Ryan Radecki just posted this little vignette on the real incidence of stroke mimics (AKA “neuroimaging negative” stroke) with the associated reference on emlitofnote: http://www.emlitofnote.com/2013/04/neuroimaging-negative-strokes-are-lie.html

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Subsequent posts will more closely examine the evidence for O₂ use in cardiac chest pain, COPD/asthma, pneumonia, sepsis and traumatic brain injury (TBI).

So let’s inhale deeply, fill our FRC with fresh air, and see where Kate takes us:

Oxygen 1: friend or foe?

Background:

I became interested in this question a couple of years ago when I was informed by an RN in a regional Australian hospital that they “aren’t allowed” to give high-flow O₂ to patients (with normal pulse-oximetry readings) presenting with cardiac-sounding chest pain “because free radicals make myocardial damage worse”.

At the time, as a very fresh consultant/attending Emergency Physician, I felt like I may have missed something important and felt somewhat chastised by my nursing colleagues. I decided to investigate the evidence for O₂ therapy in a wide range of conditions.

Traditionally, we were taught that administration of high-flow O₂ is standard practice (think back to EMST, APLS and ATLS teaching) for all patients who are critically unwell, and definitely for all cardiac patients. The exception that proved the rule was the chronic CO₂-retainer with COPD, but even then, if they were severely hypoxic, they received life-saving O₂ (high-flow if required), given the oft-quoted axiom “hypoxia kills quickly, hypercapnia kills slowly”.

But could we have got it wrong? Have we been inadvertently harming our patients?

Some of the questions arising in my quest include:

• What is ideal PaO₂? What is the definition of hyperoxia?
• What does hyperoxia and free radical generation really do, other than cause wrinkles and help sell expensive face-creams to aging women and Sydney men?
• Does ideal PaO₂ vary in individuals?
• Is there individual variation depending on biological or pathological processes that are occurring; what is that patient’s ideal PaO₂ considering the disease state they are in now?

What I discovered is that there is very limited evidence in the literature.

I was able to establish that “normal” PaO₂ on room air (FiO₂ = 0.21) at sea level is considered to be 75-100 mmHg. How this translates into individual variation throughout the course of a lifetime varies on patient factors and also disease factors (e.g. smoking, auto-immune disorders, occupational exposures, etc.). Expert consensus suggests that as long as your PaO₂ is > 50 mmHg, you’ll be OK. Looking at the Hb-O₂ dissociation curve, this roughly correlates with a SpO₂ of 85%.

Click here for a refresher on respiratory and O₂ physiology.

(If textbooks are still your thing, check out West’s Respiratory Physiology).

HbO2 curve from #physphoto118

Individuals will have times during disease burden where they actually have increased O₂ consumption. Examples include:

• Fever: with a 1^oC temperature rise, there is a 7% increase in O₂ consumption
• Seizing patients (even if given muscle relaxants): still exhibit a 300-400% increase in O₂ consumption in their brain.
• Septic patients: demonstrate 200% increase in O₂ consumption.
• In exertion/exercise (think seizure, rigors, restlessness, increased work of breathing) your O₂ consumption is also going to increase.

How does this information translate to our practice?

The effects of hyperoxia are more variable than just simple free radical production: Hyperoxia can directly affect blood vessels, causing vasoconstriction. At the level of the pulmonary vasculature, this can worsen V/Q mismatch. Vasoconstriction of coronary arteries and cerebral arteries probably isn’t really a good thing either!

How do free radicals actually cause harm? Free radicals are generally mopped up by nitric oxide (NO – the chemical that vasodilates vessels in vivo). They have direct cellular effects, including harming DNA, and can even cause apoptosis of cells.

What is the EVIDENCE for the role of free radicals?

I found this article, which I have to include:

The authors comment that:

“The use of oxygen in “severe angina pectoris” was first described in 1900 by Steele. Clinical improvement after oxygen inhalation in four patients with acute myocardial infarction was reported by Levy and Barach in 1930. Since then the use of oxygen in myocardial infarction has been advised in most standard medical texts.”

(As an aside, I am amazed that “clinical improvement” in only 4 patients in 1930 became standard of care. What else are we doing that has such profound evidence?)

The 1976 BMJ study was a double-blinded RCT which randomized 200 consecutive patients thought to have had MI to treatment with O₂ or air, administered via medium concentration mask for the first 24 hours of hospital care. 43 patients were excluded post-hoc when diagnosis of MI was revoked. None received current standard MI treatment (aspirin, thrombolysis, PCI), so the applicability to current practice is somewhat debatable.

