Since we were talking about Na-channels in the last podcast, Sean Smith suggested this video:
I had a crazy case of Tricyclic Overdose while on an overnight shift at Janus General.
Initial and Post-Treatment EKGs
List of Tricyclic Agents from Wikipedia.org
- Amitriptyline (Tryptomer, Elavil)
- Amitriptylinoxide (Amioxid, Ambivalon, Equilibrin)
- Butriptyline (Evadyne)
- Clomipramine (Anafranil)
- Demexiptiline (Deparon, Tinoran)
- Desipramine (Norpramin, Pertofrane)
- Dibenzepin (Noveril, Victoril)
- Dimetacrine (Istonil, Istonyl, Miroistonil)
- Dosulepin/Dothiepin (Prothiaden)
- Doxepin (Adapin, Sinequan)
- Imipramine (Tofranil, Janimine, Praminil)
- Imipraminoxide (Imiprex, Elepsin)
- Lofepramine (Lomont, Gamanil)
- Melitracen (Deanxit, Dixeran, Melixeran, Trausabun)
- Metapramine (Timaxel)
- Nitroxazepine (Sintamil)
- Nortriptyline (Pamelor, Aventyl, Norpress)
- Noxiptiline (Agedal, Elronon, Nogedal)
- Pipofezine (Azafen/Azaphen)
- Propizepine (Depressin, Vagran)
- Protriptyline (Vivactil)
- Quinupramine (Kevopril, Kinupril, Adeprim, Quinuprine)
- Amineptine (Survector, Maneon, Directim) Norepinephrine-dopamine reuptake inhibitor
- Iprindole (Prondol, Galatur, Tetran) 5-HT2 receptor antagonist
- Opipramol (Insidon, Pramolan, Ensidon, Oprimol) ? receptor agonist
- Tianeptine (Stablon, Coaxil, Tatinol) Selective serotonin reuptake enhancer
- Trimipramine (Surmontil) 5-HT2 receptor antagonist and moderate-potency norepinephrine reuptake inhibitor.
And of course, the non-TCA agents…
Pharmacologic Effects of TCAs
|K+ Channel Blockade||QTC Prolongation|
|NE & Serotonin Reuptake Inhibition||Initial hypertension quickly followed by hypotension|
|Na+ Channel Blockade||QRS Prolongation|
Hypotension — depresses myocardial contractility
Brugada-like findings on EKG
|Muscarinic Anticholinergic Receptor Antagonism||Anticholinergic Toxidrome|
|Antihistaminergic||CNS stimulation or sedation|
|Alpha1 Adrenergic Antagonism||Hypotension|
|GABA-A Receptor Blockade||Seizures|
This chart was taken from the excellent Resus Review Blog by Charles Bruen
Increases amount of drug in non-ionized form and may decrease binding to Na-channels 
May need many, many amps. For some reason the sodium and the bicarb don’t rise significantly in severe toxicity
My goals are QRS duration <100, hemodynamically stable, Na ~150, pH ~7.5
Beware of hypokalemia and hypocalcemia
Send VBG with lytes at least Q1 hour
To promote alkalosis
If the patient is too alkalotic or out of amps of Bicarb
Can substitute for NaBicarb. This article gives dosing recommendations and precautions. 
Intubation & Sedation
Be very careful the patient doesn’t become hypercapneic
Sedate with benzo or propofol to raise seizure threshold
Gastric Decon and/or Lavage
If time of ingestion <1 hour ago and airway is protected
We use a commercial device: the Easi-Lav system
May help, though risk of Torsades is low as long as the patient remains tachycardic
Even though lidocaine is another Na-Channel Blocker, it actually antagonizes the effects of the TCA-like mediciations. As a Vaughan Williams Class IB agent, For additional information, this review discusses the pertinent issues.
Norepi or Epi
Certainly for cardiac arrest and probably for hypotension/increasing pressor necessity
For this or any other Lipid Question, you need to go immediately to the Lipid Rescue Site
You can find the Lipid Administration Instruction Sheet there, which should be hanging somewhere on the wall of your ED.
The last resort for tox instability
My friends Sean Nordt and Stu Swadron did a great EM:RAP episode on this 2 months ago
Here is a review and guideline article.
Medcalc sent me some freebie codes for their new IOS version of the app. Join the mailing list to be in the running (see the area below to sign up for the mailing list)
Daren Lewis of leadingvisually.com designed the wonderful Janus General logo; consider him if you need any message design.
Now on to the podcast…
- K. Blackman, S.G. Brown, and G.J. Wilkes, "Plasma alkalinization for tricyclic antidepressant toxicity: a systematic review.", Emergency medicine (Fremantle, W.A.), 2001. http://www.ncbi.nlm.nih.gov/pubmed/11482860
- M.J. Neavyn, E.W. Boyer, S.B. Bird, and K.M. Babu, "Sodium Acetate as a Replacement for Sodium Bicarbonate in Medical Toxicology: a Review.", Journal of medical toxicology : official journal of the American College of Medical Toxicology, 2013. http://www.ncbi.nlm.nih.gov/pubmed/23636658
- A. Foianini, T. Joseph Wiegand, and N. Benowitz, "What is the role of lidocaine or phenytoin in tricyclic antidepressant-induced cardiotoxicity?", Clinical toxicology (Philadelphia, Pa.), 2010. http://www.ncbi.nlm.nih.gov/pubmed/20507243
You just read the post: Podcast 98 – Cyclic (Tricyclic) Antidepressant Overdose from EMCrit Blog - Emergency Department Critical Care.
Janus General Hospital
Where to Comment/Question
If it is about a blogpost/podcast, comment here on the EMCrit.org site
If it is a clinical question or discussion, go to the EMCrit G+ Community Page
If it is a quick comment or question, hit me on Twitter
If it is a problem with the EMCrit Site or the CME Site, come to the Contact Page
Direct Link to CME for Each Episode
Starting with episode 97, at the bottom of each post, there is a direct link to get CME:
So last podcast, I bashed on sodium bicarbonate or as John Kellum and David Story call it: chloride-free sodium. This episode I talk about all the good reasons to use NaBicarb.
A physiology quandary
Owen, an anaesthesia registrar, wrote with this comment:
[...On increasing minute ventilation on vented patients with any bicarb given: Great idea and probably what most of us do, but even if you don't then with each breath the patient will be getting rid of more CO2 than previously so there should be more weak acid loss.]
