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By Anonymous

Image Credit: Image by teeveesee from Pixabay.

Disclaimer: This piece is satirical. On purpose. Please do not interpret all words literally.

Spoiler Alert: I sometimes have mental health struggles! And probably so do you.

TW: Anxiety, depression, occasional swearing, poop jokes (How inclusive is this meant to be?)

.      .      .

Oh, hello there. How are you? Do you have a moment to learn about the uncomfortable details of my anxiety?

Surprise!!  I have it.

Actually, we all have it. We may not label it ‘anxiety’. Maybe we call it stress or insomnia or ineptitude (when it’s really really bad).

I’m here as your friendly neighborhood ER doctor to tell you that it’s normal. No, really!  I’m not just saying that because I have to. In the interest of full disclosure, this piece was not sponsored by Big PharmaTM (although if the makers of sertraline would like to step up, you know where to find me).

Around 20% of all adults in the US1 have some form of an anxiety disorder, which includes social anxiety, panic attacks, agoraphobia, hypochondriasis and just plain old, garden-variety generalized anxiety disorder; “GAD” for short.

GAD is a great example of how medical terminology and particularly medical acronyms can be very dumb. Imagine trying to nonchalantly explain to your Tinder date that you have a thing called GAD. Not even Gal Gadot could pull that off with charisma.

 Anxiety in all its forms is actually estimated to be the most common chronic mental health condition in the US1. I’m convinced the number is MUCH higher than 1 out of 5, but I’m also pretty sure nobody likes telling themselves they have a “disorder.” What kind of weird and ridiculous word is that, disorder?

If you’re not in the medical field (or if you are), it might surprise you to learn that the incidence of anxiety & depression are actually higher in doctors2 than in the general population. Ironically enough, the stigma around mental health issues in doctors is like the stigma around these issues in your gossipy, digital friend groups, multiplied by like, I don’t know, 17.

Probably people don’t like to think of their doctors as having mental illness. But honestly, my doctor probably has high blood pressure and hey, I’m not judging. It’s a hard job to take care of your body, lady.

The reality is, when I became a doctor, I didn’t magically become a not-human-being, though it seems that was kind of the expectation.

So, in the interest of taking care of myself, I’ve decided that I shouldn’t feel embarrassed that I sometimes struggle with anxiety and other negative emotions.  That’s just dumb!  Or Wait; I’ll try to practice better positive self-talk:

My embarrassment is not super productive and is literally bad for my health.

There, much better.

Anxiety and depression are normal emotions. However, feeling so unable to acknowledge them that you begin to question reality and find yourself awake at 2am, eating Doritos, and somehow sobbing and laughing at the same time for no apparent reason? That is decidedly not ideal.

But also, sometimes Doritos are kind of the best medicine, you know?

So anyway. This is a thing that happens to me, a real-live actual doctor who does doctor things as her job.

Is your mind blown? It’s okay, try to act natural.

I’d say that I am not anxious about sharing this but… obviously I am. Please don’t read this and just like/love/panic-wow-face it as your (imperceptibly subtle) way of showing solidarity. Please don’t comment to tell me how brave I am, because I’m not (I mean thanks, but nah). I spent literal days agonizing over this piece, and then several weeks agonizing about whether it was too self-centered or unprofessional to share in this forum.

Unfortunately, even doctors still have to be afraid that disclosing mental health issues will cost them their jobs.

I’m not actually joking about that part. Pretty messed up irony, huh?

The stigma is real. The idea that being honest about struggling with anxiety or depression could negatively impact your work or relationships or whatever else¾ that idea is actually not an irrational paranoia that only you have.

So how the hell do I get patients to trust that they can safely confide in me about mental illness if I can’t even admit to myself that sometimes I have it? I’m no chef, but I know that’s not a recipe for success.

I can easily relay empathy to patients who come to the ER with food poisoning by saying things like:

Ugh. I’m really sorry you’ve had so much diarrhea that you’re up to your eyeballs in it.  And you’ve vomited so many times the bottom of your toilet seat looks like some repulsive crime scene ¾except, you know, in a doctory and uber-professional sort of way.

But when patients come to the ER with symptoms that I suspect or even am sure are related to anxiety, depression, bipolar disorder, schizophrenia and other manifestations of extreme and/or chronic stress, I am so afraid of relating to them TOO much that my words of comfort ring hollow.

And they know it too. Because they, like I, feel very ashamed.

I am often afraid to even mention those capitalized words ‘Anxiety’ or ‘Depression’when treating patients because the stigma that we as people ALL feel is so unbearably potent that we would rather act personally offended by the words than admit it’s something we can all relate to.

