Podcast 122 – Cardiac Arrest after the Toxicology of Smoke Inhalation with Lewis Nelson


We had a case a few months ago at Janus General–very sad and very scary. The patient came in after a house fire. He had some burns, but not enough to be the cause of his arrest. Instead, it had to be the asphyxia and possible toxicology of the smoke inhalation. I wanted to get a better idea of ideal care for these patients; for that I needed a toxicologist.

Lewis NelsonFew tox folks are smarter than Lewis Nelson, MD of the NYC Poison Center.

Note: In this episode we don’t deal with the thermal injury of smoke inhalation

Cyanide Toxicity

  • Empiric administration of  Hydroxocobalamin 5 g rapid IV drip x 1
  • Even better if this can be given at the scene as soon as the patient arrests or is profoundly hypotensive
  • Messes with labs that use colorimetric probes (cooximetry, lactate, LFTs, etc.) Get blood for cooximetry before giving the med if at all possible
  • Dr. Nelson doesn’t recommend giving sodium thiosulfate in addition to the Hydroxocobalamin
  • An IM version is in the pipeline–this will be easier for EMS/emergency use


You'll need 200 ml of Saline

You’ll need 200 ml of Saline

Carbon Monoxide

  • Put the patient on 100% fiO2
  • Not much to do beyond that until the patient stabilizes
  • See LITFL for more on CO


  • Caused by Hb oxidation from the heat of the fire
  • Administer Methylene Blue 2 mg/kg x 1 IVP
  • May be worthwhile to start a drip if patient has resistant hypotension, but this is an unproven therapy

Now on to the Podcast…


EMCrit Podcast 121 – REBOA


Today, I got to interview one of the superstars at Shock Trauma on REBOA (resuscitative endovascular balloon occlusion of the aorta).

Balloon occlusion of the aorta was first described in 1954 (Surgery 1954;36(1):65). Other older articles include (Ann Emerg Med 1986;15(12):1466, J Endovasc Ther 2000;7(1):1, Endovasc Ther 2005;12(5):556).

The Shock Trauma Center (STC) Approach to REBOA

Gain Access to the Common Femoral Artery with Femoral A-line Kit

  • Just like normal, except make sure you are hitting common femoral and not superficial femoral artery

Float the Wire

  • STC uses Boston Scientific Amplatz superstiff wires (0.035in/260 cm/straight tip)
  • Measure externally from the catheter to the umblicus and then up to the level of the 2nd rib–mark this level on the wire
  • Advance the wire floppy-end first to the marked depth
  • Confirm location with either radiograph or fluoro before proceeding

Place the Sheath

  • At STC, they use a Check-Flo Performer Introducer (12 fr, 30cm)
  • Remove the femoral artery catheter
  • Measure the introducer externally from groin to just below the umbilicus
  • Dilate the vessel to accept the introducer
  • Place the introducer to the previously marked level

Place the Coda Catheter/Balloon

  • Grab a CODA balloon catheter (32 mm-balloon)
  • Measure externally; Zone 1 is measured to the xiphoid, Zone 3 is measured to just above the umbilicus

from J Trauma. 2011 Dec;71(6):1869-72


  • Remove all air from the balloon using saline syringe
  • Insert the CODA catheter
  • The wire stays stationary throughout

Inflate the Balloon

  • Use a 30 ml syringe, ideally filled with 20 ml of NS and 10 ml of omnipaque (lohexol); use just saline if contrast not available
  • Inflate until resistance goes to moderate (would love to know what luminal pressure this corresponds to). In general, this corresponds to 12-22 mls depending on the size of the aorta–but this must be individualized to the patient.

Secure Everything for Transport

  • Here’s how they do it at STC


  • Mark the levels of everything so you can verify there has been no migration

Get an Xray when time allows

Balloon in Zone-3

Balloon in Zone-3

Balloon in Zone-1

Balloon in Zone-1

Go to Definitive Management

  • The introducer sheath will need to be removed under direct observation after cutdown, with arterial repair (at least until smaller catheters are developed)

Shock Trauma Center Protocol


REBOA Articles

REBOA review article (J Trauma. 2011 Dec;71(6):1869-72)

Case series: Martinelli T et al. J Trauma 2010 Apr;68(4):942-8

Case Series: Brenner M et al. J Trauma Acute Care Surg. 2013 Sep;75(3):506

Now on to the Podcast…


Podcast 120 – The ProCESS Trial with Derek Angus


The ProCESS trial was published less than a week ago (The night before my SMACC lecture on severe sepsis–dohhh!)