There was a mortality rate of 11% in the O₂ group vs. 4% in the air group, but this did not achieve statistical significance.

They conclude that the results are suggestive that O₂ administration has a “deleterious effect”, and that administration of O₂ in patients with an uncomplicated MI does not have any benefit.

[This went unnoticed until unearthed in a systematic review (by Wijesinghe et al. in HEART 2009) of the...wait for it...two, yes, TWO relevant papers in the literature on the subject!

ILCOR and ARC ran with this in 2010-11, and an RN in a regional hospital quoted it back at Kate shortly after - Domhnall/Ed.]

Cementing our move into the 21^st century, 2012 brought this paper:

The study:

• This was a randomised, controlled trial with n = 136.
• All patients presented with an uncomplicated STEMI (i.e., no cardiogenic shock or “marked hypoxia”).
• The 2 groups were randomised to receive either “standard of care” (6L/min via medium concentration mask) or titrated O₂ aiming for SpO₂ 93-96%.
• The primary end-points were 30-day mortality, and infarct size (determined by the Troponin T level at 72 hours)
• They also utilized MRI at 4-6 weeks for a subset of patients to assess infarct size as a secondary end-point
• The result was that there was no significant difference between high-concentration O₂ vs. titrated O₂ in regard to Troponin T concentration, infarct mass or percent infarct mass.

Problems with the study:

• Small study with wide confidence intervals – the study should probably be repeated with a much larger sample size to truly determine if there is harm/benefit associated with supplemental O₂
• Unblinded study – but, primary end-points were objective measures, so shouldn’t alter the outcomes
• Pre-hospital O₂ therapy (received PRIOR to enrollment in the study) – patients averaged 62 min of pre-hospital O₂. Does this have an effect? It certainly muddies the waters for me…
• There was a significant difference in the two groups with respect to the territories infarcted: more in the high-flow group had an inferior or posterior MI, compared with those in the titrated group with an anterior MI. Those with an anterior MI tended to have higher peak troponins; however this did not lead to a statistically significant difference in the groups

Finally Nikolaou et al. in an opinion-piece in the Hellenic Journal of Cardiology, published in 2012 (53: 329-330) argue that:

“inhalation of 100% O₂ for 10-15 minutes is associated with a decreased in coronary blood flow by 20-30% through constriction of the micro vascular resistance vessels”

They hypothesise that this may be due to NO being depleted by mopping up the free radicals generated through hyperoxia. They cite an additional concern that hyperoxia may exacerbate reperfusion injury to the heart (due to increased free radicals).

They conclude that evidence is lacking, but despite this, go on to recommend that

“routine administration of high-flow O₂ for ALL acutely ill patients should clearly be abandoned and be replaced with judicious O₂ administration guided by pulse oximetry”

I’m rather (un)impressed that they have managed to draw this very concrete conclusion for acutely ill patients (with any aetiology) in a cardiology journal, based on a carefully selected 12 papers, of which 11 are specific to cardiology (the exception was the BTS guidelines for emergency O₂ use in adult patients). It really is a bit of a leap, however, this is where I stand:

My conclusions in regards to O₂ for ACS:

• We still don’t know if we cause harm, or benefit, by giving our patients high-flow oxygen when they have myocardial ischaemia.
• We just don’t have evidence to say that what we have considered as standard of care for years (i.e. 6L/min O2 via Hudson Mask) is harming or benefiting patients in this and other groups of acutely ill patients.

Will my practice change?

• I think I will probably remove more Hudson Masks now and replace with titrated nasal prongs, if required, aiming for SO₂ of 95% (why that number, I can’t say, but it’s what I feel comfortable with and it is within “physiological normalcy”).
• More importantly, it makes it a hell of a lot easier to take a good history, which will probably benefit my patient more.

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PHARM Podcast 64 : MORE Jelly Beans from SMACC 2013 with Dr Doug Lynch.

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I’ve been thinking about FOAM since SMACC2013 (Social Media and Critical Care)…thinking a lot and talking to some friends.

