Respiratory Failure and ST Depression: Is there Posterior STEMI?

The ultrasound in this case was recorded by Dr. Robert F. (Rob) Reardon, one of my partners here at Hennepin County Medical Center (HCMC) in Minneapolis, and one of the world leaders in emergency ultrasound.  He is also an editor of this great new textbook of emergency ultrasound (Ma, Mateer, Reardon, Joing, eds.), and one of the authors of the Cardiac Ultrasound chapter (other authors of this chapter are Dr. Andrew Laudenbach (also of HCMC) and Dr. Scott Joing (also of HCMC, and the creator of the outstanding FOAMed site,


A middle-age woman with a history of emphysema presented in severe respiratory distress and respiratory failure.  She was intubated emergently in the ED.  Her venous blood gas after intubation had a pH of 7.16 and pCO2 of 66.  The Chest X-ray was suggestive of pneumonia, but not pulmonary edema.  The following ECG was recorded:
There is sinus tachycardia, and ST depression that is maximal in V3 and V4, suggestive of posterior STEMI, or possibly subendocardial ischemia.  [However, subendocardial ischemia is usually diffuse, and therefore has an ST depression vector towards the apex of the heart (towards V5 and V6.  That is to say, the maximal ST depression is usually in I, II, V5, and V6, with reciprocal ST elevation in aVR.]

A posterior ECG was recorded:
There is ST elevation in posterior leads V7 and V8.  

Although this meets criteria for posterior STEMI (0.5 mm in 2 leads), there will virtually always be some ST elevation in posterior leads when there is ST depression in anterior leads, as these are opposing leads. 

[There is an exception to this rule, and that would be in pericarditis, when there is an ST elevation vector that goes from endocardium to epicardium throughout the entire heart, with an ST elevation summation vector towards the apex.  In such a case, there is diffuse ST elevation, including towards the posterior wall.]

Thus, there is probably posterior transmural ischemia.  Is this ACS with posterior MI?  The presentation of respiratory failure without pulmonary edema is not at all typical for ACS.  The patient apparently has a COPD exacerbation with pneumonia.  She could have 2 pathologies at once, but this is less likely.

An ED cardiac echo was performed at the bedside:

This subcostal view shows poor contractility at the entire base of the heart, and excellent contractility at the apex.  There is no wall motion abnormality in a coronary distribution.

Dr. Reardon made a diagnosis.  What is it?

Reverse Takotsubo!  (See below for description of Takotsubo and Reverse Takotsubo)

Case continued:

The patient was admitted to the Medical ICU.  She recovered.  Her max troponin I was 2.2 ng/mL.  Formal Echo also showed Reverse Takotsubo, with EF of 35%.  Echo 2 months later showed full recovery of EF.

She returned in respiratory distress 5 months after the first presentation, and required intubation again.  Here is her ECG from that visit:
Very concerning for Anterior STEMI
A bedside echo showed what appeared to be an anterior wall motion abnormality.  Cardiology was immediately consulted for a formal echocardiogram.  It showed an EF of 15% with a circumferential loss of function at the mid-section, with preservation of the apex and the base.  (This is called mid-ventricular stress cardiomyopathy).

Again, the troponin I peaked at 2.2 ng/mL.

An angiogram was done and showed normal coronary arteries.

The LV function eventually recovered again.

Stress Cardiomyopathy, Takotsubo and Reverse Takotsubo, and Mid-Ventricular Takotsubo Cardiomyopathy

In Takostubo stress cardiomyopathy, caused by small vessel ischemia from high catecholamine influence, there is poor contractility at the apex, causing "apical ballooning," which has the appearance of a Japanese octopus trap, or "Takotsubo"  Here is a left ventriculogram of Takotsubo SCM.
Standard Takotsubo with Apical Ballooning.
See this case for ECG and Echo video of Takotsubo Stress Cardiomyopathy that Mimics STEMI.