If you have no idea what I’m talking about, climb down from your mountain-top monastery, find a damn iphone and read this:

ProCESS Trial in the NEJM

As soon as I returned to the states, I begged and pleaded with the study author, Dr. Derek Angus, to give us his thoughts, he kindly acceded.

Derek AngusDr. Angus is chair of the Department of Critical Care Medicine and Distinguished Professor and Mitchell P. Fink Endowed Chair of Critical Care Medicine at the University of Pittsburgh Schools of the Health Sciences and UPMC Health System. His accomplishments are too numerous to list here, so check out his bio page.

I will be adding a ton of stuff to this page regarding the trial ASAP; for now I just wanted to get Dr. Angus’s interview up on the site.

Most Important Table

Updated Table S4

Updated Table S4


Other Stuff Mentioned

Supplementary Material for ProCESS (this is the corrected version)

High versus Low Blood-Pressure Target in Patients with Septic Shock

Excellent Posts in the FOAMcc World

Now on to the Podcast…


Podcast 119 – Rich Levitan on the Surgical Airway


My friend and all-around incredible guy, Rich Levitan, speaking on the Surgical Airway.


Subsequent to publication of the podcast, Rich Levitan received this letter:


I met you about 4 years ago and we had talked about airway training as you can see in the email below. First off I would like to thank you for your presentation at SOMA (or SOMSA) 2013. It was enlightening for me and I appreciated the discussion.

I am writing you about an airway lecture that you gave in a 2014 conference which was subsequently posted on EMCrit as podcast 119. Although the lecture was excellent, I would like to bring two small inconsistencies about the video portion to your attention:

1)      Just for the sake of clarity, the soldiers featured in the video were actually from the 101st airborne, which is a conventional airborne unit staged out of Ft Campbell KY and they were performing operations in Afghanistan. These are not Special Forces soldiers and in fact, are not affiliated with Special Operations at all. The medics in the video received entry level medical training at Ft Sam Houston, home to AMMED. The scope of their training is relatively narrow in comparison to that of the Special Operations Medic.

The majority of Special Operations medics are more familiar with the cricothyrotomy procedure and are competent/confident enough to perform it when the injury pattern dictates the need. In fact, the majority of the cricothyrotomies performed at the point of injury, in combat, are performed by SOF Medics and not by conventional medics. This is not to take away from the amazing work that Dr Bob Mabry has done with the entry level training at Ft Sam.

2)      The injured soldier in the video is actually an Afghan soldier working alongside American Troops. This is not one of their buddies. This is not to say that bonds never get formed between American Troops and the members of the local population because they certainly do, but a safe assumption here might be that the provider and the casualty do not even know each other’s names.

I don’t know why I am so compelled to address this, maybe it is a little bit of foolish pride in my Special Forces lineage but nevertheless being a man of science I am sure you desire the same level of accuracy in medicine as you do in all things.

Thank you again for all the support, hard work and passion you bring to emergency medicine!


Rich Levitan’s New Advanced Airway and Endoscopy Course


Now on to the Vodcast…

Podcast 118 – EMCrit Book Club – On Combat by Dave Grossman

Today I am joined by the master of all things Mind of the Resuscitationist, Cliff Reid of resus.me and the Rage Podcast. In the first ever EMCrit Book Club, we discuss a book I read years ago and recently reread:


On Combat by Dave Grossman has enormous relevance to resuscitationists. I feel the entire book is worth reading, but we zoned in on the really juicy bits.