I’ve cleared my desk literally and figuratively for a while and intend to read a lot and spend sometime away from computers and in the fresh air. But for good or ill I’m going to share some of my ruminations about FOAM post-SMACC and where it stands:

I thought SMACC was an amazing conference, and I had a fantastic time. I was inspired and challenged by many, especially some icons of the Critical Care world – Cliff Reid, Scott Weingart and Joe Lex. Meeting them, and others, as if I had known them for years, was a surreal experience. I also got a real buzz from speaking among such eminent company and not self-destructing, despite my extreme anxiety about it (or perhaps because of my anxiety – since as Myburg and Weingart say, adrenaline is “God’s own nectar”).

But among all of this enthusiasm, euphoria and exaltation, I have become aware that not everyone felt like I did about SMACC2013. Some people I have the utmost respect for, including several colleagues who I consider to be mentors in my professional life, had what they describe as a “mixed” experience. Rather than trumpet my own overwhelmingly positive experience, I thought it would a be useful exercise to explore the experience of others. So this will be an opinion piece discussing the discomfort of some with how the “Brave New World” of FOAM and #FOAMed is playing out. I think it is important to air and address these views in order to ensure that the “product” we deliver as FOAM is as good as it can be.

FOAM as espoused by SMACC is unfolding with some of the features of a new religion:

• It has a “big idea” at the core.
• It sets out to reject dogma and challenge the status quo.
• It is somewhat anti-establishment.
• It has evangelists. It has an inner circle of disciples, it has zealots and it has converts.
• Thus, it faces the same problems as a religion, and could fall into similar traps, and could eventually leave itself open to some of the same criticisms as religions are.

There are several traps FOAM could fall into, I believe:

• It could lose itself in enthusiasm, evangelism and quasi-religious fervour.
• It risks the criticism that there is a “cult of celebrity” developing (I don’t think this is true, but it is how some see things from the outside).
• It preaches openness and yet some see it as a clique. It can appear somewhat smug to the “uninitiated”
• It risks portraying itself as the “one true path.”
• SMACC spent a lot of time discussing ideas about how we can ensure that FOAM self-polices content and quality, but little time addressing the fact that there is risk that it develops into a “club” which some may not feel they can join.
• Although a version of “peer review” is important, I think this perception of a clique is a bigger threat to FOAM.

The big ideas of SMACC2013 apart from furthering FOAM as an educational movement were: challenging dogma and destroying silos – particularly those separating pre-hospital medicine, ED and ICU. But we MUST be careful that we do not replace these silos with another silo, the FOAM silo. We must not just challenge the dogma that exists and then fall into the trap of creating a replacement dogma (The central message of a certain prophet/son of god/historical figure was love, equality, rejection of dogma and openness – but his followers somehow contrived to develop a new boys club and a new dogma as exclusive and prescriptive as what preceded it).

FOAM, and conferences like SMACC, risk alienating further the slightly more open and curious skeptics precisely BECAUSE they don’t feel part of the evolving club despite taking the courageous step of attending to dip their toes in the water. For those of us who, as Scott Weingart says, “jump in and drink from the stream” it seems self evident that you get out what you put in, but not everyone feels able to commit to that degree, and we risk losing the swinging voter unless we accept and address the perception that FOAM can appear like an exclusive inner circle to the outsider. This may seem crazy to us and is light-years from the intentions and principles of FOAM, but it is definitely how some perceive us. We think we are making it easy because it worked for us, but we need to be rigorous about how open the FOAM movement is.  So what can we do?

FOAM must remain truly open and inclusive.

FOAM must listen to and embrace the uncertain and dissenting voices.

Pretty simple, and yet I suspect it will be very difficult.

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I managed to capture a screencast recording of the talk, and posted it on GMEP

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I regularly arrive on the ED floor at morning handover, and go ECG-snooping. When I hear a handover mentioning chest pain in any shape or form and the phrase “but the ECG was OK/normal/no acute changes”…etc, I complete the handover, and go and review the ECGs myself. No doubt, the residents hate me for it.

For this reason I regularly unearth “missed” abnormal and instructive ECGs which could be considered subtle (although worryingly sometimes they are barn-door obvious) and hence the “ECG sagas of subtlety” series was born in an attempt to share the lessons learned. I don’t intend criticism of the doctors involved. These are often subtle and difficult ECG findings. The one I share here was discovered on one such snoop:

The case: Chronologically a 50 year old man with 70 year old physiology, who presented with central chest and back pain. He was centrally obese, a diabetic, and had a history of prior warfarinisation for DVT, recently ceased.

