current issues in emergency medicine, reviews, opinion and curbside consults

Does anything work to reverse angioedema? If it's hereditary, then icatibant may do the trick. Otherwise, there's not much out there. Fresh frozen plasma (FFP) has it's place in angioedema lore as something that works, but the evidence in its favor is a series of case reports. Emergency physician and angioedema researcher Gentry Wilkerson gives a State of the Union on the known knowns and known unknowns of this sometimes mysterious disease.

Links mentioned in this show

Register for Essentials of Emergency Medicine

Angioedema algorithms

Cicardi, Marco, et al. "Guidance for diagnosis and treatment of acute angioedema in the emergency department: consensus statement by a panel of Italian experts." Internal and emergency medicine 9.1 (2014): 85-92. Link

Bowen, Tom, et al. "2010 International consensus algorithm for the diagnosis, therapy and management of hereditary angioedema." Allergy, Asthma & Clinical Immunology 6.1 (2010): 1-13. Link

Chiu, Alexander G., et al. "Angiotensin-converting enzyme inhibitor-induced angioedema: a multicenter review and an algorithm for airway management." Annals of Otology, Rhinology & Laryngology 110.9 (2001): 834-840. Link

Hassen, Getaw Worku, et al. "Fresh frozen plasma for progressive and refractory angiotensin-converting enzyme inhibitor-induced angioedema." The Journal of emergency medicine 44.4 (2013): 764-772. Link

Direct download: Angioedema_ercast.mp3
Category:podcasts -- posted at: 9:01pm MDT

Are you ready for REBOA? Zaf Qasim (@emeddoc) gives the ins and outs of Resusciataitve Endovascular Balloon Occlusion of the Aorta

Intro Segment:
Mel Herbert and I talk about our favorite podcasts as well as Mel's new show Shabam!

My Top 3: The Tim Ferriss ShowQuestion of the DayMen In Blazers

Mel's Top 5: Radiolab99% InvisibleCommon SenseMemory PalaceMacbreak Weekly

Episode Transcript (with some extras)

What are the steps of REBOA?

To understand REBOA you have to know a little bit of anatomy.  We talk about 3 aortic zones when we talk about REBOA.  Zone 1 is from the left subclavian artery to the celiac trunk, Zone 3 is from the lowest renal artery to the aortic bifurcation, and Zone 2 is the area in between.  We don’t like to talk about zone 2 – that’s essentially a no go zone because if you inflate the balloon here, you may not occlude the vessel that’s causing the bleeding.

So once you’ve decided to place REBOA, and we’ll talk about indications and contraindications a bit more in a second, the key step is accessing the common femoral artery and putting in a standard 18G arterial line.  Next, you’re going to be passing a long guidewire through that arterial line up to the level of the left subclavian.  We use a stiff, 260cm wire to do this, and measure it using external landmarks.  If you have the time, you’ll get a chest xray to confirm the position.  Next, you’ll replace the arterial line with an introducer sheath – the one we use is actually pretty huge, 12 French, and that allows passage of the actual balloon catheter.  You’ll need to measure the length of insertion against your external landmarks, and that’s the xiphisternum for Zone 1, and the umbilicus for Zone 3, pass the catheter over the wire through the sheath, and inflate the balloon with saline in the appropriate zone until you feel a change in resistance as the balloon abuts the aortic wall.  You should at this time see a pretty dramatic rise in your blood pressure.

Who gets this? Pelvic fractures, get that, but I’m hearing about it in any sort of hemorrhagic shock, sort of a poor man’s cross clamping of the thoracic aorta without having to crack the chest

So yeah, you hit the nail on the head – this is the alternative to cracking open the chest and putting a big clamp on the aorta just for the purposes of stopping bleeding below the diaphragm and improving cardio-cerebral perfusion.

Let’s talk first about who’s not going to get it.  If you think your patient has some sort of horrible chest injury, like a cardiac tamponade or a traumatic proximal aortic dissection, you do NOT want to put a balloon up there. That’s just going to make that patient’s day a whole lot worse.  You can easily rule those things out with what you do already in the trauma bay, the FAST and the chest xray.  If you see a tamponade, you’re going to be opening the chest.

But if you think this patient has what’s termed non-compressible torso hemorrhage, that is, devastating bleeding from areas below the diaphragm in the abdomen, pelvis, or retroperitoneum, places you can’t put a tourniquet or direct pressure to, these are the folks who will benefit from REBOA.  This can be from blunt or penetrating trauma, and even non-traumatic hemorrhage as I’ll talk about in a second.  If you’re suspecting abdominal bleeding, they’ll get a Zone 1 balloon, for pelvic bleeding it’s Zone 3.

