Maximally Aggressive Care, Everywhere
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Ahmed Samir

Discussion  - 
I am going to make a preliminary lecture about triage (for ED Nurses and some interns) w/out (mini-course/workshop if possible). I will be saying the lecture in English, then in  Arabic, depending on the Canadian classification

I 'd like to some simplified materials, ppt,  to build upon and ideas (English of course) about Triage for dummies.
Katya Evans's profile photoAhmed Samir's profile photo
thank you.I long to material depending on Canadian Triage classification
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Clifford Tucker

Discussion  - 
Any New Yorkers here?
Ulla Lei Larsen's profile photo
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Ric Solis

Discussion  - 
A call to #FOAM feedback from the comunity. Pedi CICO improvised Jet Ventilation setup. Is this feasible? Would like to get comments/feedback/constructive criticism from all.
don zweig's profile photoAhmed Samir's profile photoJesse Lang's profile photo
I had to do the surgical Cricothyroidotomy and guess what, it worked.Yet the patient died 45 minutes later in spite of securing airway due to to other injuries.
It was a helluva situation
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Adrian DAmico

Discussion  - 
Hi EmCritters, any thoughts on the role of hydralazine in the ED for emergent hypertension? Our hospitalists love it; I avoid it because of it's duration of action; am I wrong? should I be on the hydralazine bus?
Adrian DAmico's profile photoJordan Schooler's profile photo
It's convenient but dangerous.
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Discussion  - 
EMCrit originally shared:
Airway Decisions and Online Etiquette in Podcast # 148

More on the recent cric case from the perspective of airway decision making
More on the recent cric case from the perspective of airway decision making
Klint Kloepping's profile photo

Paul Tourigny

Discussion  - 
Scott--have you thought about a podcast on capnography waveforms? 

Great website with a capnography guru who might be a good guest:
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Josh Wilson

Discussion  - 
I have always said that the patients I dislike the most are the hypotensive CHF patient...aka cardiogenic shock. I like hypertensive CHF patients because I can give them large doses of NTG and often fix them.

I recently had a patient 40 YO F morbidly obese that came in with AMS, initial O2 sat mid 60s and initial BP was 99 sys. I was able to get the O2 sat up to high 80s with NRB and NC. ABG initially showed pH of 7.1 and pCO2 in the high 80s so BiPAP was started. 2L of fluid went in and we were only able to get radial pulses after that. Started levophed and titrated up but still hypotensive.

I went back and forth with the intensivist about whether to start dobutamine or dopamine...

EKG showed TWI in inferolateral leads but no STEMI. 

Performed an awake intubation after a second ABG showed worsening numbers and hyperventilated her. She made it out of our ED and got to the intensivist.

Would you have done anything differently? The big question is regarding pressors. Would you have just topped out levophed or started another agent with this?

Also, thank you Scott! I am not sure this patient would have made it out of here without some of your lectures guiding our decision making.
Josh Wilson's profile photoTrip699's profile photo
Sounds like regardless of what you did the patient was moved from ED to ICU... so you did the right things

The retrospectoscope is always 20/20 and anything I say from here is just points and not critique.

When to intubate somebody can be difficult at times to tease out. I am sure you will get lots of different answers in this scenario.  Some will argue that you should and others, like me, will argue that intubation soon would be best. 
For the following reasons.  Bipap is indicated in truely only a few instances when you look at the data.  Mild asthma, COPD exacerbations,  mild heart failure, and mild respiratory distress in patients with malignancy with mild infiltrates. 

I suspect that the combination of hypercapnia and hypoxemia warrants a sooner rather than later intubation.  I would have given fluid, started levophed, and done the intubation soon.  

Regarding dobutamine vs dopamine... I dont start dobutamine with a systolic that is too low.  A -Line is very important in this case but sometimes less possible in the ED as opposed to the ICU.