Reverse and Mid-Ventricular Takotsubo Stress Cardiomyopathy (SCM):

Reverse Takotsubo SCM is the term used when the LV dysfunction is of the base, and not the of the apex.  Thus, there is no apical ballooning. As in standard Takotsubo, the dysfunction is circumferential, not in a vascular territory, and not due to ACS.    

Reverse SCM has been described in many stressful situations, just as standard Takotsubo SCM, including sympathomimetic drug abuse, energy drinks, serotonin syndrome, anaphylaxis, high dose epinephrine (adrenaline!), pheochromocytoma, subarachnoid hemorrhage, sepsis, and dobutamine stress.

Reverse Takotsubo may be more common in younger patients, but there is little systematic data on the condition.  One small registry of 103 SCM patients, 20 of whom had reverse Takotsubo, showed that the reverse type had higher incidence of triggering stress (100% vs. 77%), less dyspnea, pulmonary edema, and cardiogenic shock, and less T-wave inversion on ECG.

Mid-ventricular Takotsubo is the term for good function of the mid LV, with poor function of BOTH the base and the apex.  It is less common than either of the other forms.

Of course, if it is SCM that does not have apical ballooning, it does not look like an octopus trap, and therefore perhaps should not be called Takotsubo at all.

There is also a claim of a 4th type, "localized" SCM (with focal wall motion abnormalities mimicking ACS).  The claim is substantiated only by case reports, such as this one, which cannot establish with certainty the absence of a thrombotic coronary lesion.

Take Home Lesson:

When the clinical situation is stress (such as respiratory failure from COPD in this case -- not from pulmonary edema), and the echocardiogram shows circumferential dysfunction, whether at the base, mid-LV, or apex, then stress cardiomyopathy is very likely the etiology of the ECG abnormalities.

Episode 46 – Social Media & Emergency Medicine Learning

In early June of this year I caught up with Dr. Rob Rogers of iTeach EM and The Teaching Course, Dr. Ken Milne of The Skeptics Guide to EM and Dr. Brent Thoma of Academic Life in EM and Boring EM at the Canadian Association of Emergency Medicine Conference in Ottawa to chat about the evolution of Social Media & Emergency Medicine Learning. In this podcast, we discuss how Social Media can enhance your career, tips on how to get the most out of FOAMed without getting overwhelmed by the volume of material, swarm-based medicine, tacit knowledge sharing, the flipped classroom, the use of FOAMed in emergency medicine training curricula, how Twitter, Google+, Google Hangout and Google Glass have changed the face of medical education, and much more.

[wpfilebase tag=file id=465 tpl=emc-play /]

[wpfilebase tag=file id=466 tpl=emc-mp3 /]

The post Episode 46 – Social Media & Emergency Medicine Learning appeared first on Emergency Medicine Cases.


There are multiple topical anesthetics that we use in the ED. The common theme is that all of these drugs with -caine cause sodium channel inhibition in nerves, which blocks axonal transmission leading to the typical numbness and and localized weakness. I admit that it can be a bit confusing as to which one you should use and when. The aim of this post is therefore to help provide some clarity.


This gel contains 4% Lidocaine, 0.1% epinephrine and 0.5% tetracaine. It is used for topical laceration repair and according to some studies can provide adequate local anesthesia for scalp and facial lacerations in up to 90% of patients. Apply 1-3mL to the open wound. It should then remain there for 20-30 minutes to allow for absorption. Cover the wound with an occlusive bandage and tell the patient not to remove it. LET is great for lacs of the face of the scalp. It is generally contraindicated in areas with end arterial supply digits, penis, nose, and ears because pi is a vasoconstrictor. In large wounds the amount needed to cover can be toxic. You can also see excess absorption if it is applied to mucous membranes – so don’t do that.  However, in most uses it is very safe. A trial of 203 children by Harman et al, in 2013 involving kids 3 mos to 17 years saw no toxicity when 3mL of LET was applied to a wound prior to tissue adhesive. The amount of lido in 3 mL of LET is approximately 135 mg – but the amount absorbed is generally way less than this and is limited by the size of the lac. Epi will lead to less absorption locally due to the vasoconstriction.