The beauty of this procedure is that you don’t have to wait for the patient to die before you proceed like you do with the thoracotomy.  You can proactively place this in the transient or non-responder.  Since you’re being proactive about this and stemming bleeding before the patient undergoes that horrendous insult called death, I think you have the potential to have a higher percentage of what you really want at the end of this - neurologically intact survivors, and this is what we’re already seeing.

At Shock Trauma we’ve also placed REBOA in witnessed traumatic cardiac arrest, but I think you really need to have witnessed that arrest for this to be a useful procedure.

People wonder how long this procedure takes to do what with all the wire and device changes that are occurring.  The answer, and we have this data from the interim analysis of an ongoing national study called AORTA, is that it is not statistically different to the time it takes to do a thoracotomy and get an aortic cross-clamp on right.  This really annoys the naysayers!

Remember, before you do this you’ll already have gotten your IV access, started your damage control resuscitation, placed the pelvic binder, done all that.  If they’re STILL circling the drain, so the transient or non-responder, and you think they’re highly likely to code, REBOA is the next step to buy them those precious minutes to get to the OR or in some cases to IR.  But don’t forget the basics!


What would it take for me to go from where I am today, a true neophyte, to REBOA operator?

I think as with any new procedure it’s critical that people get the right training to do this, as it is certainly not without risk.  Having said that, REBOA builds on skills that emergency physicians already have – the use of ultrasound to localize the common femoral artery and the use of a Seldinger technique to insert the various pieces of equipment.

Essentially the first critical step, placing the femoral arterial line, is something we have been trained to do.  The caveat is you have to be sure you’re in the common femoral artery.  It’s always a little higher than you think it will be, but with dynamic ultrasound, you can be trained to do that safely and efficiently.  My advice is place that arterial line in your sick patient early, while you still have a decent caliber vessel to access.  If they get better, hey you’ve got a central arterial line.  If not, though, you’ve already done the rate-limiting step of the procedure.

Upsizing to the 12 French sheath can be daunting – think of your usual Cordis (or introducer) but on steroids! You have to be very careful to ensure you’re inserting this without feeling any major resistance, and that your dilator doesn’t inadvertently get pushed out as you’re putting the sheath in.  But again this step builds on principles we as EPs already have.

In the US, this technique was trialed and brought out primarily by trauma surgeons, and the reason behind that was not only the way trauma care is delivered in the US but also the high potential for injury when you stick a huge sheath into the femoral artery.  Additionally, you can’t just pull that thing out at the end of the day, get the medical student to hold pressure, and go get some coffee.  No.  It needs a formal assessment and closure of the hole made in the artery as well as ensuring good limb perfusion at the end of the procedure, and that’s a skillset we as emergency physicians don’t have.  You may also need to perform a cutdown on the groin to access the artery, especially in the setting of cardiac arrest, and that’s a skill we don’t have from our training but one that CAN be learnt.

So on the back of that, the initial training courses that came out here were really also directed at the surgeons, and there were initially two in the country.  I teach one of them, the Basic Endovascular Skills for Trauma course down in Baltimore, and our candidates are primarily surgeons.  We do both simulator and cadaver work with them.  Currently the only EPs that have been trained on our course are those with dual training in critical care and affiliated with Shock Trauma.

But this will evolve and change for two reasons I think.  First, emergency physicians have already demonstrated that, with appropriate training, they can safely and effectively perform procedures with big catheters like ECMO – just look at the Reanimate course and the work out of Sharp Memorial in San Diego.  Second, and this is the most exciting news, back in October, the FDA approved a new, purpose built device called the ER-REBOA catheter (and I have no financial interest in this device by the way).  This can be placed through a much smaller 7-French sheath – that’s the size of the Cordis we all know and love.  Additionally, there’s no lengthy wire that needs to be put in before hand, you can just do your measurements using this catheter device and place it in the appropriate zone.

So to summarize, yes, emergency physicians can build on their existing skillset to learn this procedure, and with appropriate training and within a system of robust quality assurance, will be able to safely deliver this.


Is this ready for the community ED?