This is one of those situations where I was gobsmacked for a second. When I started to think about this, it seemed intuitively wrong and yet conceptually right. I knew I needed to find someone far smarter than me. I reached out to Mel Herbert, who recommended David Story. Dr Story is Chair of Anaesthesia at the Melbourne Medical School and a physiology god. Here is his response:
Dr. Story, Here is the quandary. As you saw, I did that acid-base show with Dr. Kellum discussing NaBicarb use for the critically ill. Both Dr. Kellum and I believe and the evidence bares out that in a patient who can’t get rid of the excess CO2, there will be negligible changes in pH from the bicarb administration.Now in an apneic patient, I think this is inarguable. However, in a mech. ventilated patient with no resp drive (let’s say a pt we gave NMBs to), I perpetrated the situation would be the same. In response of my listeners brought up this question: If the minute ventilation is kept the same, but the ETCO2 rises (and by extension, the return of CO2 to the alveoli), this would seem to indicate that each breath is actually eliminating more CO2. Say the ETCO2 went from 40 to 80 with the same Vt. Is more CO2 being eliminated and if so, would this alone clear the transitory excess CO2 from the bicarb? This made me think of the opioid overdose patient. As their CO2 rises, are they too eliminating more CO2 with each of their breaths? My cursory understanding has always been simply that CO2 elimination is directly proportional to minute ventilation. That is what i took from West and never really gave it much thought. Now I am thinking and it is puzzling. –Scott
Response from Dr. Story: I agree it is confusing but this is how I see it. I wrote a letter the Anesthesiology years ago on a related topic.
The short answer is it is all relative.
The universal alveolar air equation for any gas (x) is:
PAx = PIx +/- Vx / VA; where PA is alveolar partial pressure, Vx is production or consumption of the gas
For an excreted gas like CO2 this will be:
PACO2 = PICO2 + K (VCO2 / VA)
The constant is due to VCO2 being STPD and VA being BTPS and is about 800 if you are using mmHg and ml/min.
So usually PACO2 = 40, PIcO2 = 0, VCO2 = 250 ml/min and VA = 5,000 ml / min (10 X 500ml)
Also PACO2 is directly proportional to VCO2 and inversely to Va.
Now if we give NaBic and Bic forms CO2 VCO2 will increase. If it went up 50% it would be from 250 ml / min to 375 ml / min. If VA is fixed then
PACO2 = 800 X 375 / 5,000 = 60 mmHg
However I agree that Va will go up which will be due to the increase in VCO2, ie the EXPIRED VA will increase
(inspired unlikey = expired when VO2 does not equal VCO2, that is the respiratory exchange ratio does not equal 1, that is what the F in the alveolar gas equation corrects)
Therefore the VA is now 5,125 ml / min
PACO2 = 800 (375 / 5,125) = 58.5 mmHg.
We have had a 50% increase in VCO2 but only a 2.5% increase in VA this will lead to a new equilibrium point in alveolar and arterial CO2 at around 58mmHg.
I have exaggerated the effects of NaBic or as I call it chloride-free sodium to demonstrate the effects as I see it.
Therefore, yes the alveolar ventilation increases due to greater CO2 excretion but it is a relatively small effect on VA. To reduce the PACO2 back to 40 will require a 50% increase in VA. This will be transient as the VCO2 returns to the rate prior to the NaBic infusion.
I hope the above helps. If not let me know.
So what do I take from all of that? I think regardless of any increase in minute ventilation, the CO2 will eventually go back to baseline after an adminsitration of sodium bicarbonate and you will see the alkalizing effect, but unless you increase the minute ventilation it will take much longer.
Use of Sodium Bicarbonate
If not stored in glass, bicarb containing solutions exchange CO2 and become not so much bicarbonate.
When to use Bicarb
- Na Channel Blockade in Tox (Slow Push)
- Non-SIG Acidosis (Drip or IV Fluid)
- SIG Acidosis (As an IV Fluid)
- Increased ICP (Drip)
- Hyperkalemia (As an IV Fluid)
- Hyponatremia (Drip)
NaBicarb can be used as a substitute for hypertonic saline in increased ICP (Neurocrit Care 2010;13:24 & Neurocrit Care 2011;15:42). They used 85 ml of 8.4% sodium bicarb infused over 30 minutes.
Problems with Bicarbonate Drips
When not to use Bicarb
- Probably no role in Cardiac Arrest unless you feel the patient has hyperkalemia or toxicologic cause.
MDCalc is where I go when I need to remember a clinical scoring system. I was thus quite pleased to find one of the scores I use every shift appear on the site. The LLS score is how I determine the need for many interventions, but especially to decide who needs massive transfusion.
This is Part V of the EMCrit Acid-Base Talks. If you haven’t listened to the initial series, you may be better off starting there:
- Part I lays out the background of the quantitative approach
- Part II puts it in mathematical terms to allow calculation of acid base status
- Part III takes you through some real world examples
- Part IV discusses the Acid-Base Effects of IV Fluids
Today’s topic comes from a debate I have been having with Steve Smith of the amazing EKG Blog. The main thrust of the debate started with this question…
Does Bicarb Fix pH if You Can’t Increase Minute Ventilation?
When you can adjust PaCO2 to maintain a certain value (i.e. you increase minute ventilation), bicarb will lower pH as evidenced by this animal study (Crit Care Med 1996; 24:827-834). However, if you can’t blow off the CO2 then the effects on pH will not be there (J Pediatr 1977;91(2):287).
In this study, NaBicarb did not correct the pH, while CarbiCarb did (Carbicarb: an effective substitute for NaHCO3 for the treatment of acidosis. (Surgery 102:835–839).
This review article recommends against bicarb for permissive hypercapnia (Intensive Care Med (2004) 30:347–356).
This study furthers the idea that NaBicarb is not all that great in closed systems (J Pediatr 1972;80(4):671) and then this discussion explores all of the biochemical reasons why administering bicarbonate as a rapid push in a closed system is a bad idea (J Pediatr. 1972 Apr;80(4):681-2.).
Here is a quote from another review article (Anesthesiology 1990;72(6):1064):
The key concept in the equation [above] is that pH is not related to the absolute value of either bicarbonate concentration nor PCo2, but rather to their ratio.
When exogenous bicarbonate is administered during acidemia, bicarbonate reacts with hydrogen ions to form carbonic acid. Physicochemical equilibrium is shifted, favoring dissociation of carbonic acid to C02 and water. C02 partial pressure increases. The degree of alkaliniza- tion resulting from increased [HC03“] is limited by the rise in Pco2* In (open) systems where increases in PCo2 are prevented (by ventilation) alkalination occurs. When CO2 cannot be eliminated, the pH of the system is only minimally changed. Ostrea and Odel demonstrated in vitro that when isotonic sodium bicarbonate was added to whole blood in a (closed) system where generated C02 could not escape, PCo2 increased and pH was unchanged. Only when C02 was eliminated was the system alkalinized. Similarly, Steichen and Kleinman noted in hypoxic acidotic dogs that administration of 2 mEq/kg of sodium bicarbonate over 3 min when ventilation was unchanged resulted in no net change in arterial pH, although PaCo2 rose from 46 to 61 mmHg. If C02 elimination cannot keep pace with increased C02 generation, administration of bicarbonate during acidemia produces hypercarbia (respiratory acidosis) with little net improvement in pH.
How about this quote from a strong-ion approach to the use of buffers (Crit Care 2004;8:259):
When ventilation is fixed, however, as commonly occurs in mechanically ventilated patients, the effect of sodium bicarbonate may be to lower arterial pH, as was seen in patients ventilated with a lung protective strategy… [in this study-Am J Resp Crit Care Med 2000;161:1149].