You may be familiar with 5mg/kg at the ceiling for lidocaine dosing. The lack of toxicity with LET means that this number does not need to be slavishly followed. Finally, since lidocaine can lead to methemoglobinemia be cautious in using it in infants under age 1 month.


EMLA stands for eutectic mixture of local anesthetics and is comprised of 2.5% lidocaine and 2.5% prilocaine in a cream. This cream consists of microscopic droplets that penetrate intact skin up to a depth of 2-3mm via diffusion down the concentration gradient. It can reduce the pain of venous/arterial puncture, lumbar puncture, access of ports and in wound repair/abscess I&D (prior to subcutaneous injection of lidocaine).

The usual dose is 1-2 grams applied per 10 square cm of skin. Cover with an occlusive dressing for 45-60 minutes.

Per Gajraj et al, the maximum area for usage is: The maximum application areas recommended for children are [22]:

  • Less than 10 kg – 100 sq cm
  • 10 to 20 kg – 600 sq cm
  • Greater than 20 kg – 2000 sq cm

It does require approximately one hour to achieve peak effect and can last for 60-120 minutes after removal. It does not work as well in diseased/denuded skin (like eczema) with a shorter duration of action. You should not use it in patients with risk factors for methemoglobinemia (G6PD deficiency). In infants younger than 3 months be careful with how much you apply.


LMX is liposomal lidocaine and it used to be known as ELA-Max. LMX 4 is 4% lidocaine, LMX 5 is 5% lidocaine. It is designed to be applied to intact skin. It has a more rapid onset because the liposomes penetrate better and prevent metabolism. It compares foavorably with EMLA in IV stick pain. It does not technically require an occlusive dressing (but it is probably a good idea to prevent accidental removal). It takes 30 minutes to work as opposed to 60 minutes for EMLA.

The risk of significant systemic absorption is very low. Nevertheless it should only be applied to intact skin.

The dose is 1 to 2 g of LMX per 10 sq cm of skin with similar max doses to EMLA.

The post LETEMLALMX appeared first on PEM Blog.

Quantum Quandaries, Diagnostic Decoherence and Probabilisticians

So I imagine you have just read the title of this post and thought – “Casey has finally lost it!” – or something to that effect….

Diagnostic Decoherence – it sounds like the title of an obscure SMACC lecture.

So what am I rambling on about – what is this concept? Where does it come from? And why do you care?

Let me explain.

At SMACC 2013 I had the pleasure of meeting Prof. Simon Carley – a man with a brain the size of a small planet.  One evening over a beer he stumped me with a statistical problem – the Monty Hall paradox

It is a simple problem that demonstrates our often-flawed intuition when it comes to probability and decision-making.  And even smart, experienced clinicians get it wrong a lot of the time.   I recall walking away from that conversation feeling like a small part of the rug had been pulled from under my clinical gestalt.

The next morning Simon gave a great lecture on the real world application of statistics at the bedside – this talk was called “Wrestling with Risk” – you can see it on the 2013  SMACC podcast.  Free, awesomeness.

Simon’s talk was great – a beautiful illustration of  balancing risk of missing vs. over investigation and diagnosis that leads to unnecessary intervention.  It is all about understanding the imperfection of our science and being able to think past the “results” of tests. We need to be thinking about what the results really mean and how they apply to the individual in your care.  IN recent months Simon has teamed up with Dr Ian Beardsell [@docib] to produce the St. Emlyn’s podcast - the first few episodes go right to the heart of probability and testing in ED.