That’s a great question.  It’s certainly a very attention-grabbing procedure that’s in the headlines and I think ultimately this will have a key role in the community ED.  You’re essentially aiming to extend your golden hour by placing this.  Imagine you’re at a single coverage community ED and you get an unexpected drop-off who is a bad motorcycle victim who’s bleeding out from his abdomen or pelvis, you place this device, get control, and are able to ship them off to the regional level 1.  Not only that but think of the patient with a non-traumatic bleed, a ruptured ectopic for example – the same principle applies and you can use REBOA to buy them time for either your own surgeon to come into the hospital or to get them out to your local ivory tower.  That is the ultimate goal.

Are we there yet?  I think not quite.  Currently as you say REBOA is being performed at big academic centers, like the intergalactic shock trauma center.  These places are able to get the patient to the OR fairly quickly and have the complement of specialties in house or very rapidly accessible to deal with any issues or complications that may arise as a result of placing REBOA.  There are some issues that still need to be worked out before we’re ready to say that community docs within a trauma network will be able to utilize this technology.  These are primarily centered on training and system logistics.  But I think one of the major limitations is time.


What’s the treatment arc of REBOA? How long can it stay in? What should be your mindset once you place it?

The mindset once you put in REBOA is “I need to get this person to definitive care as soon as humanly possible.”  These aren’t people who will tolerate you scratching your head or rubbing your chin. They’re staring you down and saying “I’m sick as hell, fix me” Once the balloon is up you need to already have a plan in place of how you’re going to fix the problem.  You may have some time depending on how your shop is set up to get some focused imaging, but the default destination is most likely going to be the OR.  That highlights a couple of things.

First of all, you need to limit balloon inflation time.  Think about it, if you’re putting a balloon in Zone 1 and occluding flow to everything below the diaphragm, you’re taking out a lot of real estate – the kidneys, the gut, even the spinal cord.  Your patient is not going to like that.  The animal studies and the limited human studies show elevations in lactate proportional to the duration of balloon inflation.  The animal studies show that up until about the 40-60-minute mark, appropriate resuscitation will clear that lactate, but beyond that it can precipitate a devastating cycle of physiologic injury that you may not recover from.  On top of that, when you let the balloon down after prolonged inflation, you run the risk of reperfusion injury – akin to those people you treat with crush syndrome.  Zone 3 balloons are a bit better tolerated but still have the same principle to them.

The Japanese papers really highlighted this.  They have been doing REBOA much longer than we have, and their papers were showing complications not clearly evident in our limited US data.  Their system is somewhat different: they don’t see a lot of trauma and so their surgeons aren’t in house.  Their EPs are trained to put in REBOA and call the surgeon in.  Because of this their time to get to the OR may average well over an hour, and that was one reason I think those patients were having less than optimum outcomes.  The other being they sometimes resorted to using the balloon as a last-ditch, throwing the kitchen sink at the problem effort.  So it goes to further emphasize the timing issue – if you’re going to use it, use it early, and then get them to definitive care quickly.

The second thing this highlights is if you’re thinking of bringing this into your service, you need to train your team to hustle efficiently once the procedure is performed.  There can’t be delays because of rubbernecking or high-fives that you’ve done this sexy new procedure – do that after you’ve fixed the problem for sure, but not at the time.  Remember if you’re the one doing the procedure, you put on blinders and become task-focused.  You develop tunnel vision and lose that situational awareness.  This patient is still extremely sick, and so needs ongoing resuscitation.  You need to designate someone to take over and lead the resuscitation so that the blood products still go in, the right services are involved, and the team is coordinated to move this patient to the OR once the balloon has gone up.

The way I wrote the protocol at our shop for example is that in our trauma codes, the trauma surgeon will move from supporting the senior trauma resident as the team leader to becoming the proceduralist.  The emergency physician moves from supporting the airway resident at the top of the bed to becoming the designated team leader and the direct support for the trauma resident.  Our nurses help by clearly documenting times of balloon inflation.  In the OR, the anesthesiologist with help from the circulating nurse becomes tasked with reminding the surgeon using closed-loop communication about the duration of balloon inflation so that everyone is geared to limit that time the balloon is up.  That requires team training beyond just learning the procedural steps.


This has all been pixie dust and fairy parties so far, but what are the downsides of this procedure?

What’s wrong with fairy parties?!  Definitely nothing comes for free though.  We already spoke about the big issue of the physiologic consequences of balloon inflation, so keep an eye on those times.  There’s the risk of losing situational awareness which we also touched on.