But don’t believe me, let’s Get an Expert…
I got to interview John Kellum, MD, master of all things acid-base in the critically ill. You’ll hear more from him in upcoming episodes; this time I asked him the following questions:
- Does giving NaBicarb actually do anything to the patient’s pH if the patient can’t increase their minute ventilation to blow off the generated PaCO2? (Closed System)
- Let’s say you can actually can increase pH with NaBicarb, Is there any clinical advantage to actually doing this in an Anion-Gap Acidosis?
- How about in a patient that received a ton of NS in the ED, should we switch them to a bicarb drip to get SID back in balance?
Even when you Fix the pH with Bicarb, have you done any good in patients with SIG Acidosis?
Advocates of NaBicarb discuss its salutary effects on hemodynamics. However based on the available evidence, there is no reason to think there is any additional effects above those you would see giving hypertonic saline.
Small head-to-head study of NaBicarb and NS showed deleterious effects of the Bicarb (Am J Med. 1989 Jul;87(1):7-14.)
One of the best reviews is by Forsythe and Schmidt in this article (Chest 2000; 117:260–267). Table 1 demonstrating the intracellular effects is particularly relevant.
The other is by Hindman et al. (Anesthesiology 1990;72(6):1064).
If you are going to use it, use it by slow infusion while increasing minute ventilation. Boyd et al. agree and say it better than I can (Curr Opin in Crit Care 2008;14:379).
Severe Acidosis in Trauma Patients
Not fantastic evidence, but in this recent trauma paper (J Trauma 2013;74:45) giving bicarb to severely acidotic patients was associated with increased mortality.
Comments and where they Go…
- If you have a comment about a podcast, put it in the comments of that podcast–more people will see it that way
- If you have an unrelated clinical question, put on the EMCrit Google Plus Community Page.
An Amazing Conference is Coming in June 2013:
Here is a bibliography of the Literature Reviewed for this Episode
 Arieff AI, Leach, W, Park, R, et al. Systemic effects of NaHCO3 in experimental lactic acidosis in dogs. The American journal of physiology. 1982;242: F586-591.
 Bersin RM, Chatterjee, K, Arieff, AI. Metabolic and hemodynamic consequences of sodium bicarbonate administration in patients with heart disease. The American journal of medicine. 1989;87: 7-14.
 Boyd JH, Walley, KR. Is there a role for sodium bicarbonate in treating lactic acidosis from shock? Current opinion in critical care. 2008;14: 379-383.
 Cuhaci B, Lee, J, Ahmed, Z. Sodium bicarbonate controversy in lactic acidosis. Chest. 2000;118: 882-884.
 Dell RB. Acid-base effects of hypertonic sodium bicarbonate solutions: a commentary. The Journal of pediatrics. 1972;80: 681-682.
 Forsythe SM, Schmidt, GA. Sodium bicarbonate for the treatment of lactic acidosis. Chest. 2000;117: 260-267.
 Gehlbach BK, Schmidt, GA. Bench-to-bedside review: treating acid-base abnormalities in the intensive care unit – the role of buffers. Critical care. 2004;8: 259-265.
 Hindman BJ. Sodium bicarbonate in the treatment of subtypes of acute lactic acidosis: physiologic considerations. Anesthesiology. 1990;72: 1064-1076.
 Kallet RH, Jasmer, RM, Luce, JM, et al. The treatment of acidosis in acute lung injury with tris-hydroxymethyl aminomethane (THAM). American journal of respiratory and critical care medicine. 2000;161: 1149-1153.
 Omron EM, Omron, RM. A physicochemical model of crystalloid infusion on acid-base status. Journal of intensive care medicine. 2010;25: 271-280.
 Ostrea EM. The influence of bicarbonate administration on blood pH in a “closed system”: clinical implications. The Journal of pediatrics. 1972;80: 671-680.
 Rhee KH, Toro, LO, McDonald, GG, et al. Carbicarb, sodium bicarbonate, and sodium chloride in hypoxic lactic acidosis. Effect on arterial blood gases, lactate concentrations, hemodynamic variables, and myocardial intracellular pH. Chest. 1993;104: 913-918.
 Steichen JJ, Kleinman, LI. Studies in acid-base balance. I. Effect of alkali therapy in newborn dogs with mechanically fixed ventilation. The Journal of pediatrics. 1977;91: 287-291.
 Wilson RF, Spencer, AR, Tyburski, JG, et al. Bicarbonate therapy in severely acidotic trauma patients increases mortality. The journal of trauma and acute care surgery. 2013;74: 45-50; discussion 50.
Now on to the podcast…
Thomas Scalea is a legend! He is Physician-in-chief at the Shock Trauma Center in Balitmore. He started the EM program at Kings County in 1991. He is also an excellent doctor and a wonderful person. At the 2012 EMCrit Conference, he gave an amazing lecture on the cutting edge techniques they are using at Shock Trauma for intracranial pressure (ICP) management.
For the basics of ICP Management, check out this prior podcast.
Need just the mp3? Right-click here and choose save-as.
Now on to the podcast…
You just read the post: Podcast 95 – Thomas Scalea on Cutting-Edge ICP Management from EMCrit Blog - Emergency Department Critical Care.
I recently got an email from the creators of a new approach to airway management
What these two gentlemen have crafted is a paradigm called the vortex approach. It is best represented by this diagram:
And here are versions with even more information:
I could write about the method, but to do it true justice, it is better to watch this video:
The Shock Trauma Algorithm
Now you folks know I am partial to a modified-version of the Shock Trauma Algorithm for Failed Airway Management. It is bar none the simplest, most effective (and validated) algo I have come across. Or at least it was until I started parsing the Vortex Approach. The reason is that the Vortex Approach encompasses the STC algorithm in a way that is universal to all specialties and settings.
Nicholas and Peter wrote a free ebook about the concept, which is available in a number of formats.
They also have a website set up for the Vortex Approach as well as other projects on their Clinical CrEd Site. The Vortex site also has videos demonstrating the approach in action in both an emergency department and operating theater intubation.
Minh Le Cong did an interview with the two of them on his PHARM podcast site that is definitely worth a listen.
Apps I Liked
I was sent free evaluation copies of 2 IOS applications:
- The IOS version of PressorDex from the EMRA folks. The pocket-book was good; the app is even better.
- An application listing the most important critical care papers and a short summary of their impact. The app is called ICU Trials by Sean Kane. The link goes to the free lite version; if you like it buy the full version.
Now on to the Wee…
My friend Chad Meyers is an ED Intensivist from NYC. He gave this lecture at ALLNYCEM 2012, but the video sucked. He rerecorded it for the EMCritters.
I will be bringing Roger Harris, MD of SMACC and Sydney ICU fame on the show in the very near future to debate this very issue.
Need the audio-only version? Right Click Here and Choose Save-as.
CME is available for this episode
Now on to the Wee…
You just read the post: EMCrit Wee – The Holy Grail of Fluid Resuscitation is just a Tin Cup from EMCrit Blog - Emergency Department Critical Care.
SMACC 2013 was, bar none, the best Critical Care Conference I have ever attended!
I got to meet people like…
Doug Lynch (@thetopend)
Victoria Brazil (@SocraticEM)
and Most Importantly,
to all of the wonderful listeners that introduced themselves–I Love You!