Section I - Physiology of Combat

Chapter Two – Stress Responses to Combat

We briefly discuss bowel and bladder control as they relate to stress

Chapter Three – Sympathetic & Parasympathetic Responses

Parasympathetic backlash-a time of cognitive danger

“The moment of greatest vulnerability is the instant immediately after victory” –Napoleon

Adapt a 360 degree visual sweep for threats (keep looking at all of your patients vitals and remember to bag)

SWAT Team Acronym-L.A.C.E. liquids, ammunition, casualties, equipment; For us–check your team, immediate reset of resus bay, drink something, debrief

Burn off the adrenaline dump

Conflict with colleagues. Exercise, Punching Bags? If a horrible call is reported on the EMS phone, but never shows–run a sim to burn the epi.

Sleep Deprivation-Caffeine can be our friend, nicotine not so much. If you are too exhausted to perform, tell a colleague and take a nap.

Chapter Four – Colored Conditions

originally from Bruce Siddle, Sharpening the Warriors Edge

Heart rate and task performance: heart rates are a guide, getting there by exercise is not the same as by fear/stress, so HR is merely an associated marker
Yellow 90-120, Over 115 and fine motor skills performance degrades significantly
Red 120-150, a 145 HR seems to be the break-point for optimal performance of complex skills
Black >150 and badness ensues, (or >175 in the highly trained, they get a gray zone)

  • Fine motor skills-precision tasks
  • Gross Motor Skills-ape skills
  • Complex-a combination of maneuvers or use of multiple body parts

SWAT team breaking down door function in condition red (or gray), but they have trained until the necessary tasks that require fine motor have been practiced till automaticity

Unified Model of Stress and Performance

On Combat Unified Model

From Grossman On Combat

On Combat Heart Rate Diagram


We need to train how we fight
Stress Inoculation Training and (Academic Medicine 2009;84(10):S25)

We are currently wasting high fidelity simulation, it should purely be for stress training. Perhaps, we should create a hell week for our 2nd years.

Stay in yellow (alert, but with fine motor control) – yellow dot stickers to remind you

“I understand a fury in your words, but not the words” –Shakespeare from Othello

Tactical/combat breathing to stay in the color zone

Hicks’ Law – procedures should only be learned one way-preflush central lines, one way to RSI.

Section 2 – Perceptual Distortions

Chapter 1 – Auditory exclusion and tunnel vision

tunnel vision – the toilet paper tube

Chapter 2 – Auto-pilot

What is drilled in during training comes out the other end in combat, no more no less

Chapter 3 – Grab Bag

Time perception is sent awry

This is why you must not squeeze a BVM when stressed.

Chapter 4 – Memory

Memories under Stress are Suspect

Self Debriefing is flawed, debrief with your team.

Section 3 – The Call to Combat

Chapter 2 – Training warriors

Need to train the puppy brain, because the doggy will be in control

Triune Model of the Brain

  • Forebrain-Human
  • Midbrain-Puppy
  • Hindbrain-Lizard

Cleanse denial: not if, only when. Do not train to “If I get into a CICO situation,” instead, “When I get into a CICO situation.”

“In combat you do not rise to the occasion, you sink to the level of your training.” –Grossman

Principles of Training

  1. Never Kill a Warrior in Training-this only trains them to die. Every engagement should end in the proper behavior
  2. Try to never send a loser off your training site
  3. Never talk trash about your students-Punish in private, Praise in public

This is a great chapter for folks running courses/simulations

Section 4 – The Price of Combat

Chapter 5 – Tactical Breathing

Autogenic / Tactical / Combat Breathing


  • Breath in through your nose filling up your belly for 4 seconds
  • Hold for 4 seconds
  • Exhale through your mouth for 4 seconds
  • Hold for 4 seconds
  • Repeat x 4

If you read the book and have thoughts, please leave them in the comments below

Now on to the Podcast…


Podcast 117 – Everyday Emergency Kits with Keith Conover


If you are an EM:RAP listener, you have probably heard Mel Herbert’s story of 2 cars crashing right outside of his house. Mel realized he did not stock a medical kit in his house with the necessary crucial supplies for an emergency scene. I realized I don’t either (there is one in my car). So, I reached out to the master of preparedness, Dr. Keith Conover.

Everyday Emergency Kit

We spend the 1st part of the show discussing the everyday kit which Dr. Conover has with him (or in eye shot) pretty much always. He carries it in a fanny pack–I’m not sure if I can be persuaded to do this, but you should probably keep a kit with at least these items in your car or house.