Additionally, you always run the risk of vascular injury – you can put the sheath into one of the smaller branch vessels and risk shearing that off, or creating dissection flaps.  You might access the vein by mistake, guaranteed not to get you any style points.  The balloon may inadvertently migrate, or potentially fail.

But a really huge issue is the risk of critical limb ischemia and limb loss.  There are reports from abroad of this having happened, and to date, the US has not had any reported cases of limb loss.  The limb is at risk for a variety of reasons – the size of the sheath can completely occlude the main vessel to the leg, especially in smaller patients.  Also, and you wouldn’t have thought this would happen in people who are so sick, is that our surgeons are often seeing clot around the sheath at the time of removal and vessel repair, which sets it right up for ischemic and embolic problems.  I think one of the inadvertent benefits of needing to use a huge sheath currently in this country is that it dictates open repair and removal.  So the surgeons have the opportunity to check limb perfusion right there in the OR at the end of the case and make sure the flow is appropriate, and I think that’s why we don’t have any reported US cases of limb loss from the use of REBOA.  Be extra vigilant about limb perfusion – ANY difference between the two limbs, even a slightly different color, mandates vascular to come and assess that leg again.

A final point which isn’t exactly a complication but should be mentioned is the notion that REBOA is either not something worth doing or might be done for the wrong reasons and so more often than indicated.  There are certainly naysayers, and yes it’s new and still being tested but it is already showing positive results and importantly has the benefit of producing neurologically intact survivors.  It can certainly be incorporated as another tool in the box in managing these difficult patients in an attempt to get them to definitive care.  On the other hand, new toys might get used when they shouldn’t be or in lieu of good basic tenets of trauma care.  So to ameliorate that effect, bring it in within a strict protocol that undergoes a strict QA process – do it right and remember your basics.

Say I have a patient with a crushed pelvis, I put in a REBOA, is that patient OK for transfer to a bigger trauma center? Is bad pelvic fx in any way a contraindication?

Bleeding pelvic fractures are the ideal candidates to get a Zone 3 REBOA and be moved to the trauma center.  Remember you should also put on the pelvic binder and continue your usual resuscitation but these are the guys who have a high mortality in the civilian literature. They will bleed out quickly-  talk and die.  The zone 3 position may also tolerate slightly longer balloon inflation times than zone 1.


What are your take home points?

REBOA is a promising procedure for managing devastating torso hemorrhage

The skills for it build on those that we as emergency physicians already have, but need to be refined through specific training and need to be delivered within a multidisciplinary system having a robust QA process

Balloon inflation times and the potential for limb ischemia are very real threats to its use

Both the technology and the data continue to evolve, so collaborate, share your experience, and watch this space



Qasim, Zaffer, et al. "Resuscitative endovascular balloon occlusion of the aorta." Resuscitation 96 (2015): 275-279.


Direct download: REBOA_101_ERCAST.output.mp3
Category:general -- posted at: 2:05pm MDT

Ryan Radecki from EM Lit of Note is here to deconstruct the HEART score, utility of stress tests in low risk patients, and his approach to low risk chest pain. As a bonus, Ryan is also the wordsmith for the show notes.

Important stuff mentioned on this show

The Show notes...

There is no such thing as “zero-risk” chest pain:

Once you learn to stop worrying and love again, where are we going with “low-risk” chest pain?

Simply put, most of our observation chest pain evaluations represent low-value care:

  • In a study comparing CCTA and rapid stress-testing for rule-out of “low-risk” patients, only a handful had positive results.
  • In a study reviewing two years of chest pain rule-outs, again, just 1.7% of stress tests performed were positive, and 1/3rd of those were false positives. No “low-risk” patients had a positive stress.
  • A study reviewing stress test outcomes in an intermediate risk cohort (mean age 60) resulted in ~25% positive of indeterminate results, with a third of those referred for angiography – half of which received an intervention.At the micro level, why should we care? Patients make their free choice to come for comprehensive evaluation.However, on a macro level, it’s unsustainable. And, as more and more patients are shifted to HMO and ACO care and payment models – the Kaisers, Geisengers, Intermountains, Partners of the world – there will be, essentially, mandates to reduce such low-value care.So, how do we do this safely?Step 1: Highly-sensitive troponin assays.
    The evidence, of which there is ample, is of reasonable quality. Much of it, unfortunately, is sponsored by the manufactures of the assays involved, which degrades some confidence in the results. But, there are a few main summary points:
  • Sensitivity for nSTEMI is about 90% at ED presentation.
  • Specificity of any troponin elevation, however, is 50-60%.
  • The longer the time from onset of symptoms, the more reliable the sensitivity.
  • Repeating a troponin 1- or 2-hours after presentation, particularly for thosepresenting early in symptoms, will increase sensitivity for late rise – and likewise improve specificity by ruling out AMI for patients’ whose troponins do not increase.