Simon used the PE workup as an example – it is one of those diagnoses where we have good data – well-defined pretest risk assessment tools and calculated likelihood ratios for our “diagnostic tests”.  The problems we see with PE workup come from the common misunderstanding many clinicians have about the use of these tests.  For example, performing a CTPA on a Well’s Score low-risk patient is more  likely to yield a false positive over a true positive if reported as “PE”.

OK, great.  We need to teach our students and trainees all these stats – educate them about test characteristics and application to various populations.  If they knew all the LRs, scores and risks then they could make statistically-sensible decisions.  Less harms, less false diagnoses and probably a swag of money saved.

But…. here’s the problem.  We are still practicing in the Wild west of science. There are not a lot of rules, plenty of unknown unknowns and yet we need to get the job done – for most of what we do there is just not a great evidence base.  Even when we do have evidence – it is often of questionable quality or cannot be applied to our patients’ particular context.  Would lead many of us to EBM-nihlism or drink!

Ever since that talk I have been thinking – contemplating and trying to come up with a counterpoint.  Examining the way I use probability in daily practice and searching for a good analogy in another field of science.  And I think I have found it!  So here it goes…. but first a quick disclaimer.

I, Dr Casey Parker, am a total physics nerd and make no apology for this.  So the following rant makes complete sense to me and maybe a few other people I know!  This next bit is very heavy on non-medical, theoretical ideas which I believe are a nice analogy to the conundrum posed by Prof. Carley.  If this type of thing bores you to tears – stop reading now! OK, still there? Begin…

Einstein is famously quoted as stating that “God does not play dice with the Universe.”  Possibly the most famous quote from the great man – and possibly the most flawed!  Einstein was expressing his incredulity at the emerging quantum physics of the early 20th Century – he felt fundamentally uneasy with the idea that probabilistic mechanisms determined the nature of the universe.  Specifically the Copenhagen interpretation stated that: “A system is completely described by a [probability] wave function , representing the state of the system, which evolves smoothly in time, except when a measurement is made, at which point it instantaneously collapses to an eigenstate of the observable that is measured.”

Here is where the infamous thought experiment of Schrodinger’s cat comes in (or doesn’t… if it is dead ;-).  The cat exists in a state where it is both alive and dead (probabilistically) up until the point that the box is opened and an observation is made.

So when you are working up a lowish-risk PE patient – you might have a Well’s score, a modified Geneva or your trusty clinical gestalt.  You plug it into MDCalc and you get a probability of a PE being present.  The D-dimer is done… DOH!… it is “not negative” and you are unable to say “go home!”   So you decide to make an ‘observation’ ie. a CTPA – which really just changes the probability.  There is no waveform collapse, no eigenstate, no.   Medicine is not like physics – there is no absolute.

But, here is the but…  at some point you have to make a call.  We work in the real world – you cannot go to the patient and tell them that they have a 73.2% PE.  You cannot give them a 73 % dose of heparin? We need to be able to to decide who gets treated and who does not.  This is analogous to the classical-quantum divide:  we know that particles are composed of probability waves, yet when you look around you – you see objects, collisions, hard surfaces all of a predictable nature.  When your patient falls – their radius breaks, when the clot sticks, they get ST elevation.  So how can we reconcile this in our practice.

For the vast majority of diseases or problems that we see in the ED there are no numbers, no starting position – we are sailing in uncharted waters and would be lost.  I say “would”.  Because we do have our own personal onboard navigation systems – we all carry a rich library of experience and “gut instinct” around in our heads.  This is what we call “Gestalt” – that oft spoken German word which is rarely understood.  So how does this work?

Back to the quantum world… For most of the 20th century theoretical physics was stuck with a big headache.  On one hand there was a great theory that explained the big things – Einstein’s relativity.  And then there was the new kid on the block – quantum theory which used probability and wave equations to describe and predict the tiny world of the fundamental particles.  However, there was a demarcation dispute.  At some scale the particles had to start behaving like classical physical objects.  But there was no way to marry these two perfectly functional theories in such a way that made any sense.  This is where Decoherence comes in.