Great Article (CLEVELAND CLINIC JOURNAL OF MEDICINE 2011;78(10):675)
SMACC-Backs are coming…
The Clinical Stuff
- BP Rep Time
- Drip Sheets – See the EHCED drip-sheet project
- Tension Pneumo
- Bind the Pelvis
You just read the post: EMCrit WEE – SMACC 2013 Summary and Learning Points from EMCrit Blog - Emergency Department Critical Care.
Paul Mayo and I seem to have established a tradition of debating each other at the annual Greater NY Hospital Association Critical Care Controversies Conference.
This year, the topic was Should All Intubations be Performed with Video Laryngoscopy?
I think you will enjoy the debate, because we don’t mind attacking our opponent.
If you enjoyed this podcast and the others on the EMCrit site, please consider supporting the show at CME.EMCrit.org.
Need an audio-only version?
Now, on to the debate…
You just read the post: Podcast 94 – Has Video Laryngoscopy Killed the Direct Laryngoscope? from EMCrit Blog - Emergency Department Critical Care.
Cliff Reid adds to the MotR lexicon with Chicken Bombs and Muppet Factors
You just read the post: Mind of the Resuscitationist – Chicken Bombs and Muppet Factors from EMCrit Blog - Emergency Department Critical Care.
As you know, my motto is maximally aggressive care, ALWAYS! Maximally aggressive curative care and maximally aggressive palliative care. I did a podcast episode on critical care palliation a year or so ago.
At this year’s EMCrit Conference, Ashley Shreves gave the ultimate lecture on the topic. Twenty minutes jam-packed with goodness.
Need an Audio-Only version?
Now on to the Vodcast…
You just read the post: Podcast 93 – Critical Care Palliation with Ashley Shreves from EMCrit Blog - Emergency Department Critical Care.
I received a distressed email from a fan who was dismayed that other residents in her program were bashing medical podcasting; this is my response.
What is Tacit Knowledge?
Slide Show on Tacit Knowledge and Wicked Problems
Social Media as a Transmission Tool for Tacit Knowledge
- Social Media and Tacit Knowledge Sharing
- Potentials of Social Media for Tacit Knowledge Sharing – Preliminary Findings
- Conceptual Model for Social Media and Tacit Knowledge
Next horizon is to answer the question of how to solve Wicked Problems and can social media and FOAM help?
What do you think?
You just read the post: EMCrit Wee – Tacit Knowledge and Medical Podcasting from EMCrit Blog - Emergency Department Critical Care.
At the EMCrit 2013 Conference we had a Blast Competition. The BLAST rules are easy:
The winner this year was Salil Bhandari with an incredible presentation on peri-mortem caesarean section.
Here is an article:
Eur J Emerg Med. 2011 Aug;18(4):241-2. doi: 10.1097/MEJ.0b013e328344f2c5. Prehospital resuscitative hysterotomy.
Want to know more about peri-mortem c-section? Check out this insanely good post:
And here is a simulator video:
Now on to the Wee…
You just read the post: EMCrit Conference Blast Winner: Peri-Mortem C-Section from EMCrit Blog - Emergency Department Critical Care.
If you have a comment or question about one of the podcasts, chuck it into the comments section.
But I get a ton of clinical cases and questions by email or the contact form that have not been covered on a podcast yet. I love this–it exposes me to some great cases I would never hear about otherwise. Problem is, up until this point, it has been a 1 on 1 conversation. This is sort of a waste because nobody else benefits except you and me. So in the future, when you have a case or question like this, I would love it if you posted to the Google Plus EMCrit Community page. This allows a few things:
- it allows my answer to be seen by a much larger group of people
- it allows folks smarter than me to chime in as well
- it keeps a record of these case interactions so I can refer people to them in the future
So how do you do it? Easiest way to learn is to watch this video:
Since Peter Pronovost’s landmark study on how a simple checklist can nearly abolish central line infections, checklists have been the darling of the medical literature. But central lines generally are for elective procedures, allowing us the time and patience to run through the list. Can we gain the same safety and cognitive benefits in an adrenaline-laden procedure like intubation? Hell yeah!
It all starts with the EMCrit Intubation Checklist
Here is the wee on the HOp Killers: Hemodynamic Kills, Oxygenation Kills, and pH Kills
- Intubating the Hemodynamically Unstable Patient
- Intubating the Patient at Risk for Critical Hypoxemia
- Intubating the Patient with Metabolic Acidosis
RSI or Awake? · DSI? · RSA? · ICP/Vascular?
- Awake Intubation Lecture
- Awake Intubation Video
- More info on Delayed Sequence Intubation (DSI)
- Rapid Sequence Airway (RSA)
- ICP/Vascular Intubation
Are the peri-intubation medications ready?
What is the plan for unexpected difficult or failed airway?
- I use a modified version of the Shock Trauma Center Failed Airway Algorithm
- Cook Gas ILA (My preferred Extraglottic Airway)
Can the cricothyroid membrane be palpated?
What is the plan for post-intubation sedation?
- A bad sedation package traps your patient in a nightmare
Is the patient positioned adequately?from AirwayCam Site
Would the patient benefit from pre-intubation NGT?
Skills of Intubation
Post Intubation Management
Other People’s Intubation Checklists for Inspiration
Shoulders of giants and such
Did you like this post? Then tweet the hell out of it
Finally… The EMCrit Call/Response VodCast is done. Podcast 92: emcrit.org/podcasts/emcri… Now tear it apart and make it better!
— Scott Weingart (@emcrit) February 5, 2013
Need the Audio only version
Now, on to the podcast…
A listener, Brian Katan, wrote to suggest adding ondansetron to the awake intubation procedure. Now this is interesting, because I don’t want the patient to vomit from ramming things into the back of her throat, but the mechanism is not nausea–it is the gag reflex. So, the question is: does ondansetron affect the gag reflex? Turns out it does…
Evaluation of the efficacy of oral ondansetron on gag reflex in soft palate and palatine tonsil areas
So now, ondansetron 4 mg IVP has been added to the airway checklist. Thanks Brian!
My friend Chris Bond runs a blog called SOCMOB (see below for an explanation).
Like all Canadians, Chris likes to have a nice meal, drink a glass of wine, and then go to the parking lot, break a beer bottle and stab people with it. In Canada, they call this bottling. When not bottling, Chris posts on emergency medicine topics; he put together a video on how to build a cheap and dirty cric trainer. Take a look…
Here is the original SOBMOB post.
The trainer is based on this article: (Anaesthesia 2004; 59:1012–15).
A recent letter to the editor takes the model even further: (Anaesthesia, 2009, 64, pages 687–697).
Chris is also the creator of the, “Diagnosis Wenckebach” video:
What is SOCMOB?
SOCMOB = Standing on the corner, minding my own business. For any of you who work in emergency departments, you’ve likely heard this history before. Most likely the presenting complaint was trauma
The SOCMOB Algorithm
You just read the post: How to Build the Ultimate Cricothyrotomy Trainer with Chris Bond from EMCrit Blog - Emergency Department Critical Care.
The American Society of Anesthesia just released their new difficult airway guidelines. Of course, I’ll be reviewing them on the Practical Evidence Podcast.