Step 2: Shared decision-making.
After making a diagnosis regarding acute MI in the Emergency Department – or, at least, to the extent hs-Troponin permits such an answer – outcome prognostication begins.

Most folks are familiar with TIMI for risk-stratification, despite not being derived in the Emergency Department. While it is still a reasonable to assess overall risk with TIMI, most folks are moving to the HEART score, while a few other protocols/algorihtms – EDACS, MACS, Vancouver, modified Goldman – are also vying for use.


There’s a lovely synergy between identifying a patient as “low risk” and the negative predictive value of negative troponin testing in the Emergency Department. Patients discharged with negative – particularly undetectable troponins – will have event rates at a fraction of a percent, and even lower if only AMI or cardiac-death are included. This is why HEART is described, primarily, as a single-troponin strategy.

These are the sorts of numbers to present to patients in the context of shared decision-making as part of changing the routine conversation about admission into one about discharge. Returning autonomy to the patient to make an informed choice about further care – and documenting such – allows the patient to assume the risks of their self-determination. Adding mention of the frequency of false- positives in a low-risk population – roughly as frequent as the true positives – is also valuable.

There are still quirks with HEART – mostly that patients, in theory, can have ischemic EKGs or elevated troponins and still remain “low risk”. These instances ought to be extremely rare in practice – and clinicians will have to make prudent individualized decisions given the clinical context. The fantastic Stephen Smith, of Hennepin County, also frequently reminds me true unstable angina is still an important troponin-negative. These are near-critical occlusions of the coronary circulation, and the key to diagnosis – and missed diagnosis – is correctly interpreting the EKG and performing serial EKGs in the Emergency Department.

Lastly, it is important to note the AHA Guidelines, as well as prudent longitudinal medical care, recommend patients still have follow-up for additional diagnostics or management, as indicated. Patients at low-risk and with negative biomarkers are at profoundly low-risk for events in, at least, the very short term. Of 11,230 patients observed and with negative biomarkers in Ohio community hospitals, only 20 had a potentially preventable poor outcome related to hospitalization. Narrowed down to the 7,266 patients with entirely normal EKGs and vital signs, 4 had poor outcomes – 2 of which were noncardiac, and 2 of which were iatrogenic. Patients, particularly low-risk, are almost certainly safer outside the hospital than in!

Stress Test Utility Citations:
"Safety of a rapid diagnostic protocol with accelerated stress testing" 

“The Association Between Pretest Probability of Coronary Artery Disease and Stress Test Utilization and Outcomes in a Chest Pain Observation Unit” 

“The incremental value of stress testing in patients with acute chest pain beyond serial cardiac troponin testing

hs-Troponin Citations:
“Multicenter Evaluation of a 0-Hour/1-Hour Algorithm in the Diagnosis of Myocardial Infarction With High-Sensitivity Cardiac Troponin T”

“High-sensitivity cardiac troponin I at presentation in patients with suspected acute coronary syndrome: a cohort study”

“Implications of Introducing High-Sensitivity Cardiac Troponin T Into Clinical Practice

“Prospective validation of a 1-hour algorithm to rule-out and rule-in acute myocardial infarction using a high-sensitivity cardiac troponin T assay

“Does undetectable troponin I at presentation using a contemporary sensitive assay rule out myocardial infarction? A cohort study”

Direct download: Chest_pain_2016_style.mp3
Category:general -- posted at: 4:30pm MDT

What is sepsis? Even the world's experts can’t agree on what it means.  Is it infection plus organ dysfunction? That’s how surviving sepsis defines it. Is it infection with a whole body inflammatory respoinse? That’s how Wikipedia defines it. Is it two or more SIRS criteria plus infection?  All of these overlap in a Venn diagram that is what sepsis really is.