So instead, if you’ve stuck with me this long; if this lengthy mass of words resonates with you in any way, form, or poop-shaped emoticon, please…

Take a minute to put on your bravery cape and talk to somebody about it.

You can even just share this rant if you want  ¾it’s okay, you’re not lazy, even though I bet you’re sitting there contemplating it and telling yourself that you are. You’re so lazy you can’t even click a share button.

Wowza. Look at how anxiety makes us treat ourselves.

Really though, share it wherever you want. Print it out and tape it on a cool looking tree in the park. You have my permission. Tell your kids, tell your wife, tell your best friend or your worst friend or your boss’s weird cousin at the holiday party.

As my partner likes to say (in a way that used to make me roll my eyes but now I realize is probably the sagest advice I ever heard in my damn life):

“It’s only awkward if you make it awkward.”

So true it hurts and I don’t even mean that sarcastically.

If you ever feel like you’re struggling with anxiety or depression, and you’re worried (ha) that it’s reaching a breaking point, PLEASE go see a doctor. Any doctor. If it’s too awkward to see your doctor, see my doctor. I’ll give you her card.

Don’t have a doctor?  Get one.

As an ER doctor, my professional medical opinion is that primary care doctors are THE. BEST. DOCTORS. for this and any other unsettling human dysfunctions you’re experiencing.

But I promise I won’t ever be mad if you show up in the ER instead. Mental health can be an emergency too.

I love you guys, and I don’t mean that in the fake-cheesy social media way. I mean it like I became a doctor because I want to help people. And if talking about my own adventures with the ups and downs of mental illness can normalize it even a teensy tiny bit, I’m in.  Oh!  And one last thing – because if high school taught me anything ,it’s that the cleverest way to end an essay is with a thoughtful quote.  Here is one by my favorite author and secret personal hero, Tom Robbins:

“I see nothing particularly courageous in risking one’s life. So you lose it, you go to your hero’s heaven and everything is milk and honey ’til the end of time. Right? You get your reward and suffer no earthly consequences. That’s not courage. Real courage is risking something you have to keep on living with, real courage is risking something that might force you to rethink your thoughts and suffer change and stretch consciousness. Real courage is risking one’s clichés.”

So take care of yourselves.   Because if you don’t, I’ll have to.   Just kidding, but also not really.

.      .      .

1. National Institute of Mental Health


2.  Beyond blue study


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By Sean Schowalter, MD

Learning Objectives:

  1. Be able to list major structures in the anterior, medial, lateral and posterior compartments of the knee
  2. Learn components of a basic ultrasound of the knee
  3. Understand the current literature involving ultrasound for detection of meniscal tears

Anterior compartment

-Quadriceps tendon

-Suprapatellar joint recess

-Patellar tendon


-Prepatellar & infrapatellar bursitis

Medial Compartment


-Medial Meniscus (incompletely visualized)

-Pes Anserinus

Lateral Compartment

-IT Band


-Lateral Meniscus (incompletely visualized)

Posterior Compartment

-Baker cyst

-Popliteal neurovascular bundle

Anterior compartment Start with the patient in supine position and the knee slightly flexed (figure 1). Place the probe in the sagittal plane just proximal to the patella, along the long axis of the quadriceps tendon. Evaluate the complete quadriceps tendon, medial to lateral, in both the long and short axes (figures 2, 3). The tendon can be follow proximally to evaluate its four muscular components: rectus femoris, vastus medialis, vastus lateralis, and vastus intermedius (figure 4). Just deep to the quadriceps tendon is the suprapatellar recess (figure 6). Positioning the knee in slight flexion preferentially drives fluid into this recess, making it a sensitive area to evaluate for knee effusions. From here, the transducer is moved inferiorly in the sagittal plane, just distal to the patella until the patellar tendon is identified. Again evaluate the entire tendon in longitudinal and transverse orientations. This region is also evaluated for bursal fluid superficial to the patella (prepatellar bursa), and anterior to the patellar tendon (infrapatellar tendon). Remember to use light pressure in order to avoid displacing and missing fluid in this area. Lastly flex the knee to 90° and evaluate the femoral trochlear cartilage by placing the probe in a transverse orientation. The cartilage should appear hypoechoic and of uniform thickness.