Craig Rosebrock MD
pulmonary and critical care 
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Jeffrey Reed

Discussion  - 
Scott, as a FP doc in an Emergency Med fellowship, I have listened to your podcasts, and read what you've suggested, knowing it would help me care for sick patients. Recently at "Janis General" I had the privilege of caring for a crashing dialysis patient who came obtunded, septic (lactate 8.6), with pneumonia and sarcoidosis, previous PE, filter and all. When I used delayed sequence intubation, apneic oxygenation, and tips with the glidescope you have given...especially the one about having the perfect view on the monitor and not being able to pass the tube...then the laryngoscope as a murder weapon...and when to pause the attempt, bag them back up off the steep part of the curve...watching the HR, pressure and sats, knowing I am 30 secs delayed...using the vent tips and keeping the plateau pressures in range despite the underlying process. Scott, you were in the room with me. There was NO ICU bed available. For seven hours I worked with her. When the ICU took her, lactate was <3. Pressure and sats good. Thank you. I could not have done this without you. We saved her together. You absolutely ROCK.
Khalid Bahar's profile photoEMCrit's profile photoMinh Le Cong's profile photoBill Hinckley's profile photo
Massive... How nice! 
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Naveen Sundaram

Discussion  - 
55 years old lady, presented with epigastric and chest pain, HR-130, BP- 60/?, RR-35, SpO2-96% on 15 L O2, GCS-15/15, pH-6.9, pCO2-48, pO2-82, HCO3-10.

Over the following one hour her RR decreased to 20-25.

Patient was not intubated till she died 2 hours after admission, received 2 litres fluid, Didnot receive any vasopressor infusion, fluid assessment not done. though the teams working diagnosis was aortic dissection, autopsy showed hollow viscus perforation.

My senior's arguement:

Patient would have died irrespective of the management and was happy with what we did.

My arguement:

Patient needed RSI for 2 reasons:

To wash out CO2 atleast as a rescue measure for a short time, to prevent worsening of acidosis.

To prevent 40% of cardiac output getting wasted in the work of breathing.

Though BP was very low, push dose pressors could have been used peri RSI, instead of just giving fluids alone and no other intervention was done.
Carl Horsley's profile photocraig ro's profile photoJay Matthew's profile photo
The point by the senior that the patient would have died regardless seems a bit presumptive ...

I would have intubated and treated with fluids and pressors till I figured out what was going on.
My two cents

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David Dansky

Discussion  - 
Hi Scott,
   Thanks as always for your amazing podcast!

 This is a question about the pain-free ED. Sergey Motov mentioned using ketamine for recalcitrant pain management cases. It would seem that it is not just in the ED that we need to control their pain, but to create an acute pain management plan at home as well.... or they will just bounce right back.
So, following a successful low dose ketamine infusion for pain, what does the patient then get discharged home on? Most of my patients who arrive in pain are understandably concerned about what to do when the pain returns after their discharge home, Since most of us are not prepared to prescribe Special K for home use... does the addition of clonidine (poor man's Precedex) or neurontin help?
    Thanks for any thoughts you might have.

Dave Dansky
Emergency Dept.
Community Hospital of the Monterey Peninsula
Monterey CA
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About this community

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


Discussion  - 
Would like peoples opinions: 65 yrs female present with sudden crushing retro sternal pain 7/10 that woke her up in the middle of the night. Only hx of HTN and mechanical valve ( i believe mitral). No hx of a-fib. Present with the first ecg in what seem rapid a-fib. Trial of adenosine with no success, cardioversion with no success x3. Started on amiodarone drip. After the bolus it decreased the rate to the second ecg and CP only 2/10. My questions: wouldn't the first ecg show concern for a Left main blockage?? If so, would it be sufficient to activate a cath lab??
Minh Le Cong's profile photo
I presume woman is adequately anticoagulated for her mechanical valve, hence decision to cardiovert?
not sure why adenosine trialled?
yes 1st ECG looks like STE in AVR. with reciprocal depression in lateral leads. despite resolution in 2nd ECG, the persisting chest pain is concerning and warrants cath lab activation.

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Jason Boitnott

Discussion  - 
Hey fellow EmCritters,
I was hoping maybe ya'll could add some insight into a patient case I was recently involved in. The details have been changed of course. So I am an ED RN/Paramedic at Janis General and a few weeks ago a 54 YOM came into the ED due to unresponsiveness by EMS. He had come from a alcohol rehab facility, he was of course unresponsive to pain and had a GCS of 7 (Eye-1, Verbal-2, Motor-4). The patient had a NPA in with NC and NRB on 15 LPM (love our local EMS who believe in NoDesat and preox even if they can't field RSI). What was interesting was that he was mottled from the nipple line up upon arrival. After much back and forth the patient was intubated via RSI. From what I remember on the ABG pre intubation (the part of the story is changed by memory) pH 6.8, PaCO2 71, PaO2 13 and Lactate of 17 (do not remember much else). The labs did start to correct a while after intubation.