Those guidelines are a bit too involved for Emergency Medicine and Intensive Care. For us, I recommend the Shock Trauma Algorithm. I modified it somewhat to fit my own prejudices (as usual).
The approach was validated in this study:
[Stephens CT, Kahntroff S, Dutton RP. The success of emergency endotracheal intubation in trauma patients: a 10-year experience at a major adult trauma referral center. Anesth Analg. 2009 Sep;109(3):866-72.]
Couldn’t be easier to remember and use.
This podcast was originally posted on the Practical Evidence Podcast
The 2012 SSC Guidelines were just published and I saw the preview in Puerto Rico
2012 Surviving Sepsis Campaign Guidelines
See the Guidelines at (CCM 2013;41(2):580)
Diagnosis of Sepsis
Diagnosis of Severe Sepsis
The New Bundles
A. Initial Resuscitation
- Protocolized, quantitative resuscitation of patients with sepsis- induced tissue hypoperfusion (defined in this document as hypotension persisting after initial fluid challenge or blood lactate concentration ? 4 mmol/L). Goals during the first 6 hrs of resuscitation:
- Central venous pressure 8–12 mm Hg
- Mean arterial pressure (MAP) ? 65 mm Hg
- Urine output ? 0.5 mL/kg/hr
- Central venous (superior vena cava) or mixed venous oxygen saturation 70% or 65%, respectively (grade 1C).
- In patients with elevated lactate levels targeting resuscitation to normalize lactate (grade 2C).
B. Screening for Sepsis and Performance Improvement
- Routine screening of potentially infected seriously ill patients for severe sepsis to allow earlier implementation of therapy (grade 1C).
- Hospital–based performance improvement efforts in severe sepsis (UG).
- Cultures as clinically appropriate before antimicrobial therapy if no significant delay (> 45 mins) in the start of antimicrobial(s) (grade 1C). At least 2 sets of blood cultures (both aerobic and anaerobic bottles) be obtained before antimicrobial therapy with at least 1 drawn percutaneously and 1 drawn through each vascular access device, unless the device was recently (<48 hrs) inserted (grade 1C).
- Use of the 1,3 beta-D-glucan assay (grade 2B), mannan and anti-mannan antibody assays (2C), if available and invasive candidiasis is in differential diagnosis of cause of infection.
- Imaging studies performed promptly to confirm a potential source of infection (UG).
D. Antimicrobial Therapy
- Administration of effective intravenous antimicrobials within the first hour of recognition of septic shock (grade 1B) and severe sepsis without septic shock (grade 1C) as the goal of therapy.
- Initial empiric anti-infective therapy of one or more drugs that have activity against all likely pathogens (bacterial and/or fungal or viral) and that penetrate in adequate concentrations into tissues presumed to be the source of sepsis (grade 1B). Antimicrobial regimen should be reassessed daily for potential deescalation (grade 1B).
- Use of low procalcitonin levels or similar biomarkers to assist the clinician in the discontinuation of empiric antibiotics in patients who initially appeared septic, but have no subsequent evidence of infection (grade 2C).
- Combination empirical therapy for neutropenic patients with severe sepsis (grade 2B) and for patients with difficult-to-treat, multidrugresistant bacterial pathogens such as Acinetobacter and Pseudomonas spp. (grade 2B). For patients with severe infections associated with respiratory failure and septic shock, combination therapy with an extended spectrum beta-lactam and either an aminoglycoside or a fluoroquinolone is for P. aeruginosa bacteremia (grade 2B). A combination of beta-lactam and macrolide for patients with septic shock from bacteremic Streptococcus pneumoniae infections (grade 2B). Empiric combination therapy should not be administered for more than 3–5 days. De-escalation to the most appropriate single therapy should be performed as soon as the susceptibility profile is known (grade 2B).
- Duration of therapy typically 7–10 days; longer courses may be appropriate in patients who have a slow clinical response, undrainable foci of infection, bacteremia with S. aureus; some fungal and viral infections or immunologic deficiencies, including neutropenia (grade 2C).
- Antiviral therapy initiated as early as possible in patients with severe sepsis or septic shock of viral origin (grade 2C).
- Antimicrobial agents should not be used in patients with severe inflammatory states determined to be of noninfectious cause (UG).
E. Source Control
- A specific anatomical diagnosis of infection requiring consideration for emergent source control be sought and diagnosed or excluded as rapidly as possible, and intervention be undertaken for source control within the first 12 hr after the diagnosis is made, if feasible (grade 1C).
- When infected peripancreatic necrosis is identified as a potential source of infection, definitive intervention is best delayed until adequate demarcation of viable and nonviable tissues has occurred (grade 2B).
- When source control in a severely septic patient is required, the effective intervention associated with the least physiologic insult should be used (eg, percutaneous rather than surgical drainage of an abscess) (UG).
- If intravascular access devices are a possible source of severe sepsis or septic shock, they should be removed promptly after other vascular access has been established (UG).
F. Infection Prevention
- Selective oral decontamination and selective digestive decontamination should be introduced and investigated as a method to reduce the incidence of ventilator-associated pneumonia; This infection control measure can then be instituted in health care settings and regions where this methodology is found to be effective (grade 2B).
- Oral chlorhexidine gluconate be used as a form of oropharyngeal decontamination to reduce the risk of ventilator-associated pneumonia in ICU patients with severe sepsis (grade 2B).
G. Fluid Therapy of Severe Sepsis
- Crystalloids as the initial fluid of choice in the resuscitation of severe sepsis and septic shock (grade 1B).
- Against the use of hydroxyethyl starches for fluid resuscitation of severe sepsis and septic shock (grade 1B).
- Albumin in the fluid resuscitation of severe sepsis and septic shock when patients require substantial amounts of crystalloids (grade 2C).
- Initial fluid challenge in patients with sepsis-induced tissue hypoperfusion with suspicion of hypovolemia to achieve a minimum of 30 mL/kg of crystalloids (a portion of this may be albumin equivalent). More rapid administration and greater amounts of fluid may be needed in some patients (grade 1C).
- Fluid challenge technique be applied wherein fluid administration is continued as long as there is hemodynamic improvement either based on dynamic (eg, change in pulse pressure, stroke volume variation) or static (eg, arterial pressure, heart rate) variables (UG).
- Vasopressor therapy initially to target a mean arterial pressure (MAP) of 65 mm Hg (grade 1C).
- Norepinephrine as the first choice vasopressor (grade 1B).
- Epinephrine (added to and potentially substituted for norepinephrine) when an additional agent is needed to maintain adequate blood pressure (grade 2B).
- Vasopressin 0.03 units/minute can be added to norepinephrine (NE) with intent of either raising MAP or decreasing NE dosage (UG).
- Low dose vasopressin is not recommended as the single initial vasopressor for treatment of sepsis-induced hypotension and vasopressin doses higher than 0.03–0.04 units/minute should be reserved for salvage therapy (failure to achieve adequate MAP with other vasopressor agents) (UG).
- Dopamine as an alternative vasopressor agent to norepinephrine only in highly selected patients (eg, patients with low risk of tachyarrhythmias and absolute or relative bradycardia) (grade 2C).