Figure 1. Probe/knee positioning for evaluation of anterior knee. Knee should be flexed 20-30°. Figure 2. Quadriceps tendon longitudinal. Image from Alves et al. US of the Knee: Scanning Techniques, Pitfalls, and Pathologic Conditions. RadioGraphics. 2016. Figure 3. Quad tendon transverse – VM is vastus medialis. C is Femoral trochlear cartilage. Image from Alves et al. US of the Knee: Scanning Techniques, Pitfalls, and Pathologic Conditions. RadioGraphics. 2016. Figure 4. Quadriceps muscles. VM is vastus medialis. RF is rectus femoris, VI is vastus intermedius, VL is vastus lateralis.Image from Alves et al. US of the Knee: Scanning Techniques, Pitfalls, and Pathologic Conditions. RadioGraphics. 2016. Figure 5. Patellar Tendon longitudinal. HF is hoffa fat pad. TT is tibial tuberosity. Image from Alves et al. US of the Knee: Scanning Techniques, Pitfalls, and Pathologic Conditions. RadioGraphics. 2016. Figure 6. Simple joint effusion in suprapatellar recess, deep to quadiceps tendon.Image from Alves et al. US of the Knee: Scanning Techniques, Pitfalls, and Pathologic Conditions. RadioGraphics. 2016.

Medial Knee

Evaluation is begun in coronal plane by finding the MCL along the medial aspect of the joint line. Evaluate the entire extent of the MC in long & short axes. The medial meniscus can also be seen deep to the MCL, between the femur and tibia (figure 8). The medial meniscus should appear triangular and hyperechoic. The probe can then be moved anteriorly and posteriorly to evaluate the anterior & posterior horns of the meniscus. Finally, evaluate the pes anserine tendons by moving distally along the MCL to about 4-5cm beyond the joint line and slightly anteriorly (figure 9). Here the insertions of the pes anserine tendons (sartorius, gracilis, and semitendinosus) can be evaluated, as well as the bursal fluid below them. The sartorius is the most anterior tendon, the semitendinosus is the most posterior tendon, and the gracilis is between the two.

Figure 7. Position the leg in external rotation and slightly flex knee (Line represents probe position) Figure 8. MCL Longitudinal. MM is medial meniscus. Image from Alves et al. US of the Knee: Scanning Techniques, Pitfalls, and Pathologic Conditions. RadioGraphics. 2016. Figure 9. Pes Anserine tendons in longitudinal, superficial to MCL. Appears as single entity at this level but can be followed proximally to see demarcation of the different tendons. Image from Alves et al. US of the Knee: Scanning Techniques, Pitfalls, and Pathologic Conditions. RadioGraphics. 2016.

Lateral Knee

Start on the patellar tendon in long axis and move probe laterally. The first longitudinal structure will be the IT band (figure 11). Follow the IT band proximally, focal thickening or surrounding fluid at the distal femur can indicate IT band friction syndrome. Once evaluation of the IT band is finished, the transducer can be moved further laterally in the coronal plane until the LCL is visualized (figure 13). Along the joint line the lateral meniscus should also be visualized. Move the probe anteriorly and posteriorly to observe the anterior and posterior horns. As with the medial meniscus, the lateral meniscus should appear triangular and hyperechoic.

Figure 10: Position the leg in internal rotation and slightly flex knee (Rectangle represents probe position). Image from Alves et al. US of the Knee: Scanning Techniques, Pitfalls, and Pathologic Conditions. RadioGraphics. 2016. Figure 11. T band longitudinal view. Just lateral to patella. Image from Alves et al. US of the Knee: Scanning Techniques, Pitfalls, and Pathologic Conditions. RadioGraphics. 2016.
Figure 12. Probe placement for LCL evaluation. Proximal end of transducer at popliteal groove (surface of lateral femoral condyle where popliteus muscle originates)

Figure 13. LCL in longitudinal. Image from Alves et al. US of the Knee: Scanning Techniques, Pitfalls, and Pathologic Conditions. RadioGraphics. 2016.
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By Natalija Farrell, PharmD, BCPS, DABAT

*Editor’s Note: This is the first post from our wonderful ED Pharmacist colleagues, and by our in-house toxicologist no less!


Hereditary angioedema (HAE) is a rare genetic disorder that results in recurrent episodes of well-demarcated angioedema attacks without urticaria

  • Results in C1 inhibitor (C1-INH) deficiency (HAE-1) or dysfunction (HAE-2)
  • Less commonly, the C1-INH is normal (HAE-3)
  • HAE attacks are bradykinin mediated
  Signs and Symptoms Treatment
Laryngeal Attacks Laryngeal edema, upper airway obstruction On Demand Therapy, Intubation
Gastrointestinal (GI) Attacks GI colic, nausea, vomiting, diarrhea , bowel wall edema, debilitating pain On Demand Therapy
Cutaneous Attacks Edema of the extremities, torso, face, and genitalia that results in functional impairment On Demand Therapy

On Demand Treatment Options:

  • Early recognition and treatment is essential
  • Onset of treatment effect is ~30-60 minutes
    • Treatment prevents further swelling initially and will reverse the existing swelling prior to treatment with time
      • Do not delay intubation for on demand treatment with HAE laryngeal attacks
  • 2nd dose of therapy  is not warranted unless HAE attack begins to worsen
  • Available on-demand treatments have not been studied head-to-head
  • For certain on demand treatments, patients are instructed to have them readily accessible (e.g. ecallantide)
  • Fresh Frozen Plasma (FFP) or solvent detergent-treated plasma (SDP) is only recommended if treatment specific on-demand options are not available
  • Depending on the presentation, additional adjunct therapy may be needed (e.g. IV fluids, analgesics, antiemetics, etc)
  Dose Admin Repeat Dose Mechanism Adverse Effects
pdC1-INH (Berinert) 20 units/kg IV   (round to the nearest 500 units) IV at 4 ml/min 2 hours Inhibits plasma kallikrein, coagulation factors XIIa and Xia, C1s, C1r, MASP-1, MASP-2, and plasmin Well tolerated (Nausea, Headache, Fever)
pdC1-INH (Cinryze) 1000 units IV   Repeat 1000 units in 2 hours PRN IV at 1 ml/min 2 hours (same as above) Well tolerated (Nausea, Headache, Fever)
rhC1-INH (Ruconest) 50 units/kg IV  [max:  4200 units] Slow IV push over 5 minutes 2 hours   Max 4200 units/24 hr Relapse not reported (same as above) Hypersensitivity reactions (rabbit), Headache, Nausea, Diarrhea
Ecallantide (Kalbitor) 30 mg SC     3, 10mg SC injections at separate sites preferably in the abdomen   Max:  60mg/24 hr Max:  2 doses/24 hr As early as 1 hr Inhibits plasma kallikrein Hypersensitivity reaction (rare), Prolonged PTT, Headache, Nausea, Diarrhea, Fatigue
Icatibant (Firazyr) 30 mg SC   May repeat 2nd dose in 6 hr (max of 3 doses/day) Slow SC preferably in the abdomen 6 hour Max:  3 doses/24 hr Bradykinin B2 receptor antagonist Local injection site reactions, Abdominal pain, Nausea, Headache, Dizziness, Fever, Asthenia, Increased transaminases
Fresh Frozen Plasma (FFP) ~2 units IV Administer via standard Y blood infusion set N/A Inhibits plasma kallikrein, coagulation factors XIIa and Xia, C1s, C1r, MASP-1, MASP-2, and plasmin Sudden worsening of HAE attacks, Infusion reactions, Possible transmission of infectious agents


  • HAE attacks are a potentially life-threatening medical emergency
  • Early recognition and treatment of HAE attacks is essential
  • Be familiar with which HAE on demand treatments are available at your institution
    • Due to cost and utilization considerations, FFP may be the only option at your institution
    • Consider establishing patient-specific treatment protocols in patients with known HAE that utilize your institution


  1. Zuraw BL, et al. US hereditary angioedema association medical advisory board 2013 recommendations for the management of hereditary angioedema due to C1 inhibitor deficiency.  J Allergy Clin Immunol:  In Practice 2013;1:458-67.
  2. Craig T, et al. A focused parameter update:  hereditary angioedema, acquired C1 inhibitor deficiency, and angiotensin-converting enzyme inhibitor associated angioedema. J Allergy Clin Immunol 2013;131(6):1491-3.
  3. Craig T, et al. WAO Guideline for the Management of Hereditary Angioedema. World Allergy Organ J 2012;5(12):182-99.
  4. Nasr IH, et al. Optimizing hereditary angioedema management through tailored treatment approaches. Expert Rev Clin Immunol 2015; doi: 10.1586/1744666X.2016.1100963
  5. Wu MA, et al. Current treatment options for hereditary angioedema due to C1 inhibitor deficiency. Expert Opinion on Pharmacotherapy 2015; doi:  10.1517/14656566.2016.1104300
  6. Zanichelli A, et al. The safety of treatments for angioedema with hereditary C1 inhibitor deficiency. Expert Opin Drug Safety 2015;doi:  10.1517/14740338.2015.1094053
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By Liz Mitchell, MD

Just take a moment in my shoes

and feel the heat the bodies lying,

sitting, falling, standing in our halls

this crowded ever louder crush of

humans crying, moaning, sometimes cursing

with their fists outstretched to punch or grab a nurse

and sandwiched in so close

they hear the other patients’ private pain.

There is no HIPPA here

there is no place for modesty or shame.