Take Home Points

  • Modified SIRS criteria: T>100.4 or <96.8 that’s over 38 or under 36 C, HR>90, RR>20, O2sat<90%, MAP<65, newALOC. Two or more plus infection/suspected infection = sepsis
  • Lactate is your buddy. Your clinical gestalt in sepsis isn't as good as you think. Use the lactate as part of your decision making in determining severity of sepsis
  • Resuscitate patients before intubating. Your patient is breathing hard (can increase venous return) and  hyper-adrenergic. Take those away and your patient will become hypotensive. They may have  sepsis induced cardiomyopathy. Positive pressure ventilation can cause hypotension. Be prepared for the blood pressure to crash. Before intubating, fluid resuscitate, start pressors (if needed) or at least have pressors ready.
  • Beware of transient hypotension in the seemingly not sick septic patient. It may be a warning sign that your patient is heading toward a bad outcome.
  • Get the right antibiotics on board early

Important stuff mentioned on this show

Direct download: Sepsis_ERCast.output.mp3
Category:general -- posted at: 12:18pm MDT

Emergency Medicine legend Amal Mattu reveals his deepest secrets

  • How he became "Too Tall Amal"
  • Al Sacchetti does a bait and switch- setting up Amal for a huge career in emergency cardiology
  • The unexpected path to becoming the world's leading educator on EKGs
  • The Mattu Top 5 movies of all time
  • Rituals before going onstage
  • Giving a great lecture is easier than you think

Bonus Content

How to do peripheral pressors like a pro with Scott Weingart




What to do with trauma patients who have a "seat belt sign" with Kenji Inaba




Direct download: Amal_Mattu_on_being_too_tall_and_giving_a_kick_ass_lecture.output.mp3
Category:general -- posted at: 5:01pm MDT

Reuben Strayer from is our guest to discuss proper dosing of ketamine.

Take home message: At very low dose, you get analgesia with minimal effect on perception and emotion. At a very high dose, you’re going to get dissociation. In between high and low doses, you don’t know what kid of response you’re going to get.  It depends on the patient’s mood, what other drugs are on board, and the alignment of the stars in the sky. This is why using sub-dissociative ketamine as monotherapy for sedation is not a good idea- it might chill someone out, or it might take a crazy agitated patient and make them a crazy agitated patient now tripping on ketamine. Don’t use sub-dissociative ketamine alone for routine agitation; ketamine is not for routine agitation, it’s for tranquilization of the uncontrollably violent patient in full dissociative doses. For analgesia, use LOW DOSE - 10 or 15 mg in an adult. Do not push more than that or you will end up in recreational range or partial dissociation (which is not what you want).

Ketamine Dosing

Analgesic dose (0.1-0.3 mg/kg)

Recreational dose (0.2-0.5 mg/kg)

Partially dissociated dose (0.4-0.8 mg/kg)

Dissociative dose (>0.7 mg/kg)


Reuben's kick ass links

Here is a detailed review of the Ketamine Brain Continuum

The Amazing Intubation Checklist

Procedural Sedation Checklist

Direct download: The_Ketamine_Brain_Continuum_final.mp3
Category:podcasts -- posted at: 8:16am MDT

Jeff Kline is one of the world's leading researchers in thromboembolism. He's also a dad, bodybuilder, former wrestler, and philosopher. 

Direct download: Jeff_Kline_and_the_Art_of_Wrestling.output.mp3
Category:podcasts -- posted at: 12:42pm MDT

What I do in the in the first 90 seconds of a code…

We want to avoid simultaneous action paralysis: the feeling that multiple things need to happen at once and then nothing gets done. In a code, it seems like everything has to HAPPEN RIGHT THIS SECOND. While it can feel that way, it’s not the case.

My sequence of events in an emergency department cardiac arrest

When the medics roll in, I am listening for five pieces of information. 

  • What happened, preferably in one sentence
  • What was the initial rhythm
  • What have they done (actions, meds, etc)
  • What was the last rhythm
  • How long has the patient been down, unconscious, and presumably in cardiac arrest.

While that report is coming, I keep my eye on the patient's chest to make sure CPR is not stopping. Continuous quality CPR in the first 90 seconds is important because there is so much potential to pause it: transfer to the stretcher, putting on leads, or “Can you stop it for a second for this or that.” Ideally, I’ll have the LUCAS set up so I can take the cognitive load of thinking about CPR out of the picture. 
We’re  about 30 seconds in, and I’ve got general a look at the patient: what's the airway situation, what’s the vascular access. Now is the first decision point. Do I check the rhythm, secure an ET tube, get vascular access? Well, what makes a difference? Electricity is the first thing that comes to mind. So I have the CPR continue while the patient is settled on our stretcher, keeping the EMS chest pads on, keeping the patient attached to their monitor. At this stage, changing over to our monitor (if they’re already on a perfectly good one) makes no sense. Once we’re ready, stop CPR and check the rhythm while simultaneously using the ultrasound for subxiphoid view of the heart. 