- Phenylephrine is not recommended in the treatment of septic shock except in circumstances where (a) norepinephrine is associated with serious arrhythmias, (b) cardiac output is known to be high and blood pressure persistently low or (c) as salvage therapy when combined inotrope/vasopressor drugs and low dose vasopressin have failed to achieve MAP target (grade 1C).
- Low-dose dopamine should not be used for renal protection (grade 1A).
- All patients requiring vasopressors have an arterial catheter placed as soon as practical if resources are available (UG).
I. Inotropic Therapy
- A trial of dobutamine infusion up to 20 micrograms/kg/min be administered or added to vasopressor (if in use) in the presence of (a) myocardial dysfunction as suggested by elevated cardiac filling pressures and low cardiac output, or (b) ongoing signs of hypoperfusion, despite achieving adequate intravascular volume and adequate MAP (grade 1C).
- Not using a strategy to increase cardiac index to predetermined supranormal levels (grade 1B).
- Not using intravenous hydrocortisone to treat adult septic shock patients if adequate fluid resuscitation and vasopressor therapy are able to restore hemodynamic stability (see goals for Initial Resuscitation). In case this is not achievable, we suggest intravenous hydrocortisone alone at a dose of 200 mg per day (grade 2C).
- Not using the ACTH stimulation test to identify adults with septic shock who should receive hydrocortisone (grade 2B).
- In treated patients hydrocortisone tapered when vasopressors are no longer required (grade 2D).
- Corticosteroids not be administered for the treatment of sepsis in the absence of shock (grade 1D).
- When hydrocortisone is given, use continuous flow (grade 2D).
K. Blood Product Administration
- Once tissue hypoperfusion has resolved and in the absence of extenuating circumstances, such as myocardial ischemia, severe hypoxemia, acute hemorrhage, or ischemic heart disease, we recommend that red blood cell transfusion occur only when hemoglobin concentration decreases to <7.0 g/dL to target a hemoglobin concentration of 7.0 –9.0 g/dL in adults (grade 1B).
- Not using erythropoietin as a specific treatment of anemia associated with severe sepsis (grade 1B).
- Fresh frozen plasma not be used to correct laboratory clotting abnormalities in the absence of bleeding or planned invasive procedures (grade 2D).
- Not using antithrombin for the treatment of severe sepsis and septic shock (grade 1B).
- In patients with severe sepsis, administer platelets prophylactically when counts are <10,000/mm3 (10 x 109/L) in the absence of apparent bleeding. We suggest prophylactic platelet transfusion when counts are < 20,000/mm3 (20 x 109/L) if the patient has a significant risk of bleeding. Higher platelet counts (?50,000/mm3 [50 x 109/L]) are advised for active bleeding, surgery, or invasive procedures (grade 2D).
- Not using intravenous immunoglobulins in adult patients with severe sepsis or septic shock (grade 2B).
- Not using intravenous selenium for the treatment of severe sepsis (grade 2C).
N. History of Recommendations Regarding Use of Recombinant Activated Protein C (rhAPC)
A history of the evolution of SSC recommendations as to rhAPC (no longer available) is provided.
O. Mechanical Ventilation of Sepsis-Induced Acute Respiratory Distress Syndrome (ARDS)
- Target a tidal volume of 6 mL/kg predicted body weight in patients with sepsis-induced ARDS (grade 1A vs. 12 mL/kg).
- Plateau pressures be measured in patients with ARDS and initial upper limit goal for plateau pressures in a passively inflated lung be ?30 cm H2O (grade 1B).
- Positive end-expiratory pressure (PEEP) be applied to avoid alveolar collapse at end expiration (atelectotrauma) (grade 1B).
- Strategies based on higher rather than lower levels of PEEP be used for patients with sepsis- induced moderate or severe ARDS (grade 2C).
- Recruitment maneuvers be used in sepsis patients with severe refractory hypoxemia (grade 2C).
- Prone positioning be used in sepsis-induced ARDS patients with a Pao2/Fio2 ratio ? 100 mm Hg in facilities that have experience with such practices (grade 2B).
- That mechanically ventilated sepsis patients be maintained with the head of the bed elevated to 30–45 degrees to limit aspiration risk and to prevent the development of ventilator-associated pneumonia (grade 1B).
- That noninvasive mask ventilation (NIV) be used in that minority of sepsis-induced ARDS patients in whom the benefits of NIV have been carefully considered and are thought to outweigh the risks (grade 2B).
- That a weaning protocol be in place and that mechanically ventilated patients with severe sepsis undergo spontaneous breathing trials regularly to evaluate the ability to discontinue mechanical ventilation when they satisfy the following criteria: a) arousable; b) hemodynamically stable (without vasopressor agents); c) no new potentially serious conditions; d) low ventilatory and end-expiratory pressure requirements; and e) low Fio2 requirements which can be met safely delivered with a face mask or nasal cannula. If the spontaneous breathing trial is successful, consideration should be given for extubation (grade 1A).
- Against the routine use of the pulmonary artery catheter for patients with sepsis-induced ARDS (grade 1A).
- A conservative rather than liberal fluid strategy for patients with established sepsis-induced ARDS who do not have evidence of tissue hypoperfusion (grade 1C).
- In the absence of specific indications such as bronchospasm, not using beta 2-agonists for treatment of sepsis-induced ARDS (grade 1B).
P. Sedation, Analgesia, and Neuromuscular Blockade in Sepsis
- Continuous or intermittent sedation be minimized in mechanically ventilated sepsis patients, targeting specific titration endpoints (grade 1B).
- Neuromuscular blocking agents (NMBAs) be avoided if possible in the septic patient without ARDS due to the risk of prolonged neuromuscular blockade following discontinuation. If NMBAs must be maintained, either intermittent bolus as required or continuous infusion with train-of-four monitoring of the depth of blockade should be used (grade 1C).
- A short course of NMBA of not greater than 48 hours for patients with early sepsis-induced ARDS and a Pao2/Fio2 < 150 mm Hg (grade 2C).
Q. Glucose Control
- A protocolized approach to blood glucose management in ICU patients with severe sepsis commencing insulin dosing when 2 consecutive blood glucose levels are >180 mg/dL. This protocolized approach should target an upper blood glucose ?180 mg/dL rather than an upper target blood glucose ? 110 mg/dL (grade 1A).
- Blood glucose values be monitored every 1–2 hrs until glucose values and insulin infusion rates are stable and then every 4 hrs thereafter (grade 1C).
- Glucose levels obtained with point-of-care testing of capillary blood be interpreted with caution, as such measurements may not accurately estimate arterial blood or plasma glucose values (UG).
R. Renal Replacement Therapy
- Continuous renal replacement therapies and intermittent hemodialysis are equivalent in patients with severe sepsis and acute renal failure (grade 2B).
- Use continuous therapies to facilitate management of fluid balance in hemodynamically unstable septic patients (grade 2D).
S. Bicarbonate Therapy
- Not using sodium bicarbonate therapy for the purpose of improving hemodynamics or reducing vasopressor requirements in patients with hypoperfusion-induced lactic acidemia with pH ?7.15 (grade 2B).