Take in the smell of food and bile

and sometimes something worse

like bleeding guts or rotting feet

or socks still soaked in weeks of rain

with yeasty thickened nails uncovered on our beds.

Walk past the pale blue curtains blowing in and out,

a scent of gas comes spilling into stations where we work.

If you could find the time somehow

carve out some space as walls close in

and while I race from “what’s your name”

to “who are you?” and “anybody know

where this one is” the board says hallway 3

but there are now 3 people more out there,

their gurneys pushed up tight against the walls

and doors, to where we sometimes go to pee

and shit! there is no way to get inside

the stretchers lie across that spot and

block the only place I have to sit

and rest my soul and still my weary aching feet.

I want to see you walk one day

inside my shoes and down these crowded halls.

The truth would tumble you from where you sit

your well-intentioned money conscious management

might take a hit from perilous conditions we abhor

inside our gritty world

where sadness, pain and sickness lie

in hopes of something more.

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By Zaid Altawil, MD.

Technology in medicine is advancing at ever faster rates, thanks to impressive (and exponential) progress in both cost and scale. Connected “Things” are getting smaller, cheaper, and more ubiquitous. If you don’t believe me, check your heart rate on your smartwatch.

Not you, grandpa.

Technological advances impact how we deliver care in our emergency rooms. While medicine has traditionally been slow on the uptake, we are seeing increasing examples of medical technology in action in the emergency department (ED). Connectivity is rapidly embedding itself in patient care, from how patients pursue care (ex. patient self-presenting because their holter monitor registered a 6 beat pause and they were contacted by the monitoring company) to how we monitor them in the emergency department (Bay 6’s bed is beeping, he’s trying to make run for it!)

Quick, distract him with that salty goodness.

As reflected in recent pop-culture phenomena such as the Netflix Original “Black Mirror” or USA Network’s “Mr. Robot”, the looming specter of malicious intent is ever present when technology is involved. As our care becomes intertwined with the internet-of-things (or recently coined internet of medical things), security becomes ever more important. Want can we do as emergency physicians?

Let’s start with awareness.

“Im in.”

Imagine this scenario, you are called to the resuscitation room to evaluate a patient with symptomatic bradycardia. The patient reports that he was reading his favorite journal in a coffee shop when he suddenly began to feel palpitations and shortness of breath. He begins to lose consciousness, and you rifle through your Advanced Cardiac Life Support (ACLS) algorithms. But what caused this? Well it turns out that his pacemaker is malfunctioning, and it’s not due to lead issues (ex. dislodgment), pocket issues (ex. migration, erosion), or battery failure.

While no actual cases have been documented in the literature, these flaws were demonstrated in 2012 when hacker BarnabyJack reverse engineered a pacemaker’s transmitter to deliver an 850-volt shock. Reports of this vulnerability go back as far 2007, when Dick Cheney’s physician disabled the wireless function on the then vice president’s pacemaker, fearing a terrorist could assassinate the vice president by sending a deadly signal to his device a.

If it could happen to Dick Cheney, it could happen to that guy in Bay 7.

Despite the theoretical threat, and the paucity of literature reports, this flaw has had real world implications. In 2017, the FDA recalled nearly 500,000 pacemakers when a vulnerability was discovered that could allow hackers to reprogram pace makers to slow down or even stop b.

The old man was right!

The good news is that as of April 2018, the FDA approved a firmware update for many Abbott (formerly St. Jude) ICDs (implantable cardioverter defibrillator) and CRTs (cardiac resynchronization therapy)c.The update requires any external devices attempting to communicate with the ICD/CRTs to provide authorization. This authorization can only be provided by their proprietary programmers and transmitters, such as those found in clinic and in their home monitoring systems. Abbott has also gone so far as to offer the option of disabling radiofrequency communication for some of its older devices that cannot handle an update. The downside however is that this will prevent data from being accessed by the users and their physicians.

For now, as EM physicians, we can do our part in recognizing the possibility of such an event occurring, and gently reminding our patients to get their devices updated, if they have not already done so.  

Consider another scenario where a patient is brought in by paramedics in a combative altered mental state. The patient is diaphoretic, screaming and needs four security guards to tie him down. You have given him intramuscular glucagon, intraosseous D50 many times and only now secured IV access to hang a continuous infusion of D50. Yet the patient remains in refractory hypoglycemia. What is going on??

“There’s a national shortage on Dextrose, so we’re just giving him saline with the word ‘sugar’ plastered on the label. Heh.”

