Maximally Aggressive Care, Everywhere
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George Edwards

Discussion  - 
 
Hi,

I'm currently in the military and have a question about Fentanyl and it effects on mental status of a patient with combat wounds. About half of the medics I work with believe that it effects the mental status just like morphine would, and the other half believe that fentanyl has no effects on the patient mental status.

Thank you for any information
1
Jordan Schooler's profile photodon zweig's profile photo
2 comments
 
Could also cause euphoria

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Brandon Hill

Discussion  - 
 
Looking for a good procedural and/or airway course to send our physicians to. Which ones give you the most bang for your buck? I am aware of Levitan's airway course. 
1
EMCrit's profile photo
EMCrit
 
rich's cadaver course is the one
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Jason X

Discussion  - 
 
My question is about push-dose epinephrine in critically ill asthma exacerbation patients. I am looking for literature regarding this. I have seen the recommendation on the EMCrit site for push dose pressors (http://emcrit.org/podcasts/bolus-dose-pressors/) and the comment listed in the comments section that it is "great for asthma."

I have also heard talks on EMRAP describing the "dirty Epi drip" and I have seen the webpage referencing push dose Epi for anaphylaxis (http://circ.ahajournals.org/content/112/24_suppl/IV-143).

But do you know of any literature supporting push dose Epi specifically for asthma? 
1
Jordan Schooler's profile photo
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DSI Extension and Poor's man BiPAP

Hi Guys !

I had an interesting case 1 week ago, and a lot of questions ;-) !

I got a call from the paramedics for a 34 years old male who jumped from a 4th floor on concrete because he saw a "ghost" while on amphetamine.
When the guy arrive, the scene is quite surreal. He is in a wild adrenergic toxidrome, with complex facial fracture screaming : #pain, #needhelp, #f*ckyoudoc
There is 4 paramedics trying to restraint him, but he is sitting down spitting blood on everyone..
He was given a dose of 5mg IM of midazolam on arrival with no effect
It was impossible to get any vitals
I wanted to take control of the situation quickly, it was obvious that this guy needed intubation but i didn't want to rush things

So i gave him 1mg/kg of ketamine and 2 subsequent boluses of 0.5mg/kg
He became fully dissociated so i was able to do my bedside ultrasound assessment and make sure there was no pneumo/hemothorax/free fluid/tamponnade.
I put him on NRB and Nasal Canula 15L and got a sat of around 95%
I wasn't fully satisfied of the sat at that point so i put the peep valve on the BVM and it climbed to 99%
I then gave him a full dose of roc and intubated him without any problems

So here's my thoughts and questions

1) Do you think the concept of DSI would apply not only to optimise the preoxygenation but also to potentially optimise preload or detect a pneumothorax before intubation ?. Have you ever use it in trauma ? It was my first experience of DSI in trauma and everyone were amazed of how fast we gained control of the chaotic resus.

2) The respiratory therapist were once again completely against the "Poor's man CPAP thing" . They feared the patient would "suffocate"
Tell me if i'm wrong, but i think it's true that there is no flow of air on a BVM if you don't squeeze. So it implied that the patient have to initiate a breath to trigger the valve to open. Is it possible for a very weak patient to be unable to trigger the valve ? Is the nasal canula helping to trigger the valve ?

3) Finally, i am not sure why we don't put a PEEP valve on every single intubation ?. From Scott article, you first look if the sat is below 95% with 100% FiO2 to see if there is a shunt physiology,. But considering the patient is sick and not taking full vital capacity breath, wouldn't PEEP be helpful to fully recruit the patient even if his sat is 95% ?
Could we prolong the time to desaturation by driving the PaO2 further up with peep even on patient sating at 100% ?

Sorry for the lenght, thanks for your thoughs ;-)

Fred




4
EMCrit's profile photoFrédéric Lemaire's profile photo
2 comments
 
+EMCrit Thx for your input ! I reread your DSI article and found you used it in a couple of case for the placement NG tube in upper GI bleed. So i get that DSI is not solely for preoxygenation, but do you have any personnal experience of DSI in trauma as in my case ? 
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Yogesh Apte

Discussion  - 
1
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Andrew Haynes

Discussion  - 
 
Hi all,

Open forum question about a case we had in our ED the other day.

32y male attends 24 hours after falling while intoxicated and sustaining a right sided chest injury. Progressive increasing breathing difficulty since then. Arrives in triage with SpO2 of 86% on air and brought to resus.