When we take a history and examine a patient – we are building up a set of probabilistic waves.  Each piece of data increases or decreases the amplitude of the wave.  Each wave carries the probability of a diagnosis – and to reach the threshold of action / reality / or the “treatment threshold” the wave must break over the wall.  Stick with me – it gets clearer soon.

Simon has beautifully described how various factors create waves of various amplitude in the work up of chest pain.  Check out his SMACC Gold lecture from 2014 - on risk factors.  When we take the history from a chest pain patient – we know that the typical atherosclerosis risk factors are poor predictors of acute coronary syndromes.  In other words – they produce only small waves, they are subtle ripples in the ACS pond.  In order to get over the threshold – we need a collection of waves which positively interfere with one another in order to make it to an “actionable” probability.  Chest pain is easy – we have good data to measure the waves and the amplitude of the threshold.  Alas, when you are floating on the “non-specific abdo pain pond” the waters are choppy.  Lots of waves interfering with one another – leaving us with murky water.  That is why these patients seem tougher to sort out.  And by the way – no matter what the Surg Reg tells you – the white cell count is merely a ripple on that pond!

Now of course, some of our “tests” create big waves – think about “thunderclap headaches”, “shingles rash” or a “3 mm of ST elevation pattern in II, III and aVF”.  These features create waves that easily carry us over the “action threshold”.  This is the stuff we all learn in Med School.  Sometimes it is wrong – for example – Framingham risk factors and ACS – no real wave in the ACS setting.  However, more often it is just plain messy.

When the quantum physicists look at probability waves – they isolate a couple of particles and do complex probability wave calculations  - very smart.  But if you try and do this with more than 3 particles (waves) at a time – the numbers get crazily complex – it is just too messy.  And yet we all do this intuitively on a daily basis.   One of my mentors believed in “Diagnostic Triads” – the idea that many diseases could be reduced to 3 symptoms – this is an example of three simple probability waves interfering to create an ‘eigendisease’ -e.g.  fever, jaundice plus (R)UQ pain = cholangitis.  Unfortunately during our daily grind in the ED the act of taking a clinical history and exam is an infinitely complex assessment in which we are constantly integrating new data and probability waves into the mix.  At some point the waves may coalesce into a meaningful reality – and this is what a quantum physicist might describe as Decoherence.  The waves become a real thing – something that we can name, refer, incise or thromobolyse.

So in summary – I agree with Simon. [ 'twould be daft not to! ]  We are probabilisticians rather than diagnosticians.  However, the math is far more complex than our textbooks and teachers would have us believe.   Medical students have always struggled with the complexity of clinical diagnosis.  There are just too many variables for even the brightest minds to integrate into a cohesive model of what is going on in most patients.  Of course – spending more time, doing more tests can give us more data points and help us “realise” a diagnosis.  And as we gain experience we learn to recognise “disease scripts” – patterns in the waves that we recognise as “a thing” before they reach the threshold.

Now – one might read all of this and get a sense of nihilism.  It all just seems too complex and hard.  But I think there is a way forward.  Here is what I believe we should do:

1.  We need more research to define the probabilities – clinical medicine is full of dogmatic belief in our clinical skills.  E.g.  “the chest is clear – therefore no pneumonia….”  In reality the negative LR for auscultation in pneumonia is close to 1.0.  Utterly useless!  By knowing and teaching the reality of our skills we can do better, make more reasoned decisions.

2.  We need to teach probability to Medical Students – personally I am a fan of the Bayesian approach and teach likelihood ratios as the most easily applied stats to keep in the back of one’s head.  These are more intuitive than sensitivity or specificity.  They tell you more about the “test” and can be applied directly tot he individual patient in front of you.