T. Deep Vein Thrombosis Prophylaxis
- Patients with severe sepsis receive daily pharmacoprophylaxis against venous thromboembolism (VTE) (grade 1B). This should be accomplished with daily subcutaneous low-molecular weight heparin (LMWH) (grade 1B versus twice daily UFH, grade 2C versus three times daily UFH). If creatinine clearance is <30 mL/min, use dalteparin (grade 1A) or another form of LMWH that has a low degree of renal metabolism (grade 2C) or UFH (grade 1A).
- Patients with severe sepsis be treated with a combination of pharmacologic therapy and intermittent pneumatic compression devices whenever possible (grade 2C).
- Septic patients who have a contraindication for heparin use (eg, thrombocytopenia, severe coagulopathy, active bleeding, recent intracerebral hemorrhage) not receive pharmacoprophylaxis (grade 1B), but receive mechanical prophylactic treatment, such as graduated compression stockings or intermittent compression devices (grade 2C), unless contraindicated. When the risk decreases start pharmacoprophylaxis (grade 2C).
U. Stress Ulcer Prophylaxis
- Stress ulcer prophylaxis using H2 blocker or proton pump inhibitor be given to patients with severe sepsis/septic shock who have bleeding risk factors (grade 1B).
- When stress ulcer prophylaxis is used, proton pump inhibitors rather than H2RA (grade 2D)
- Patients without risk factors do not receive prophylaxis (grade 2B).
- Administer oral or enteral (if necessary) feedings, as tolerated, rather than either complete fasting or provision of only intravenous glucose within the first 48 hours after a diagnosis of severe sepsis/septic shock (grade 2C).
- Avoid mandatory full caloric feeding in the first week but rather suggest low dose feeding (eg, up to 500 calories per day), advancing only as tolerated (grade 2B).
- Use intravenous glucose and enteral nutrition rather than total parenteral nutrition (TPN) alone or parenteral nutrition in conjunction with enteral feeding in the first 7 days after a diagnosis of severe sepsis/septic shock (grade 2B).
- Use nutrition with no specific immunomodulating supplementation rather than nutrition providing specific immunomodulating supplementation in patients with severe sepsis (grade 2C).
W. Setting Goals of Care
- Discuss goals of care and prognosis with patients and families (grade 1B).
- Incorporate goals of care into treatment and end-of-life care planning, utilizing palliative care principles where appropriate (grade 1B).
- Address goals of care as early as feasible, but no later than within 72 hours of ICU admission (grade 2C).
Lower Dp/Dt and Blood Pressure
Control Pain with fentanyl
Control Heart Rate/Inotropy with esmolol
See the esmolol drip sheet (YOU MUST CHECK ALL NUMBERS WITH YOUR OWN PHARMACY)
Control Blood Pressure
With in order of preference: clevidipine, nicardipine, nitroprusside, nitroglycerin
What about if the patient can’t get beta-blockers?
What about labetalol?
Why is the Patient’s Blood Pressure Low?
Andy Neill thankfully addressed my erroneous assumption that MIs in Dissection would only be right coronary infarctions
and check out this article as well (J Emerg Trauma Shock 2011;4:273-278)
Site of Blood Pressure Measurement
Rupture of the Aorta
Do a high-icp/vascular intubation (More to come on this)
Monday’s show will be on aortic dissection. The show two weeks from now will be a unveiling and discussion of an intubation checklist I have been working on for the past couple of months. I wanted to send it out early to get comments and see if you folks can find anything that can be corrected.
It is a call/response checklist. The idea is only the top half of page 1 would actually be used during the intubation and the checklist should be folded in half to reduce cognitive load. It has been inspired by the incredible work of the safer intubation project and emupdate’s EDICT sheet.
Let me know your thoughts…
Cliff Reid is the prototypical resuscitationist; he rocks! He has discussed his philosophies on previous episodes:
And of course, Cliff’s blog, resus.me, is some of the best retrieval and resuscitation information around.
I brought Cliff up to speak in my Critical Care Track at the 2012 Essentials of Emergency Medicine. Mel Herbert was kind enough to give me permission to post the lecture here. I think you’ll love it as much as I do.
Now, on to the podcast…
Thanks for Listening and Supporting EMCrit!
Got this email from a listener:
Merry Christmas. So here I am sitting here sipping my coffee on a quiet Christmas morning and I’m writing YOU a complete stranger, a Christmas email. Well not a complete stranger but you can tell how obsessed I am with airway stuff when I’m writing this on Christmas morning! Besides this is one of the few quiet moments I’ve had in many months to collects some thoughts before the troops wake up. I started writing you this email a while back but some how erased it and haven’t gotten back to it. In any case kudos to you for keeping up the stellar podcasts. I really like how you have aligned yourselves with other outstanding minds in our field and created a more or less free forum to put out some incredible educational points for Crit Care and ER medicine.
One of my pet peeves is getting people to really understand the real benefits and proper technique of VL. I’ve seen and heard some of your stuff on this but I thought I’d chime in with a few of my tips and tricks that I teach on an airway course we give here in the Middle East called AIME. Originally designed and created by Adam Law an anaesthetist that hails from Canuck land. Adam has shared with me some invaluable tips in using the VL which just these subtle things can make this technique so easy anyone can do it first or second try.
One of the first things people need to understand is DL is LINE OF SIGHT. We have to have a STRAIGHT shot at the cords to be able to see and put the tube in. That’s why we align the oral and laryngeal axes. And that’s why we need to do the ears to sternal notch. WE CAN’t SEE AROUND CORNERS WE SEE IN STRAIGHT LINES. This is what the standard straight bougie was designed to help us with. So it drives me crazy when I’ve heard some people talk about using a regular bougie with VL. Yes it’s flexible but standard bougies don’t hold a bend, they’re meant to follow along the line of sight and be able to help us with those CL grade 2 and 3 views while doing DIRECT LARYNGOSCOPY (and yes I still teach that you should use it on grade I views to get the hang of it but really it’s for the later). The other thing that people must understand that it isn’t a “blind mans cane” for grade 4 views and shouldn’t be used as such. If all you see is tongue you don’t blindly kep shoving the bougie up and down hunting for clicks (sorry I know this is obvious to you but I’m just on a bit of a rant) . The last point is STANDARD BOUGIES AREN’T MEANT OR DESIGNED FOR VIDEO LARYNGOSCOPY. Ok you could argue that for a King vision or Pentax AWS a bougie is great to guide down the channel but that’s not what a lot of VL’s have and so a bougie is not the tool to use.
So ultimately VL is to look AROUND the corner and therefore we don’t have to just “slightly” extend the neck in trauma; something we’re all guilty of (just getting “that little bit more extension” to get the tube in). Alternatively someone stabilizes the neck while we do the Herculean lift to squish the tongue through the submandibular space to get our line of sight. So I think it was either Minh or Cliff who said that they really don’t use VL in the field yet, I really think they need to begin to see the benefits of this.
