G. T., & Miller, J. M. (2008). New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm, 5(1), 89-98.
[7]Szelényi, Zsuzsanna, et al. "Comparison of the “Real‐life” Diagnostic Value of Two Recently 
 Published Electrocardiogram Methods for the Differential Diagnosis of Wide QRS Complex Tachycardias." Academic Emergency Medicine 20.11 (2013): 1121-1130.
[8] Jastrzebski, M., Kukla, P., Czarnecka, D., & Kawecka-Jaszcz, K. (2012). Comparison of five electrocardiographic methods for differentiation of wide QRS-complex tachycardias. Europace, 14(8), 1165-1171.

Still up for a little more learning? Here is a summary of three of the algorithms for distinguishing SVT with aberrancy vs. Vtach.  Below is a summary of three of them as well as links to additional resources.

i. The Brugada algorithm:  One of the most well-known criteria for differentiating SVT with aberrancy vs Vtach.  It comprises a series of four questions.  If the answer to any question is "Yes" then the diagnosis is Ventricular tachycardia [5].
Brugada algorithm; Figure 1 from Reference 5.
You can link to the PV Card from ALiEM for the Brugada criteria here.

ii. R-wave to peak time at DII: This algorithm (also from Brugada) was published in 2010 as an attempt to develop simpler criteria utilizing only one lead [6].  It was developed using an EP study as a gold standard.  The basic premise is that if the R wave to peak time (duration from the onset of QRS depolarization onset until the first change of polarity) is > 50 ms in lead II, the diagnosis is Vtach.  The authors reported a sensitivity and specificity for Vtach of 0.93 and 0.99, respectively.

RWPT in lead II measurement.  Figures 5 & 6 from Reference 6.

One thing that you can see from their example (above) is that measuring RWPT really is not that straightforward.  And practically speaking, a sensitivity of 93% really is not good enough.  You can read more about this method at ALiEM here.

iii. Vereckei's algorithm for lead aVR, published in 2008, uses lead aVR to differentiate from Vtach vs. SVT with aberrancy:

The last step of this algorithm, Step 4, requires a calculated comparison of the distance traveled during the initial and concluding impulses of the QRS complex:
In the initial study, they reported a 96.5% sensitivity for the diagnosis of Ventricular tachycardia.

Wednesday, March 4, 2015

As Low As Reasonably Achievable

Your patient is a 40-something female who has never been to your facility before but reports a history of chronic abdominal pain of undetermined etiology. She has had an appendectomy and a cholecystectomy. She is now presenting with two days of right-sided cramping abdominal pain associated with nausea without vomiting and lightheadedness. Screening labs protocoled by the triage nurse are unremarkable, and a bedside RUQ ultrasound is negative for significant pathology. After two doses of morphine she is still visibly uncomfortable in the stretcher. The team is reticent to pursue further diagnostics, but given the fact that she currently carries no diagnosis for her symptoms and is still in considerable distress, and the lack of any prior imaging in your EMR, the decision is made to order a CT abdomen/pelvis with contrast.

Clinical Question:

Given the fact that the pre-test probability for finding significant pathology in this patient is low, how worried should you be about exposing your patient to further ionizing radiation?

Monday, March 2, 2015

EKG Challenge No. 11 - Mmmm.... That looks sort of fast...

You are working one evening in the emergency department when a 60-something year old female is slotted for a room.  Her chief complaint?  "Fever, weakness, vomiting".    Seeing that her triage heart rate was 157, you leave your granola bar where it is and immediately walk into the room to assess her.  You see an elderly-appearing female in moderate respiratory distress.  Her temperature is 38.2,  blood pressure is 125/87, RR is 32, oxygen saturation is 93% on 5L NC.  She has a history of a bone-marrow transplant and is chronically immunosuppressed. She endorses poor PO intake and several episodes of emesis over the last few days.  She says that she came in today when she developed some shortness of breath as well.  She denies any chest pain or palpitations.  On exam, her mucous membranes are dry, her abdomen non-tender, and her breath sounds are decreased in the right base.  You are a bit disturbed by the looks of her rhythm strip on the monitor so you get a 12-lead EKG:

Interpret the EKG.  What is your differential?  What would you do next?  

See the case conclusion here