No other medical history or medication of relevance.

Chest US shows a lung point in the right apex and CXR shows a significant pneumothorax, almost all of which was apical.

The consultant running ED directed for a seldinger chest drain to be placed, which was attempted in the standard space by myself. The problem was that at the 5th IC space there was no air gap between the plura, as the pneumothorax was all in the apex. On US in the 5th IC space you could see good pleural sliding. Up in the axilla and on the anterior chest wall at the 2nd/3rd space the pneumothorax was evident.

Further discussion with the ED consultant at which point I suggested doing a surgical (blunt) drain that could be placed without needing to be able to aspirate air via needle, but was told instead to place a seldinger drain in the 3rd IC space mid-axil line. Now this seemed like a bad idea to me given the proximity to various things that you can hit... This was further attempted with direct US visualisation of the needle (since it made me feel better!) with the same problem - the air gap between the pleural was tiny and you could only aspirate 1-2ml of air via the needle before it stopped (presumably due to visceral pleura on the needle tip). Both myself (PGY5) and the other resident (PGY8?) weren't happy to wire through this needle when we couldn't aspirate air to check placement.

Further discussion with the ED consultant and we ended up doing a simple needle aspiration in the 2nd IC space anteriorly (which worked fine) and leaving the surgical team to place whatever drain they felt like!

To my mind it seemed like by far the best option would have been to bail out when we couldn't place the fist seldinger drain and just place a conventional drain where you can confirm with your finger that it isn't going into lung tissue, but I might be missing something. Any comment greatly appreciated!


1
1
EMCrit's profile photoAndrew Haynes's profile photo
3 comments
 
Thanks for the replies. 2nd ICS anterior sounds generally good although I can imagine everyone in my unit getting totally freaked out by the non-standard placement. I like the idea of the "semi-open" approach since you end up with the acceptable looking seldinger in the end.

I should have mentioned that the CT showed a significant amount of anterior air that you couldn't see on plain film due to projection. 
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We are currently using phillips intellivue MP70 monitors in critical care. A coworker pointed out that we are able to change the "cal factor" number when using art lines. I scoured the internet and couldn't find much information. Does anyone know what this means? and when/why would we want to change the value?   Thanks!
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Jennifer Leckie's profile photo
 
The "cal factor" is the calibration factor. You change it when the transducer type you're using doesn't match the default. For instance, when my complicated high-risk dual valve surgery comes back from the OR they use a different cal factor than the one that comes up from cath lab. Just look up the number in the manual/bedside book/website to see which one you're supposed to be using. 
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Steven York

Discussion  - 
 
Hi all,

I am a flight medic on board with a fantastic flight program and there is a big question going around in regards to Beta Blocker use in STEMI setting. One of the questions I had posed was why not use nicardipine instead of metoprolol in the AMI setting since nicardipine not only controls rate but had coronary artery dilations, vs metoprolol that really only gives rate control. Ive only found a few articles that touch on and allude to this topic, but nothing that I think would apply in the flight/prehospital environment.  I have had some pretty bad experiences with metoprolol which is why I am inquiring about the nicardipine instead.
I am a long time listener of the podcast and your podcasts have been pivotal in pushing me from being a routine ground medic to a critical care flight medic, and I truly can't thank you enough for your work!
-Steve
1
Vince DiGiulio's profile photoSteven York's profile photo
2 comments
 
Do you have any experience with Esmolol vs Metoprolol on this either? Another thought being tossed around is that once metoprolol is given, you cant take it back. At least with the esmolol, you can stop the drip if you have unwanted affects and titrate. Again, this is a transport setting so I can understand the thoughts behind esmolol and how stopping it in transport could be beneficial, if needed. Any thoughts?
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Oskar Sandqvist

Discussion  - 
 
What skills are most important for your advanced airway assistant?

I’m preparing an introductory airway course for nurses in the beginning of their Master in intensive care at Uppsala University. The focus of the course are skills needed to be an effective team member during RSI in the ICU/ED. I’d very much like to get input and opinions from all of you.