Almost all video laryngoscope blades are much more curved than standard mac blades. WHY? AGAIN It’s because they’re designed to LOOK AROUND THE CORNER! The only bougie that will help you with this (if you want to use a bougie) is I think the pocket bougie from Bomimed. Now I haven’t used the pocket bougie but from what I’ve seen on Jim Ducanto’s video it can be bent or is bent to go AROUND THE CORNER. This is the only bougie that I’ve seen that does this. Using a STANDARD bougie may work if you’re using a VL to do Direct laryngoscopy but again the blade wasn’t designed to help you to see directly, the flatter, less curved mac blade was. But if you load an ETT with a properly formed stylet in almost all cases you really don’t need a curved bougie with VL and especially NOT a straight bougie. I actually think we do our students a disservice by watching them do a DIRECT laryngoscopy while we watch on the Glidescope screen because the blade is so curved that the mechanics and placement of the VL blade tip in the Vallecula like you should with a regular mac blade are VERY different. Because a VL blade is so curved if you put it in the vallecula and pull in the direction of the handle like we teach with a regular mac blade, they are not pulling in the same direction as with a standard mac blade and I think that in a difficult scenario will at best won’t make things easier and at worse might injure the perilaryngeal structures. People should teach DL with a standard blade NOT a VL blade. Use the right tool for the application it was designed for.
The way I teach VL is as follows.
First and foremost you must use an introducer and that introducer needs to be bent exactly in the shape of the VL blade
Because both blade and tube are so curved some times it’s difficult to slide them in straight. I often tell the students to scissor their right index finger and thumb on upper and lower incisors respectively to open the mouth. Then with the blade handle pointed to 9 o clock, insert the blade. When the blade is towards the back of the tongue, rotate the handle to 12 o’clock. Now look at the screen as you slowly advance…
I agree with your “mouth, screen, mouth, screen” reminder to prevent injuries with blade and tube insertion.
I don’t tell students to get the blade tip in the vallecula like with DL, it just makes VL harder because then end up pulling the larynx to anterior which just compounds the problems of passing the tube. As you and I both know seeing the cords isn’t the problem, getting the tube in is. When students in their excitement of seeing that grade I view (often for the very first time!!) love to keep this view at the expense of making getting the tube in very difficult.
What I teach is a grade II view is all you need and is actually what you want. Once you get this, similar to inserting the blade you insert the tube with the long axis pointing to 3 o’clock and watch the tip go into the mouth and past the back of the tongue. Now look at the screen and keep advancing slowly. Once you can see a hint of plastic on the screen, rotate the tube to 12 o’clock and presto, the tube tip is right at the cords.
The last hold up is when they try and ram the tube and introducer in. Invariably the tube and introducer gets rammed into the anterior larynx. So the student needs to bring the tube tip to the cords and maybe just a little past. Have someone hold the introducer and continue to slide the tube off and down. If it gets hung up on the anterior larynx this is where the student can slowly twist the tube 90-180 degrees to pass the tube. Even watching Dr. Ducanto push the pocket bougie in with it’s big bend he gets hung up on his video and has to do the multiple twists with the bougie to get it to pass down the trachea.
So that’s my Christmas rant. I feel much better. Have a good one.
Harold, Great comments/teaching tips. I would say that we need to make a clear separation between the indirect vision video blades (Glidescope, CMAC D, etc.) and the standard/displacing blade shapes (Standard CMAC). In the latter, a standard bougie works just fine; for the former the pocket bougie seems to be the best thing out there.
let Harold and I know what you think
We have hit the 10,000 patient mark in the NYC STOP Sepsis collaborative. Here are some of the lessons learned…
Want to See the Protocols?
- Let nurses handle recognition
- Send lots of lactates
- Lactate turn-around 30 minutes or get Point-of-Care
- Run the lactates on a blood gas machine
- Make lactate >=4 a panic value
- Prompt palliative vs. curative
- Non-invasive protocols have evidence and seem to be working
Want to See the Protocols?
Early appropriate antibiotics
- Empiric Abx Guidelines
- First dose of those antibiotics in the ED
- Simultaneous Infusions
- Safe Intubation
- Echo Assessment of Cardiac Output
- IVC ultrasound (Also check out the Stone Debate)
- If empiric fluid-loading, give 4-6 liters
- Do a sterile neck line or a non-sterile femoral (which should be yanked and replaced as soon as the patient gets upstairs)
- Norepi should be your 1st pressor choice
Check Your Work
- Mandate repeat lactates
More Sepsis Resources
- Manny Rivers on Early Goal Directed Therapy
- A tirade on Sepsis Care in the ED (And additional follow-up) Back then there was no Non-Invasive Path
- That was until Alan Jones published his lactate clearance study
- Find a ton of evidence and other good stuff on the EMCrit Severe Sepsis Deep Dive Pages
The Proposed NQF Measure
Please contact the folks in your hospital that will be voting on the measure
On a Side Note…
EMCrit just broke the 3 Million Downloads mark. Yeah!!!!
Like this post? Then tweet the hell out of it
Lessons learned from 10,000 patients with severe sepsis on EMCrit Podcast 89: emcrit.org/podcasts/lesso…
— Scott Weingart (@emcrit) December 26, 2012
You just read the post: Podcast 89 – Lessons from the STOP Sepsis Collaborative from EMCrit Blog - Emergency Department Critical Care.
A premed asked what literature should one read to develop the mindset and tiger’s eye of a resuscitationist. Knowing when to consult my betters, I threw the question to @precordialthump. And Nickson responded thusly:
These days less and less is learnt from books… however there are some books mentioned in what follows.
Learn about Osler – the ultimate role model for how to succeed as human being and where all good medicine begins:
Read “Blood of Strangers” by Frank Huyler – the best tales from the ER by a great writer
Check out these talks:
2012/10/joe-lex-an-old-fogey- speaks-45-years-on-the-front- lines/
2010/04/peter-rosen- beginnings-of-emergency- medicine/
Read anything by croskerry on cognitive errors such as http://1.usa.gov/xPfmhA
Read LITFL :
Oh, and listen to EMCrit too!
Lots of martial arts, stoic and eastern philospohy, military works, and mountaineering/ survival books have obvious parallels to what we do (at least to some of us).
I would add that reading Sherlock Holmes would probably serve you well as well. This BMJ article summarizes why…
White coats and fingerprints: diagnostic reasoning in medicine and investigative methods of fictional detectives
The MOPETT Trial took sub-massive PE patients and randomized them to half-dose tPA vs. standard care. No bleeds in either group. 41% ARR of pulmonary hypertension at 28 months.
Study Description from the Author
Does this change your game?
- Latency of Pulse Oximetry Signal with use of Digitial Probes Associated with Inappropriate Extubation (J Emerg Med 2012;42(4):424)
- Latency and loss of pulse oximetry signal with the use of digital probes during prehospital rapid-sequence intubation. (Prehosp Emerg Care. 2011 Jan-Mar;15(1):18-22.)
- Rate of decline in oxygen saturation at various pulse oximetry values with prehospital rapid sequence intubation. (Prehosp Emerg Care. 2008 Jan-Mar;12(1):46-51.)
Dan Davis at his best:
Did you like this episode? Then tweet the hell out of it…
Now on to the Podcast…
You just read the post: EMCrit Podcast 88 – Oxygen Physiology with Daniel Davis from EMCrit Blog - Emergency Department Critical Care.