So here is the interesting part, post intubation (20 minutes or so) the patient's body was completely mottled, lips were blue, extremities were ice cold. I actually flashed back to my days on the street because he looked like a DOS to me and not the patient he was...with a heartbeat and functional perfusing rhythm. Patient was transferred to the ICU where he eventually died after going into an initial V-Tach arrest that converted to asystole. The patient yo-yo'd between systole and ROSC 5 different times (Code was about 30 or so minutes). Now my question is what are the differential diagnosis on this case? The two ruling differentials were PE and some sort of Hystotoxic Hypoxia. Normally I would just ask my ED Physician and the ICU Intensivist but both of them shrugged their shoulders. So has been bugging me about differentials and interventions. What do ya'll think?
craig ro's profile photoJason Boitnott's profile photo
Wow thanks yall, I do have some studying to do on aortic root tears. His bp was garbage and we had him on norepi (sorry remembering more details) and we were simultaneously working him up for sepsis and some other alcohol intoxication (can't remember the drugs name). The whole case was a head scratcher.
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Chetan Bharel

Discussion  - 
Hi All
So our hospital is going to be tying in a portion of our bonus to ED implementation of the Canadian Head CT rules. They are doing this to reduce head CT ordering in the ED.

does anyone know if these guidelines are the best way to do this? (ie is New Orleans better or maybe some other derivation rule out there)

Eric Schneider's profile photo
You have to check the literature yourself. Decent basics review at on both.

For my money, Canadian (ccth) rules are what I want. Might miss a nonoperative but no operative and significantly decrease # cts. Biggest difference = can exclude even if they have a headache.

Also "trauma above clavicles" in New Orleans (NO) rules. Useful with ccth allows no ct on broken nose and headache, you see?

Or if you're more concerned about Someone with a broken nose, scan 'em. Like David Newman said: if you have 2 validated decision 'tools' (for Ken Milne), you can use the one that fits your narrative- and either way, you're right (or wrong if applied to wrong pt)
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Derrick Clay

Discussion  - 
Which paralytic & dose would you use for RSI following physostigmine administration?

Had an ER patient who received a total of 3mg of physostigmine for anticholinergic crisis following an antihistamine OD.  Patient's agitation continued to worsen so the decision was made to intubate for airway protection. Pt. was RSI'd with Etomidate + Sux (1.3mg/kg) which resulted in the patient being paralyzed for a really long time (at least 90 mins, maybe longer).

In theory, a cholinesterase inhibitor should potentiate the effects of Sux but antagonize the effects of Roc. After discussing this with the doc, we decided a low dose of Sux or a really high dose of Roc would be options. Thoughts?

Randy Sharp's profile photoWill Angus's profile photo
Tricky one. The danger here is that sux could worsen the anticholinergic crisis by causing depolarisation. But equally you might find your rocuronium less effective.

In someone who is cardiovascularly unstable from an anticholinergic toxidrome I'd probably go for high dose rocuronium over suxamethonium. But not sure if there's any literature to support this.
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Ashes Mukherjee

Discussion  - 
Had a 63 yr old man otherwise fit with submassive PE.

Dyspnoea but not severe. RR-20. SpO2-80% on RA. 96% on O2. HR-120.

Point of care Echo- RVD with no TR, Septal bowing.

BP-130/80. ECG RBBB. Troponin raised.

2 weeks ago had a bone graft on ankle and is in a BK cast. No further operative history available.

CTPA- bilateral pulmonary artery PE with large clot burden.

Would you consider thrombolysis? 
Graham Johnson's profile photoAshes Mukherjee's profile photo
It was a shared decision Graham. All the last 5 patients that I have thrombolysed in the past 10 years had significantly more dyspnoea. Just the day before that, I had a 83 yr old with similar presentation again shared conservative decision. This was one of those where it was borderline decision and kept me thinking.
This discussion surely helped.
An interesting thing also was, he had been put on Aspirin post-op! 
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Jeffrey Davis

Discussion  - 
I am a critical care transport medic, former flight medic but on a ground unit right now.  Our hospital is facing a major CMS survey, so things are a little tense to say the least.  Mandatory restraint training, mandatory blah blah blah.  