Oskar Sandqvist
Nurse Anesthetist & Intensive care specialist, MSN
Uppsala University Hospital, Sweden
1
David Pecora's profile photoOskar Sandqvist's profile photo
4 comments
 
Thanks David! I got the litterature and research. Just looking for opinions. Mainly experiences of useful non-technical skills and practical tips.
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Peter Smulowitz

Discussion  - 
 
I've seen some recent discussion/lectures about delaying intubation for patients with severe metabolic acidosis (e.g. DKA, aspirin, metformin lactic acidosis, etc) under the thought that intubation can precipitate cardiac arrest. I came across this recently with a patient with probably AKA and metformin toxicity with a pH of 6.6.  Any thoughts on this topic and any idea of literature on the topic?
1
don zweig's profile photo
 
one of emcrits first few podcasts covers this topic nicely
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About this community

The place for EMCritters to share cases and ideas on resuscitation, ED critical care, and trauma.

Ramani Balu

Discussion  - 
 
Hi all, I'm a neurointensivist who's been thinking a lot about acid base problems recently, especially the drop in pH that is expected when bicarbonate is administered rapidly without changing minute ventilation.

The explanation usually given is that the abrupt NaHCO3 bolus drives CO2 generation, which creates a transient respiratory acidosis. Makes sense, but the more I think about it, unless something else is going on I would expect H+ to go down overall even if CO2 production is increased. Also, if you plug in data from a published paper the numbers don't always add up.

I plugged values from the attached table (AJRCCM 2000; 161:1149, referenced in podcast #86) into the Henderson Hasselbalch Equation to calculate the expected HCO3 pre and post bicarb administration. When you do this, in several patients (Case 1, 5, 9) the calculated HCO3 post bicarb administration is LOWER than before administration. For instance, in case 5, HCO3 before is 16.86, whereas expected HCO3 after is 10.69. How could bicarb administration actually decrease the bicarb levels? I'm wondering if there's some other process being missed?

Any thoughts are appreciated.

1
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Jim MacMillan

Discussion  - 
 
So I am a CCU nurse at a top 20 US News hospital. And of course we still aren't staffed with a proper CCM. Not only that as a teaching institution at night we are only staffed with a cardiac fellow (and depending on their interest in critical care vs say wanting to go into cardiac imagining can well...truly suck AKA they are asleep by midnight). Oh and of course the intern and the resident.

Anyway I am curious about bicarb and the very sick crashing patient. I see two patient populations that end up needing bicarb in general. The post arrest that received a ton of NS (probably cold) and now has a hyperchloremic metabloic acidosis and is on pressors (that are no longer working) or just a very sick patient (cariogenic/septic/mixed) acidotic and again pressors just are refusing to work. .

So old school nursing says push. I generally try to advocate for LR sooner rather then later in these pts but that tends to fall on deaf ears. So now we are at the point where MD's and RN's want to push bicarb.

So...would it make sense for me to advocate to hyperventilate the pt via bagging at that point to eliminate the C02? Or increasing their set rate on the vent? Or am I barking up the wrong tree?


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Jim MacMillan's profile photodon zweig's profile photo
3 comments
 
They will need to be bagged more or turn up rate to bliw off co2. I find it very hard to change bicarb giving behavior of surgeons and even our icu docs. It is a good volume expander an is ok for renal tubular acidisis


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don zweig

Discussion  - 
 
When intubating and trying to preoxygenate do u have tips for when we cant get a good wave form and thus cant see what saturation is?
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EMCrit's profile photodon zweig's profile photo
3 comments
 
we tried all that except the digital block. ill do that next time. the bp was map over 60. if you assume its a low sat does that mean you give ketamine and try bagging or bipap (aka dsi?)
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Hi Scott. In your article "Managing Initial Mechanical Ventilation in the Emergency Department" Annals of Emergency Medicine 2016 you say....

"Set the initial tidal volume to 8 mL/kg. This initial
setting is appropriate for all intubated ED patients. The
weight used is the patient’s predicted body weight (based
on patient’s height) rather than actual body weight."

I wonder what your reasoning is for this figure. Some of the research you used for this article give ranges of tidal volumes from 6ml/kg-8ml/kg PBW.