3.  We need to change the language that we use when we talk to our patients.  A while back I defined the Zeroth Law of Diagnostics - “there is no such thing as Zero risk”.  And I believe that we ought to fess up to our patients – certainty is a rare beast in Medicine.  We should tell our patients this.  We can have a reasonable belief that they do not have a PE, or that they do have ‘smouldering diverticulitis’ – however, there is a real chance that we are wrong.  If things change, or they get new symptoms [waves - new waves ] then they need a review and rethink.  The catch phrase for this is = “shared decision-making”… or as we in GP-land call it : consultation.  The patient is the one with the disease [or not] and they take the risk.

4.  We need a bit of Dogmalysis – there are a lot of pseudo axioms and long-held truths in our game that need re-examination.  David Newman has produced a nice series of podcasts on this topic – check it out at SMART EM.

5.  We need to develop a healthy insight into the way we think – I believe the buzz word is metacognition.  Understanding the sources of error and recognising the false waves will help us to make better, more accurate decisions – and to do better by our patients.

Ok.  That was quite a ramble.  Back to something more concrete soon!   Or is that concrete really just the summation of a pile of waves of probable concrete particles ?

Let me know what you think.

Andif you want to read more about Decoherence in quantum physics – I recommend reading this quick review paper.  For more reading check out the Decoherence website here.  Or just go outside and get some sun ;-)


Red in the Face

A nurse from triage presents a case to you of a 43 year old woman that he believes is having an allergic reaction.  When you evaluate the pain, you notice her skin is bright red from her face to her ankles.  She denies any pruritis, and you do not appreciate any hives.  She denies any difficulty breathing/swallowing, sensation of throat tightness, or changes in voice.   She denies any chest or abdominal pain.  No nausea or vomiting.  She reports she feels anxious.

She reports a past medical history of hyperlipidemia, and states she was diagnosed with C diff (two weeks ago diagnosed by positive stool culture), for which she was started on Flagyl (PO) at home.  She denies use of any other medications at home or any new exposures.  She denies any history of allergies to food or medications.  She denies cigarette or illicit drug use.  She reports occasional alcohol use, and reports she had two glasses of red wine with dinner.

Her vital signs are as follows:

T = 98.7, BP = 132/79, HR = 88, RR = 16, O2 = 98% room air

Her exam is remarkable for:

Anxious appearing female

Diffuse erythema, no hives or other rashes

Coarse bilateral UE tremors

What do you think is going on, and what would you do next?

This is a classic disulfiram-like reaction with metronidazole and ethanol.

Other important differential diagnoses to consider (in addition to an allergic reaction) include other toxin ingestion/overdose (i.e. anticholinergic toxidrome), SJS, TEN, serotonin syndrome, sepsis (always!), etc.

Patients with this reaction can present with flushing, nausea, vomiting, hypotension, and tachycardia.

The mechanism of this effect is not entirely clear, it is thought to be secondary to inhibition of aldehyde dehydrogenase, however some studies suggest it may be secondary to a “toxic serotonin syndrome.”

Of note, there are other medications have have been noted to cause disulfram-like reactions when used in combination with alcohol: tinidazole, bactrim, nitroglycerin, isosorbide dinitrate, glyburide, chlorpropamide, tolbutamide

Treatment for this is supportive care – IV fluid hydration, etc., in addition to cessation of the offending agent until symptom resolution.


How long after use of the above agents can patients drink alcohol?

Flagyl – 24 hours after last dose

Bactrim + tinidazole – 72 hours after last dose



Karamanakos PN, Pappas P, Boumba VA, Thomas C, Malamas M, Vougiouklakis T, Marselos M, Pharmaceutical Agents Known to Produce Disulfiram-like Reaction: Effects on Hepatic Ethanol Metabolism and Brain Monoamines, Int J Toxicology, 26(5): 423-32, 2007.

Weathermon R, Crabb DW. Alcohol and Medication Interactions. Alcohol Research and Health. 1999 (23);1:40-54.