In 2017, programmers at Rapid 7, a cybersecurity consulting firm, announced vulnerabilities in the Animas OneTouch Ping insulin pump system d. The system uses wireless communication between its pump and its glucometer to transmit glucose values in real time without requiring the user to input the amount of insulin needed. The programmers found that these communications were delivered using clear text without any encryption, opening to the possibility that anybody in close proximity could listen in to the communications and potentially trick the pump into believing that their own external messages were actually coming from the glucometer itself. This could allow ‘hackers’ to prompt the pump to deliver an extra-large dose of insulin when none was required. Consider the video below, where Jay Radcliffe wirelessly programs a OneTouch pump to deliver a 20U insulin bolus:

Insulin Pumps vulnerable to cyber attacks - YouTube
Copyright Jay Radcliffe,  Rapid7

These disclosures were released after communication with Animas. For their part, Animas have relayed the warning to their customers. However, it is unclear whether security on these pumps has been tightened. What does this mean for us as emergency physicians?  Well for one, it involves being more cognizant of the patient’s medical history, particularly with respect to what kind of hardware they are carrying. The risk of this sort of incident is pretty low given the relatively low prevalence of patients presenting with medical devices that are susceptible to security vulnerabilities, and it does require a significant amount of technical expertise. For now, it is an interesting tidbit of information to help keep your medical students on their toes. But it can happen.

“I don’t care if its 2019 or 2119, I’m not putting hacking on my differential”- medical student who hates you.

On another hypothetical difficult (quote horrible) shift, your charge nurse hurriedly runs over to tell you that EVERY, SINGLE infusion pump in the ED is beeping like crazy. Blood pressures are going low on nicardipine, and others are blowing through the roof on norepinephrine. As you frantically tell her to literally disconnect every line, you start to panic about how to deliver titrated medicines to patients who need them. What’s going on??

It could be gremlins. But that’s another blog post.

In 2015, the FDA released a security advisory recommending that consumers avoid using a particular brand of wireless infusion pumps due to security vulnerabilities that would allow those with malicious intent to access the pump and deliver fatal doses of medications e. This security vulnerability was demonstrated in a video produced by Blackberry (yes, that blackberry) where a security expert was able to access a PCA pump and deliver many times the safe dose of morphine. While that particular type of pump was discontinued by its manufacturer for different reasons back in 2015, the threat is still present, as evidenced when security vulnerabilities were uncovered in a different brand of infusion pumps in 2017 f.

These examples serve to show the many ways in which cybersecurity compromises can affect patient care. While thankfully no cases of direct patient harm have been reported, the threat remains a real possibility. The FDA has been doing its part to address these cybersecurity concerns. It has held public workshops, webinars, as well as releasing new guidelines on submissions for software contained in medical devices g. Hospital systems are also preparing for potential cyber-security attacks that could threaten patient care systems. While slow on the uptake, they face many challenges including a wide array of potential targets, third-party software and hardware that make security compliance difficult. Most importantly the human element is particularly challenging to account for, as demonstrated by the uncountable phishing attacks that occur every year h. These attacks are invited in by the system’s users themselves, whenever they click on links with malicious attachments, supply their passwords to fraudulent links by accident, or reply to emails asking for more information.

Reasons is good enough for me. *Click*.
Image by  Selling_illegal_pepe, reddit.com

 The emergence of disaster protocols similar to those put in place for natural disasters and mass shooting is necessary, as the trend is towards ever more connectivity. Is not hard to imagine a future where all medical machines are connected wirelessly. As our patients become more connected to the internet of (medical) things, it is our responsibility as providers to become more cognizant of the potential dangers they are exposed to.  


  1. Gupta, S. (2013). Dick Cheney’s heart. [online] Cbsnews.com. Available at: https://www.cbsnews.com/news/dick-cheneys-heart/ [Accessed 21 Jun. 2018].
  2. Fda.gov. (2018). Firmware Update to Address Cybersecurity Vulnerabilities Identified in Abbott’s (formerly St. Jude Medical’s) Implantable Cardiac Pacemakers: FDA Safety Communication. [online] Available at: https://www.fda.gov/MedicalDevices/Safety/AlertsandNotices/ucm573669.htm [Accessed 5 Jun. 2018].
  3. Fda.gov. (2018). Battery Performance Alert and Cybersecurity Firmware Updates for Certain Abbott (formerly St. Jude Medical) Implantable Cardiac Devices: FDA Safety Communication. [online] Available at: https://www.fda.gov/MedicalDevices/Safety/AlertsandNotices/ucm604706.htm [Accessed 21 Jun. 2018].
  4. Rapid7 Blog. (2018). R7-2016-07: Multiple Vulnerabilities in Animas OneTouch Ping Insulin Pump. [online] Available at: https://blog.rapid7.com/2016/10/04/r7-2016-07-multiple-vulnerabilities-in-animas-onetouch-ping-insulin-pump/ [Accessed 21 Jun. 2018].
  5. U.S. (2018). UPDATE 1-FDA warns of security flaw in Hospira infusion pumps. [online] Available at: https://www.reuters.com/article/hospira-fda-cybersecurity/update-1-fda-warns-of-security-flaw-in-hospira-infusion-pumps-idUSL1N10B2MA20150731 [Accessed 5 Jun. 2018].
  6. MDDI Online. (2017). Why Infusion Pumps Are So Easy to Hack. [online] Available at: https://www.mddionline.com/why-infusion-pumps-are-so-easy-hack [Accessed 21 Jun. 2018].
  7. Fda.gov. (2018). Cybersecurity. [online] Available at: https://www.fda.gov/medicaldevices/productsandmedicalprocedures/ucm373213.htm [Accessed 21 Jun. 2018].
  8. SC Media UK. (2018). Devastating phishing attacks dominate 2017. [online] Available at: https://www.scmagazineuk.com/devastating-phishing-attacks-dominate-2017/article/685213/ [Accessed 27 Jun. 2018].