On the topic of fanny packs…

Well anyhooooo, here is the list

Keith Conover's Everyday Kit

We also discussed the Daypack Medical Kit for your House/Car

Digital Intubation

Equipment we Discussed



The CAT Tourniquet is the best one yet

Disposable Laryngoscopes for Kits


I recommend the Zebralights, this is the one I use:


Zebralight H502W

SAM Splint


The SAM Splint is EMS standard stock

Trauma Bag

In his trunk, Dr. Conover has this prestocked trauma kit.

Pelvic Binder

Dr. Conover actually carries a pelvic binder in his trunk as well (no comment), he stocks the SAM II Pelvic Splint.

Other Crucial Links

Stuff EMCrit Likes – The Anesthetic Crisis Manual

I reached out to the creator of the Anaesthetic (Anesthetic) Crisis Manual after I saw a post on LITFL.

This book is amazing! It fulfills what Joe Novak was talking about on EMCrit Podcast ; this is the manual you want in the OR/OT after you go through the no-shitters. Waterproof, unrippable, and easy to find the crucial info you need–good stuff. Please go read the full review on LITFL.

Go to the ACM Website and check it out. I took no money (would I ever?) for this plug; but the author sent me a bunch of books to distribute to you folks.


Podcast 116 – the tPA for Ischemic Stroke Debate


Here is one of my favorite segments from the 2014 EMCrit/ISMMS Conference. My chair Dr. Andy Jagoda debates my friend Dr. Anand Swaminathan.

The debate seemed relevant because ACEP, a major US emergency medicine organization, released clinical guidelines markedly increasing stress on thrombolysing stroke. These clinical guidelines were sent back by ACEP’s council for further commentary and assessment, a move unprecedented in the history of the organization.

ACEP Clinical Guidelines from 2013

Pro Side

Dr. Jagoda took the Pro stance.

Here are his slides

Con Side

Dr. Swaminathan took the con stance. Check out his site, EM Lyceum for more FOAM goodness.

Here is his slideset

Now on to the Podcast…

Podcast 115 – A New Paradigm for Post-Intubation Pain, Agitation, and Delirium


All the way back on Podcast 21, I advocated for better post-intubation sedation in the ED. Well, now it turns out that if you are still using just lorazepam and vecuronium you are now even further from the ideal.

It is all about Sleep and Orientation

Bad sedation strategies destroy sleep architecture and orientation, then patients become crazy.


  • The impact of delirium in the intensive care unit on hospital length of stay. Intensive Care Med 2001; 27:1892–1900
  • Delirium as a predictor of mortality in mechanically ventilated patients in the intensive care unit. JAMA 2004; 291:1753–1762
  • Occurrence of delirium is severely underestimated in the ICU during daily care. Intensive Care Med 2009; 35:1276–1280
  • Delirium leads to long-term cognitive impairment (N Engl J Med 2013; 369:1306-1316) HT to @icudelirium
  • Days of delirium are associated with 1-year mortality in an older intensive care unit population. Am J Respir Crit Care Med 2009; 180:1092–1097

It doesn’t matter if we screw it up Downstairs, they can Fix it in the ICU

Ummm, not so much if you believe the SPICE Study-In 251 critically ill patients at multiple centers, we identified deep sedation within 4 hours of commencing ventilation as an independent negative predictor of the time to extubation, hospital death, and 180-day mortality. The early phase of ICU sedation is usually unaccounted for in randomized controlled trials due to late randomization. (Am J Respir Crit Care Med Vol 2012;186(8):724–731)(10.1164/rccm.201203-0522OC)

A1 Sedation – Analgesia First

Stick your finger down your throat–now leave it there

Strom et al. evaluated this: RCT of 140 patients-analgesia vs. analgesia+sedation. Analgesia only showed shorter vent time and ICU LOS.(20116842)

Analgosedation: a paradigm shift in intensive care unit sedation practice,(10.1345/aph.1Q525).

Just put patients on a fentanyl drip. If not go with dilaudad IV. When remifentanil is cheap, we’ll switch to that in a bunch of patient categories.(15329588)

Then evaluate pain and decide if the patient needs additional pushes of pain meds.