This is his time-zero ECG (apologies for reproduction quality, but click on it and it should be discernable):

with chest and back pain at time zero

The night crew spotted the ST depression in III and aVF, called it “ischaemia” and treated the patient as ACS. I came on in the morning, heard the story and heard that the ECG was “OK,” and went snooping.

What do you think about this ECG?

• Sinus rhythm, normal axis, etc…
• There is indeed ST depression in III and aVF as previously noted
• There is subtle saggy ST depression in V6
• As frequently mentioned by Steve Smith, ST depression DOES NOT LOCALISE ischaemia. So this COULD represent subendocardial ischaemia BUT:

WHEN YOU SEE ST DEPRESSION YOU SHOULD ALWAYS LOOK FOR THE ST ELEVATION THAT IT MAY BE RECIPROCAL TO

Is there any here?

• Yes – aVL shows 0.5mm of ST elevation
• There may be a hint (read retrospective “eye of faith” hint) of ST elevation in I
• This is a high lateral STEMI, and is likely to represent occlusion of either the diagonal or circumflex coronary artery or branch thereof

Unfortunately this went unrecognised. The patient was given 300mg of aspirin and 2 sprays of GTN. He had some improvement in his anterior chest pain, however his back pain was more severe than the chest pain and was ongoing. The following ECG was recorded 2 hours later in the context of ongoing pain:

with ongoing back pain

What is your interpretation of this ECG?

• The ST depression has largely settled (there may be a smidge persisting in III)
• The ST elevation is now barely perceptible in aVL which has also developed a Q-wave and T-wave inversion
• The T-waves in I and V6 are MUCH flatter, but the T-waves in III and aVF are MUCH more peaked
• This may reflect some reperfusion but in the context of ongoing pain with dynamic ST changes, the cath lab should be activated

I met this man about 2 hours after this second ECG, four hours into his presentation. He had ongoing back pain and looked uncomfortable. He was given further antiplatelet therapy and anticoagulated, then referred to cardiology. His troponin peaked at 3.5.

This man had a “missed” high lateral STEMI. Did missing this have adverse consquences? Hard to know really. We may have saved a bit more myocardium if he’d gotten to PCI earlier. There were further delays to PCI and the case was somewhat frustrating. If you are interested in reading further on high lateral STEMI, click on this link to the always enlightening Steve Smith’s take on the topic. To quote Steve:

“When there is inferior ST depression, one is tempted to diagnose “inferior ischemia”. However (paradoxically and mysteriously) there is no correlation between location of subendocardial ischemia on the ECG and the location of the ischemia in the heart. When there is subendocardial ischemia, the ST depression tends to be diffuse.

So what does “inferior” ST depression represent?

It is reciprocal to high (lateral) ST elevation until proven otherwise“

The denouement is of course the cath result - click here to reveal it:

• diffuse CAD
• obstruction of 1st LAD diagonal branch
• anterior wall hypokinesis, mild-mod LV dysfunction

And there you have it. His discharge letter from the treating team is still calling this an NSTEMI. For me, it is a STEMI with the D1 vessel being the culprit lesion that correlates nicely with the ECG changes

The post ECG sagas of subtlety 2 appeared first on Underneath EM.

Screaming
human?
Patchwork
Scarred
Scared
Amphetamine fuelled
Pulsing rage,

With a syringe of midazolam
-fantazaslam!

Invoking the Mental Health Act,
As if I believe in it
-The gospel according to psychiatry

I realise this does not rest easy
Beside the mumbled Greek of Hippocrates,

Sworn in a marbled hall in another life,
When we all believed in it.

The post The Hypocritic Corpus appeared first on Underneath EM.

By way of a shoutout and a thank you, I’d just like to preface this by saying that there is no question that the erudite teachings of Steve Smith and Amal Mattu in the dark arts of deeper ECG understanding via FOAM have allowed me to tease these cases out.

Click on the questions (blue bold text) to reveal my drop-down answers and discussions. As usual, details have been changed to protect the innocent and this is not meant to be a blame game, but a learning opportunity (for me, too!). Please comment if you disagree.