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An 86 year old male with a complicated past cardiac and GI history rolls into the resuscitation bay. He has a known history of afib on apixaban, prior esophageal cancer s/p esophagectomy and multiple significant GI bleeds of unknown origin. He is sitting on the stretcher with a bag of coffee ground emesis in his lap and actively vomiting dark red blood. Quickly, 2 large bore IVs are established, 40 mg IV pantoprazole is given, GI is stat paged and unmatched blood is on its way. As you are resuscitating the patient and discussing the need for airway management, the nurse points out a wide complex tachycardia on the monitor.

An EKG shows persistent monomorphic ventricular tachycardia. BP is 110/80 and now the patient has stopped vomiting. He is sitting up and talking to you with a seemingly normal mental status and denying chest pain or shortness of breath.

The first critical decision point is stable vs unstable. This patient has a high likelihood of decompensation but currently has an appropriate blood pressure (greater than 90/60) and adequate perfusion evidenced by a normal mental status and denial of chest pain and shortness of breath. So, for now he can be considered stable (1).

After that decision, there is the more complicated decision of what agent to reach for to terminate the ventricular tachycardia. The available choices are amiodarone, procainamide, lidocaine and adenosine. This review will discuss the benefits of procainamide over amiodarone and how to dose both in the Emergency Department.

Amiodarone is a popular choice for an antiarrhythmic that acts on sodium channels, beta adrenergic receptors, potassium channels and calcium channels (it is a class I, II, III and IV drug) to varying degrees. Despite its popularity, it carries a Class IIb recommendation from the AHA (1). Procainamide is a Class Ia antiarrhythmic agent that carries a Class IIa recommendation from the AHA (1). It is an older drug but it has been directly compared to Amiodarone in a head to head trial with favorable results (2).

Given the AHA recommendation and available evidence, I use it as a first line agent for termination of stable ventricular tachycardia.

The PROCAMIO trial was a multicenter, randomized and prospective trial that compared IV procainamide vs IV amiodarone for stable ventricular tachycardia (2). The doses used were:

  • IV procainamide 10mg/kg over 20 min
  • IV amiodarone 5mg/kg over 20 min

It spanned six years and was a relatively small clinical study (74 patients recruited). 

Outcome Procainamide Amiodarone OR 95% CI (p-value)
Major Cardiac Adverse Events 9% 41% 0.1 0.03-0.6 (0.006)
V-tach termination (within 40 minutes) 67% 38% 3.3 1.2-9.3 (0.026)
Adverse Events Within 24 Hours 18% 31% 0.49 0.15-1.61 (0.017)

It is worth noting that this trial was done in Europe and the dosing was slightly different that what you may be familiar with in the US. A more common dose at our Trauma Center in Boston is to give procainamide at 17 mg/kg with a max rate of 50 mg/min or to give 100 mg IV over 2 minutes every 5 minutes until you convert the rhythm. Amiodarone can be administered by a loading dose of 150 mg IV over 10 minutes, followed by an infusion.  

The most common adverse event with both drugs was hypotension (2). When this happens, you should be ready to cardiovert, so pad placement prior to drug administration is critical. In the above patient, we were able to convert the patient to normal sinus rhythm with 17 mg/kg of procainamide. The patient was intubated post conversion for emergent EGD and despite the love for it in our department, ketamine was carefully avoided given the sympathomimetic surge associated with its use as an induction agent.