Mostly I could care less, but then something happened that directly impacted our department and as I see it potentially affects our patient care.  They took our succinylcholine away and replaced it with rocuronium.  Some of us have been pushing to get roc for a while now, but not at the expense of succs.  If anything, we wanted them to toss vecuronium from the box because (IMHO) we don't need such a long acting paralytic in the transport environment.  

The decision was supposedly made in response to a CMS requirement that anyone using succs have dantrolene readily available in case of malignant hyperthermia induced by the depolarizing paralytic.  To me this seems overly paranoid at the least, silly at best, and potentially dangerous since most of the people in our department have little to no experience using roc and what RSI's they have done have all been with etomidate and succs.  Unfortunately, this decision is sticking despite several of us voicing concerns.  

From my own past experience, I like the etomidate/succs combo or the ketamine/roc cocktail because of the comparable duration of action of the pairings.  Unfortunately, we do not have ketamine on our units, although "they''re working on it."  

I was wondering what your take is, Dr. Weingart and the rest of the forum, since I can't think of anyone else more vocal about airway management and LAMW.  Has anyone else had this experience?  I know other (maybe all?) CCT/flight programs are carrying succs without dantrolene, so how are they "getting around" the CMS rules?

Don't worry, I am not going to take any comments back to the powers that be here and try to use them to reverse their decision.  I know better than to try and fix things, since I am just a knuckle-dragging paramedic ambulance driver.  I am just trying to wrap my head around the situation.
Trip699's profile photoErik Rubach's profile photo
Jeff, at least you know your place as an "ambulance driver."  (says another former ambulance driver).

Directly from the Malignant Hyperthermia Association of the United States:  

"The exact incidence of MH is unknown. Epidemiologic studies reveal that MH complicates one in about 100,000 surgeries in adults and one in about 30,000 surgical procedures in children. The incidence varies depending on the concentration of MH families in a given geographic area. High incidence areas in the United States include Wisconsin, Nebraska, West Virginia and Michigan."

I can't speak to CMS requirements, but both flight programs with which I've been involved over the last 3 years (one is hospital based and directly subject to CMS) carry all 3 paralytics...Vec, Roc, and Succs--without Dantrolene.  I'd say whatever is creating the need for RSI is much more likely to kill a patient versus an almost infinitesimally small risk of MH.
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Erik Rubach

Discussion  - 
Scott et al., 

I am a former medic, flight nurse, and ACNP student (who knows just enough to get me in trouble) stuck in a situation where I am 6 weeks back in the hospital as a bedside ICU RN and the decisions/care being provided goes completely against my training, experience, and what's I've learned from EMCrit over the years....  Thank you in advance for any constructive critique, suggestions, or thoughts.

Yesterday I landed a morbidly obese, post abdominal surgical patient who had small bowel hernias on top of her small bowel hernias.  The surgeon resected several sections of her necrotic small bowel, and left her belly open for another go, in a day or two.  She was 5'1 and had a generous ideal body weight of no more than 60kg (but weighed more like 160kg).  An extensive history included DM, HTN, CKD, and likely undiagnosed COPD after smoking for 45 years.

She was clearly septic based on symptoms before surgery, and came out with a lactate of 11.6, metabolically acidotic (bicarb of 11 and pH of 7.1), profoundly hypotensive (art line showing systolic pressures in the mid 60s when she arrived), and tachycardic in the 150s.  HGB was 11.6 after 1 unit of PRBCs during the surgery.  And then one of our pulmonologist-“intensivists” got involved...

These pulmonologists have never heard of lung protective ventilation and EVERY patient in the ICU is on AC with 10-12 mL/kg of volume with Pplats often above 30.  When the patients are ready to be weaned they go straight from AC to CPAP.  Even patients who are conscious, alert, and able to answer questions are on AC and left in misery, sometimes with sedation but never with analgesia.