(The first of these cases may be familiar to you if you happen to also follow me on Twitter, where it was first discussed, and indeed I will incorporate some of the Twitter comments from folk to expand the perspective somewhat)

On to the case and the first ECG:

Male; 50; T2DM diet “controlled;” heavy smoker; typical chest pain for about an hour. ECG on arrival with pain:

Describe and interpret the ECG:

Let's have another go at interpreting this initial ECG:

Minh le Cong quite rightly asked for right sided and posterior leads when this appeared on Twitter and these were done, however at my shop, scanning of ECGs to the record is ad hoc and misses out some serial ECGs done close together in time, so I don’t have images for these (this is somewhat frustrating and has the potential for patient harm – we are trying to change it). I can tell you that there was similar subtle ST elevation in V4R, but the posterior leads were too low voltage to say anything definitive

A second ECG was recorded 30 minutes later after aspirin, clopidogrel, GTN infusion and heparin bolus

The second ECG with improving but not absent pain:

I had handed over the patient and left the hospital assuming the team would take him to the lab as a STEMI (albeit not meeting DANAMI 2 ECG criteria). The ECG findings are now as follows:

• There is now clear T-wave inversion in III and aVF
• Lead III has developed a Q-wave
• The ST depression in aVL has resolved
• The ST elevation and markedly upright positive T-wave in V1 has flattened right out
• The cardiology registrar continued to reject that this had been a STEMI! (he accepted that these were dynamic changes, but he still refused to accept their real significance – in fact he was unable to even have a sensible discussion on the subject, essentially dismissing ED without listening)

This clearly reflects the idea that many STEMIs are labelled non-STEMIs by virtue of the timing of ECGs (i.e. not done often enough or just missing the one ECG which met criteria) or the rigid adherence to specific voltage criteria, as if the pathophysiology carried a ruler or calipers (see Steve Smith on the subject here). The fact is, this ECG represents the occlusion of a coronary artery, and PCI is indicated urgently - however:

• There was no urgent primary PCI
• The first troponin was normal – the cardiologists were reassured and his cath was delayed until next day
• In the interim his troponin bumped to 9
• The PCI done about a day later demonstrated ”extensive coronary artery disease…culprit lesion was felt to be an 80% RCA stenosis (DES placed)…additional 40% and 60% stenoses of LAD and Cx respectively”

Minh le Cong suggested looking for Q-waves to retrospectively confirm the diagnosis:

So what are the take-home points from this case?

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The idea of three parallel hospitals was first introduced to me by a mentor and colleague, Dean Powell, and I believe addressing it with top-down leadership is the key to unlocking some of our greatest problems.

The three hospitals are:

• The hospital the administrators and the board think they are running
• The hospital the consultants think they are running
• The real hospital – the one run by junior doctors that comes out to play after hours

In the specialty of Emergency Medicine we are probably the only group of specialists who recognise and truly understand the parallel hospital issue. Things go bump(y) in the night. Unfortunately most of our patients experience this third hospital too.

Until this is also widely acknowledged and addressed by administrators and inpatient consultants, things like obstructiveness, bullying, overinvestigation, undertreatment, delays to decision making, ED length of stay, and ultimately access block will continue to plague our attempts to provide a consistent service to the acute healthcare of our population. We are doomed to failure in meeting the NEAT (National Emergency Access Target) unless we are realistic about the real hospital.

We in ED need to start by consistently and firmly defining what our specialty is to inpatient junior docs. The first step is convincing specialty juniors that coming to ED to admit a patient is NOT THE SAME as consulting a patient on the wards. My ideas about our role are listed below:

1. We are, above all things, advocates for the patient in a service industry
2. We are not your resident or intern or your clerk or secretary
3. We are not just extended triage, and we are not just the department of available medicine
4. More importantly, we will not just be defined by what we do not do
5. We ARE resuscitationists, and doing your non-urgent inpatient related duties for you interferes with doing this properly
6. We ARE dispositionists, and we can and will decide (largely correctly) where people should GO and under WHOM. We are prepared to get this wrong and we will wear that
7. Occasionally definitive diagnosis helps, and tests will inform points 5. and 6., but I won’t be adding on your serum rhubarb for you, nor will I be calling you back to re-refer after all the tests are done
8. We will assess and treat all comers, but we will stop and give them to you when we no longer value-add to a given patient’s care, and you do. We will define this transition point, then we’ll let you know

So lets define the limits of what we do, rather than let it be defined by what others won’t do or are used to having done for them. A culture change needs to be led from the top. ED shouting from the basement can only do so much. Administrators and hospital consultants need to stand up, and if they won’t, in the words of Greg Henry, let us “bring our lion’s heart into our lion’s throat and give a roar in defence of the patient.”

Remember, in Greg’s words, we are the last doctors who deserve to carry the staff of Ascelapius. Let us wield it.

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