The head-to-head trial is the best evidence available for procainamide over amiodarone. However, prior to this study, there were several retrospective case series that indicated similar results and prior studies that demonstrated the efficacy of procainamide over lidocaine (3, 4, 5).  So, even though your pharmacist may have to run out of the resus bay to grab this “very old drug”, consider it for your next stable patient with ventricular tachycardia.


  1. Neumar RW, Otto CW, Link MS, et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122(Suppl 3): S729–67.
  2. Ortiz M et al. Randomized Comparison of Intravenous Procainamide vs. Intravenous Amiodarone for the Acute Treatment of Tolerated Wide QRS Tachycardia: the PROCAMIO Study. Eur Heart J 2016. PMID: 27354046
  3. Marill KA, et al. Amiodarone is poorly effective for the acute termination of ventricular tachycardia. Ann Emerg Med. 2006 Mar;47(3):217-24.
  4. Desouza IS, et al. Antidysrhythmic drug therapy for the termination of stable, monomorphic ventricular tachycardia: a systematic review.Emerg Med J. 2013;0:1-7.
  5. K Komura S, Chinushi M, Furushima H, et al. Efficacy of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. Circ J May 2010;74:864–9.

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There are only a few things I know about the world. Sunrise in the east, sunset in the west. Death and taxes. Cheese is definitely ok to toss on to your baby in a high chair, but probably not ok to toss on somebody else’s baby.

TL:DR – You need to consider the patient when you get an ECG, and you need to look for a few specific things on an ECG ordered for syncope. Have a plan, or a mnemonic. #cheesechallenge.

Your patient came to the ED after passing out. Now what do you do?  You could do a lot, including cbc for anemia, chemistry for electrolyte abnormalities, BNP for cardiogenic cause, head CT for SAH, CT PA for PE, MRI for TIA/CVA, CTA for dissection or ruptured AAA, and probably some others. We won’t go through a whole syncope algorithm tonight, but you can certainly find many out there, including some clinical decision guidelines1,2,3.

Tonight, suffice to say that everybody should get a POC glucose, POC pregnancy (women only please), and an ECG, the star of tonight’s post.

Over the last month or so of overnights, I’ve been focusing on the ECG reading in Syncope. Probably shouldn’t ever present a case of syncope without an ECG. Definitely shouldn’t ever present a case without reading the ECG that’s already done.

Again, we’re only going over how I (and maybe you) should review the ECG in the patient who has had an episode of syncope (or near syncope)

  1. You should read the ECG – i.e. however you usually read ECGs (rate, rhythm, axis, etc.) you should start there.
  2. You should read the ECG looking for ECG abnormalities that might explain the syncope.

This is my routine.

I start by looking at:

  1. intervals (which is nice because it is near the end of my regular ECG routine). In particular, short PR phenomena like WPW or LGL. Which can devolve into VF/VT from aberrant conduction.


  2. Long QT (short QT too) – over 500 QTc is interesting, over 525 might be concerning. Which can lead to TdP.
  3. High degree blocks – 2° type 2, and 3°. Can lead to pauses that lead to syncope, which requires pacer placement. BTW, you should have already diagnosed this because you already read it already, in step 1 above.
  4. Bundle blocks can lead to paroxysmal AV block as the cause.

Then I look for micropathology:

  1. Brugada – Sodium channel mutation. Linked with sudden cardiac death. ‘Coved’ (I call it “shark fin”) ST into inverted T or ‘saddleback’ ST in early precordial leads.  


  1. ARVD – Arrhythmogenic Right Ventricular Dysplasia (or ARVC – cardiomyopathy) – fibrofatty deposits, leads to VT/VF arrests, young healthy sudden deaths often during exercise/stress/illness.The Epsilon wave is often hard to see (tucked in to the end of QRS), but if you have the right patient, and you think it might be there, consider zooming in.  That is double the rate and amplitude of the ECG machine. 50mm/s and 20mm/mV. Or take a pic with your phone and zoom in with your fingers you crazy millennial.

Next, macropathologies:

  1. LVH which may be related to Aortic Stenosis, or HOCM. http://hqmeded-ecg.blogspot.com/2014/06/history-of-hypertrophic-cardiomyopathy.html


  2.  Dilated Cardiomyopathy – often with critically low EF (can’t see this on ECG).


Finally, I look for some Right heart stuff:

  1. Right heart strain – PE, Pulmonary hypertension, etc. https://marlin-prod.literatumonline.com/cms/attachment/2119497220/2094433195/gr1_lrg.jpg


  2. STE in aVR. Could be RV MI or Left Main/3 vessel disease, these people look sick, and are likely in profound shock http://hqmeded-ecg.blogspot.com/2018/02/st-elevation-in-avr-with-diffuse-st.html

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