But I digress.  My patient was conscious and responsive within 30mins of arrival to the ICU, was being ventilated at 600, AC at 20, 80%, and 10 of peep, and was over-breathing the vent at a rate of 30 and had an SaO2 of 100%.  She had gotten only 2L of fluid in the OR (just maintenance drips prior to surgery), and came out on 15 of Levo and 5 of Dopamine.  1 more liter of fluid was ordered (which hypothetically might have stretched it to 2L) and I was instructed to titrate the Levo up to improve the pt's BP.  With the 2 additional liters in, and Levo now at 20, her pressure was only up to the upper 70s.  Oh yeah, and her lung sounds were dramatically diminished on the L (assessing chest rise was impossible with her body habitus), but they wouldn’t pull back the tube until a CXR was shot.  No air on the right and the tube came back 3cm and voilà, she has bilateral lung sounds, slightly coarse (she probably spent the entire surgery in the right main-stem).  Over the 4 hours I had her in the ICU she also got an additional unit of PRBCs, 4 amps of Bicarb, and was put on a bicarb drip.  Urine output was in the toilet (pun intended).

RNs are not allowed to touch the vents, but hypothetically I may have adjusted it to 400mL and 4 of peep to see what would happen.  Her Pplat dropped from 37 to 26, SaO2 to 98%, and her systolic pressure increased to 99, and she nodded yes when asked if she was more comfortable.  When I turned it back to the ordered settings, her pressure tanked back to the upper 70s and she went back to grimacing and banging on the bedrails.  

With no other options ordered, I started the Vasopressin just so I could give the patient something in an attempt to make her comfortable (Precedex).  I tried to assess IVC collapse (as she was getting 10mL/kg of volume) with a Sonosite machine (again, without orders to do so—I’ve never seen it used but to place central lines) but was unable to visualize the IVC.  I don’t have a ton of experience doing so and am not sure if the foam dressing they had left under the top part of the incision that was partially closed (she was cut from just below her xiphoid process to below her umbilicus) got in my way, or if the IVC was just so collapsed I couldn’t see it.  All I could see was the bottom of the heart moving.  

At 1900 I handed the very uncomfortable, conscious, and miserable patient off to the oncoming RN.  She increased the Levo to 30, called to get orders, and was instructed by an on-call doc who had never seen the patient to add an epi drip.  Without doing anything to assess fluid volume.

My suspicion was the patient was without likely short on fluid volume, was being inappropriately ventilated, and likely didn’t need so many vasopressors had she be ventilated properly.  But I feel hamstrung to do anything (like change vent settings or order more labs, maybe to assess serum osmolality) to prove my suspicions.  My questions:

1. Are there some treatment guidelines of which I am unaware that don’t match my prior experience/training?  
2. Did she need that much peep considering the likely reduction in preload?  That much ventilator volume?
3. Can anyone offer any other suggestions or how they would have managed her differently from my local docs?
4. Help!  
Erik Rubach's profile photoJason Boitnott's profile photo
Ya'll are great, thank you +Trip699 and +Erik Rubach, being an ED Nurse, I wish our ED Physicians and Intensivists understood how different our education is. The Nursing education really does not provide for understanding or knowledge like this. 
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Lamar Moody

Discussion  - 
I am curious about the Angel Catheter. Have you had a chance to play with it or use it? Any difficulty with placement? opinion? Conceptually promising and beneficial.
EMCrit's profile photo
never been in a hospital that had them so I can't say. It is a cool idea
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Shane Barclay

Discussion  - 
HI Steve
Love your podcasts!
I hope this question has not been answered already but I have searched your site and think listened to most of the podcasts.
In any event, I had a case of Rt Vent infarct a while ago, with the usual hypotension, brady and rather severe chest pain. We managed to get him thrombolysed within 12 minutes of the door, however his pain and hypotension was a real issue. My concern was giving him nitro with resultant further BP drop ( I eventually did a 'dribble' nitro drip with small bolus N/S)
I can't seem to get consensus from the literature however,  which/if/how a pressure could be used. ie dobutamine, dopamine, norepi etc. Some say yes, other sources say never dopamine etc etc.
I work in a rural, 20 bed hospital,  in Canada, and so don't have the luxury of a lot of the things you often discuss. Our critical pts are helicoptered out and that day took nearly 3 hrs to get a chopper.
Your comments and those of others, as usual, would be greatly appreciated.
Shane Barclay
Salt Spring Island, B.C.
EMCrit's profile photo
norepi is prob. best choice for cardiogenic shock at this stage. Has an actual study demonstrating mortality (albeit subgroup)

I like small dose fentanyl for this situation for the pain treatment
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Ahmed Samir

Discussion  - 
I want some info about benchmarking ED Performance/ performance indicators..elaborate, please
roberto cosentini's profile photoAhmed Samir's profile photo
Any more....
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