Consider using the Behavioral Pain Scale (Crit Care Med 2001;29(12):2258) HT to Nikolay Yusupov


Myth – We can prevent PTSD if we Black Out the ICU Experience

just the other way around

Myth – Benzos are just Swell

Not so much-Benzos lead to longer length of stay, longer vent time, and increased delirium.

Benzodiazepine versus nonbenzodiazepine-based sedation for mechanically ventilated, critically ill adults: a systematic review and meta-analysis of randomized trials,(10.1097/CCM.0b013e3182a16898).

Myth – Short-Acting Sedatives and Analgesics Go Away Quickly

You need a goal, like RASS

Here is the RASS Scale from the amazing ICU Delirium Site

Myth-Pain is a Great Pressor

Patients should never be undersedated due to hemodynamics

Patient Scenarios

Standard Critically Ill Patients

Fentanyl and Dexmedetomidine


Dan Herr's Method of Dex Titration

Dan Herr’s Method of Dex Titration

Neuro Patients/DTs

If you have ICP issues, propofol and fentanyl

Hemodynamically Compromised Patients

Fentanyl and then,

Ketamine drip or intermittent boluses

What are they doing in the ICU?


In patients with protocolized sedation, daily sedation interruptions (holidays) did not lead to demonstrable benefit. The SLEAP Study (JAMA 2012;308(19):1985)(10.1097/CCM.0b013e3182a168c5)

The SCCM Guidelines

Barr et al. Clinical Practice Guidelines for the Management of Pain, Agitation, and Delirium in Adult Patients in the Intensive Care Unit

A Lecture on the SCCM Guidelines

By a masterful teacher, Dann Herr. Courtesy of the Maryland CC Project

Must Read Reviews

Now, On to the Podcast…



Best of 2013 – Eight is Enough & Social Media Update


Social Media Update

  • Use either RSS or the email updates feature (find both on the home page)
  • If you have a comment on an EMCrit Podcast or Post, please put it on the blogpost on emcrit.org
  • If you have something pithy to say, use twitter
  • If you have a case or a question unrelated to an EMCrit Podcast or Post, use Google Plus or post to the FOAMcc Google Community
  • If you like being screwed and having your information manipulated, use Facebook


Best of 2013


Niche Sites


Social Media Guidelines

Previous Year’s Best ofs

A Product I Recommend



by Brian Kloss and Travis Bruce

Happy Solstice Everyone! and now on to the Podcast…



Another Comment from Our Semi-Retired Critical Care Doctor on Fluids and the Lymphatics


If you hadn’t already read John (Last Name Not Given), go immediately to this post and read it.

A physiology master comments on the sepsis talks

The comment was in response to the two podcasts on Dr. Paul Marik’s Fluids in Sepsis Talk

The Role of the Lymphatics

In the light of our ‘improved’ understanding of the capillary fluid dynamics of which lymphatics play a significant part (I know, I am sounding like a broken record when it comes to the role of lymphatics!), a few points need to be addressed…..

Optimal fluid resuscitation involves the maintenance of adequate microcirculatory flow coupled with prevention of development of interstitial edema. Edema develops when the capillary hydrostatic pressure increases, coupled with a reduction in removal of interstitial fluid. There is always a normal extravasation of fluid from the intracapillary space to the extracapillary (interstitial) space, otherwise the cells would starve. This extravasation happens along the entire length of the non-fenestrated, non-sinusoidal capillaries and not just at the arteriolar end, as previously thought ( Tom W’s fantastic article!!).

A normally functioning lymphatic system is crucial for returning this fluid back to the central circulation, otherwise edema would ensue.

Normal Lymphatic Function

Let us have a very brief outline of the normal lymphatic structure in this context. I find it useful to think about the arrangement as a kind of a bronchial tree in reverse ….