Is your choice of 8ml/kg influenced by the type of ventilator or patient or indeed both? Having had this discussion with some of my critical care colleagues, it would seem that their volume of choice would be lower i.e more likely 6mls/kg

Thank you

Jonathan Downham (@ccpractitioner)
1
Trip699's profile photoEMCrit's profile photo
2 comments
EMCrit
 
for a patient without ALI it would be a waste of ventilatory efficiency to put a patient on 6 ml/kg. Recommending 8 ml is already below the norm for patients with unaffected lungs.
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don zweig

Discussion  - 
 
Any tips for keeping needle in IJ in very dehydrated patient. Vessel collapse so easy it becomes pancake an i have trouble passing wire. 
1
Jordan Schooler's profile photodon zweig's profile photo
4 comments
 
Tried lots of T-berg (took me some time to figure that abbreviation)? I had her hum but she couldn't hold a tune.:) I finally got it with inline as opposed to transverse sono.. I like the subclavian with fluids running in arm.
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Justin Riedel

Discussion  - 
 
Does anyone have any solid studies or opinions based on studies about the treatment of hypertension in the prehospital environment?
1
don zweig's profile photo
 
I would not recommend it unless the patient has a very long transport time and the symptoms are clearly due to the high bp and they are significant (MI, acs, stroke, encephalopathy) and i am not sure how this can be determined. Bottom line don't
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terse2010

Discussion  - 
 
Hi all,

When we say FOAM, we mean free meducation for all medical staff: doctors, physician assistants, and nurses. If you have a seminar at your hospital on Neuro, Cardiovascular, Infection or other medical topic, do you care who comes? is it open for any health care provider who are interested in the topic or just for specific staff from your hospital?

My request to attend one of the free seminars at Stanford hospital was refused by the educator who is responsible for this event. I wonder why.
1
don zweig's profile phototerse2010's profile photo
7 comments
 
Yes. Thank you! They are my favorite. Also EM Basic by Steve Carroll.
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terse2010

Discussion  - 
 
Hi all,
How aggressive are you when you treat the elderly patient with new onset of atrial flutter with RVR if the patient is asymptomatic and HR is in 140-150s? how long do you feel it is ok for the patient to have this HR? what is your approach if atrial flutter with RVR is persistent?
I greatly appreciate your input.

Inessa
2
don zweig's profile phototerse2010's profile photo
4 comments
 
Thank you for sharing! greatly appreciate your input.

Inessa
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Mark Rostash

Discussion  - 
 
As always, thanks Scott and all of the contributors to emcrit. I was hoping someone could direct me the root literature supporting the practice of serial ECGs for ED patients. Unfortunately my ED has totally misinterpreted the literature and we are doing an insane amount of ECGs on inappropriate patient populations (based on my understanding of the literature). Any help would be appreciated
1
Vince DiGiulio's profile photoBenjamin Dowdy's profile photo
2 comments
 
I think Dr. Smith's book available online at his blog, includes the literature on serial or continuous ST segment monitoring. My best understanding is that its clearest indication is on patients at high risk of spontaneous reocclusion, i.e. Wellen's. I also will use it on NSTEMI patients who are pain-free after opiates, just so I can document whether they've had ECG evidence of reduced ischemia with aggressive medical management; however, I don't have citations ready at hand to support that use.
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Marlin Boomkamp

Discussion  - 
 
Hi Scott!

About the emcrit podcast in 2009 on SCAPE NIV and nitro.
I just gave a lecture about this, but there were some questions of my supervisors I didn't know how to answer:
1) We are talking about cardiogenic pulmonary edema and a symphatatic overdrive, but what if it's pulmonary edema from ARDS or other causes, aren't you doing harm with the nitro?
2)What about aortic stenosis, only found a study were adverse advents were still 25%. Do you ultrasound first in the ED before starting nitro? Or do you do it anyway?

Thank you in advance
1
Marlin Boomkamp's profile photoAndrew Haynes's profile photo
5 comments
 
I've used some really really high does nitro on many occasions in ED since in the UK most EDs can't deliver their own intubation without ITU/anaesthetics coming down to help out.

I think the chances of confusing ARDS and SCAPE are really small - it's highly unlikely someone can get ARDS over a period of a few hours without an obvious precipitating factor (trauma would really be the only thing that would go that fast) so unless you literally have no history at all you should be able to filter out those that have had progressive worsening of Sx over a period of days and may not be SCAPE. Further, we routinely treat ARDS with furosemide so I'm not massively convinced that a few doses of nitro will be that harmful unless they started hypotensive (which is often) and then (I hope) they wouldn't get it anyway...

If you really have no history at all then the combination of high BP, cool peripheries, severe sympathetic overdrive Sx (sweating, tachy) respiratory distress and many many B-lines bilaterally and in all zones on chest US should be a good enough set of signs to make SCAPE by far the most likely Dx. Not treating because of a 1% risk your Dx is wrong doesn't fly in the ED because we make more errors than that all the time due to the environment, and you wouldn't treat anyone!
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