Now I’ve got the rhythm and direct visualization of any cardiac activity.  Whatever the rhythm, I know what I'm going to do. 

We're 90 seconds in and I’m moving to intubate/get ETCO2. I that’s already done, I just keep a finger on the femoral pulse while the CPR is happening. Why do I do this? I want to have my hands on the patient but not do be a primary operator of CPR, bag valve mask squeezing, vascular access - just watching and thinking. The room is quiet, there are no raised voices - tone and volume are conversational and calm.

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Direct download: How_to_not_freak_out.output.mp3
Category:podcasts -- posted at: 11:13am MDT

Torsades de pointes is very bad.  It easily degenerates into Ventricular Fibrillation (VF) and that’s sudden cardiac death.  How many cases of torsades have you seen in your career? Are your ready for it when you see it? Let’s see, there’s magnesium...uh, and then I seem to recall that drug isoproterenol (that I’ve never used) and then..oh yeah...I’m supposed to do ‘OVERDRIVE pacing’.  Got it. Ummm, how do you do overdrive pacing? How does it work? DOES it work?  

First. Let's set the record straight: emergency doctors don’t do overdrive pacing.  How do I know that? Because there is only one indication for “overdrive pacing” in the ED: torsades de pointes.  But the rate of torsades is 150-250 BPM.  And the most commonly used pacemaker in US ED’s is the Medtronic single-chamber Pacer, which has a maximum RATE of 180 BPM. So how were you planning to OVERDRIVE Torsades, which is running at 250 BPM, when your max pacer rate is 180?  See? You can’t even DO overdrive pacing.  What are you really supposed to do?

Ventricular Tachycardia: 2 flavors

  1. Monomorphic VT
  2. Polymorphic VT
    1. Normal QT
    2. Long QT ----- BEWARE! This is Torsades de pointes

Torsades de Pointes = Polymorphic VT with long QT

  • Torsades occurs when a PVC occurs during the T Wave  (R on T)
  • THIS explains WHY ‘overdrive pacing’ works - see Treatment below

The QT conundrum:

The QT is heart rate-dependent.  When the heart rate is slower, the QT is longer, and vice versa.  In order to determine whether your patient truly has a long QT, the QTc was developed as a calculation that that attempts to normalize the QT interval to a rate of 60 BPM.  

The bottom line: the QTc is number you should look at.  There are several calculations available- even MDCalc has one.  But just look at the top of the EKG. It turns out the EKG computer does a fine job of calculating the QTc. Use the QTc.

What is a long QTc

The dirty definition:   Long QT = QT > 500 ms 

Beware the patient with syncope or near-syncope with a QTc longer than 500.  You might be staring straight at a patient who just had polymorphic VT with long QTc.  You might be staring at torsades.  Torsades likes to degenerate into VF, and VF is a less than desirable rhythm.

Treatment of Torsades

  1. Stabilize the cardiac myocyte and treat hypomagnesemia: Magnesium 2gm IV q15m
  2. Increase the resting heart rate. Increasing the HR narrows the QT. Narrowing the QT narrows the T wave (ventricular repolarization). A narrow T wave means your ventricle is spending less time repolarizing.  If your T wave is narrow, the chances of throwing a PVC on top of a T (R on T) is much less likely.  So....just increase the heart rate. Oh wait...increase the heart rate AFTER you’ve cardioverted them from polymorphic VT.

Drugs to use after sinus rhythm achieved and you want to speed the heart rate


  • nonselective beta agonist
  • Inotropic, chronotropic, dromotropic
  • dose: 10-20 mcg IVP or drip


Dopamine drip

**Transvenous Pacing: RATE = 110 BPM

Bonus: Hollywood Weingart

Show notes by Joe Bellezzo from the ED ECMO podcast

Direct download: Torsades_De_PointesTorsades.mp3
Category:podcasts -- posted at: 6:05pm MDT

Mel Herbert is arguably the most influential medical educator of our time. He sat down with ERCast to discuss...

Direct download: Mel_Herbert_This_Wont_Hurt_A_Bit_ERCast.output.mp3
Category:general -- posted at: 3:45pm MDT