Initial lymphatics, rich in numbers and deeply embedded in tissue parenchyma, consist of pure endothelial channels without perivascular cells (e.g., pericytes) and smooth muscle cells. They have overlapping cell junctions forming primary valves in addition to traditional secondary lymph valves, and they rely on surrounding tissue motions to achieve periodic lymph channel expansion and compression for collection of interstitial fluid and fluid transport inside the lymphatics.
By contrast, the contractile lymphatics, (calcium dependant) are equipped with rows of bileaflet valves and contract by a specialized smooth muscle phenotype unique to the lymphatics to carry fluid from the initial lymphatics to the lymph nodes. Each pair of upstream and downstream valves in contractile lymphatics forms a lymphangion, facilitating unidirectional lymph fluid during periodic contraction. Contractile lymphatics have many of the vascular control mechanisms present in the arterioles, from classical myogenic contraction to neurogenic, purinergic, and endothelial-dependent and -independent controls.

The microenvironment surrounding collecting lymphatic vessels is a determinant of lymphatic function. Under physiological conditions, NO produced by eNOS in endothelial cells is required for periodic contraction and lymph flow; removing NO caused a reduction in contraction strength. Under inflammatory conditions, iNOS overproduces NO, overwhelms the subtle flow-dependent NO production from eNOS, and prevents contraction. At least in mouse models, higher levels of NO production stimulated by ACh evoked dilation, decreased tone, slowed contraction frequency and reduced fractional pump flow. The situation facilitates lymph edema, reduces antigen delivery into lymph nodes, and consequently, reduces antigen-presenting cells and T-cell activation. It is interesting to note that the effect of nitric oxide and therefore Nitroglycerin are completely different in normal circumstances and in inflammation!
Suppression of lymphatic function by CD11b-positive myeloid cells is a mechanism of self-protection from autoreactive responses during on-going inflammation. To initiate an immune response, antigen and antigen-presenting cells arrive in lymph nodes within hours on antigen encounter. Myeloid cells may accumulate at an inflammatory site and inhibit collecting lymphatic function, suppressing additional immune response to self-antigen by reducing antigen transport into the lymph node.

Some good references on this point are ..

Glycocalyx Protection

Now, on to the aspect of glycocalyx protection,

Injudicious fluid administration in resuscitation practices can cause edema to develop by a variety of mechanisms.
A rapid fluid bolus can cause significant shear stress on the delicate glycocalyx, disrupting it and breaking down the barriers to extravasation.

Colloids and hyperoncotic stuff can themselves cause dessication and compaction of the glycocalyx, by sucking up its water content.

Hypervolemia itself can cause atrial stretch, causing the release of ANP and BNP (evil twins of volume overload.) The actions of both peptides include natriuresis and diuresis, a decrease in systemic blood pressure, and inhibition of the renin–angiotensin–aldosterone system. Further, ANP and BNP elicit increases in blood microvessel permeability sufficient to cause protein and fluid extravasation into the interstitium to reduce the vascular volume. They have a rather differential action on the lymphatics, interms of altering either the permeability or the contractility. Notably, ANP abolishes spontaneous contraction amplitude while BNP augments both parameters by ?2-fold . In aggregate, the consensus is that an increase in collecting lymphatic permeability opposes the absorptive function of the lymphatic capillaries, and aids in the retention of protein and fluid in the interstitial space to counteract volume expansion. The works of Joshua P. Scallan, Michael J. Davis and Virginia H. Huxley, in this regard are noteworthy.

One can see the possible pitfalls of using Nitroglycerine at a micro-circulatory level….

One, by causing vasodilatation, it can aggravate edema..(increased capillary hydrostatic pressure)

Two, by knocking off lymphatics, (through the NO synthase mechanisms) it might perpetuate interstitial fluid retention.

Hope this helps.
“Semi retired critical care doc”.

It does indeed help, but…!

Now, an alternative view is to go to the actual clinical data (albeit preliminary), for instance

Spronk PE, Ince C, Gardien MJ, Mathura KR, Oudemans-van Straaten HM, Zandstra DF. Nitroglycerin in septic shock after intravascular volume resuscitation. Lancet. 2002 Nov 2;360(9343):1395-6.

His letter of response to questions also has additional references for the mode of action that may be beneficial

These two fantastic review articles on microcirculatory resuscitation are must reads:

  • Intensive Care Med 2002;28:1208
  • Critical Care 2006;10:221

What do you think?